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ESP: PubMed Auto Bibliography 31 Jul 2026 at 01:54 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-07-29
The Methicillin-Resistant S pseudintermedius Crisis: Are We Out of Options to Treat the Most Common Canine Pathogen?.
The Veterinary clinics of North America. Small animal practice pii:S0195-5616(26)00085-9 [Epub ahead of print].
S pseudintermedius is a leading cause of canine pyoderma and an important pathogen in small animal skin, soft tissue, otic, wound, and postoperative infections. The emergence of methicillin-resistant S pseudintermedius (MRSP) has made recurrent infections more difficult to manage by combining multidrug resistance, biofilm-associated persistence, treatment failure, and repeated antimicrobial exposure. This article reviews MRSP emergence and epidemiology, mechanisms of resistance and recurrence, and the limitations of current treatment options. It discusses emerging therapeutic strategies, including phage-based therapies, microbiome-directed interventions, immune modulation, nanomaterials, photodynamic therapy, and antimicrobial peptides, that serve as adjuncts to standard care and reduce reliance on systemic antimicrobials.
Additional Links: PMID-42527298
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@article {pmid42527298,
year = {2026},
author = {Pluta, DH and Gilbertie, JM},
title = {The Methicillin-Resistant S pseudintermedius Crisis: Are We Out of Options to Treat the Most Common Canine Pathogen?.},
journal = {The Veterinary clinics of North America. Small animal practice},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cvsm.2026.06.004},
pmid = {42527298},
issn = {1878-1306},
abstract = {S pseudintermedius is a leading cause of canine pyoderma and an important pathogen in small animal skin, soft tissue, otic, wound, and postoperative infections. The emergence of methicillin-resistant S pseudintermedius (MRSP) has made recurrent infections more difficult to manage by combining multidrug resistance, biofilm-associated persistence, treatment failure, and repeated antimicrobial exposure. This article reviews MRSP emergence and epidemiology, mechanisms of resistance and recurrence, and the limitations of current treatment options. It discusses emerging therapeutic strategies, including phage-based therapies, microbiome-directed interventions, immune modulation, nanomaterials, photodynamic therapy, and antimicrobial peptides, that serve as adjuncts to standard care and reduce reliance on systemic antimicrobials.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Clostridium innocuum Bacteremia: Case Report and Systematic Review.
South Dakota medicine : the journal of the South Dakota State Medical Association, 79(6):271-273.
Clostridium innocuum is an anaerobic gram-positive spore-forming bacteria, a commensal member of the human gut microbiome. We encountered a case of bacteremia with this organism as a complication of a foot ulcer in a middle-aged patient with diabetes, end-stage renal disease, and malnutrition. A systematic review of the limited number of previously reported cases of C. innocuum bacteremia is presented, along with a brief narrative review the organism's association with other diseases, ranging from diarrhea and local infections to modulating inflammatory bowel disease and kidney disease.
Additional Links: PMID-42527363
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@article {pmid42527363,
year = {2026},
author = {de Matos-Konrad, C and Chima, N and Huntington, MK},
title = {Clostridium innocuum Bacteremia: Case Report and Systematic Review.},
journal = {South Dakota medicine : the journal of the South Dakota State Medical Association},
volume = {79},
number = {6},
pages = {271-273},
pmid = {42527363},
issn = {0038-3317},
mesh = {Humans ; *Clostridium Infections/diagnosis/drug therapy/microbiology ; *Bacteremia/microbiology/drug therapy/diagnosis ; *Clostridium/isolation & purification ; Middle Aged ; Anti-Bacterial Agents/therapeutic use ; *Diabetic Foot/complications ; Male ; Kidney Failure, Chronic/complications ; },
abstract = {Clostridium innocuum is an anaerobic gram-positive spore-forming bacteria, a commensal member of the human gut microbiome. We encountered a case of bacteremia with this organism as a complication of a foot ulcer in a middle-aged patient with diabetes, end-stage renal disease, and malnutrition. A systematic review of the limited number of previously reported cases of C. innocuum bacteremia is presented, along with a brief narrative review the organism's association with other diseases, ranging from diarrhea and local infections to modulating inflammatory bowel disease and kidney disease.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Clostridium Infections/diagnosis/drug therapy/microbiology
*Bacteremia/microbiology/drug therapy/diagnosis
*Clostridium/isolation & purification
Middle Aged
Anti-Bacterial Agents/therapeutic use
*Diabetic Foot/complications
Male
Kidney Failure, Chronic/complications
RevDate: 2026-07-29
Sex-specific modulation of lung function and transcriptome in neonate mice exposed to thirdhand electronic-cigarette aerosols.
Pediatric research [Epub ahead of print].
BACKGROUND: Vaping is increasingly prevalent among young adults at age for starting families. Thirdhand e-cigarette aerosols (THEA) are persistent residues that adhere to indoor surfaces and can resuspend in air. Since lung development continues after birth, infants from homes with adults who vape, are vulnerable to THEA exposures.
METHODS: Neonate mice were exposed to THEA with nicotine or nicotine + tobacco-flavoring from terrycloth and carpet for the first 21 days of life. We assessed broncho-alveolar lavage cytology, lung morphometry, gene expression, and intestinal microbiomes at 21 days. At 10 weeks, we evaluated lung function.
RESULTS: We showed that exposures to THEA during alveologenesis, a critical window of lung development, induced sex-specific alterations in pulmonary inflammatory and developmental trajectories. Females exhibited acute pulmonary neutrophilic inflammation with a resolving cytokine profile. In contrast, males exhibited upregulation of genes associated with pulmonary inflammation and epithelial mesenchymal transition, plus delayed lung development, leading to lung dysfunction in adulthood. Male gut microbiomes showed reduced abundance of taxa associated with xenobiotic biotransformation, suggesting host-microbial detoxification capacity as a target of THEA exposure.
CONCLUSION: Low-level of THEA exposures in early life can alter lung inflammation, structure, and function, increasing susceptibility to respiratory dysfunction later in life.
IMPACT: Early-life exposures to nicotine and carbonyls from thirdhand e-cigarette aerosols (THEA) may induce alterations in lung alveologenesis and augment susceptibility to lung conditions later in life. Using a preclinical model of pediatric airways, we showed that THEA exposures caused neutrophilic inflammation in neonate female mice. In neonate male mice, THEA exposures led to alterations in lung structure, gene expression, and gut microbiome dysbiosis. Adult male mice exposed to THEA as neonates exhibited decline in lung function characteristic of obstructive pulmonary physiology.
Additional Links: PMID-42527537
PubMed:
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@article {pmid42527537,
year = {2026},
author = {Zaman, A and Cook, T and Mabou, DB and Schexnayder, M and Xiao, R and Perveen, Z and Penn, AL and Noël, A},
title = {Sex-specific modulation of lung function and transcriptome in neonate mice exposed to thirdhand electronic-cigarette aerosols.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42527537},
issn = {1530-0447},
abstract = {BACKGROUND: Vaping is increasingly prevalent among young adults at age for starting families. Thirdhand e-cigarette aerosols (THEA) are persistent residues that adhere to indoor surfaces and can resuspend in air. Since lung development continues after birth, infants from homes with adults who vape, are vulnerable to THEA exposures.
METHODS: Neonate mice were exposed to THEA with nicotine or nicotine + tobacco-flavoring from terrycloth and carpet for the first 21 days of life. We assessed broncho-alveolar lavage cytology, lung morphometry, gene expression, and intestinal microbiomes at 21 days. At 10 weeks, we evaluated lung function.
RESULTS: We showed that exposures to THEA during alveologenesis, a critical window of lung development, induced sex-specific alterations in pulmonary inflammatory and developmental trajectories. Females exhibited acute pulmonary neutrophilic inflammation with a resolving cytokine profile. In contrast, males exhibited upregulation of genes associated with pulmonary inflammation and epithelial mesenchymal transition, plus delayed lung development, leading to lung dysfunction in adulthood. Male gut microbiomes showed reduced abundance of taxa associated with xenobiotic biotransformation, suggesting host-microbial detoxification capacity as a target of THEA exposure.
CONCLUSION: Low-level of THEA exposures in early life can alter lung inflammation, structure, and function, increasing susceptibility to respiratory dysfunction later in life.
IMPACT: Early-life exposures to nicotine and carbonyls from thirdhand e-cigarette aerosols (THEA) may induce alterations in lung alveologenesis and augment susceptibility to lung conditions later in life. Using a preclinical model of pediatric airways, we showed that THEA exposures caused neutrophilic inflammation in neonate female mice. In neonate male mice, THEA exposures led to alterations in lung structure, gene expression, and gut microbiome dysbiosis. Adult male mice exposed to THEA as neonates exhibited decline in lung function characteristic of obstructive pulmonary physiology.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Gut microbiota restricts intestinal lipid uptake via modulation of bile phosphatidylcholine metabolism in mice.
Nature microbiology, 11(8):2349-2364.
The gut microbiota influences host metabolism, but the mechanisms of lipid uptake from food remain mysterious. Here we used stable isotope-labelled tracers in gnotobiotic mouse models, which revealed that host uptake of dietary lipids depends on microbial colonization. Systemic lipid metabolism modelling predicted that the gut microbiota restricts intestinal lipid absorption, and labelled lipid administration verified that the gut contents of microbiota-colonized mice contained up to 12-fold more lipids than those of germ-free animals. A combination of lipidomics and proteomics showed that gut microbes trigger Myd88 signalling, leading to a downregulation of hepatic Cyp7b1 activity and increased taurocholate production. Taurocholate stimulates phospholipase A1 activity in bile, causing the degradation of phosphatidylcholine that is essential for luminal micelle formation and lipid uptake. A diverse microbiome was associated with lower phosphatidylcholine content. This previously unrecognized host-gut microbiota interplay via enzymes in bile could provide future targets to modulate dietary lipid absorption.
Additional Links: PMID-42527633
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Citation:
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@article {pmid42527633,
year = {2026},
author = {Brunner, S and Plagge, J and Zimmermann-Kogadeeva, M and Höring, M and Liebisch, G and Basic, M and Bolsega, S and Janssen, KP and Slack, E and von Gamm, S and Viehof-Beckmann, A and Clavel, T and Zimmermann, M and Heeren, J and Giansanti, P and Weiss, AS and Hermeling, S and Dupont, A and Ullrich, AL and Jokisch, F and Seeliger, C and Bleich, A and Hidrobo, M and Stecher, B and Coleman, OI and Moresi, C and Greter, G and Arnoldini, M and Scheiber, J and Matysik, S and Klingenspor, M and Küster, B and Haller, D and Burkhardt, R and Kuipers, F and Ecker, J},
title = {Gut microbiota restricts intestinal lipid uptake via modulation of bile phosphatidylcholine metabolism in mice.},
journal = {Nature microbiology},
volume = {11},
number = {8},
pages = {2349-2364},
pmid = {42527633},
issn = {2058-5276},
support = {395357507-SFB 1371, P13//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 446175916//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; INST 95/1650-1 FUGG//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 395357507-SFB 1371//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 279971426//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; },
mesh = {Animals ; *Phosphatidylcholines/metabolism ; Mice ; *Bile/metabolism ; *Lipid Metabolism ; *Gastrointestinal Microbiome/physiology ; Germ-Free Life ; Taurocholic Acid/metabolism ; Mice, Inbred C57BL ; Liver/metabolism ; Male ; Intestinal Absorption ; Intestinal Mucosa/metabolism ; },
abstract = {The gut microbiota influences host metabolism, but the mechanisms of lipid uptake from food remain mysterious. Here we used stable isotope-labelled tracers in gnotobiotic mouse models, which revealed that host uptake of dietary lipids depends on microbial colonization. Systemic lipid metabolism modelling predicted that the gut microbiota restricts intestinal lipid absorption, and labelled lipid administration verified that the gut contents of microbiota-colonized mice contained up to 12-fold more lipids than those of germ-free animals. A combination of lipidomics and proteomics showed that gut microbes trigger Myd88 signalling, leading to a downregulation of hepatic Cyp7b1 activity and increased taurocholate production. Taurocholate stimulates phospholipase A1 activity in bile, causing the degradation of phosphatidylcholine that is essential for luminal micelle formation and lipid uptake. A diverse microbiome was associated with lower phosphatidylcholine content. This previously unrecognized host-gut microbiota interplay via enzymes in bile could provide future targets to modulate dietary lipid absorption.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Phosphatidylcholines/metabolism
Mice
*Bile/metabolism
*Lipid Metabolism
*Gastrointestinal Microbiome/physiology
Germ-Free Life
Taurocholic Acid/metabolism
Mice, Inbred C57BL
Liver/metabolism
Male
Intestinal Absorption
Intestinal Mucosa/metabolism
RevDate: 2026-07-29
Short-chain fatty acids.
Nature metabolism [Epub ahead of print].
Short-chain fatty acids (SCFAs), principally acetate, propionate and butyrate, are produced by the gut microbiota through the fermentation of non-digestible carbohydrates. Beyond serving as energy substrates, SCFAs act as signalling molecules that influence metabolism, immune function and physiological homeostasis across multiple organ systems. This Review consolidates the fragmented literature on SCFAs and provides an overview of their production, metabolism and physiological actions. We discuss the microbial and dietary determinants of SCFA production, including the roles of the gut microbiome, cross-feeding interactions and dietary carbohydrates. We then examine the mechanisms through which SCFAs exert their effects, focusing on receptor-mediated signalling, epigenetic regulation and tissue-specific physiological functions. Finally, we evaluate the current evidence linking SCFAs to metabolic health and disease and consider the translational potential of targeting SCFA pathways through dietary and therapeutic approaches. At a time when inadequate dietary fibre intake is a growing public health concern, this Review highlights the physiological importance of SCFAs and their potential role in metabolic health and disease prevention.
Additional Links: PMID-42527661
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Citation:
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@article {pmid42527661,
year = {2026},
author = {Dagbasi, A and Cai, M and Hirdaramani, A and Hanyaloglu, A and Morrison, DJ and Frost, G},
title = {Short-chain fatty acids.},
journal = {Nature metabolism},
volume = {},
number = {},
pages = {},
pmid = {42527661},
issn = {2522-5812},
support = {BB/N016947/1//RCUK | Biotechnology and Biological Sciences Research Council (BBSRC)/ ; },
abstract = {Short-chain fatty acids (SCFAs), principally acetate, propionate and butyrate, are produced by the gut microbiota through the fermentation of non-digestible carbohydrates. Beyond serving as energy substrates, SCFAs act as signalling molecules that influence metabolism, immune function and physiological homeostasis across multiple organ systems. This Review consolidates the fragmented literature on SCFAs and provides an overview of their production, metabolism and physiological actions. We discuss the microbial and dietary determinants of SCFA production, including the roles of the gut microbiome, cross-feeding interactions and dietary carbohydrates. We then examine the mechanisms through which SCFAs exert their effects, focusing on receptor-mediated signalling, epigenetic regulation and tissue-specific physiological functions. Finally, we evaluate the current evidence linking SCFAs to metabolic health and disease and consider the translational potential of targeting SCFA pathways through dietary and therapeutic approaches. At a time when inadequate dietary fibre intake is a growing public health concern, this Review highlights the physiological importance of SCFAs and their potential role in metabolic health and disease prevention.},
}
RevDate: 2026-07-29
Impact of labor before delivery on necrotizing enterocolitis in very low birth weight infants.
Journal of neonatal-perinatal medicine [Epub ahead of print].
BackgroundNecrotizing Enterocolitis (NEC) is multifactorial, and the gut microbiome may contribute. Neonatal gut colonization differs by delivery mode; while delivery mode has not been linked to NEC in prior studies, the impact of labor prior to delivery is unknown. Our objective was to investigate the impact of labor prior to delivery on NEC incidence in very low birth weight (VLBW, <1500 g) infants.MethodsWe performed a single-center retrospective cohort study of VLBW infants 23 0/7-34 6/7 weeks gestation born at our center between 03/25/2012 and 12/31/2023. Infants with congenital anomalies or who died prior to admission were excluded. Labor was defined as uterine contractions with cervical dilation or effacement. When cervical exam was undocumented, labor was determined by presence of regular contractions >1 h before delivery. Multivariable logistic regression evaluated the association between labor before delivery and NEC after adjusting for baseline differences.ResultsAmong 1,951 infants, 1,175 (60.2%) were exposed to labor before delivery. Groups differed by gestational age, birth weight, chorioamnionitis, maternal diabetes, multiple gestation, and small for gestational age. Exposure to labor had lower odds of NEC (odds ratio [OR] = 0.606, 95% confidence interval [CI]: 0.407-0.902, p = 0.01), compared to those unexposed. This association remained significant after adjustment (adjusted OR = 0.614, 95% CI: 0.384-0.983, p = 0.04). There was no difference in surgical NEC.ConclusionsLabor prior to delivery was associated with lower odds of NEC in this VLBW cohort, highlighting the potential importance of perinatal microbial exposures and suggesting new avenues for NEC risk stratification and prevention.
Additional Links: PMID-42527892
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PubMed:
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@article {pmid42527892,
year = {2026},
author = {Dhawan, N and Yasrebi, S and Hagan, J and Brasher, MI and Patil, MS},
title = {Impact of labor before delivery on necrotizing enterocolitis in very low birth weight infants.},
journal = {Journal of neonatal-perinatal medicine},
volume = {},
number = {},
pages = {19345798261475330},
doi = {10.1177/19345798261475330},
pmid = {42527892},
issn = {1878-4429},
abstract = {BackgroundNecrotizing Enterocolitis (NEC) is multifactorial, and the gut microbiome may contribute. Neonatal gut colonization differs by delivery mode; while delivery mode has not been linked to NEC in prior studies, the impact of labor prior to delivery is unknown. Our objective was to investigate the impact of labor prior to delivery on NEC incidence in very low birth weight (VLBW, <1500 g) infants.MethodsWe performed a single-center retrospective cohort study of VLBW infants 23 0/7-34 6/7 weeks gestation born at our center between 03/25/2012 and 12/31/2023. Infants with congenital anomalies or who died prior to admission were excluded. Labor was defined as uterine contractions with cervical dilation or effacement. When cervical exam was undocumented, labor was determined by presence of regular contractions >1 h before delivery. Multivariable logistic regression evaluated the association between labor before delivery and NEC after adjusting for baseline differences.ResultsAmong 1,951 infants, 1,175 (60.2%) were exposed to labor before delivery. Groups differed by gestational age, birth weight, chorioamnionitis, maternal diabetes, multiple gestation, and small for gestational age. Exposure to labor had lower odds of NEC (odds ratio [OR] = 0.606, 95% confidence interval [CI]: 0.407-0.902, p = 0.01), compared to those unexposed. This association remained significant after adjustment (adjusted OR = 0.614, 95% CI: 0.384-0.983, p = 0.04). There was no difference in surgical NEC.ConclusionsLabor prior to delivery was associated with lower odds of NEC in this VLBW cohort, highlighting the potential importance of perinatal microbial exposures and suggesting new avenues for NEC risk stratification and prevention.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-30
Astrovirus infection alters gut microbial communities in a widespread neotropical bat across human-modified landscapes.
BMC microbiology, 26(1):.
Astroviruses are becoming a growing concern in public and veterinary health. In humans, astrovirus infections can cause severe diarrhea and may lead to neuropathological encephalitis, whereas in wildlife, these enteropathogenic viral infections often lack overt symptoms and thus remain unnoticed. Yet their close interaction with the host's gastrointestinal microbiome might drive cascading effects with disadvantages for host health. Bats harbor many zoonotic viruses without showing signs of disease, and many species move freely along the gradient from pristine to agricultural landscapes. To better understand the impact of astrovirus (AstV) infection under a One Health framework, we investigated the gut microbiome of naturally AstV-infected Seba's short-tailed bats (Carollia perspicillata, n = 234) inhabiting old-growth lowland forests or forest fragments embedded in an agricultural matrix in Panama. AstV prevalence was higher in forest fragments. We observed that AstV infection is associated with a shift in microbial beta but not alpha diversity, which points towards the replacement of common gut microbial taxa when infected. Indeed, potentially beneficial bacteria, such as Lactococcus, decreased in abundance, whereas potentially pathogenic bacteria from the Helicobacter genus increased in AstV-positive bats. Two Helicobacter haplotypes closely related to avian Helicobacter species were identified. We conclude that even though the impact of infection on the microbiome was not amplified in forest fragments, the higher infection likelihood in landscapes altered by humans implies more frequent or prolonged health repercussions for bats.
Additional Links: PMID-42527911
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@article {pmid42527911,
year = {2026},
author = {Brändel, SD and Melville, DW and Wilhelm, K and Corman, VM and Page, R and Drosten, C and Tschapka, M and Sommer, S and Wasimuddin, },
title = {Astrovirus infection alters gut microbial communities in a widespread neotropical bat across human-modified landscapes.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {42527911},
issn = {1471-2180},
mesh = {Animals ; *Chiroptera/microbiology/virology ; *Astroviridae Infections/veterinary/virology/epidemiology ; *Gastrointestinal Microbiome ; *Bacteria/classification/genetics/isolation & purification ; Panama ; *Astroviridae/isolation & purification ; Humans ; RNA, Ribosomal, 16S/genetics ; Forests ; Sequence Analysis, DNA ; Feces/microbiology/virology ; Phylogeny ; Biodiversity ; },
abstract = {Astroviruses are becoming a growing concern in public and veterinary health. In humans, astrovirus infections can cause severe diarrhea and may lead to neuropathological encephalitis, whereas in wildlife, these enteropathogenic viral infections often lack overt symptoms and thus remain unnoticed. Yet their close interaction with the host's gastrointestinal microbiome might drive cascading effects with disadvantages for host health. Bats harbor many zoonotic viruses without showing signs of disease, and many species move freely along the gradient from pristine to agricultural landscapes. To better understand the impact of astrovirus (AstV) infection under a One Health framework, we investigated the gut microbiome of naturally AstV-infected Seba's short-tailed bats (Carollia perspicillata, n = 234) inhabiting old-growth lowland forests or forest fragments embedded in an agricultural matrix in Panama. AstV prevalence was higher in forest fragments. We observed that AstV infection is associated with a shift in microbial beta but not alpha diversity, which points towards the replacement of common gut microbial taxa when infected. Indeed, potentially beneficial bacteria, such as Lactococcus, decreased in abundance, whereas potentially pathogenic bacteria from the Helicobacter genus increased in AstV-positive bats. Two Helicobacter haplotypes closely related to avian Helicobacter species were identified. We conclude that even though the impact of infection on the microbiome was not amplified in forest fragments, the higher infection likelihood in landscapes altered by humans implies more frequent or prolonged health repercussions for bats.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Chiroptera/microbiology/virology
*Astroviridae Infections/veterinary/virology/epidemiology
*Gastrointestinal Microbiome
*Bacteria/classification/genetics/isolation & purification
Panama
*Astroviridae/isolation & purification
Humans
RNA, Ribosomal, 16S/genetics
Forests
Sequence Analysis, DNA
Feces/microbiology/virology
Phylogeny
Biodiversity
RevDate: 2026-07-30
Rhizosphere Engineering by Root Exudates: High-Yielding Alfalfa Recruits Functional PGPR to Sustain Soil Nutrient Availability Under Long-Term Cultivation.
Plant, cell & environment [Epub ahead of print].
Soil nutrient transformation capacity is a critical determinant of sustainable productivity in perennial cropping systems; however, the extent to which high-yielding crops actively regulate rhizosphere microbial assembly to maintain nutrient availability remains poorly understood. We investigated whether root exudates from high-yielding alfalfa (Medicago sativa L.) selectively recruit plant growth-promoting rhizobacteria (PGPR) to enhance nutrient transformation. In an 8-year continuous alfalfa system (2018-2025), high-yielding cultivars increased soil organic carbon by 8.64%, total nitrogen by 6.01%, and moderately labile phosphorus fractions by 1.62%. Rhizobox experiments demonstrated that root exudates enhanced growth only with an active microbiome. High-yielding alfalfa enriched PGPR communities, specifically Ensifer, Pseudomonas, and Bacillus. Isolated strains exhibited N fixation, P solubilisation, and IAA production. Metabolomic profiling revealed that exudates were enriched in specific sugars and amino acids. Maltopentaose, maltotetraose, taurine, N-acetyl-L-leucine, and asparagine functioned as chemoattractants, stimulating PGPR proliferation and biofilm formation. These findings demonstrate that root exudate-mediated, targeted recruitment of functional PGPR enhances N fixation and P transformation, thereby supporting sustained high alfalfa productivity. This study demonstrates a key rhizosphere mechanism underlying the long-term sustainability of high-yielding perennial legume systems and provides a mechanistic basis for microbiome-informed sustainable alfalfa production and management.
Additional Links: PMID-42528084
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PubMed:
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@article {pmid42528084,
year = {2026},
author = {Sun, Y and Wei, K and Yang, K and Hui, J and Xia, D and Wang, X and Cartmill, AD and López, IF and Ma, C and Zhang, Q},
title = {Rhizosphere Engineering by Root Exudates: High-Yielding Alfalfa Recruits Functional PGPR to Sustain Soil Nutrient Availability Under Long-Term Cultivation.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70631},
pmid = {42528084},
issn = {1365-3040},
support = {2023B02031//Xinjiang Uygur Autonomous Region Key R&D Task Special Project/ ; 2026DB001//Science and Technology Program of XPCC/ ; 32260347//National Natural Science Foundation of China/ ; //T. R. Ellett Agricultural Research Trust/ ; },
abstract = {Soil nutrient transformation capacity is a critical determinant of sustainable productivity in perennial cropping systems; however, the extent to which high-yielding crops actively regulate rhizosphere microbial assembly to maintain nutrient availability remains poorly understood. We investigated whether root exudates from high-yielding alfalfa (Medicago sativa L.) selectively recruit plant growth-promoting rhizobacteria (PGPR) to enhance nutrient transformation. In an 8-year continuous alfalfa system (2018-2025), high-yielding cultivars increased soil organic carbon by 8.64%, total nitrogen by 6.01%, and moderately labile phosphorus fractions by 1.62%. Rhizobox experiments demonstrated that root exudates enhanced growth only with an active microbiome. High-yielding alfalfa enriched PGPR communities, specifically Ensifer, Pseudomonas, and Bacillus. Isolated strains exhibited N fixation, P solubilisation, and IAA production. Metabolomic profiling revealed that exudates were enriched in specific sugars and amino acids. Maltopentaose, maltotetraose, taurine, N-acetyl-L-leucine, and asparagine functioned as chemoattractants, stimulating PGPR proliferation and biofilm formation. These findings demonstrate that root exudate-mediated, targeted recruitment of functional PGPR enhances N fixation and P transformation, thereby supporting sustained high alfalfa productivity. This study demonstrates a key rhizosphere mechanism underlying the long-term sustainability of high-yielding perennial legume systems and provides a mechanistic basis for microbiome-informed sustainable alfalfa production and management.},
}
RevDate: 2026-07-30
Comparison of the effects of four commercially available prescription diet regimens on the fecal microbiome in healthy cats.
The Journal of veterinary medical science [Epub ahead of print].
Diet significantly influences the gut microbiota, with variations in macronutrient content (proteins, fats, and carbohydrates) and the presence of non-digestible carbohydrates, such as fiber, playing crucial roles in shaping microbial composition. This study investigated the effects of four commercial prescription diets (low-carbohydrate, weight-loss, high soluble fiber, and renal) on the fecal microbiome of five healthy domestic cats using a 4×4 Latin square design. Fecal samples were analyzed using Illumina sequencing of the bacterial 16S rRNA gene to assess bacterial community structure and diversity. Results showed that cats fed the renal diet (low protein, high carbohydrate, high fat) were associated with higher relative abundances of the phylum Actinobacteria, particularly Bifidobacterium. The low-carbohydrate diet was associated with higher relative abundances of Adlercreutzia, Collinsella, and Slackia. The high-soluble fiber diet was associated with a higher relative proportion of Streptococcaceae. In contrast, the renal diet was associated with lower relative abundances of Blautia and Erysipelotrichaceae. No significant differences were observed in alpha-diversity indices among diets, whereas beta-diversity analysis showed significant differences in microbial community composition among dietary groups. These findings suggest that dietary composition may influence the fecal microbiome in healthy cats. However, given the exploratory design and compositional nature of the sequencing data, these findings should be interpreted cautiously and considered hypothesis-generating.
Additional Links: PMID-42528237
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PubMed:
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@article {pmid42528237,
year = {2026},
author = {Komiya, T and Koyama, K and Akiyama, R and Oda, H and Gokita, K and Sako, T and Mori, A},
title = {Comparison of the effects of four commercially available prescription diet regimens on the fecal microbiome in healthy cats.},
journal = {The Journal of veterinary medical science},
volume = {},
number = {},
pages = {},
doi = {10.1292/jvms.24-0494},
pmid = {42528237},
issn = {1347-7439},
abstract = {Diet significantly influences the gut microbiota, with variations in macronutrient content (proteins, fats, and carbohydrates) and the presence of non-digestible carbohydrates, such as fiber, playing crucial roles in shaping microbial composition. This study investigated the effects of four commercial prescription diets (low-carbohydrate, weight-loss, high soluble fiber, and renal) on the fecal microbiome of five healthy domestic cats using a 4×4 Latin square design. Fecal samples were analyzed using Illumina sequencing of the bacterial 16S rRNA gene to assess bacterial community structure and diversity. Results showed that cats fed the renal diet (low protein, high carbohydrate, high fat) were associated with higher relative abundances of the phylum Actinobacteria, particularly Bifidobacterium. The low-carbohydrate diet was associated with higher relative abundances of Adlercreutzia, Collinsella, and Slackia. The high-soluble fiber diet was associated with a higher relative proportion of Streptococcaceae. In contrast, the renal diet was associated with lower relative abundances of Blautia and Erysipelotrichaceae. No significant differences were observed in alpha-diversity indices among diets, whereas beta-diversity analysis showed significant differences in microbial community composition among dietary groups. These findings suggest that dietary composition may influence the fecal microbiome in healthy cats. However, given the exploratory design and compositional nature of the sequencing data, these findings should be interpreted cautiously and considered hypothesis-generating.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Biomarkers From the Microbiome to Predict ALD Progression and Its Severity: A Comprehensive Review.
Mediators of inflammation, 2026(1):e7244952.
Alcohol use is a major global health issue, causing about 3.3 million deaths each year, or roughly 5.9% of all deaths worldwide. Alcohol-related liver disease develops in stages: steatosis, steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. If alcohol consumption is discontinued at early stages, alcohol-related fatty liver disease can be reversed; however, continued exposure leads to progressive liver injury and increased mortality risk. Current diagnostic tools lack sufficient sensitivity and specificity to detect early-stage disease or accurately assess disease progression. This highlights the need for reliable and mechanistically relevant biomarkers for early diagnosis and staging. This review examines alterations in gut microbiota across different stages of alcohol-associated liver disease and evaluates gut microbiota-associated biomarkers, including microbial metabolites, in the context of their potential diagnostic and prognostic utility. In addition, the review discusses the limitations of existing biomarkers and highlights the emerging role of microbiome-derived signals in reflecting disease mechanisms. These findings suggest that gut microbiota-related biomarkers may provide a promising but still evolving approach for improving early detection and understanding disease progression in alcohol-associated liver disease.
Additional Links: PMID-42528288
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Citation:
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@article {pmid42528288,
year = {2026},
author = {Mishra, S and Solanki, H and Mandal, P},
title = {Biomarkers From the Microbiome to Predict ALD Progression and Its Severity: A Comprehensive Review.},
journal = {Mediators of inflammation},
volume = {2026},
number = {1},
pages = {e7244952},
pmid = {42528288},
issn = {1466-1861},
mesh = {Humans ; *Biomarkers/metabolism ; Disease Progression ; *Gastrointestinal Microbiome/physiology ; *Microbiota ; *Liver Diseases, Alcoholic/metabolism/microbiology ; Animals ; },
abstract = {Alcohol use is a major global health issue, causing about 3.3 million deaths each year, or roughly 5.9% of all deaths worldwide. Alcohol-related liver disease develops in stages: steatosis, steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. If alcohol consumption is discontinued at early stages, alcohol-related fatty liver disease can be reversed; however, continued exposure leads to progressive liver injury and increased mortality risk. Current diagnostic tools lack sufficient sensitivity and specificity to detect early-stage disease or accurately assess disease progression. This highlights the need for reliable and mechanistically relevant biomarkers for early diagnosis and staging. This review examines alterations in gut microbiota across different stages of alcohol-associated liver disease and evaluates gut microbiota-associated biomarkers, including microbial metabolites, in the context of their potential diagnostic and prognostic utility. In addition, the review discusses the limitations of existing biomarkers and highlights the emerging role of microbiome-derived signals in reflecting disease mechanisms. These findings suggest that gut microbiota-related biomarkers may provide a promising but still evolving approach for improving early detection and understanding disease progression in alcohol-associated liver disease.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Biomarkers/metabolism
Disease Progression
*Gastrointestinal Microbiome/physiology
*Microbiota
*Liver Diseases, Alcoholic/metabolism/microbiology
Animals
RevDate: 2026-07-30
CmpDate: 2026-07-30
Multivariate functional linear discriminant analysis with feature selection: an application to inflammatory bowel disease classification.
Biostatistics (Oxford, England), 27(1):.
Inflammatory Bowel Disease (IBD), including Crohn's Disease (CD) and Ulcerative Colitis (UC), presents significant public health challenges due to its complex etiology. Motivated by the IBD study of the Integrative Human Microbiome Project, our objective is to identify microbial pathways that distinguish between CD, UC, and non-IBD over time. Most current research relies on simplistic analyses that examine 1 variable or time point at a time, or address binary classification problems, limiting our understanding of the dynamic interactions within the microbiome over time. To address these limitations, we develop a novel functional data analysis approach for discriminant analysis of multivariate functional data that can effectively handle multiple high-dimensional predictors, sparse time points, and categorical outcomes. Our method seeks linear combinations of functions (ie discriminant functions) that maximize separation between 2 or more classes over time. We impose a sparsity-inducing penalty when estimating the discriminant functions, allowing us to identify relevant discriminating variables over time. Applications of our method to the motivating data identified microbial features related to mucin degradation, amino acid metabolism, and peptidoglycan recognition, which are implicated in the progression and development of IBD. Furthermore, our method highlighted the role of multiple vitamin B deficiencies in the context of IBD. By moving beyond traditional analytical frameworks, our innovative approach holds the potential for uncovering clinically meaningful discoveries in IBD research.
Additional Links: PMID-42528381
PubMed:
Citation:
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@article {pmid42528381,
year = {2026},
author = {Liu, L and Wang, G and Safo, SE},
title = {Multivariate functional linear discriminant analysis with feature selection: an application to inflammatory bowel disease classification.},
journal = {Biostatistics (Oxford, England)},
volume = {27},
number = {1},
pages = {},
pmid = {42528381},
issn = {1468-4357},
support = {/NH/NIH HHS/United States ; },
mesh = {Humans ; Discriminant Analysis ; *Inflammatory Bowel Diseases/classification/microbiology ; Multivariate Analysis ; Colitis, Ulcerative/microbiology/classification ; },
abstract = {Inflammatory Bowel Disease (IBD), including Crohn's Disease (CD) and Ulcerative Colitis (UC), presents significant public health challenges due to its complex etiology. Motivated by the IBD study of the Integrative Human Microbiome Project, our objective is to identify microbial pathways that distinguish between CD, UC, and non-IBD over time. Most current research relies on simplistic analyses that examine 1 variable or time point at a time, or address binary classification problems, limiting our understanding of the dynamic interactions within the microbiome over time. To address these limitations, we develop a novel functional data analysis approach for discriminant analysis of multivariate functional data that can effectively handle multiple high-dimensional predictors, sparse time points, and categorical outcomes. Our method seeks linear combinations of functions (ie discriminant functions) that maximize separation between 2 or more classes over time. We impose a sparsity-inducing penalty when estimating the discriminant functions, allowing us to identify relevant discriminating variables over time. Applications of our method to the motivating data identified microbial features related to mucin degradation, amino acid metabolism, and peptidoglycan recognition, which are implicated in the progression and development of IBD. Furthermore, our method highlighted the role of multiple vitamin B deficiencies in the context of IBD. By moving beyond traditional analytical frameworks, our innovative approach holds the potential for uncovering clinically meaningful discoveries in IBD research.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Discriminant Analysis
*Inflammatory Bowel Diseases/classification/microbiology
Multivariate Analysis
Colitis, Ulcerative/microbiology/classification
RevDate: 2026-07-30
CmpDate: 2026-07-30
Coexist or eliminate? Antibody-based functional silencing versus eradication in gut microbiome- targeted therapy.
Frontiers in immunology, 17:1903103.
BACKGROUND: Dominant anti-infective strategies equate therapeutic success with pathogen eradication, yet in the gut most clinically relevant "pathogens" are pathobionts that cause disease only under specific ecological conditions. Antibiotics resolve infection but decimate commensal communities and select for resistance.
SCOPE AND APPROACH: We review antibody-based interventions, native mucosal antibodies (IgA, IgM), monoclonal antibodies, and immunoglobulin Y (IgY), as mechanistic test cases for a functional silencing paradigm, in which pathobiont virulence is attenuated through non-bactericidal mechanisms while preserving community architecture.
KEY FINDINGS: Drawing on randomized trial data (bezlotoxumab in Clostridioides difficile recurrence prevention, MODIFY I/II, n = 2,655), preclinical and early clinical IgY studies in enteric infections, and long-term IgY deployment in aquaculture, we find that functional silencing delivers durable benefit when disease is driven by discrete virulence factors. However, evolutionary risks, including phase variation, conformational switching, and the theoretical framework of "imperfect immunity", identify conditions under which retained pathobionts may re-emerge as threats.
CONCLUSIONS: Eradication and functional silencing are best understood as complementary strategies whose optimal deployment depends on host immune status, barrier integrity, and the nature of pathobiont virulence. Defining the boundary between safe coexistence and evolutionary rebound constitutes the field's central unresolved challenge.
Additional Links: PMID-42528616
PubMed:
Citation:
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@article {pmid42528616,
year = {2026},
author = {El-Kafrawy, SA and Abbas, AT and El-Kafrawy, AS and El-Daly, MM and Azhar, EI},
title = {Coexist or eliminate? Antibody-based functional silencing versus eradication in gut microbiome- targeted therapy.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1903103},
pmid = {42528616},
issn = {1664-3224},
mesh = {Humans ; Animals ; *Gastrointestinal Microbiome/immunology/drug effects ; *Antibodies, Monoclonal/therapeutic use ; Clostridioides difficile/immunology ; Immunoglobulins/immunology/therapeutic use ; *Clostridium Infections/immunology/microbiology/therapy ; },
abstract = {BACKGROUND: Dominant anti-infective strategies equate therapeutic success with pathogen eradication, yet in the gut most clinically relevant "pathogens" are pathobionts that cause disease only under specific ecological conditions. Antibiotics resolve infection but decimate commensal communities and select for resistance.
SCOPE AND APPROACH: We review antibody-based interventions, native mucosal antibodies (IgA, IgM), monoclonal antibodies, and immunoglobulin Y (IgY), as mechanistic test cases for a functional silencing paradigm, in which pathobiont virulence is attenuated through non-bactericidal mechanisms while preserving community architecture.
KEY FINDINGS: Drawing on randomized trial data (bezlotoxumab in Clostridioides difficile recurrence prevention, MODIFY I/II, n = 2,655), preclinical and early clinical IgY studies in enteric infections, and long-term IgY deployment in aquaculture, we find that functional silencing delivers durable benefit when disease is driven by discrete virulence factors. However, evolutionary risks, including phase variation, conformational switching, and the theoretical framework of "imperfect immunity", identify conditions under which retained pathobionts may re-emerge as threats.
CONCLUSIONS: Eradication and functional silencing are best understood as complementary strategies whose optimal deployment depends on host immune status, barrier integrity, and the nature of pathobiont virulence. Defining the boundary between safe coexistence and evolutionary rebound constitutes the field's central unresolved challenge.},
}
MeSH Terms:
show MeSH Terms
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Humans
Animals
*Gastrointestinal Microbiome/immunology/drug effects
*Antibodies, Monoclonal/therapeutic use
Clostridioides difficile/immunology
Immunoglobulins/immunology/therapeutic use
*Clostridium Infections/immunology/microbiology/therapy
RevDate: 2026-07-30
CmpDate: 2026-07-30
Microbial dysbiosis and wound healing in diabetic foot ulcers: a mini review with a note on the role of artificial intelligence.
Frontiers in cellular and infection microbiology, 16:1891884.
Diabetic foot ulcers (DFUs) are a serious diabetes-related complication characterized by high rates of amputation and mortality. Emerging evidence suggests that DFUs are not simply the result of infection, but also involve microbiome dysbiosis, which impairs healing. Systemically, disturbances to the gut microbiota via the gut-skin axis promote systemic inflammation and metabolic dysfunction. Locally, skin microbial diversity is significantly reduced, allowing opportunistic pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa to form resilient biofilms. These biofilms resist antibiotics and host immunity, while microbial virulence factors exacerbate tissue damage and disrupt the healing cascade. This synergy between host pathology and dysbiosis perpetuates chronic ulceration. Novel therapeutic strategies therefore aim to modulate this aberrant ecology by shifting from broad-spectrum eradication to targeted restoration. Promising approaches include probiotics, phage therapy, traditional Chinese medicine, and faecal microbiota transplantation, which seek to recalibrate the microbiome and promote healing. However, translation into clinical practice requires more robust evidence from large-scale trials. Future perspectives point towards personalized microbial medicine, integrating multi-omics data and artificial intelligence to match interventions with specific microbial ecotypes, which may reduce the global burden of DFUs.
Additional Links: PMID-42528685
PubMed:
Citation:
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@article {pmid42528685,
year = {2026},
author = {Yu, X and Liu, Q and Huang, Y and Wang, Q and Wang, Y and Zhao, G},
title = {Microbial dysbiosis and wound healing in diabetic foot ulcers: a mini review with a note on the role of artificial intelligence.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1891884},
pmid = {42528685},
issn = {2235-2988},
mesh = {Humans ; *Diabetic Foot/microbiology/therapy ; *Dysbiosis/microbiology/therapy ; *Wound Healing ; *Artificial Intelligence ; Biofilms/growth & development ; Probiotics/therapeutic use ; Gastrointestinal Microbiome ; Animals ; Skin Microbiome ; },
abstract = {Diabetic foot ulcers (DFUs) are a serious diabetes-related complication characterized by high rates of amputation and mortality. Emerging evidence suggests that DFUs are not simply the result of infection, but also involve microbiome dysbiosis, which impairs healing. Systemically, disturbances to the gut microbiota via the gut-skin axis promote systemic inflammation and metabolic dysfunction. Locally, skin microbial diversity is significantly reduced, allowing opportunistic pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa to form resilient biofilms. These biofilms resist antibiotics and host immunity, while microbial virulence factors exacerbate tissue damage and disrupt the healing cascade. This synergy between host pathology and dysbiosis perpetuates chronic ulceration. Novel therapeutic strategies therefore aim to modulate this aberrant ecology by shifting from broad-spectrum eradication to targeted restoration. Promising approaches include probiotics, phage therapy, traditional Chinese medicine, and faecal microbiota transplantation, which seek to recalibrate the microbiome and promote healing. However, translation into clinical practice requires more robust evidence from large-scale trials. Future perspectives point towards personalized microbial medicine, integrating multi-omics data and artificial intelligence to match interventions with specific microbial ecotypes, which may reduce the global burden of DFUs.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Diabetic Foot/microbiology/therapy
*Dysbiosis/microbiology/therapy
*Wound Healing
*Artificial Intelligence
Biofilms/growth & development
Probiotics/therapeutic use
Gastrointestinal Microbiome
Animals
Skin Microbiome
RevDate: 2026-07-30
CmpDate: 2026-07-30
Ecological and functional roles of plant microbiomes in environmental detoxification.
Frontiers in microbiology, 17:1883316.
Plant-associated microbiomes play a crucial role in environmental detoxification by influencing the degradation, immobilization, and resistance to toxins in polluted settings. The ecological and functional activity of endogenous microbial communities, such as rhizobacteria and endophytic microorganisms, is not well studied when examining contaminants and their environments, despite the fact that plant-mediated bioremediation has garnered a lot of research attention. The majority of previously published research focuses on a single biodegradation route or solitary plant-microbe interactions. Our knowledge of how the microbiome's composition, functional diversity, and ecological stability of microbial communities work together to produce detoxifying results in practical applications is currently lacking. To advance understanding of how plant microbiomes cooperatively mediate environmental detoxification through metabolic interactions, adaptive responses, and host-microbiome communication, this review integrates insights from microbial ecology and functional microbiology. Its primary objective is to synthesize current knowledge on key microbial functions, including metal sequestration, xenobiotic degradation, redox regulation, and modulation of plant responses to biotic stress, while linking these functions to ecological processes such as host specificity, niche specialization, and community assembly. A distinctive aspect of this review is its ecosystem-level perspective, which shifts the focus from individual microbial taxa to the functional resilience of microbial communities in determining detoxification efficiency. The information provided in this review has a scope to provide framework to develop ecologically-sustaining, microbiome-based strategies for the detoxification of the environment and for conducting future bioremediation research.
Additional Links: PMID-42528698
PubMed:
Citation:
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@article {pmid42528698,
year = {2026},
author = {Selim, S and Adhikary, K and Sarkar, R and Ganguly, K and Misra, A and Kashmiry, AA and Alshareef, SA and Alkhatib, SN and Hagagy, N and Maiti, R},
title = {Ecological and functional roles of plant microbiomes in environmental detoxification.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1883316},
pmid = {42528698},
issn = {1664-302X},
abstract = {Plant-associated microbiomes play a crucial role in environmental detoxification by influencing the degradation, immobilization, and resistance to toxins in polluted settings. The ecological and functional activity of endogenous microbial communities, such as rhizobacteria and endophytic microorganisms, is not well studied when examining contaminants and their environments, despite the fact that plant-mediated bioremediation has garnered a lot of research attention. The majority of previously published research focuses on a single biodegradation route or solitary plant-microbe interactions. Our knowledge of how the microbiome's composition, functional diversity, and ecological stability of microbial communities work together to produce detoxifying results in practical applications is currently lacking. To advance understanding of how plant microbiomes cooperatively mediate environmental detoxification through metabolic interactions, adaptive responses, and host-microbiome communication, this review integrates insights from microbial ecology and functional microbiology. Its primary objective is to synthesize current knowledge on key microbial functions, including metal sequestration, xenobiotic degradation, redox regulation, and modulation of plant responses to biotic stress, while linking these functions to ecological processes such as host specificity, niche specialization, and community assembly. A distinctive aspect of this review is its ecosystem-level perspective, which shifts the focus from individual microbial taxa to the functional resilience of microbial communities in determining detoxification efficiency. The information provided in this review has a scope to provide framework to develop ecologically-sustaining, microbiome-based strategies for the detoxification of the environment and for conducting future bioremediation research.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Decoding the gut-adipose-ovary axis in polycystic ovary syndrome: from metabolic dysregulation to oncological risk modulation.
Frontiers in microbiology, 17:1882127.
Polycystic ovary syndrome (PCOS) is traditionally managed as a localized reproductive disorder, but emerging evidence redefines it as a systemic metabolic-endocrine continuum with profound long-term health implications. This review comprehensively synthesizes the pathogenic role of the nutrition-mediated "gut-adipose-ovary axis" in bridging PCOS-associated metabolic dysfunction with an elevated risk of gynecological malignancies. Aberrant nutritional intake acts as the primary environmental catalyst, driving gut microbiota dysbiosis and metabolic endotoxemia. These gut-derived signals provoke visceral adipose tissue dysfunction, initiating a self-reinforcing cascade of systemic insulin resistance, hyperandrogenism, and chronic low-grade inflammation. Crucially, the convergence of these systemic insults continuously remodels the localized ovarian microenvironment. By sustaining proliferative signaling, forcing metabolic reprogramming, and fostering immune evasion, these convergent insults may contribute to a permissive pre-neoplastic microenvironment in susceptible patients with PCOS. To dismantle this pathogenic network, we outline a multi-dimensional therapeutic framework that integrates precision nutrition, microbiome modulation, and targeted pharmacological agents. Ultimately, this systems-biology perspective mandates a paradigm shift in clinical practice: moving beyond empirical symptom palliation toward proactive, risk-stratified interventions that interrupt the disease continuum and reduce long-term oncological risk in appropriately stratified women with PCOS.
Additional Links: PMID-42528754
PubMed:
Citation:
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@article {pmid42528754,
year = {2026},
author = {Guo, L and Lu, J and Liu, L and Zhang, M and Yu, N and Lu, L and Yang, T and Zhou, J and Hou, B and Chen, Y and Geng, Y},
title = {Decoding the gut-adipose-ovary axis in polycystic ovary syndrome: from metabolic dysregulation to oncological risk modulation.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1882127},
pmid = {42528754},
issn = {1664-302X},
abstract = {Polycystic ovary syndrome (PCOS) is traditionally managed as a localized reproductive disorder, but emerging evidence redefines it as a systemic metabolic-endocrine continuum with profound long-term health implications. This review comprehensively synthesizes the pathogenic role of the nutrition-mediated "gut-adipose-ovary axis" in bridging PCOS-associated metabolic dysfunction with an elevated risk of gynecological malignancies. Aberrant nutritional intake acts as the primary environmental catalyst, driving gut microbiota dysbiosis and metabolic endotoxemia. These gut-derived signals provoke visceral adipose tissue dysfunction, initiating a self-reinforcing cascade of systemic insulin resistance, hyperandrogenism, and chronic low-grade inflammation. Crucially, the convergence of these systemic insults continuously remodels the localized ovarian microenvironment. By sustaining proliferative signaling, forcing metabolic reprogramming, and fostering immune evasion, these convergent insults may contribute to a permissive pre-neoplastic microenvironment in susceptible patients with PCOS. To dismantle this pathogenic network, we outline a multi-dimensional therapeutic framework that integrates precision nutrition, microbiome modulation, and targeted pharmacological agents. Ultimately, this systems-biology perspective mandates a paradigm shift in clinical practice: moving beyond empirical symptom palliation toward proactive, risk-stratified interventions that interrupt the disease continuum and reduce long-term oncological risk in appropriately stratified women with PCOS.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Trained immunity in chronic rhinosinusitis: epigenetic reprogramming of innate immune memory as a driver of mucosal inflammation and recurrence.
Frontiers in immunology, 17:1822395.
Chronic rhinosinusitis (CRS) is a highly prevalent and debilitating inflammatory condition of the upper airway, affecting 5-28% of the global population and imposing a substantial socioeconomic burden. Despite major advances in endoscopic sinus surgery, pharmacological management, and targeted biologic therapies, long-term disease recurrence following treatment remains an unresolved clinical challenge. Current pathophysiological frameworks centered on adaptive type 2 immunity, eosinophilic inflammation, and pathogen persistence fail to fully account for the chronification and therapy resistance of CRS. Emerging evidence positions trained immunity (the epigenetic and metabolic reprogramming of innate immune cells enabling non-antigen-specific functional memory) as a fundamental and previously underappreciated mechanism driving CRS recurrence. Persistent sinonasal microbial colonizers, including Staphylococcus aureus biofilms and fungal components, along with viral pathogens and dysbiotic microbiome communities, function as potent epigenetic training stimuli that reprogram sinonasal macrophages, group 2 innate lymphoid cells (ILC2s), and epithelial progenitor cells. The recent identification of a TLR4+ trained ILC2 subset in nasal polyp tissue, sustained by AP-1-driven chromatin remodeling at the Tlr4 locus, exemplifies the cellular specificity of this phenomenon. Concurrently, nasal basal stem cells acquire heritable pro-inflammatory chromatin states following type 2 cytokine exposure, encoding an epithelial inflammatory memory that perpetuates mucosal dysfunction independent of ongoing stimulation. This review systematically examines the microbial triggers, epigenetic mechanisms, key cellular mediators, and therapeutic implications of trained immunity in CRS, proposing a new framework for disease-modifying strategies targeting the sinonasal epigenetic inflammatory landscape.
Additional Links: PMID-42528773
PubMed:
Citation:
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@article {pmid42528773,
year = {2026},
author = {Huang, GJ and Li, LJ and Li, PS and Fan, ZJ and Lu, BQ},
title = {Trained immunity in chronic rhinosinusitis: epigenetic reprogramming of innate immune memory as a driver of mucosal inflammation and recurrence.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1822395},
pmid = {42528773},
issn = {1664-3224},
mesh = {Humans ; *Rhinosinusitis/immunology/genetics ; *Trained Immunity ; *Immunity, Innate ; Chronic Disease ; *Immunologic Memory ; *Epigenesis, Genetic ; Animals ; Recurrence ; Inflammation/immunology ; *Nasal Mucosa/immunology ; Immunity, Mucosal ; },
abstract = {Chronic rhinosinusitis (CRS) is a highly prevalent and debilitating inflammatory condition of the upper airway, affecting 5-28% of the global population and imposing a substantial socioeconomic burden. Despite major advances in endoscopic sinus surgery, pharmacological management, and targeted biologic therapies, long-term disease recurrence following treatment remains an unresolved clinical challenge. Current pathophysiological frameworks centered on adaptive type 2 immunity, eosinophilic inflammation, and pathogen persistence fail to fully account for the chronification and therapy resistance of CRS. Emerging evidence positions trained immunity (the epigenetic and metabolic reprogramming of innate immune cells enabling non-antigen-specific functional memory) as a fundamental and previously underappreciated mechanism driving CRS recurrence. Persistent sinonasal microbial colonizers, including Staphylococcus aureus biofilms and fungal components, along with viral pathogens and dysbiotic microbiome communities, function as potent epigenetic training stimuli that reprogram sinonasal macrophages, group 2 innate lymphoid cells (ILC2s), and epithelial progenitor cells. The recent identification of a TLR4+ trained ILC2 subset in nasal polyp tissue, sustained by AP-1-driven chromatin remodeling at the Tlr4 locus, exemplifies the cellular specificity of this phenomenon. Concurrently, nasal basal stem cells acquire heritable pro-inflammatory chromatin states following type 2 cytokine exposure, encoding an epithelial inflammatory memory that perpetuates mucosal dysfunction independent of ongoing stimulation. This review systematically examines the microbial triggers, epigenetic mechanisms, key cellular mediators, and therapeutic implications of trained immunity in CRS, proposing a new framework for disease-modifying strategies targeting the sinonasal epigenetic inflammatory landscape.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Rhinosinusitis/immunology/genetics
*Trained Immunity
*Immunity, Innate
Chronic Disease
*Immunologic Memory
*Epigenesis, Genetic
Animals
Recurrence
Inflammation/immunology
*Nasal Mucosa/immunology
Immunity, Mucosal
RevDate: 2026-07-30
CmpDate: 2026-07-30
The diet-microbiota-inflammation axis and colorectal cancer.
Frontiers in oncology, 16:1895753.
BACKGROUND: Colorectal cancer (CRC) is still one of the leading causes of cancer morbidity and mortality worldwide. There is increasing evidence that diet, gut microbiota, microbial metabolites and chronic inflammation are important factors in colorectal carcinogenesis and may provide novel opportunities for prevention, diagnosis and treatment.
AIM: To provide a comprehensive review of the current evidence on the role of diet, nutrition, microbial metabolism and chronic inflammation in CRC, with emphasis on emerging translational applications including microbiome-based biomarkers and microbiota-targeted therapeutic strategies.
METHODS: A literature search was performed with PubMed, Scopus and the Cochrane Library. Relevant studies on diet-microbiota interactions, microbial metabolites, inflammatory mechanisms, colorectal carcinogenesis, microbiome-derived biomarkers, and microbiota-targeted interventions were identified and reviewed. Preclinical and clinical studies and high quality reviews and meta-analyses were considered.
RESULTS: Dietary patterns have been shown to have a major impact on the composition and function of the gut microbiota. Rich-fiber diets and short-chain fatty acids (SCFAs) production seem protective against CRC, while western dietary patterns, ultra-processed foods and dysbiosis-associated metabolites promote a pro-inflammatory environment associated with carcinogenesis. Some microorganisms such as Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis and pks-positive Escherichia coli have been associated with CRC by inflammatory, genotoxic and immune-modulatory mechanisms. Recent advances in sequencing technologies and multi-omics approaches have enabled the identification of microbial signatures with potential diagnostic and prognostic value. Moreover, microbiota-targeted interventions such as probiotics, prebiotics, postbiotics, faecal microbiota transplantation, and next-generation microbial therapies have yielded promising preclinical and early clinical results.
CONCLUSIONS: The diet-microbiota-inflammation axis is a key player in colorectal carcinogenesis and a promising target for translational research. Microbiome-based biomarkers and microbiota-targeted therapies may have a role in future precision prevention and personalised management strategies of colorectal cancer despite significant challenges in terms of causation, standardisation and translation into clinical practice.
Additional Links: PMID-42528838
PubMed:
Citation:
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@article {pmid42528838,
year = {2026},
author = {Kossenas, K and Damaskos, C and Garmpis, N},
title = {The diet-microbiota-inflammation axis and colorectal cancer.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1895753},
pmid = {42528838},
issn = {2234-943X},
abstract = {BACKGROUND: Colorectal cancer (CRC) is still one of the leading causes of cancer morbidity and mortality worldwide. There is increasing evidence that diet, gut microbiota, microbial metabolites and chronic inflammation are important factors in colorectal carcinogenesis and may provide novel opportunities for prevention, diagnosis and treatment.
AIM: To provide a comprehensive review of the current evidence on the role of diet, nutrition, microbial metabolism and chronic inflammation in CRC, with emphasis on emerging translational applications including microbiome-based biomarkers and microbiota-targeted therapeutic strategies.
METHODS: A literature search was performed with PubMed, Scopus and the Cochrane Library. Relevant studies on diet-microbiota interactions, microbial metabolites, inflammatory mechanisms, colorectal carcinogenesis, microbiome-derived biomarkers, and microbiota-targeted interventions were identified and reviewed. Preclinical and clinical studies and high quality reviews and meta-analyses were considered.
RESULTS: Dietary patterns have been shown to have a major impact on the composition and function of the gut microbiota. Rich-fiber diets and short-chain fatty acids (SCFAs) production seem protective against CRC, while western dietary patterns, ultra-processed foods and dysbiosis-associated metabolites promote a pro-inflammatory environment associated with carcinogenesis. Some microorganisms such as Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis and pks-positive Escherichia coli have been associated with CRC by inflammatory, genotoxic and immune-modulatory mechanisms. Recent advances in sequencing technologies and multi-omics approaches have enabled the identification of microbial signatures with potential diagnostic and prognostic value. Moreover, microbiota-targeted interventions such as probiotics, prebiotics, postbiotics, faecal microbiota transplantation, and next-generation microbial therapies have yielded promising preclinical and early clinical results.
CONCLUSIONS: The diet-microbiota-inflammation axis is a key player in colorectal carcinogenesis and a promising target for translational research. Microbiome-based biomarkers and microbiota-targeted therapies may have a role in future precision prevention and personalised management strategies of colorectal cancer despite significant challenges in terms of causation, standardisation and translation into clinical practice.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Integrated metagenomic and metabolomic insights into microbial metabolic reprogramming in the rhizosphere of the invasive plant Praxelis clematidea under low-temperature stress.
Frontiers in microbiology, 17:1852122.
A primary factor preventing the spread of the invasive plant Praxelis clematidea to higher latitudes and altitudes is the low-temperature stress induced by global climate change. The present study investigated the impact of low-temperature stress on the rhizosphere soil micro-ecosystem of P. clematidea, with the aim of examining its adaptive micro-ecological mechanisms via a comprehensive multi-omics approach. The rhizosphere soils of plants were compared under low-temperature (LT, 5 °C) or normal-temperature (HT, 25 °C) treatments. Using soil physicochemical analysis, enzyme activity assay, metagenomics, and non-targeted metabolomics, we observed that LT stress did not significantly alter microbial alpha diversity but strongly shifted the community structure. This change enriched cold-tolerant bacterial taxa, including Nocardiopsis, Sphingobium and Azoarcus. The LT stress was associated with altered carbon and nitrogen cycling, as indicated by increased soil urease activity but decreased alkaline phosphatase and catalase activities. The nitrate-N and ammonium-N levels increased, but total nitrogen, total organic carbon, and organic matter were reduced. Additionally, metagenomic study revealed overexpression of major microbial carbon metabolism genes (e.g., TCA cycle and glycolysis) and downregulation of nitrogen assimilation genes (e.g., glnA and NasA). Furthermore, metabolomics indicated a rise in carbohydrates and vitamins, along with a notable accumulation of stress-resistant secondary metabolites such as phenolic acids, flavonoids, and terpenes in the rhizosphere soils under LT stress. Correlation analysis indicated strong positive associations between the enriched cold-tolerant genera and these stress-resistant metabolites (e.g., costunolide and choline sulfate). Functional enrichment analysis suggested a metabolic reprogramming signature coupled with low-temperature treatment. Finally, this integrated multi-omics study reveals that P. clematidea is associated with an altered rhizosphere microbiome, differential functional gene abundance, and reorganized metabolic networks under low-temperature conditions. These findings offer a vital micro-ecological elucidation for P. clematidea effective colonization and propagation in novel, colder habitats.
Additional Links: PMID-42528952
PubMed:
Citation:
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@article {pmid42528952,
year = {2026},
author = {Liu, X and Cheng, W and Li, C and Dessie, W and Qi, C and Ayaz, M and Xu, X},
title = {Integrated metagenomic and metabolomic insights into microbial metabolic reprogramming in the rhizosphere of the invasive plant Praxelis clematidea under low-temperature stress.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1852122},
pmid = {42528952},
issn = {1664-302X},
abstract = {A primary factor preventing the spread of the invasive plant Praxelis clematidea to higher latitudes and altitudes is the low-temperature stress induced by global climate change. The present study investigated the impact of low-temperature stress on the rhizosphere soil micro-ecosystem of P. clematidea, with the aim of examining its adaptive micro-ecological mechanisms via a comprehensive multi-omics approach. The rhizosphere soils of plants were compared under low-temperature (LT, 5 °C) or normal-temperature (HT, 25 °C) treatments. Using soil physicochemical analysis, enzyme activity assay, metagenomics, and non-targeted metabolomics, we observed that LT stress did not significantly alter microbial alpha diversity but strongly shifted the community structure. This change enriched cold-tolerant bacterial taxa, including Nocardiopsis, Sphingobium and Azoarcus. The LT stress was associated with altered carbon and nitrogen cycling, as indicated by increased soil urease activity but decreased alkaline phosphatase and catalase activities. The nitrate-N and ammonium-N levels increased, but total nitrogen, total organic carbon, and organic matter were reduced. Additionally, metagenomic study revealed overexpression of major microbial carbon metabolism genes (e.g., TCA cycle and glycolysis) and downregulation of nitrogen assimilation genes (e.g., glnA and NasA). Furthermore, metabolomics indicated a rise in carbohydrates and vitamins, along with a notable accumulation of stress-resistant secondary metabolites such as phenolic acids, flavonoids, and terpenes in the rhizosphere soils under LT stress. Correlation analysis indicated strong positive associations between the enriched cold-tolerant genera and these stress-resistant metabolites (e.g., costunolide and choline sulfate). Functional enrichment analysis suggested a metabolic reprogramming signature coupled with low-temperature treatment. Finally, this integrated multi-omics study reveals that P. clematidea is associated with an altered rhizosphere microbiome, differential functional gene abundance, and reorganized metabolic networks under low-temperature conditions. These findings offer a vital micro-ecological elucidation for P. clematidea effective colonization and propagation in novel, colder habitats.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Microbiota-directed therapies for atopic dermatitis: a three-tier framework for inflammation control, immune modulation, and microbiome restoration.
Frontiers in immunology, 17:1873455.
The pathogenesis of atopic dermatitis (AD) involves cutaneous barrier dysfunction, immune dysregulation, and microbiota imbalance. Although microbiota-directed therapeutic approaches have garnered increasing attention, current evidence is heterogeneous, encompassing probiotics, postbiotics, microbial metabolites, local microbial interventions, antimicrobials and ecological modulation strategies. This narrative review does not aim to provide clinical guidelines, but rather seeks to synthesise existing evidence within a three-tier conceptual framework. This framework classifies interventions into three categories: those primarily addressing local inflammation and barrier-associated microbiota dysbiosis; those exerting systemic immunomodulation via gut-derived microbial signals; and those modulating the skin microbiota ecology. It should be noted that human clinical data are still limited and heterogeneous, and much mechanistic insight is derived from preclinical research. By clarifying mechanistic layers and evidentiary gaps, this framework may facilitate future research to evaluate the sequencing or combination of anti-inflammatory therapy, barrier restoration, and microbiota ecological modulation.
Additional Links: PMID-42529037
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Citation:
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@article {pmid42529037,
year = {2026},
author = {Zhao, Y and Gao, Q and Li, G and Zhou, Q and Yang, F and Zhu, X},
title = {Microbiota-directed therapies for atopic dermatitis: a three-tier framework for inflammation control, immune modulation, and microbiome restoration.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1873455},
pmid = {42529037},
issn = {1664-3224},
mesh = {Humans ; *Dermatitis, Atopic/therapy/immunology/microbiology ; Skin Microbiome ; Animals ; *Immunomodulation ; Inflammation/therapy/immunology ; Probiotics/therapeutic use ; *Microbiota/immunology ; Dysbiosis/immunology/therapy ; *Gastrointestinal Microbiome/immunology ; Skin/microbiology/immunology ; },
abstract = {The pathogenesis of atopic dermatitis (AD) involves cutaneous barrier dysfunction, immune dysregulation, and microbiota imbalance. Although microbiota-directed therapeutic approaches have garnered increasing attention, current evidence is heterogeneous, encompassing probiotics, postbiotics, microbial metabolites, local microbial interventions, antimicrobials and ecological modulation strategies. This narrative review does not aim to provide clinical guidelines, but rather seeks to synthesise existing evidence within a three-tier conceptual framework. This framework classifies interventions into three categories: those primarily addressing local inflammation and barrier-associated microbiota dysbiosis; those exerting systemic immunomodulation via gut-derived microbial signals; and those modulating the skin microbiota ecology. It should be noted that human clinical data are still limited and heterogeneous, and much mechanistic insight is derived from preclinical research. By clarifying mechanistic layers and evidentiary gaps, this framework may facilitate future research to evaluate the sequencing or combination of anti-inflammatory therapy, barrier restoration, and microbiota ecological modulation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dermatitis, Atopic/therapy/immunology/microbiology
Skin Microbiome
Animals
*Immunomodulation
Inflammation/therapy/immunology
Probiotics/therapeutic use
*Microbiota/immunology
Dysbiosis/immunology/therapy
*Gastrointestinal Microbiome/immunology
Skin/microbiology/immunology
RevDate: 2026-07-30
CmpDate: 2026-07-30
Shotgun metagenomic analysis reveals taxonomic and functional alterations in the gut microbiome across prodromal and symptomatic Lewy body disease.
Frontiers in microbiomes, 5:1834726.
BACKGROUND: Lewy body disease (LBD) is a progressive neurodegenerative a-synucleinopathy, whereas isolated REM sleep behavior disorder (iRBD) is recognized as a prodromal stage of LBD. Although growing evidence implicates the gut-brain axis in neurodegeneration, the taxonomic and functional roles of the gut microbiome across the prodromal-to-symptomatic LBD continuum remain poorly defined.
METHODS: Here, we performed shotgun metagenomic sequencing on stool samples from 25 patients with LBD (10 mild cognitive impairment due to LBD [MCI-LB] and 15 dementia with Lewy bodies [DLB]), 10 individuals with iRBD, and their household matched cohabitant controls to characterize disease-associated microbial alterations while minimizing environmental confounding.
RESULTS: Despite no significant differences in global microbial diversity, we identified convergent shifts in microbial taxa, metabolic pathways, and gene families across disease stages. Both LBD and iRBD showed increased abundance of microbial taxa potentially associated with gut barrier disruption, as well as higher abundance of functional pathways related to lipopolysaccharide biosynthesis. LBD showed lower abundance of pathways related to complex carbohydrate fermentation, and both groups showed lower abundance of pathways associated with neurotransmitter-related metabolism. In particular, pathways and gene families associated with starch degradation were reduced in LBD, and those associated with histidine-to-glutamate/ GABA metabolism were reduced in both groups.
DISCUSSION: These exploratory findings represent the first high-resolution, shotgun metagenomic characterization of gut microbiome alterations across the LBD continuum, highlighting functional patterns that may serve as candidate markers of disease progression in future longitudinal and mechanistic studies.
Additional Links: PMID-42529077
PubMed:
Citation:
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@article {pmid42529077,
year = {2026},
author = {Zhao, X and McCarter, SJ and Gupta, VK and Grant, KM and St Louis, EK and Kantarci, K and Savica, R and Hill, M and Vuong, HE and Staley, C and Boeve, BF and Ross, OA and Teigen, LM and Sung, J},
title = {Shotgun metagenomic analysis reveals taxonomic and functional alterations in the gut microbiome across prodromal and symptomatic Lewy body disease.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1834726},
pmid = {42529077},
issn = {2813-4338},
abstract = {BACKGROUND: Lewy body disease (LBD) is a progressive neurodegenerative a-synucleinopathy, whereas isolated REM sleep behavior disorder (iRBD) is recognized as a prodromal stage of LBD. Although growing evidence implicates the gut-brain axis in neurodegeneration, the taxonomic and functional roles of the gut microbiome across the prodromal-to-symptomatic LBD continuum remain poorly defined.
METHODS: Here, we performed shotgun metagenomic sequencing on stool samples from 25 patients with LBD (10 mild cognitive impairment due to LBD [MCI-LB] and 15 dementia with Lewy bodies [DLB]), 10 individuals with iRBD, and their household matched cohabitant controls to characterize disease-associated microbial alterations while minimizing environmental confounding.
RESULTS: Despite no significant differences in global microbial diversity, we identified convergent shifts in microbial taxa, metabolic pathways, and gene families across disease stages. Both LBD and iRBD showed increased abundance of microbial taxa potentially associated with gut barrier disruption, as well as higher abundance of functional pathways related to lipopolysaccharide biosynthesis. LBD showed lower abundance of pathways related to complex carbohydrate fermentation, and both groups showed lower abundance of pathways associated with neurotransmitter-related metabolism. In particular, pathways and gene families associated with starch degradation were reduced in LBD, and those associated with histidine-to-glutamate/ GABA metabolism were reduced in both groups.
DISCUSSION: These exploratory findings represent the first high-resolution, shotgun metagenomic characterization of gut microbiome alterations across the LBD continuum, highlighting functional patterns that may serve as candidate markers of disease progression in future longitudinal and mechanistic studies.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Dose Titration of Plant-Based Flavonoid Blend Supplementation on Performance, Digestibility, Gut Microbiome, Blood Biomarkers, and Meat Quality of Growing Rabbits.
Food science & nutrition, 14(8):e72156.
Rabbit meat is increasingly valued for its high nutritional quality, driving growing interest in enhancing its production through phytobiotics like plant-based flavonoid blend (PFB). So, this study looked at how a PFB at different doses influences the performance, digestibility, gut microbiota, blood biomarkers, liver health, and meat quality of growing rabbits. Sixty rabbits (body weight 552.63 ± 13.44 g) were assigned at random to five dietary groups, having twelve replicates per group. The rabbits were fed a basal diet as a total mixed ration having 17.02% crude protein and 11.60 MJ metabolizable energy/kg dry matter (DM), supplemented with PFB (g/kg diet) at 0.0 (control), 0.20, 0.40, 0.60, and 0.80. Following a 2 weeks adjustment period, the feeding trial was conducted for 5 weeks. When the trial was over, rabbits were sacrificed to collect digesta, blood, and meat samples for further analysis. Supplementation with PFB at 0.60 g/kg diet (range: 0.50-0.70 g/kg) showed a better final body weight (p = 0.01), weight gain (p < 0.001), and feed conversion ratio (p < 0.001), while significantly improving DM, nitrogen-free extract (p < 0.001), and ether extract (p = 0.02) digestibility. Besides, supplementation with PFB presented a linear reduction in Escherichia coli (p = 0.003), accompanied by linear improvement in Lactobacillus spp. (p < 0.001) and serum high density lipoprotein-cholesterol (HDL-C; p = 0.001). Broken-line analysis indicated optimal PFB supplementation levels of 0.60, 0.47, and 0.60 g/kg diet for E. coli, Lactobacillus spp., and HDL-C, respectively. However, feed intake, serum triglycerides, other cholesterols, total protein, albumin, globulin, and uric acid remained unchanged across the groups. Furthermore, supplementation with PFB with an estimated breakpoint of 0.55 g PFB/kg of diet effectively (p ≤ 0.02) reduced serum liver enzymes (aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase) indicating better liver health. In addition, PFB supplementation linearly reduced meat ether extract content and improved meat redness (p < 0.001), with optimal responses at 0.58 and 0.60 g/kg diet, respectively, while having no impacts on meat protein, ash, lightness, or yellowness. Therefore, dietary inclusion of PFB at 0.55 g-0.60 g per kg diet optimized growth performance through enhanced weight gain, feed efficiency, and nutrient digestibility, while favorably modulating cecum microbiome, serum cholesterol, liver enzyme activities, and ameliorated meat quality.
Additional Links: PMID-42529078
PubMed:
Citation:
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@article {pmid42529078,
year = {2026},
author = {Rahman, MA and Hasan, MM and Hashem, MA and Siddique, MP and Chowdhury, R},
title = {Dose Titration of Plant-Based Flavonoid Blend Supplementation on Performance, Digestibility, Gut Microbiome, Blood Biomarkers, and Meat Quality of Growing Rabbits.},
journal = {Food science & nutrition},
volume = {14},
number = {8},
pages = {e72156},
pmid = {42529078},
issn = {2048-7177},
abstract = {Rabbit meat is increasingly valued for its high nutritional quality, driving growing interest in enhancing its production through phytobiotics like plant-based flavonoid blend (PFB). So, this study looked at how a PFB at different doses influences the performance, digestibility, gut microbiota, blood biomarkers, liver health, and meat quality of growing rabbits. Sixty rabbits (body weight 552.63 ± 13.44 g) were assigned at random to five dietary groups, having twelve replicates per group. The rabbits were fed a basal diet as a total mixed ration having 17.02% crude protein and 11.60 MJ metabolizable energy/kg dry matter (DM), supplemented with PFB (g/kg diet) at 0.0 (control), 0.20, 0.40, 0.60, and 0.80. Following a 2 weeks adjustment period, the feeding trial was conducted for 5 weeks. When the trial was over, rabbits were sacrificed to collect digesta, blood, and meat samples for further analysis. Supplementation with PFB at 0.60 g/kg diet (range: 0.50-0.70 g/kg) showed a better final body weight (p = 0.01), weight gain (p < 0.001), and feed conversion ratio (p < 0.001), while significantly improving DM, nitrogen-free extract (p < 0.001), and ether extract (p = 0.02) digestibility. Besides, supplementation with PFB presented a linear reduction in Escherichia coli (p = 0.003), accompanied by linear improvement in Lactobacillus spp. (p < 0.001) and serum high density lipoprotein-cholesterol (HDL-C; p = 0.001). Broken-line analysis indicated optimal PFB supplementation levels of 0.60, 0.47, and 0.60 g/kg diet for E. coli, Lactobacillus spp., and HDL-C, respectively. However, feed intake, serum triglycerides, other cholesterols, total protein, albumin, globulin, and uric acid remained unchanged across the groups. Furthermore, supplementation with PFB with an estimated breakpoint of 0.55 g PFB/kg of diet effectively (p ≤ 0.02) reduced serum liver enzymes (aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase) indicating better liver health. In addition, PFB supplementation linearly reduced meat ether extract content and improved meat redness (p < 0.001), with optimal responses at 0.58 and 0.60 g/kg diet, respectively, while having no impacts on meat protein, ash, lightness, or yellowness. Therefore, dietary inclusion of PFB at 0.55 g-0.60 g per kg diet optimized growth performance through enhanced weight gain, feed efficiency, and nutrient digestibility, while favorably modulating cecum microbiome, serum cholesterol, liver enzyme activities, and ameliorated meat quality.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Diversity and taxonomic differences in the oral microbiota of stroke patients: a systematic review and meta-analysis.
Frontiers in microbiology, 17:1874193.
BACKGROUND: In recent years, a growing body of evidence suggests that stroke may be associated with an imbalance in the oral microbiome. To further elucidate this potential link, this study aims to systematically compare differences in the oral microbiome between stroke patients and healthy individuals.
OBJECTIVE: To systematically evaluate the differences in oral microbiota diversity and taxonomic composition between stroke patients and healthy controls.
METHOD: From the date each database was established up to 20 February 2026, we conducted searches in CNKI, Wanfang, PubMed, Embase, SinoMed, Web of Science, the Cochrane Library and grey literature databases, with the aim of identifying studies reporting on the oral microbiota of stroke patients and healthy individuals. The Newcastle-Ottawa Scale (NOS) was used to assess the risk of bias in the included studies, and meta-analysis was performed using RevMan 5.4 software. The pooled effect size was calculated as the standardized mean difference (SMD) and a parallel Z-test was conducted; heterogeneity was assessed using Cochran's Q test and the I[2] statistic.
RESULT: This meta-analysis of 11 studies (746 stroke patients, 552 controls) showed upward trends in Observed species (SMD = 0.39, 95% CI: 0.05-0.72, I[2] = 84%) and Shannon (SMD = 0.31, 95% CI: 0.02-0.61, I[2] = 82%) indices, though these findings were not robust in sensitivity analyses. Chao1 and Simpson showed no significant differences. Eight of nine β-diversity studies reported significant differences between groups. Meta-analysis showed higher Bacteroidota (SMD = 0.36, 95% CI: 0.18-0.54, 3 studies; I[2] = 44%). Higher abundances of Firmicutes, Spirochaetes, and several genera were suggested by descriptive synthesis but should be considered exploratory.
CONCLUSION: The oral microbiota of stroke patients exhibits characteristic changes, which may provide preliminary clues for understanding post-stroke oral microbial alterations and offer a theoretical basis for oral care, but require validation in prospective studies.
Unique Identifier: CRD420251235256, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251235256.
Additional Links: PMID-42529147
PubMed:
Citation:
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@article {pmid42529147,
year = {2026},
author = {Chen, Y and Tian, Y and Jin, Y and Wu, X and Li, X and Du, W and Li, W and Li, J},
title = {Diversity and taxonomic differences in the oral microbiota of stroke patients: a systematic review and meta-analysis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1874193},
pmid = {42529147},
issn = {1664-302X},
abstract = {BACKGROUND: In recent years, a growing body of evidence suggests that stroke may be associated with an imbalance in the oral microbiome. To further elucidate this potential link, this study aims to systematically compare differences in the oral microbiome between stroke patients and healthy individuals.
OBJECTIVE: To systematically evaluate the differences in oral microbiota diversity and taxonomic composition between stroke patients and healthy controls.
METHOD: From the date each database was established up to 20 February 2026, we conducted searches in CNKI, Wanfang, PubMed, Embase, SinoMed, Web of Science, the Cochrane Library and grey literature databases, with the aim of identifying studies reporting on the oral microbiota of stroke patients and healthy individuals. The Newcastle-Ottawa Scale (NOS) was used to assess the risk of bias in the included studies, and meta-analysis was performed using RevMan 5.4 software. The pooled effect size was calculated as the standardized mean difference (SMD) and a parallel Z-test was conducted; heterogeneity was assessed using Cochran's Q test and the I[2] statistic.
RESULT: This meta-analysis of 11 studies (746 stroke patients, 552 controls) showed upward trends in Observed species (SMD = 0.39, 95% CI: 0.05-0.72, I[2] = 84%) and Shannon (SMD = 0.31, 95% CI: 0.02-0.61, I[2] = 82%) indices, though these findings were not robust in sensitivity analyses. Chao1 and Simpson showed no significant differences. Eight of nine β-diversity studies reported significant differences between groups. Meta-analysis showed higher Bacteroidota (SMD = 0.36, 95% CI: 0.18-0.54, 3 studies; I[2] = 44%). Higher abundances of Firmicutes, Spirochaetes, and several genera were suggested by descriptive synthesis but should be considered exploratory.
CONCLUSION: The oral microbiota of stroke patients exhibits characteristic changes, which may provide preliminary clues for understanding post-stroke oral microbial alterations and offer a theoretical basis for oral care, but require validation in prospective studies.
Unique Identifier: CRD420251235256, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251235256.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Gut microbiota and intestinal permeability in rheumatoid arthritis: pathogenic mechanisms.
Frontiers in immunology, 17:1887782.
Rheumatoid arthritis is a chronic systemic autoimmune disease in which the earliest breaks in immune tolerance may arise at mucosal surfaces before the clinical onset of synovitis. Among these sites, the gut has emerged as a particularly compelling candidate because it integrates microbial, epithelial, metabolic, and immune pathways with the potential to shape systemic inflammation. In this review, we examine the biological foundations of the gut-joint axis in rheumatoid arthritis, focusing on intestinal barrier structure, microbiome alterations, mucosal immune crosstalk, and mechanisms of barrier dysfunction. Current human evidence links rheumatoid arthritis to heterogeneous shifts in gut microbial composition, depletion of beneficial metabolite-producing commensals, altered immune-metabolic signaling, and biomarker patterns consistent with epithelial injury and microbial-product translocation. At the same time, available data do not support the existence of a single, universal microbial or permeability signature that defines the disease across populations. Recent longitudinal studies further challenge the concept of stable, long-standing dysbiosis and instead suggest a late, transient phase of ecological instability arising close to symptom onset. Experimental models provide stronger mechanistic support, showing that dysbiotic microbial communities, impaired barrier integrity, and strain-specific host-microbe interactions can promote T helper 17-skewed immunity and aggravate arthritis. Collectively, these findings support a context-dependent contribution of the gut to rheumatoid arthritis pathogenesis while underscoring the need for longitudinal, strain-resolved, and multi-omic human studies to clarify causality, refine disease models, and identify clinically meaningful windows for intervention.
Additional Links: PMID-42529164
PubMed:
Citation:
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@article {pmid42529164,
year = {2026},
author = {Bilski, J and Schramm-Luc, AI and Szczepanik, M and Pierzchalski, P and Krawczyk, A and Luc, K},
title = {Gut microbiota and intestinal permeability in rheumatoid arthritis: pathogenic mechanisms.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1887782},
pmid = {42529164},
issn = {1664-3224},
mesh = {Humans ; *Arthritis, Rheumatoid/immunology/microbiology/metabolism ; Intestinal Barrier Function ; *Gastrointestinal Microbiome/immunology ; Animals ; Dysbiosis/immunology ; *Intestinal Mucosa/immunology/microbiology/metabolism ; Permeability ; },
abstract = {Rheumatoid arthritis is a chronic systemic autoimmune disease in which the earliest breaks in immune tolerance may arise at mucosal surfaces before the clinical onset of synovitis. Among these sites, the gut has emerged as a particularly compelling candidate because it integrates microbial, epithelial, metabolic, and immune pathways with the potential to shape systemic inflammation. In this review, we examine the biological foundations of the gut-joint axis in rheumatoid arthritis, focusing on intestinal barrier structure, microbiome alterations, mucosal immune crosstalk, and mechanisms of barrier dysfunction. Current human evidence links rheumatoid arthritis to heterogeneous shifts in gut microbial composition, depletion of beneficial metabolite-producing commensals, altered immune-metabolic signaling, and biomarker patterns consistent with epithelial injury and microbial-product translocation. At the same time, available data do not support the existence of a single, universal microbial or permeability signature that defines the disease across populations. Recent longitudinal studies further challenge the concept of stable, long-standing dysbiosis and instead suggest a late, transient phase of ecological instability arising close to symptom onset. Experimental models provide stronger mechanistic support, showing that dysbiotic microbial communities, impaired barrier integrity, and strain-specific host-microbe interactions can promote T helper 17-skewed immunity and aggravate arthritis. Collectively, these findings support a context-dependent contribution of the gut to rheumatoid arthritis pathogenesis while underscoring the need for longitudinal, strain-resolved, and multi-omic human studies to clarify causality, refine disease models, and identify clinically meaningful windows for intervention.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Arthritis, Rheumatoid/immunology/microbiology/metabolism
Intestinal Barrier Function
*Gastrointestinal Microbiome/immunology
Animals
Dysbiosis/immunology
*Intestinal Mucosa/immunology/microbiology/metabolism
Permeability
RevDate: 2026-07-30
CmpDate: 2026-07-30
Beyond scarring: immune-epithelial crosstalk in wound-induced hair follicle neogenesis.
Frontiers in immunology, 17:1872547.
Wound-induced hair follicle neogenesis (WIHN) represents a remarkable regenerative phenomenon observed in adult mammalian skin (predominantly studied in mice), in which large full-thickness wounds bypass fibrotic scarring to generate fully functional de novo hair follicles. This process reflects the context-dependent reactivation of embryonic morphogenetic programs, driven by a coordinated tripartite immune-microbial-epithelial axis (defined here as the integrated multi-directional signaling network among localized immune cells, epithelial stem cells, and the skin microbiota/fibroblasts). Mechanistically, γδ T cells initiate dermal fibroblast reprogramming through an FGF9-Wnt feed-forward loop, while macrophages promote AKT/β-catenin signaling in Lgr5[+] epithelial stem cells via TNF-α-driven non-canonical pathways. Regulatory T cells (Tregs) further support follicular morphogenesis by delivering Jagged1/Notch signals. In parallel, the skin microbiota acts as a key amplifier of regeneration, modulating the wound microenvironment through the IL-1β/MyD88 signaling axis. Taken together, WIHN illustrates the remarkable functional plasticity of immune signaling, which can be repurposed from host defense to orchestrating tissue regeneration. By elucidating this dynamic murine skin-immune dialogue, this mini-review provides a conceptual framework for speculative precision immunomodulatory therapies and emerging translational approaches-such as laser-assisted tissue remodeling-aimed at treating inflammatory and scarring alopecia, as well as achieving scarless and functionally restorative wound healing.
Additional Links: PMID-42529170
PubMed:
Citation:
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@article {pmid42529170,
year = {2026},
author = {Ma, YM and Shen, W and Xie, XL and Tang, SL and Wu, Y and Zhong, HJ and Yan, Q and Sun, H},
title = {Beyond scarring: immune-epithelial crosstalk in wound-induced hair follicle neogenesis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1872547},
pmid = {42529170},
issn = {1664-3224},
mesh = {Animals ; *Hair Follicle/immunology ; Humans ; *Wound Healing/immunology ; *Cicatrix/immunology ; Signal Transduction ; Regeneration/immunology ; Skin Microbiome ; Skin/immunology ; *Epithelial Cells/immunology/metabolism ; },
abstract = {Wound-induced hair follicle neogenesis (WIHN) represents a remarkable regenerative phenomenon observed in adult mammalian skin (predominantly studied in mice), in which large full-thickness wounds bypass fibrotic scarring to generate fully functional de novo hair follicles. This process reflects the context-dependent reactivation of embryonic morphogenetic programs, driven by a coordinated tripartite immune-microbial-epithelial axis (defined here as the integrated multi-directional signaling network among localized immune cells, epithelial stem cells, and the skin microbiota/fibroblasts). Mechanistically, γδ T cells initiate dermal fibroblast reprogramming through an FGF9-Wnt feed-forward loop, while macrophages promote AKT/β-catenin signaling in Lgr5[+] epithelial stem cells via TNF-α-driven non-canonical pathways. Regulatory T cells (Tregs) further support follicular morphogenesis by delivering Jagged1/Notch signals. In parallel, the skin microbiota acts as a key amplifier of regeneration, modulating the wound microenvironment through the IL-1β/MyD88 signaling axis. Taken together, WIHN illustrates the remarkable functional plasticity of immune signaling, which can be repurposed from host defense to orchestrating tissue regeneration. By elucidating this dynamic murine skin-immune dialogue, this mini-review provides a conceptual framework for speculative precision immunomodulatory therapies and emerging translational approaches-such as laser-assisted tissue remodeling-aimed at treating inflammatory and scarring alopecia, as well as achieving scarless and functionally restorative wound healing.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Hair Follicle/immunology
Humans
*Wound Healing/immunology
*Cicatrix/immunology
Signal Transduction
Regeneration/immunology
Skin Microbiome
Skin/immunology
*Epithelial Cells/immunology/metabolism
RevDate: 2026-07-30
CmpDate: 2026-07-30
Correlation of preoperative gut microbiota and postoperative delirium in patients undergoing minimally invasive direct coronary artery bypass grafting.
Frontiers in microbiology, 17:1854098.
BACKGROUND: Postoperative delirium (POD) is a common complication after cardiac surgery, but the role of preoperative gut microbiota, especially the mycobiome, in POD susceptibility remains unclear. This study investigated the association between preoperative gut bacterome and mycobiome profiles and POD in elderly patients undergoing minimally invasive direct coronary artery bypass grafting (MIDCABG).
METHODS: Preoperative fecal samples from 31 elderly patients scheduled for MIDCABG were analyzed via 16S rRNA and ITS high-throughput sequencing. POD was assessed twice daily using the 3D-CAM scale. Patients were divided into delirium (M, n = 7) and control (C, n = 24) groups. Microbial diversity, composition, and bacteria-fungi correlations were systematically evaluated.
RESULTS: POD incidence was 22.58%. No baseline differences were observed between groups. Group M exhibited significantly lower gut microbiome health index and higher microbial dysbiosis index at both bacterome and mycobiome levels. Alpha/beta diversity did not differ significantly. LEfSe revealed bacterial enrichment of Clostridium and Intestinibacter in Group M, and Bifidobacterium in Group C. Fungally, Aspergillus and Basidiomycota predominated in Group M, while Saccharomyces and Ascomycota were enriched in Group C. candida showed the highest abundance in Group M and was a key node in the fungal co-occurrence network. Correlation analysis revealed positive associations between bacterial genera (Klebsiella, Enterococcus, Roseburia) and fungal taxa (Wickerhamomyces, Pichia, Geotrichum), suggesting ecological interactions potentially linked to POD.
CONCLUSION: Preoperative dysbiosis of gut bacterome and mycobiome is associated with POD in elderly MIDCABG patients. Several bacterial and fungal taxa, including Clostridium, Intestinibacter, Aspergillus, Saccharomyces, and Candida, were identified as candidate microbial biomarkers associated with POD and may contribute to future microbiota-based risk stratification strategies.
Additional Links: PMID-42529203
PubMed:
Citation:
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@article {pmid42529203,
year = {2026},
author = {Hu, R and Fang, Y and Han, P and Han, Y and Wang, J and Liu, H and Shi, Y and Li, Z and Zhang, L},
title = {Correlation of preoperative gut microbiota and postoperative delirium in patients undergoing minimally invasive direct coronary artery bypass grafting.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1854098},
pmid = {42529203},
issn = {1664-302X},
abstract = {BACKGROUND: Postoperative delirium (POD) is a common complication after cardiac surgery, but the role of preoperative gut microbiota, especially the mycobiome, in POD susceptibility remains unclear. This study investigated the association between preoperative gut bacterome and mycobiome profiles and POD in elderly patients undergoing minimally invasive direct coronary artery bypass grafting (MIDCABG).
METHODS: Preoperative fecal samples from 31 elderly patients scheduled for MIDCABG were analyzed via 16S rRNA and ITS high-throughput sequencing. POD was assessed twice daily using the 3D-CAM scale. Patients were divided into delirium (M, n = 7) and control (C, n = 24) groups. Microbial diversity, composition, and bacteria-fungi correlations were systematically evaluated.
RESULTS: POD incidence was 22.58%. No baseline differences were observed between groups. Group M exhibited significantly lower gut microbiome health index and higher microbial dysbiosis index at both bacterome and mycobiome levels. Alpha/beta diversity did not differ significantly. LEfSe revealed bacterial enrichment of Clostridium and Intestinibacter in Group M, and Bifidobacterium in Group C. Fungally, Aspergillus and Basidiomycota predominated in Group M, while Saccharomyces and Ascomycota were enriched in Group C. candida showed the highest abundance in Group M and was a key node in the fungal co-occurrence network. Correlation analysis revealed positive associations between bacterial genera (Klebsiella, Enterococcus, Roseburia) and fungal taxa (Wickerhamomyces, Pichia, Geotrichum), suggesting ecological interactions potentially linked to POD.
CONCLUSION: Preoperative dysbiosis of gut bacterome and mycobiome is associated with POD in elderly MIDCABG patients. Several bacterial and fungal taxa, including Clostridium, Intestinibacter, Aspergillus, Saccharomyces, and Candida, were identified as candidate microbial biomarkers associated with POD and may contribute to future microbiota-based risk stratification strategies.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
The forehead and glabella show pronounced Cutibacterium relative abundance differences between acne and healthy groups: a regional facial 16S rRNA gene sequencing study.
Frontiers in microbiology, 17:1853291.
INTRODUCTION: Acne vulgaris is a prevalent chronic inflammatory skin disease, and Cutibacterium overproliferation is a core pathogenic factor, yet findings remain controversial, partly due to single anatomical area sampling bias.
METHODS: We conducted a crosssectional study with anatomically paired sampling across multiple facial anatomical areas in 85 subjects (30 healthy subjects, 55 acne subjects), analyzing 763 samples from 6 facial anatomical areas for 16S rRNA V4 region sequencing and microbial community analysis.
RESULTS: At the whole-face level, acne subjects had a significantly higher relative abundance of Cutibacterium and Staphylococcus compared with healthy subjects. Critically, Cutibacterium enrichment was highly dependent on facial anatomical areas: only the forehead and glabella showed significant intergroup differences, with the forehead showing a 127% higher median relative abundance (adjusted q = 0.043) and the glabella showing a 53% higher median relative abundance (adjusted q = 0.043), while Staphylococcus enrichment was widespread (present in 5 of 6 areas, except the jaw), and Corynebacterium showed no intergroup differences in any facial area, although LEfSe classified it as a health-associated taxon. Tax4Fun-based functional prediction suggested upregulated antimicrobial resistance and adaptation pathways, and downregulated core metabolic pathways, in acne-associated microbiota.
DISCUSSION: This study demonstrates the facial anatomical area specificity of Cutibacterium enrichment, identifies the forehead and glabella as the areas with pronounced relative abundance differences between acne and healthy groups.
Additional Links: PMID-42529208
PubMed:
Citation:
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@article {pmid42529208,
year = {2026},
author = {Zha, W and Li, K and Qian, Y and Zhao, L and Cheung, S and Huang, J and Miao, F and Shen, J and Yu, Y and Hu, X and Wang, H and Lyu, T and Shi, L},
title = {The forehead and glabella show pronounced Cutibacterium relative abundance differences between acne and healthy groups: a regional facial 16S rRNA gene sequencing study.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1853291},
pmid = {42529208},
issn = {1664-302X},
abstract = {INTRODUCTION: Acne vulgaris is a prevalent chronic inflammatory skin disease, and Cutibacterium overproliferation is a core pathogenic factor, yet findings remain controversial, partly due to single anatomical area sampling bias.
METHODS: We conducted a crosssectional study with anatomically paired sampling across multiple facial anatomical areas in 85 subjects (30 healthy subjects, 55 acne subjects), analyzing 763 samples from 6 facial anatomical areas for 16S rRNA V4 region sequencing and microbial community analysis.
RESULTS: At the whole-face level, acne subjects had a significantly higher relative abundance of Cutibacterium and Staphylococcus compared with healthy subjects. Critically, Cutibacterium enrichment was highly dependent on facial anatomical areas: only the forehead and glabella showed significant intergroup differences, with the forehead showing a 127% higher median relative abundance (adjusted q = 0.043) and the glabella showing a 53% higher median relative abundance (adjusted q = 0.043), while Staphylococcus enrichment was widespread (present in 5 of 6 areas, except the jaw), and Corynebacterium showed no intergroup differences in any facial area, although LEfSe classified it as a health-associated taxon. Tax4Fun-based functional prediction suggested upregulated antimicrobial resistance and adaptation pathways, and downregulated core metabolic pathways, in acne-associated microbiota.
DISCUSSION: This study demonstrates the facial anatomical area specificity of Cutibacterium enrichment, identifies the forehead and glabella as the areas with pronounced relative abundance differences between acne and healthy groups.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Rethinking the hepatoprotective potential of vegetarian diets in dysfunction-associated steatotic liver disease/metabolic-associated fatty liver disease: a critical narrative review.
Frontiers in nutrition, 13:1902349.
Dietary intervention is central to the management of metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as metabolic-associated fatty liver disease (MAFLD). Although vegetarian dietary patterns are widely considered hepatoprotective, emerging evidence indicates that certain individuals following non-standardized vegetarian diets may fail to obtain the expected hepatic benefits-a phenomenon termed the "vegetarian hepatoprotection paradox." This critical narrative examines the putative mechanisms underlying this paradox. Excessive intake of high-glycemic carbohydrates and fructose, which is common in some vegetarian diets, may activate hepatic de novo lipogenesis. Furthermore, incomplete plant proteins may contribute to impaired very low-density lipoprotein (VLDL)-mediated lipid export, while an imbalanced n-6:n-3 fatty acid ratio may promote hepatic inflammation. These dietary factors may interact with genetic susceptibility, including patatin-like phospholipase domain-containing protein 3 (PNPLA3) I148M and transmembrane 6 superfamily member 2 (TM6SF2) E167K variants, disrupting hepatic lipid homeostasis. Additionally, gut dysbiosis may propagate metabolic disturbance through chronic inflammation. Accordingly, a shift from the categorical vegetarian labeling toward an emphasis on plant-based dietary quality-reflecting the principle that dietary quality matters more than the vegetarian label itself-may be warranted. This review discusses evidence-based dietary patterns, including the Mediterranean diet, the Green Mediterranean diet, and the Dietary Approaches to Stop Hypertension (DASH) diet, together with chrononutrition strategies. A precision nutrition approach integrating genetic, metabolic, and microbiome characteristics may represent an emerging but still investigational framework for individualized MASLD/MAFLD interventions.
Additional Links: PMID-42529254
PubMed:
Citation:
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@article {pmid42529254,
year = {2026},
author = {Jiang, W and Yang, Z and Cui, Y and Huang, N and Dong, L and Sun, T and Zhang, B},
title = {Rethinking the hepatoprotective potential of vegetarian diets in dysfunction-associated steatotic liver disease/metabolic-associated fatty liver disease: a critical narrative review.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1902349},
pmid = {42529254},
issn = {2296-861X},
abstract = {Dietary intervention is central to the management of metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as metabolic-associated fatty liver disease (MAFLD). Although vegetarian dietary patterns are widely considered hepatoprotective, emerging evidence indicates that certain individuals following non-standardized vegetarian diets may fail to obtain the expected hepatic benefits-a phenomenon termed the "vegetarian hepatoprotection paradox." This critical narrative examines the putative mechanisms underlying this paradox. Excessive intake of high-glycemic carbohydrates and fructose, which is common in some vegetarian diets, may activate hepatic de novo lipogenesis. Furthermore, incomplete plant proteins may contribute to impaired very low-density lipoprotein (VLDL)-mediated lipid export, while an imbalanced n-6:n-3 fatty acid ratio may promote hepatic inflammation. These dietary factors may interact with genetic susceptibility, including patatin-like phospholipase domain-containing protein 3 (PNPLA3) I148M and transmembrane 6 superfamily member 2 (TM6SF2) E167K variants, disrupting hepatic lipid homeostasis. Additionally, gut dysbiosis may propagate metabolic disturbance through chronic inflammation. Accordingly, a shift from the categorical vegetarian labeling toward an emphasis on plant-based dietary quality-reflecting the principle that dietary quality matters more than the vegetarian label itself-may be warranted. This review discusses evidence-based dietary patterns, including the Mediterranean diet, the Green Mediterranean diet, and the Dietary Approaches to Stop Hypertension (DASH) diet, together with chrononutrition strategies. A precision nutrition approach integrating genetic, metabolic, and microbiome characteristics may represent an emerging but still investigational framework for individualized MASLD/MAFLD interventions.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Dominant Role of Habitat Transformation in Driving the Divergence of Health-Risk Related Microbial Functional Genes in Karst Mountain Parks: A Metagenomic Study.
Ecology and evolution, 16(8):e74112.
The transformation of natural forests into urban parks has had a profound impact on subterranean ecosystems. Nevertheless, the underlying mechanisms by which this land use change affects human health through alterations in soil microbial functional genes remain to be elucidated. Focusing on a karst mountain park in Guiyang, China, we used metagenomic sequencing to compare the abundance and composition of antibiotic resistance genes (ARGs), pathogen-host interaction genes (PHIs), and virulence factor genes (VFs) between remnant forests and artificial green spaces, and examined how plant diversity and soil chemometrics drove their variation. Habitat type emerged as the strongest driver of gene composition. PHIs and VFs were more abundant in remnant forests and positively correlated with native plant diversity, while ARGs were enriched in artificial green spaces. All three gene categories showed positive correlations with soil nitrogen content in artificial green spaces. Remnant forests harbored microbial functions linked to complex plant-microbe interactions, whereas intensive management in artificial green spaces selects for antibiotic resistance and nutrient-adaptive genes. These findings reveal distinct health risks across habitats, suggesting that differentiated park management strategies are needed to mitigate public health risks while maintaining ecological sustainability.
Additional Links: PMID-42529303
PubMed:
Citation:
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@article {pmid42529303,
year = {2026},
author = {Wang, W and Cen, C and Yang, J},
title = {Dominant Role of Habitat Transformation in Driving the Divergence of Health-Risk Related Microbial Functional Genes in Karst Mountain Parks: A Metagenomic Study.},
journal = {Ecology and evolution},
volume = {16},
number = {8},
pages = {e74112},
pmid = {42529303},
issn = {2045-7758},
abstract = {The transformation of natural forests into urban parks has had a profound impact on subterranean ecosystems. Nevertheless, the underlying mechanisms by which this land use change affects human health through alterations in soil microbial functional genes remain to be elucidated. Focusing on a karst mountain park in Guiyang, China, we used metagenomic sequencing to compare the abundance and composition of antibiotic resistance genes (ARGs), pathogen-host interaction genes (PHIs), and virulence factor genes (VFs) between remnant forests and artificial green spaces, and examined how plant diversity and soil chemometrics drove their variation. Habitat type emerged as the strongest driver of gene composition. PHIs and VFs were more abundant in remnant forests and positively correlated with native plant diversity, while ARGs were enriched in artificial green spaces. All three gene categories showed positive correlations with soil nitrogen content in artificial green spaces. Remnant forests harbored microbial functions linked to complex plant-microbe interactions, whereas intensive management in artificial green spaces selects for antibiotic resistance and nutrient-adaptive genes. These findings reveal distinct health risks across habitats, suggesting that differentiated park management strategies are needed to mitigate public health risks while maintaining ecological sustainability.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Integrated microbiomic and proteomic profiling reveals distinct ocular surface molecular and microbial landscapes in dry eye after SMILE surgery.
Frontiers in cellular and infection microbiology, 16:1858069.
OBJECTIVES: The aim of this study is to investigate the microbial and proteomic features of the ocular surface following small incision lenticule extraction (SMILE) surgery and to elucidate their association with the development of postoperative dry eye disease (DED).
METHODS: This study comprised a prospective cohort for baseline assessment and a cross-sectional postoperative assessment. We enrolled two sets of participants: a preoperative cohort (PG) consisting of patients scheduled for SMILE; and a postoperative cohort,consisting of patients who had undergone SMILE. The postoperative cohort was further categorized into non-dry eye group (NDEG) and dry eye group (DEG) groups based on examination. Conjunctival swabs and tear samples were collected for 16S rRNA gene sequencing (V3-V4 region) and label-free quantitative proteomics, respectively.
RESULTS: A total of 52 subjects were included. Microbiome analysis revealed significantly lower α-diversity (Chao1, Shannon) in the DEG than in the PG and/or NDEG (p < 0.05). β-diversity analysis showed significant structural differences between the DEG and both the PG and NDEG. Staphylococcus and Corynebacterium were enriched in the DEG, while commensals such as Clostridia and Bacteroidota showed higher relative abundances in the NDEG. DEG exhibited specific activation of stress pathways (NF-κB signaling, macroautophagy) and a bidirectional dysregulation of the coagulation-complement system, a pattern suggestive of a potential "thromboinflammation"-like state. Weighted gene co-expression network analysis delineated three axes: an overactive "Metabolism-Stress Axis", and impaired "Homeostatic Regulation Axis" and "Orderly Repair Axis" in the DEG.
CONCLUSIONS: In this cross-sectional analysis, the presence of DED after SMILE is associated with a distinct shift in the ocular surface microbiome towards a pro-inflammatory state and a concomitant breakdown of host proteomic homeostasis. The observed correlation between microbial dysbiosis and dysregulation of host pathways, particularly the coagulation-complement system, suggests a potential integrated mechanism for postoperative dry eye. These findings identify candidate biomarkers for risk prediction and new therapeutic targets.
Additional Links: PMID-42529330
PubMed:
Citation:
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@article {pmid42529330,
year = {2026},
author = {Zhang, L and Chen, P and Han, P and Fu, H and Sun, B},
title = {Integrated microbiomic and proteomic profiling reveals distinct ocular surface molecular and microbial landscapes in dry eye after SMILE surgery.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1858069},
pmid = {42529330},
issn = {2235-2988},
mesh = {Humans ; *Dry Eye Syndromes/microbiology/etiology/metabolism ; *Proteomics ; *Microbiota ; Female ; Tears/microbiology/chemistry ; Cross-Sectional Studies ; Male ; RNA, Ribosomal, 16S/genetics ; Prospective Studies ; Adult ; *Bacteria/classification/genetics/isolation & purification ; Conjunctiva/microbiology ; *Proteome/analysis ; Middle Aged ; Multiomics ; *Postoperative Complications/microbiology ; },
abstract = {OBJECTIVES: The aim of this study is to investigate the microbial and proteomic features of the ocular surface following small incision lenticule extraction (SMILE) surgery and to elucidate their association with the development of postoperative dry eye disease (DED).
METHODS: This study comprised a prospective cohort for baseline assessment and a cross-sectional postoperative assessment. We enrolled two sets of participants: a preoperative cohort (PG) consisting of patients scheduled for SMILE; and a postoperative cohort,consisting of patients who had undergone SMILE. The postoperative cohort was further categorized into non-dry eye group (NDEG) and dry eye group (DEG) groups based on examination. Conjunctival swabs and tear samples were collected for 16S rRNA gene sequencing (V3-V4 region) and label-free quantitative proteomics, respectively.
RESULTS: A total of 52 subjects were included. Microbiome analysis revealed significantly lower α-diversity (Chao1, Shannon) in the DEG than in the PG and/or NDEG (p < 0.05). β-diversity analysis showed significant structural differences between the DEG and both the PG and NDEG. Staphylococcus and Corynebacterium were enriched in the DEG, while commensals such as Clostridia and Bacteroidota showed higher relative abundances in the NDEG. DEG exhibited specific activation of stress pathways (NF-κB signaling, macroautophagy) and a bidirectional dysregulation of the coagulation-complement system, a pattern suggestive of a potential "thromboinflammation"-like state. Weighted gene co-expression network analysis delineated three axes: an overactive "Metabolism-Stress Axis", and impaired "Homeostatic Regulation Axis" and "Orderly Repair Axis" in the DEG.
CONCLUSIONS: In this cross-sectional analysis, the presence of DED after SMILE is associated with a distinct shift in the ocular surface microbiome towards a pro-inflammatory state and a concomitant breakdown of host proteomic homeostasis. The observed correlation between microbial dysbiosis and dysregulation of host pathways, particularly the coagulation-complement system, suggests a potential integrated mechanism for postoperative dry eye. These findings identify candidate biomarkers for risk prediction and new therapeutic targets.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Dry Eye Syndromes/microbiology/etiology/metabolism
*Proteomics
*Microbiota
Female
Tears/microbiology/chemistry
Cross-Sectional Studies
Male
RNA, Ribosomal, 16S/genetics
Prospective Studies
Adult
*Bacteria/classification/genetics/isolation & purification
Conjunctiva/microbiology
*Proteome/analysis
Middle Aged
Multiomics
*Postoperative Complications/microbiology
RevDate: 2026-07-30
CmpDate: 2026-07-30
Comprehensive Assessment of the Health and Nutritional Status of Active-Duty United States Army Soldiers: The Military Health and Nutrition Examination Study Protocol.
Current developments in nutrition, 10(8):109420.
BACKGROUND: The Military Health and Nutrition Examination Study (MHANES) is modeled after the National Health and Nutrition Examination Survey (NHANES). NHANES does not enroll active-duty Service Members, who are exposed to unique and adverse occupational challenges compared with civilians. Therefore, NHANES data are not generalizable to Service Members.
OBJECTIVES: The objective of MHANES is to fill this gap by assessing dietary intake, cardiometabolic health, body composition, biomarkers of nutritional status and health, mental well-being, injury prevalence, genetics, gut microbiome composition, and physical performance in a representative sample of Army Soldiers.
METHODS: MHANES recruited Soldiers (n = 648) from Army installations across the United States. Participants attended an in-person visit to complete a 24-h dietary recall and questionnaires regarding demographics, physical and mental health, physical activity and performance, and dietary supplement and medication use. Height, weight, blood pressure, resting heart rate variability, physical activity, sleep, resting metabolic rate, hemoglobin mass, and blood volume were measured. Body composition was assessed using bioelectrical impedance, 3-dimensional body imaging, dual-energy X-ray absorptiometry, and circumference measurements. Blood and urine samples were collected to measure biomarkers of nutritional status, health, and genetics. Stool samples were collected to assess microbial diversity and composition. A second 24-h dietary recall was administered 3 to 10 d after the in-person visit.
CONCLUSIONS: Data collected will be used to determine disease risk and prevalence and to investigate relationships between dietary intake, nutritional status, and markers of health and disease in Army Soldiers. Findings will guide evidence-based screening, education, intervention strategies, and policy decisions to improve Army health. Although the current study is focused exclusively on United States Army Soldiers, a long-term goal is to expand this research to other service branches and include additional sampling cycles similar to NHANES.This trial was registered at clinicaltrials.gov as NCT06380322.
Additional Links: PMID-42529388
PubMed:
Citation:
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@article {pmid42529388,
year = {2026},
author = {Berryman, CE and Bukhari, AS and Rood, JC and Hughes, DA and Lowe, AC and Niclou, AM and Beckner, ME and Weschenfelder, C and Riley, TM and Barney, DE and Dugan, C and Bukhari, SB and Bukhari, FH and Smith, MP and Turner, BS and Sanford, CM and Karl, JP and McClung, JP and Smith, TJ and Owens, BA and Beyl, RA and Heymsfield, SB and Greenway, FL and Hennigar, SR and Lieberman, HR},
title = {Comprehensive Assessment of the Health and Nutritional Status of Active-Duty United States Army Soldiers: The Military Health and Nutrition Examination Study Protocol.},
journal = {Current developments in nutrition},
volume = {10},
number = {8},
pages = {109420},
pmid = {42529388},
issn = {2475-2991},
abstract = {BACKGROUND: The Military Health and Nutrition Examination Study (MHANES) is modeled after the National Health and Nutrition Examination Survey (NHANES). NHANES does not enroll active-duty Service Members, who are exposed to unique and adverse occupational challenges compared with civilians. Therefore, NHANES data are not generalizable to Service Members.
OBJECTIVES: The objective of MHANES is to fill this gap by assessing dietary intake, cardiometabolic health, body composition, biomarkers of nutritional status and health, mental well-being, injury prevalence, genetics, gut microbiome composition, and physical performance in a representative sample of Army Soldiers.
METHODS: MHANES recruited Soldiers (n = 648) from Army installations across the United States. Participants attended an in-person visit to complete a 24-h dietary recall and questionnaires regarding demographics, physical and mental health, physical activity and performance, and dietary supplement and medication use. Height, weight, blood pressure, resting heart rate variability, physical activity, sleep, resting metabolic rate, hemoglobin mass, and blood volume were measured. Body composition was assessed using bioelectrical impedance, 3-dimensional body imaging, dual-energy X-ray absorptiometry, and circumference measurements. Blood and urine samples were collected to measure biomarkers of nutritional status, health, and genetics. Stool samples were collected to assess microbial diversity and composition. A second 24-h dietary recall was administered 3 to 10 d after the in-person visit.
CONCLUSIONS: Data collected will be used to determine disease risk and prevalence and to investigate relationships between dietary intake, nutritional status, and markers of health and disease in Army Soldiers. Findings will guide evidence-based screening, education, intervention strategies, and policy decisions to improve Army health. Although the current study is focused exclusively on United States Army Soldiers, a long-term goal is to expand this research to other service branches and include additional sampling cycles similar to NHANES.This trial was registered at clinicaltrials.gov as NCT06380322.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Spatial organization of cutaneous microbiomes reveals putative microbial contributions to host chemical defenses in the American toad.
Frontiers in microbiology, 17:1860796.
Chemical defenses are widely evolved throughout the tree of life. Animals can exploit mutualisms with toxin-producing symbionts as a mechanism of chemical defense. However, this has only begun to be explored in depth, and how these mutualisms may relate to how animals synthesize or acquire their toxins has been even less studied. True toads synthesize their own toxins and offer a novel system to study the interplay between the cutaneous skin microbiome and how it may contribute to toxin synthesis or biotransformation. In this study, we investigated whether the cutaneous microbiome of the American toad (Anaxyrus americanus) was spatially structured across body surfaces in relation to toxin storage and secretion and assessed whether microbial communities exhibit distinctive bacterial taxa involved in toxin-related biochemical pathways. To do this, we used 16S rRNA gene sequencing, diversity metrics, differential abundance comparisons, functional pathway predictions, and ecological interaction networks. Our results indicate that the dorsal and ventral cutaneous surfaces harbor distinct bacterial assemblages, with the dorsal surface being enriched for bacterial taxa associated with the predicted potential to degrade or transform structurally complex organic compounds. This study provides insights into how the toad skin microbiome may contribute to the chemical defenses of toads and could reveal novel aspects of host-microbiome interactions in amphibians.
Additional Links: PMID-42529424
PubMed:
Citation:
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@article {pmid42529424,
year = {2026},
author = {McCammon, SD and Chen See, JR and Wright, JR and Anderson, SLC and Russell, TJ and Lamendella, RM and Firneno, TJ},
title = {Spatial organization of cutaneous microbiomes reveals putative microbial contributions to host chemical defenses in the American toad.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1860796},
pmid = {42529424},
issn = {1664-302X},
abstract = {Chemical defenses are widely evolved throughout the tree of life. Animals can exploit mutualisms with toxin-producing symbionts as a mechanism of chemical defense. However, this has only begun to be explored in depth, and how these mutualisms may relate to how animals synthesize or acquire their toxins has been even less studied. True toads synthesize their own toxins and offer a novel system to study the interplay between the cutaneous skin microbiome and how it may contribute to toxin synthesis or biotransformation. In this study, we investigated whether the cutaneous microbiome of the American toad (Anaxyrus americanus) was spatially structured across body surfaces in relation to toxin storage and secretion and assessed whether microbial communities exhibit distinctive bacterial taxa involved in toxin-related biochemical pathways. To do this, we used 16S rRNA gene sequencing, diversity metrics, differential abundance comparisons, functional pathway predictions, and ecological interaction networks. Our results indicate that the dorsal and ventral cutaneous surfaces harbor distinct bacterial assemblages, with the dorsal surface being enriched for bacterial taxa associated with the predicted potential to degrade or transform structurally complex organic compounds. This study provides insights into how the toad skin microbiome may contribute to the chemical defenses of toads and could reveal novel aspects of host-microbiome interactions in amphibians.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Gut bacterial O-demethylation in microbiome-dependent drug response.
Gut microbes reports, 3(1):2709263.
The gut microbiota is recognized as an important contributor to drug metabolism and therapeutic variability. By directly transforming orally administered drugs, gut microbes can influence drug exposure, efficacy, and toxicity. Among these microbial reactions, O-demethylation of methoxy-containing drugs remains relatively underexplored, despite the prevalence of this structural motif in many therapeutic agents. Recent studies suggest that gut bacterial O-demethylation can alter parent-drug exposure and generate metabolites with distinct biological activities, with potential consequences for therapeutic efficacy and toxicity across clinical settings. In this mini-review, we discuss gut bacterial O-demethylation as a distinct mechanism in microbiome-dependent pharmacology, with emphasis on its chemical logic, microbial basis, pharmacokinetic and toxicologic consequences, and translational potential for microbiome-targeted interventions and biomarker development.
Additional Links: PMID-42529721
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@article {pmid42529721,
year = {2026},
author = {Chiang, CK and Dibello, BS and Park, J and Rondinella, J and Wu, Q},
title = {Gut bacterial O-demethylation in microbiome-dependent drug response.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2709263},
pmid = {42529721},
issn = {2993-3935},
abstract = {The gut microbiota is recognized as an important contributor to drug metabolism and therapeutic variability. By directly transforming orally administered drugs, gut microbes can influence drug exposure, efficacy, and toxicity. Among these microbial reactions, O-demethylation of methoxy-containing drugs remains relatively underexplored, despite the prevalence of this structural motif in many therapeutic agents. Recent studies suggest that gut bacterial O-demethylation can alter parent-drug exposure and generate metabolites with distinct biological activities, with potential consequences for therapeutic efficacy and toxicity across clinical settings. In this mini-review, we discuss gut bacterial O-demethylation as a distinct mechanism in microbiome-dependent pharmacology, with emphasis on its chemical logic, microbial basis, pharmacokinetic and toxicologic consequences, and translational potential for microbiome-targeted interventions and biomarker development.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
The maternal microbiome-epigenome axis in gestational diabetes: pathogenesis, diagnosis, and emerging therapies.
Journal of developmental origins of health and disease, 17:e35 pii:S2040174426100695.
Gestational diabetes mellitus (GDM) is a common pregnancy complication with profound short- and long-term consequences for both mother and offspring. Beyond transient hyperglycemia, GDM represents a multifactorial metabolic condition shaped by the interplay of genetic predisposition, epigenetic regulation, and alterations in the maternal microbiome. Dysbiosis of the gut and reproductive tract microbiota contributes to inflammation, insulin resistance, and dyslipidemia during pregnancy, while microbial metabolites influence placental physiology and epigenetic remodeling of key metabolic and imprinted genes. These modifications, including changes in DNA methylation and non-coding RNA expression, link maternal hyperglycemia and microbial shifts to persistent alterations in gene expression that affect trophoblast activity, fetal growth trajectories, and long-term metabolic risk in offspring. Vertical transmission of maternal microbiota further imprints the neonatal microbiome, establishing an early-life foundation for reproductive and metabolic health. Although current diagnostic criteria and biomarkers remain inconsistent across populations, recent advances highlight the microbiome-epigenome axis as a promising source of predictive markers and therapeutic targets. Interventions such as probiotics, prebiotics, synbiotics, and dietary modulation show potential for improving maternal glycemic control, shaping placental function, and modulating fetal programming, although evidence for long-term efficacy is still emerging. Viewing GDM as both a metabolic stress test and a window of reproductive opportunity underscores the importance of early diagnosis and precision strategies. Integrating microbiome research and epigenetic insights into clinical practice offers new avenues to improve maternal outcomes, optimize fetal development, and reduce the intergenerational transmission of reproductive and metabolic disease risk.
Additional Links: PMID-42529871
Publisher:
PubMed:
Citation:
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@article {pmid42529871,
year = {2026},
author = {Rizvi, AA and Abbas, M and Ansari, AI and Verma, S and Sinha, A and Mahdi, F},
title = {The maternal microbiome-epigenome axis in gestational diabetes: pathogenesis, diagnosis, and emerging therapies.},
journal = {Journal of developmental origins of health and disease},
volume = {17},
number = {},
pages = {e35},
doi = {10.1017/S2040174426100695},
pmid = {42529871},
issn = {2040-1752},
mesh = {Humans ; Pregnancy ; Female ; *Diabetes, Gestational/therapy/diagnosis/microbiology/genetics ; *Microbiota/physiology ; *Epigenesis, Genetic ; *Epigenome ; Developmental Origins of Health and Disease ; Fetal Development ; *Gastrointestinal Microbiome/physiology ; Dysbiosis ; },
abstract = {Gestational diabetes mellitus (GDM) is a common pregnancy complication with profound short- and long-term consequences for both mother and offspring. Beyond transient hyperglycemia, GDM represents a multifactorial metabolic condition shaped by the interplay of genetic predisposition, epigenetic regulation, and alterations in the maternal microbiome. Dysbiosis of the gut and reproductive tract microbiota contributes to inflammation, insulin resistance, and dyslipidemia during pregnancy, while microbial metabolites influence placental physiology and epigenetic remodeling of key metabolic and imprinted genes. These modifications, including changes in DNA methylation and non-coding RNA expression, link maternal hyperglycemia and microbial shifts to persistent alterations in gene expression that affect trophoblast activity, fetal growth trajectories, and long-term metabolic risk in offspring. Vertical transmission of maternal microbiota further imprints the neonatal microbiome, establishing an early-life foundation for reproductive and metabolic health. Although current diagnostic criteria and biomarkers remain inconsistent across populations, recent advances highlight the microbiome-epigenome axis as a promising source of predictive markers and therapeutic targets. Interventions such as probiotics, prebiotics, synbiotics, and dietary modulation show potential for improving maternal glycemic control, shaping placental function, and modulating fetal programming, although evidence for long-term efficacy is still emerging. Viewing GDM as both a metabolic stress test and a window of reproductive opportunity underscores the importance of early diagnosis and precision strategies. Integrating microbiome research and epigenetic insights into clinical practice offers new avenues to improve maternal outcomes, optimize fetal development, and reduce the intergenerational transmission of reproductive and metabolic disease risk.},
}
MeSH Terms:
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Humans
Pregnancy
Female
*Diabetes, Gestational/therapy/diagnosis/microbiology/genetics
*Microbiota/physiology
*Epigenesis, Genetic
*Epigenome
Developmental Origins of Health and Disease
Fetal Development
*Gastrointestinal Microbiome/physiology
Dysbiosis
RevDate: 2026-07-30
Functional roles and nutritional potential of human milk oligosaccharides in swine gut health.
The British journal of nutrition pii:S0007114526107776 [Epub ahead of print].
Human milk oligosaccharides (HMOs) are a prominent class of bioactive glycans recognized for their pivotal roles as prebiotics, anti-adhesive antimicrobials, and immunomodulators in neonatal development. While traditionally studied in the context of infant nutrition, scalable biotechnological production now allows for their evaluation in swine production to address the relatively lower structural complexity of the porcine milk glycome compared to humans. This review critically evaluates the structural diversity and biosynthesis of HMOs, detailing how specific fucosylated and sialylated structures modulate the porcine gut microbiome and reinforce intestinal barrier integrity. We synthesize current evidence regarding the metabolic fate of these glycans in the piglet and address the translational relevance of using swine as high-fidelity models for human gastrointestinal physiology. Furthermore, the review identifies critical knowledge gaps, specifically the lack of large-scale longitudinal studies and comprehensive cost-benefit analyses required to validate the economic feasibility of HMOs in commercial agriculture. By consolidating these mechanistic insights within the context of global efforts to reduce reliance on antibiotic growth promoters, this work underscores the potential of HMOs as precision nutritional tools to enhance resilience and productivity in sustainable animal production systems.
Additional Links: PMID-42529941
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PubMed:
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@article {pmid42529941,
year = {2026},
author = {El Bouhi, R and Hu, Q and Zhong, J and Zhou, P and Zhang, Y and Liu, L and Yan, H},
title = {Functional roles and nutritional potential of human milk oligosaccharides in swine gut health.},
journal = {The British journal of nutrition},
volume = {},
number = {},
pages = {1-44},
doi = {10.1017/S0007114526107776},
pmid = {42529941},
issn = {1475-2662},
abstract = {Human milk oligosaccharides (HMOs) are a prominent class of bioactive glycans recognized for their pivotal roles as prebiotics, anti-adhesive antimicrobials, and immunomodulators in neonatal development. While traditionally studied in the context of infant nutrition, scalable biotechnological production now allows for their evaluation in swine production to address the relatively lower structural complexity of the porcine milk glycome compared to humans. This review critically evaluates the structural diversity and biosynthesis of HMOs, detailing how specific fucosylated and sialylated structures modulate the porcine gut microbiome and reinforce intestinal barrier integrity. We synthesize current evidence regarding the metabolic fate of these glycans in the piglet and address the translational relevance of using swine as high-fidelity models for human gastrointestinal physiology. Furthermore, the review identifies critical knowledge gaps, specifically the lack of large-scale longitudinal studies and comprehensive cost-benefit analyses required to validate the economic feasibility of HMOs in commercial agriculture. By consolidating these mechanistic insights within the context of global efforts to reduce reliance on antibiotic growth promoters, this work underscores the potential of HMOs as precision nutritional tools to enhance resilience and productivity in sustainable animal production systems.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Remembering stress, shaping resilience: plant adaptation across scales.
Essays in biochemistry, 70(1):1-3.
Plants face unprecedented environmental challenges arising from climate change, including increasing temperatures, altered nutrient availability, shifting seasonal patterns, and intensified biotic pressures. The present editorial introduces the special issue Plant Adaptation to Changing Environments, which brings together reviews examining plant adaptation from molecular to ecosystem levels. Collectively, these articles highlight how resilience emerges through the integration of signalling networks, metabolic regulation, developmental plasticity, ecological interactions, and environmental history. Together, they emphasise the need for interdisciplinary approaches to understand, predict, and enhance plant resilience in a rapidly changing world.
Additional Links: PMID-42530007
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PubMed:
Citation:
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@article {pmid42530007,
year = {2026},
author = {Luna, E},
title = {Remembering stress, shaping resilience: plant adaptation across scales.},
journal = {Essays in biochemistry},
volume = {70},
number = {1},
pages = {1-3},
doi = {10.1042/EBC20260069},
pmid = {42530007},
issn = {1744-1358},
support = {NE/V021346/1//UK Research and Innovation (UKRI)/ ; },
mesh = {*Stress, Physiological ; *Adaptation, Physiological ; *Plant Physiological Phenomena ; Climate Change ; *Plants/metabolism ; Ecosystem ; },
abstract = {Plants face unprecedented environmental challenges arising from climate change, including increasing temperatures, altered nutrient availability, shifting seasonal patterns, and intensified biotic pressures. The present editorial introduces the special issue Plant Adaptation to Changing Environments, which brings together reviews examining plant adaptation from molecular to ecosystem levels. Collectively, these articles highlight how resilience emerges through the integration of signalling networks, metabolic regulation, developmental plasticity, ecological interactions, and environmental history. Together, they emphasise the need for interdisciplinary approaches to understand, predict, and enhance plant resilience in a rapidly changing world.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Stress, Physiological
*Adaptation, Physiological
*Plant Physiological Phenomena
Climate Change
*Plants/metabolism
Ecosystem
RevDate: 2026-07-30
It takes a village: how plant-associated bacterial communities socialise to shape plant growth and health.
Essays in biochemistry pii:237875 [Epub ahead of print].
Plants outsource many functions to an associated microbiome, an 'outside gut' composed of socially interacting bacterial communities that support plant growth and health. These dynamic and diverse microbiomes span different plant microenvironments and form complex networks shaped by the environmental context and the plant's genetics. While some microbes cause disease, many others contribute to essential functions, influencing plant fitness, survival, and ultimately soil health. Although the host genetics and abiotic factors structure these communities, the functional diversity and ecological roles of plant-associated bacteria are ultimately shaped by microbe-microbe interactions. These interactions also play a critical role in the successful colonisation of plant tissues. Beneficial members of these communities enhance plant nutrient uptake, modulate phytohormones to shape root architecture, or prime plant systemic immunity to repel pathogens. Deciphering how plant-associated bacterial communities assemble and interact, both with their host and with one another, is essential for uncovering the mechanisms that underpin bacterial social behaviours within the plant holobiont, such as quorum sensing, metabolite exchange, and contact-dependent interactions. Here we review several recent publications that shed new light on the social lives of plant-associated bacteria, with a particular focus on their competition mechanisms and strategies for colonisation and establishment. In this context, we highlight how the rational design of plant bioinoculants based on microbial consortia represents a powerful strategy for promoting sustainable agriculture in a rapidly changing environment.
Additional Links: PMID-42530018
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PubMed:
Citation:
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@article {pmid42530018,
year = {2026},
author = {Escudero-Martínez, C and Tkacz, A and Albareda, M and Sánchez-Cañizares, C},
title = {It takes a village: how plant-associated bacterial communities socialise to shape plant growth and health.},
journal = {Essays in biochemistry},
volume = {},
number = {},
pages = {},
doi = {10.1042/EBC20250038},
pmid = {42530018},
issn = {1744-1358},
support = {PID2024-162207NA-I00//Ministerio de Ciencia, Innovación y Universidades (MCIU)/ ; OTR15203//Programa de Atraccion de Talento de la Fundacion Salamanca Ciudad de Cultura y Saberes y Ayuntamiento de Salamanca/ ; Alianzas 25CLEX-A-01//CLU-2025-2-02 "Unit of Excellence IRNASA-CSIC", from the regional Government of Junta Castilla y Leon/ ; UID/04326/2025, UID/PRR/04326/2025 and LA/P/0101/2020//MEC | Fundação para a Ciência e a Tecnologia (FCT)/ ; PID2021-1059124344OB-I00//Ministerio de Ciencia e Innovación (MCIN)/ ; },
abstract = {Plants outsource many functions to an associated microbiome, an 'outside gut' composed of socially interacting bacterial communities that support plant growth and health. These dynamic and diverse microbiomes span different plant microenvironments and form complex networks shaped by the environmental context and the plant's genetics. While some microbes cause disease, many others contribute to essential functions, influencing plant fitness, survival, and ultimately soil health. Although the host genetics and abiotic factors structure these communities, the functional diversity and ecological roles of plant-associated bacteria are ultimately shaped by microbe-microbe interactions. These interactions also play a critical role in the successful colonisation of plant tissues. Beneficial members of these communities enhance plant nutrient uptake, modulate phytohormones to shape root architecture, or prime plant systemic immunity to repel pathogens. Deciphering how plant-associated bacterial communities assemble and interact, both with their host and with one another, is essential for uncovering the mechanisms that underpin bacterial social behaviours within the plant holobiont, such as quorum sensing, metabolite exchange, and contact-dependent interactions. Here we review several recent publications that shed new light on the social lives of plant-associated bacteria, with a particular focus on their competition mechanisms and strategies for colonisation and establishment. In this context, we highlight how the rational design of plant bioinoculants based on microbial consortia represents a powerful strategy for promoting sustainable agriculture in a rapidly changing environment.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Dual Roles of Free Fatty Acids in Gout Pathogenesis: Inflammatory Drivers and Metabolic Mediators.
International journal of rheumatic diseases, 29(8):e70799.
Gout, a prototypical crystal-induced arthropathy, is characterized by a complex interaction between metabolic dysregulation and inflammatory activation. Although monosodium urate (MSU) crystal deposition remains the central pathognomonic feature, accumulating evidence suggests that free fatty acids (FFAs) play a significant role as co-modulators in the disease's pathogenesis. This review systematically examines the dual role of FFAs in gout pathophysiology: (1) their pro-inflammatory effects during gout flares through direct modulation of innate immune responses, and (2) their role as metabolic modulators contributing to disease comorbidities. We explore the molecular mechanisms by which saturated and n-6 polyunsaturated fatty acids (PUFAs) promote NLRP3 inflammasome activation, ultimately leading to cytokine storm formation and acute inflammatory responses. Paradoxically, short-chain fatty acids and n-3 polyunsaturated fatty acids exhibit anti-inflammatory properties and confer protection against gout flares via distinct immunomodulatory pathways. The review further examines FFA-mediated metabolic disturbances associated with gout, such as insulin resistance, renal fibrosis, and non-alcoholic fatty liver disease. Additionally, this review provides novel insights into targeted therapeutic strategies for the adjuvant treatment of gout, including lipid-targeted therapy, microbiome modulation, and dietary recommendations regarding polyunsaturated fatty acids.
Additional Links: PMID-42530131
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@article {pmid42530131,
year = {2026},
author = {Lin, N and Shao, C},
title = {Dual Roles of Free Fatty Acids in Gout Pathogenesis: Inflammatory Drivers and Metabolic Mediators.},
journal = {International journal of rheumatic diseases},
volume = {29},
number = {8},
pages = {e70799},
pmid = {42530131},
issn = {1756-185X},
mesh = {Humans ; *Gout/metabolism/immunology/drug therapy/physiopathology ; *Inflammation Mediators/metabolism/immunology ; *Fatty Acids, Nonesterified/metabolism/immunology ; Animals ; Inflammasomes/metabolism/immunology ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/immunology ; Signal Transduction ; Immunity, Innate ; },
abstract = {Gout, a prototypical crystal-induced arthropathy, is characterized by a complex interaction between metabolic dysregulation and inflammatory activation. Although monosodium urate (MSU) crystal deposition remains the central pathognomonic feature, accumulating evidence suggests that free fatty acids (FFAs) play a significant role as co-modulators in the disease's pathogenesis. This review systematically examines the dual role of FFAs in gout pathophysiology: (1) their pro-inflammatory effects during gout flares through direct modulation of innate immune responses, and (2) their role as metabolic modulators contributing to disease comorbidities. We explore the molecular mechanisms by which saturated and n-6 polyunsaturated fatty acids (PUFAs) promote NLRP3 inflammasome activation, ultimately leading to cytokine storm formation and acute inflammatory responses. Paradoxically, short-chain fatty acids and n-3 polyunsaturated fatty acids exhibit anti-inflammatory properties and confer protection against gout flares via distinct immunomodulatory pathways. The review further examines FFA-mediated metabolic disturbances associated with gout, such as insulin resistance, renal fibrosis, and non-alcoholic fatty liver disease. Additionally, this review provides novel insights into targeted therapeutic strategies for the adjuvant treatment of gout, including lipid-targeted therapy, microbiome modulation, and dietary recommendations regarding polyunsaturated fatty acids.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gout/metabolism/immunology/drug therapy/physiopathology
*Inflammation Mediators/metabolism/immunology
*Fatty Acids, Nonesterified/metabolism/immunology
Animals
Inflammasomes/metabolism/immunology
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/immunology
Signal Transduction
Immunity, Innate
RevDate: 2026-07-30
Rome V criteria for pediatric disorders of gut - brain interaction: key updates and clinical implications.
Expert review of gastroenterology & hepatology [Epub ahead of print].
INTRODUCTION: The Rome criteria have provided the acclaimed global standard for diagnosing pediatric functional gastrointestinal disorders. With the release of Rome criteria V in 2026, the field has undergone a major transformation. The notable changes are the replacement of the term functional gastrointestinal disorders with disorders of gut - brain interaction (DGBIs) and shifting from age-based subdivisions to an anatomical and symptom cluster framework.
AREA COVERED: We reviewed pediatric Rome V documents and available evidence to cover both upper and lower gastrointestinal disorders of gut-brain interaction (DGBI). The new diagnostic entities such as reflux hypersensitivity, reflux negative esophageal pain disorder, supragastric belching, functional pediatric feeding disorders, centrally mediated abdominal pain syndrome, biliary pain syndrome, proctalgia fugax, functional diarrhea, functional bloating, and infant distress syndrome were discussed in detail.
EXPERT OPINION: Rome V provides clinicians with a more precise diagnostic framework. However, many new entities remain descriptive, highlighting the urgent need for epidemiological studies, mechanistic research, and biomarker discovery. Large multicenter trials, in DGBI should be conducted using physiological studies, microbiome analysis, and psychosocial profiles to generate robust evidence on pathophysiology, and management strategies. Ultimately, Rome V should be seen as a launchpad for discovery - transforming descriptive categories into mechanically defined, therapeutically actionable disorders that improve outcomes for children worldwide.
Additional Links: PMID-42530324
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PubMed:
Citation:
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@article {pmid42530324,
year = {2026},
author = {Rajindrajith, S and Devanarayana, N and Hathagoda, W and Benninga, M},
title = {Rome V criteria for pediatric disorders of gut - brain interaction: key updates and clinical implications.},
journal = {Expert review of gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1080/17474124.2026.2712930},
pmid = {42530324},
issn = {1747-4132},
abstract = {INTRODUCTION: The Rome criteria have provided the acclaimed global standard for diagnosing pediatric functional gastrointestinal disorders. With the release of Rome criteria V in 2026, the field has undergone a major transformation. The notable changes are the replacement of the term functional gastrointestinal disorders with disorders of gut - brain interaction (DGBIs) and shifting from age-based subdivisions to an anatomical and symptom cluster framework.
AREA COVERED: We reviewed pediatric Rome V documents and available evidence to cover both upper and lower gastrointestinal disorders of gut-brain interaction (DGBI). The new diagnostic entities such as reflux hypersensitivity, reflux negative esophageal pain disorder, supragastric belching, functional pediatric feeding disorders, centrally mediated abdominal pain syndrome, biliary pain syndrome, proctalgia fugax, functional diarrhea, functional bloating, and infant distress syndrome were discussed in detail.
EXPERT OPINION: Rome V provides clinicians with a more precise diagnostic framework. However, many new entities remain descriptive, highlighting the urgent need for epidemiological studies, mechanistic research, and biomarker discovery. Large multicenter trials, in DGBI should be conducted using physiological studies, microbiome analysis, and psychosocial profiles to generate robust evidence on pathophysiology, and management strategies. Ultimately, Rome V should be seen as a launchpad for discovery - transforming descriptive categories into mechanically defined, therapeutically actionable disorders that improve outcomes for children worldwide.},
}
RevDate: 2026-07-30
Microbial Diversity in Odontogenic Sinusitis: Next-Generation Sequencing Versus Culture.
American journal of rhinology & allergy [Epub ahead of print].
BackgroundOdontogenic sinusitis (ODS) is a common cause of unilateral infectious maxillary sinusitis but is frequently underdiagnosed due to nonspecific symptoms, subtle dental findings on imaging, and limitations of traditional bacterial cultures-particularly for anaerobic organisms. Next-generation DNA sequencing (NGS) may enhance detection of odontogenic bacteria.ObjectiveThis study compared bacterial detection between standard cultures versus NGS in patients with confirmed ODS.MethodsTwenty consecutive adults with confirmed ODS were enrolled. Maxillary sinus purulence was collected endoscopically and submitted for routine aerobic and anaerobic bacterial cultures and for NGS-based microbial profiling using 16S rRNA gene sequencing. Detected organisms were categorized by aerotolerance and ODS relationship, and likely nasal colonizers were excluded from analyses. Alpha diversity, beta diversity, and compositional differences between methods were analyzed statistically.ResultsNGS detected significantly more bacterial species per specimen than culture (mean 4.9 vs 2.7; P = .0015). Compared to cultures, NGS identified more anaerobic bacteria (4.2 vs 0.9; P = .00004) and more ODS-related species (4.4 vs 1.0; P = .0001), while detection of aerobic species was similar between methods. Cultures also often yielded nonspeciated results, whereas NGS consistently revealed polymicrobial communities dominated by oral anaerobes. Microbial composition differed significantly between detection methods.ConclusionIn confirmed ODS, NGS detected significantly more anaerobic and ODS-related species than culture from the same specimens. These findings suggest that culture alone may underestimate odontogenic contributions to purulent sinusitis. Future studies should explore he utility of NGS as an adjunctive tool to facilitate diagnosis and treatment in the setting of possible ODS.
Additional Links: PMID-42530539
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PubMed:
Citation:
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@article {pmid42530539,
year = {2026},
author = {Abdurrob, A and Cho, DY and Eide, JG and Ray, A and Ancira, JS and Tipton, C and Hanna, Z and Craig, J},
title = {Microbial Diversity in Odontogenic Sinusitis: Next-Generation Sequencing Versus Culture.},
journal = {American journal of rhinology & allergy},
volume = {},
number = {},
pages = {19458924261474104},
doi = {10.1177/19458924261474104},
pmid = {42530539},
issn = {1945-8932},
abstract = {BackgroundOdontogenic sinusitis (ODS) is a common cause of unilateral infectious maxillary sinusitis but is frequently underdiagnosed due to nonspecific symptoms, subtle dental findings on imaging, and limitations of traditional bacterial cultures-particularly for anaerobic organisms. Next-generation DNA sequencing (NGS) may enhance detection of odontogenic bacteria.ObjectiveThis study compared bacterial detection between standard cultures versus NGS in patients with confirmed ODS.MethodsTwenty consecutive adults with confirmed ODS were enrolled. Maxillary sinus purulence was collected endoscopically and submitted for routine aerobic and anaerobic bacterial cultures and for NGS-based microbial profiling using 16S rRNA gene sequencing. Detected organisms were categorized by aerotolerance and ODS relationship, and likely nasal colonizers were excluded from analyses. Alpha diversity, beta diversity, and compositional differences between methods were analyzed statistically.ResultsNGS detected significantly more bacterial species per specimen than culture (mean 4.9 vs 2.7; P = .0015). Compared to cultures, NGS identified more anaerobic bacteria (4.2 vs 0.9; P = .00004) and more ODS-related species (4.4 vs 1.0; P = .0001), while detection of aerobic species was similar between methods. Cultures also often yielded nonspeciated results, whereas NGS consistently revealed polymicrobial communities dominated by oral anaerobes. Microbial composition differed significantly between detection methods.ConclusionIn confirmed ODS, NGS detected significantly more anaerobic and ODS-related species than culture from the same specimens. These findings suggest that culture alone may underestimate odontogenic contributions to purulent sinusitis. Future studies should explore he utility of NGS as an adjunctive tool to facilitate diagnosis and treatment in the setting of possible ODS.},
}
RevDate: 2026-07-30
Clinical applications of gut microbiome for non-invasive diagnosis of colorectal neoplasia.
Journal of gastroenterology [Epub ahead of print].
Colorectal cancer (CRC) is the third most common malignancy and the second leading cause of cancer-related death worldwide. While screening programs have reduced mortality, current stool-based tests such as the faecal immunochemical test (FIT) and tumour marker assays, remain limited in sensitivity for adenoma detection and rely on relatively later-stage biological signals in the carcinogenic process. False positives lead to unnecessary invasive procedures, whilst missed adenomas continue to progress, highlighting the need for alternative strategies. Accumulating evidence implicates the gut microbiome in CRC pathogenesis, which involves tumour-associated dysbiosis and microbial ecosystem shifts. Multinational metagenomic studies have consistently identified reproducible microbial signatures that can serve as biomarkers of disease and may predate the biological signals used in conventional screening. PCR-based microbial markers have emerged as practical tools for clinical application, enabling sensitive and specific detection of adenomas and CRC. A recent microbial panel incorporating Fusobacterium nucleatum, Hungatella hathewayi, Christensenella hongkongensis, and a novel bacterial gene marker m3 from Lachnoclostridium demonstrated improved sensitivity for adenomas whilst maintaining comparable accuracy for CRC. International guidelines have begun to recommend combining microbiome-based assays with FIT into integrated screening programs that target multiple biologic processes across the pathogenesis. Microbiome-based stool testing represents a promising non-invasive approach that improves detection of adenomas in early-stage disease, often missed by FIT alone and could enable more refined risk stratification. Further validation across diverse populations, assessment of cost-effectiveness, and integration into established screening infrastructures will be critical for broad clinical adoption.
Additional Links: PMID-42530606
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Citation:
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@article {pmid42530606,
year = {2026},
author = {Cui, C and Shi, H and Naito, Y and Otani, K and Chan, FKL},
title = {Clinical applications of gut microbiome for non-invasive diagnosis of colorectal neoplasia.},
journal = {Journal of gastroenterology},
volume = {},
number = {},
pages = {},
pmid = {42530606},
issn = {1435-5922},
abstract = {Colorectal cancer (CRC) is the third most common malignancy and the second leading cause of cancer-related death worldwide. While screening programs have reduced mortality, current stool-based tests such as the faecal immunochemical test (FIT) and tumour marker assays, remain limited in sensitivity for adenoma detection and rely on relatively later-stage biological signals in the carcinogenic process. False positives lead to unnecessary invasive procedures, whilst missed adenomas continue to progress, highlighting the need for alternative strategies. Accumulating evidence implicates the gut microbiome in CRC pathogenesis, which involves tumour-associated dysbiosis and microbial ecosystem shifts. Multinational metagenomic studies have consistently identified reproducible microbial signatures that can serve as biomarkers of disease and may predate the biological signals used in conventional screening. PCR-based microbial markers have emerged as practical tools for clinical application, enabling sensitive and specific detection of adenomas and CRC. A recent microbial panel incorporating Fusobacterium nucleatum, Hungatella hathewayi, Christensenella hongkongensis, and a novel bacterial gene marker m3 from Lachnoclostridium demonstrated improved sensitivity for adenomas whilst maintaining comparable accuracy for CRC. International guidelines have begun to recommend combining microbiome-based assays with FIT into integrated screening programs that target multiple biologic processes across the pathogenesis. Microbiome-based stool testing represents a promising non-invasive approach that improves detection of adenomas in early-stage disease, often missed by FIT alone and could enable more refined risk stratification. Further validation across diverse populations, assessment of cost-effectiveness, and integration into established screening infrastructures will be critical for broad clinical adoption.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Quorum-sensing, microbiome interactions, and emerging artificial intelligence-assisted anti-virulence strategies in Salmonella Typhi: a critical review of translational opportunities and challenges.
Archives of microbiology, 208(10):.
Typhoid fever, caused by Salmonella enterica subsp. enterica serovar Typhi (Salmonella Typhi), remains a significant global health challenge that is increasingly complicated by the emergence and spread of multidrug-resistant (MDR) and extensively drug-resistant strains. Growing limitations of antibiotic-centered treatment strategies have stimulated interest in anti-virulence approaches targeting bacterial regulatory networks rather than viability alone. Among these, quorum-sensing (QS), particularly the LuxS-mediated autoinducer-2 (AI-2) signaling system, has emerged as a potential regulator of virulence-associated phenotypes, biofilm formation, stress adaptation, microbial communication, and host-associated persistence. This review critically evaluated the current understanding of QS biology in S. Typhi while distinguishing experimentally validated findings from evidence extrapolated from non-typhoidal Salmonella and other enteric bacteria. We examine the ecological interplay between QS, gut microbiome dynamics, and host responses, highlighting how microbial communication networks influence pathogen adaptation and colonization resistance. Emerging anti-QS strategies, including microbiome-mediated quorum quenching, probiotics, postbiotics, phytochemicals, antimicrobial peptides, bacteriophage-associated approaches, signal-degrading enzymes, and nucleic acid-based interventions, are comparatively assessed with respect to their mechanisms, evidence strength, translational readiness, and limitations. The review further explores the role of artificial intelligence (AI), multi-omics integration, and systems-level analytical frameworks in target identification, microbial network reconstruction, biomarker discovery, and therapeutic prioritization. Despite promising advances, substantial barriers remain, including limited in vivo validation, insufficient mechanistic evidence in S. Typhi, lack of clinically validated QS-associated biomarkers, microbiome variability, ecological safety concerns, and challenges related to delivery, scalability, and regulatory approval. Collectively, current evidence supports QS-targeted interventions as promising but predominantly investigational strategies that may complement existing antimicrobial, vaccine-based, and public-health approaches for typhoid control.
Additional Links: PMID-42530739
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Citation:
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@article {pmid42530739,
year = {2026},
author = {Bhuiyan, MNI and Saha, BK and Miah, MAS},
title = {Quorum-sensing, microbiome interactions, and emerging artificial intelligence-assisted anti-virulence strategies in Salmonella Typhi: a critical review of translational opportunities and challenges.},
journal = {Archives of microbiology},
volume = {208},
number = {10},
pages = {},
pmid = {42530739},
issn = {1432-072X},
mesh = {*Quorum Sensing ; *Salmonella typhi/pathogenicity/physiology/drug effects/genetics ; Virulence/drug effects ; Humans ; *Artificial Intelligence ; *Typhoid Fever/microbiology ; *Microbiota ; Animals ; Anti-Bacterial Agents/pharmacology ; Homoserine/analogs & derivatives ; Lactones ; },
abstract = {Typhoid fever, caused by Salmonella enterica subsp. enterica serovar Typhi (Salmonella Typhi), remains a significant global health challenge that is increasingly complicated by the emergence and spread of multidrug-resistant (MDR) and extensively drug-resistant strains. Growing limitations of antibiotic-centered treatment strategies have stimulated interest in anti-virulence approaches targeting bacterial regulatory networks rather than viability alone. Among these, quorum-sensing (QS), particularly the LuxS-mediated autoinducer-2 (AI-2) signaling system, has emerged as a potential regulator of virulence-associated phenotypes, biofilm formation, stress adaptation, microbial communication, and host-associated persistence. This review critically evaluated the current understanding of QS biology in S. Typhi while distinguishing experimentally validated findings from evidence extrapolated from non-typhoidal Salmonella and other enteric bacteria. We examine the ecological interplay between QS, gut microbiome dynamics, and host responses, highlighting how microbial communication networks influence pathogen adaptation and colonization resistance. Emerging anti-QS strategies, including microbiome-mediated quorum quenching, probiotics, postbiotics, phytochemicals, antimicrobial peptides, bacteriophage-associated approaches, signal-degrading enzymes, and nucleic acid-based interventions, are comparatively assessed with respect to their mechanisms, evidence strength, translational readiness, and limitations. The review further explores the role of artificial intelligence (AI), multi-omics integration, and systems-level analytical frameworks in target identification, microbial network reconstruction, biomarker discovery, and therapeutic prioritization. Despite promising advances, substantial barriers remain, including limited in vivo validation, insufficient mechanistic evidence in S. Typhi, lack of clinically validated QS-associated biomarkers, microbiome variability, ecological safety concerns, and challenges related to delivery, scalability, and regulatory approval. Collectively, current evidence supports QS-targeted interventions as promising but predominantly investigational strategies that may complement existing antimicrobial, vaccine-based, and public-health approaches for typhoid control.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Quorum Sensing
*Salmonella typhi/pathogenicity/physiology/drug effects/genetics
Virulence/drug effects
Humans
*Artificial Intelligence
*Typhoid Fever/microbiology
*Microbiota
Animals
Anti-Bacterial Agents/pharmacology
Homoserine/analogs & derivatives
Lactones
RevDate: 2026-07-30
CmpDate: 2026-07-30
Bacterial-based cancer therapy: mechanisms and therapeutic advances.
Molecular biomedicine, 7(1):.
Targeted cancer therapies increasingly require platforms that can penetrate poorly perfused tumor regions while minimizing systemic toxicity. Bacteria, owing to their intrinsic tumor tropism, genetic programmability, and immunostimulatory properties, have re-emerged as versatile anticancer agents, ranging from attenuated tumor-colonizing strains to highly engineered "living therapeutics." In this review, we synthesize the mechanistic foundations and therapeutic advances of bacterial-based cancer therapy through four major themes. First, we examine foundational mechanisms, including tumor-selective colonization, direct oncolysis and cytotoxicity, activation of innate and adaptive immunity, and remodeling of the tumor microenvironment. Second, we discuss engineering strategies that enable controllable delivery of therapeutic payloads, such as cytokines, antibodies and nanobodies, enzyme-prodrug systems, toxins, and nucleic-acid therapeutics, while also improving biosafety and biocontainment. Third, we evaluate combination strategies integrating bacteria with chemotherapy, radiotherapy, phototherapy, and immunotherapy, with emphasis on how bacteria complement conventional modalities by targeting hypoxic, necrotic, and immunologically refractory tumor niches. Fourth, we summarize translational progress, including representative early-phase clinical experiences, manufacturing challenges, and major safety constraints. We also highlight emerging microbiome-disease databases and computational resources that may support target selection, biomarker discovery, and therapy-response stratification. Current evidence supports bacteria as a promising precision modality, particularly for immunologically "cold" or hypoxic tumors; however, major challenges remain in the predictability of intratumoral distribution, host clearance, genetic stability, and long-term safety. Addressing these barriers through rigorous engineering, standardized manufacturing, and clinically meaningful endpoints will be essential for the next generation of bacterial therapeutics in oncology.
Additional Links: PMID-42530837
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@article {pmid42530837,
year = {2026},
author = {Sharifi, AH and Phong, NHT and Marek, A and Kamal, MA and Al-Kodmany, S and Tran, DB and Yamada, T},
title = {Bacterial-based cancer therapy: mechanisms and therapeutic advances.},
journal = {Molecular biomedicine},
volume = {7},
number = {1},
pages = {},
pmid = {42530837},
issn = {2662-8651},
support = {R01CA272564/CA/NCI NIH HHS/United States ; R01CA289701/CA/NCI NIH HHS/United States ; R21CA280814/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; *Neoplasms/therapy/immunology ; *Bacteria/genetics/metabolism ; Animals ; Tumor Microenvironment ; Immunotherapy/methods ; },
abstract = {Targeted cancer therapies increasingly require platforms that can penetrate poorly perfused tumor regions while minimizing systemic toxicity. Bacteria, owing to their intrinsic tumor tropism, genetic programmability, and immunostimulatory properties, have re-emerged as versatile anticancer agents, ranging from attenuated tumor-colonizing strains to highly engineered "living therapeutics." In this review, we synthesize the mechanistic foundations and therapeutic advances of bacterial-based cancer therapy through four major themes. First, we examine foundational mechanisms, including tumor-selective colonization, direct oncolysis and cytotoxicity, activation of innate and adaptive immunity, and remodeling of the tumor microenvironment. Second, we discuss engineering strategies that enable controllable delivery of therapeutic payloads, such as cytokines, antibodies and nanobodies, enzyme-prodrug systems, toxins, and nucleic-acid therapeutics, while also improving biosafety and biocontainment. Third, we evaluate combination strategies integrating bacteria with chemotherapy, radiotherapy, phototherapy, and immunotherapy, with emphasis on how bacteria complement conventional modalities by targeting hypoxic, necrotic, and immunologically refractory tumor niches. Fourth, we summarize translational progress, including representative early-phase clinical experiences, manufacturing challenges, and major safety constraints. We also highlight emerging microbiome-disease databases and computational resources that may support target selection, biomarker discovery, and therapy-response stratification. Current evidence supports bacteria as a promising precision modality, particularly for immunologically "cold" or hypoxic tumors; however, major challenges remain in the predictability of intratumoral distribution, host clearance, genetic stability, and long-term safety. Addressing these barriers through rigorous engineering, standardized manufacturing, and clinically meaningful endpoints will be essential for the next generation of bacterial therapeutics in oncology.},
}
MeSH Terms:
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Humans
*Neoplasms/therapy/immunology
*Bacteria/genetics/metabolism
Animals
Tumor Microenvironment
Immunotherapy/methods
RevDate: 2026-07-30
Phase-dependent Disruption of Microbiome-Metabolome Coordination Is Associated with Diet-Induced MASLD.
American journal of physiology. Gastrointestinal and liver physiology [Epub ahead of print].
Metabolic-dysfunction-associated steatotic liver disease (MASLD) is typically attributed to caloric overload, lipotoxicity, and static gut dysbiosis, but how chronic diet alters the temporal organization of gut-liver communication remains unclear. We combined a phase stratified multi omics framework, cecal 16S rRNA profiling, dual compartment (cecum and serum) metabolomics, and hepatic clock and lipogenic gene expression in C57BL/6J male mice fed a high fat, palmitate and cholesterol enriched (FPC) diet containing high sucrose for 22 weeks. FPC feeding was associated with severe MASLD and markedly attenuated homeostatic phase dependent differences in hepatic clock and lipogenic transcripts, consistent with a persistently lipogenic transcriptional state across the light-dark cycle. This temporal disruption coincided with reduced phase structured ecological organization in the cecal microbiome and the emergence of a constrained, dysbiotic community dominated by a few taxa. Dual-compartment metabolomics revealed that, despite retaining overall phase structure, local (cecal) and systemic (serum) metabolite pools showed misalignment: pro inflammatory and bile acid species showed exaggerated luminal variations but flattened, persistently elevated profiles in serum. High-stringency covariance network analysis identified diet-associated differences in microbiome-metabolome covariance patterns. These findings are consistent with a model in which diet-induced MASLD is associated with altered spatial and phase-dependent coordination across microbiome-host metabolic and transcriptional networks, suggesting disruption of integrated microbiome-host organization beyond static dysbiosis and lipotoxic stress.
Additional Links: PMID-42531150
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@article {pmid42531150,
year = {2026},
author = {De, AJ and Upadhyaya, B and Aich, P},
title = {Phase-dependent Disruption of Microbiome-Metabolome Coordination Is Associated with Diet-Induced MASLD.},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.00163.2026},
pmid = {42531150},
issn = {1522-1547},
support = {NA//Department of Atomic Energy, Government of India (DAE)/ ; },
abstract = {Metabolic-dysfunction-associated steatotic liver disease (MASLD) is typically attributed to caloric overload, lipotoxicity, and static gut dysbiosis, but how chronic diet alters the temporal organization of gut-liver communication remains unclear. We combined a phase stratified multi omics framework, cecal 16S rRNA profiling, dual compartment (cecum and serum) metabolomics, and hepatic clock and lipogenic gene expression in C57BL/6J male mice fed a high fat, palmitate and cholesterol enriched (FPC) diet containing high sucrose for 22 weeks. FPC feeding was associated with severe MASLD and markedly attenuated homeostatic phase dependent differences in hepatic clock and lipogenic transcripts, consistent with a persistently lipogenic transcriptional state across the light-dark cycle. This temporal disruption coincided with reduced phase structured ecological organization in the cecal microbiome and the emergence of a constrained, dysbiotic community dominated by a few taxa. Dual-compartment metabolomics revealed that, despite retaining overall phase structure, local (cecal) and systemic (serum) metabolite pools showed misalignment: pro inflammatory and bile acid species showed exaggerated luminal variations but flattened, persistently elevated profiles in serum. High-stringency covariance network analysis identified diet-associated differences in microbiome-metabolome covariance patterns. These findings are consistent with a model in which diet-induced MASLD is associated with altered spatial and phase-dependent coordination across microbiome-host metabolic and transcriptional networks, suggesting disruption of integrated microbiome-host organization beyond static dysbiosis and lipotoxic stress.},
}
RevDate: 2026-07-30
CmpDate: 2026-07-30
Longitudinal omics study of transcriptional dynamics in Lactobacillus crispatus.
PloS one, 21(7):e0354930 pii:PONE-D-26-11487.
BACKGROUND: The vaginal microbiome is an important component of female reproductive health. Community State Type I (CST-I), which is dominated by Lactobacillus crispatus, is generally considered to be closely associated with a healthy vaginal microecological state. Although the taxonomic composition of CST-I communities remains relatively stable, the transcriptional dynamics of Lactobacillus crispatus across different phases of the menstrual cycle remain unclear.
METHODS: A healthy reproductive-age woman with a stable CST-I vaginal microbiome was enrolled in this longitudinal study. Vaginal secretion samples were collected at six non-menstrual time points throughout a menstrual cycle. Third-generation full-length 16S rRNA gene sequencing and metatranscriptomic sequencing were performed. Differential transcript expression analysis, KEGG pathway enrichment analysis, and Mfuzz time-series clustering were applied to systematically characterize the transcriptional dynamics of the vaginal microbiome across different phases.
RESULTS: Full-length 16S rRNA gene sequencing confirmed that Lactobacillus crispatus remained the dominant species at all six sampling time points, with no substantial changes in overall community composition. However, metatranscriptomic analysis revealed pronounced phase-specific transcriptional reprogramming. During the pre-ovulatory phase, pathways involved in DNA replication, biosynthesis, and central carbon metabolism were upregulated. On the first day after ovulation, pathways associated with carbohydrate utilization, quorum sensing, and redox homeostasis were selectively upregulated. During the mid-to-late luteal phase, pathways related to cell proliferation and growth were generally downregulated, whereas pathways involved in cofactor biosynthesis, the pentose phosphate pathway, and D-amino acid metabolism showed increased expression. Mfuzz clustering further revealed distinct phase-specific functional transitions in L. crispatus that were absent in non-L. crispatus lactobacilli.
CONCLUSION: The ecological dominance of Lactobacillus crispatus is maintained not solely through numerical abundance, but also through rhythmic and phase-specific transcriptional regulation. Dynamic functional remodeling and metabolic plasticity may represent important mechanisms underlying its long-term persistence and ecological dominance within healthy CST-I vaginal communities.
Additional Links: PMID-42531262
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@article {pmid42531262,
year = {2026},
author = {Ren, S and Jiang, H and Liu, X and Zhou, D and Liu, L and Wang, L and Lan, Y and Xiao, Y and Tang, L},
title = {Longitudinal omics study of transcriptional dynamics in Lactobacillus crispatus.},
journal = {PloS one},
volume = {21},
number = {7},
pages = {e0354930},
doi = {10.1371/journal.pone.0354930},
pmid = {42531262},
issn = {1932-6203},
mesh = {*Lactobacillus crispatus/genetics/metabolism ; Female ; RNA, Ribosomal, 16S/genetics ; *Vagina/microbiology ; Humans ; Longitudinal Studies ; Microbiota/genetics ; *Transcription, Genetic ; Gene Expression Profiling ; Transcriptome ; Gene Expression Regulation, Bacterial ; },
abstract = {BACKGROUND: The vaginal microbiome is an important component of female reproductive health. Community State Type I (CST-I), which is dominated by Lactobacillus crispatus, is generally considered to be closely associated with a healthy vaginal microecological state. Although the taxonomic composition of CST-I communities remains relatively stable, the transcriptional dynamics of Lactobacillus crispatus across different phases of the menstrual cycle remain unclear.
METHODS: A healthy reproductive-age woman with a stable CST-I vaginal microbiome was enrolled in this longitudinal study. Vaginal secretion samples were collected at six non-menstrual time points throughout a menstrual cycle. Third-generation full-length 16S rRNA gene sequencing and metatranscriptomic sequencing were performed. Differential transcript expression analysis, KEGG pathway enrichment analysis, and Mfuzz time-series clustering were applied to systematically characterize the transcriptional dynamics of the vaginal microbiome across different phases.
RESULTS: Full-length 16S rRNA gene sequencing confirmed that Lactobacillus crispatus remained the dominant species at all six sampling time points, with no substantial changes in overall community composition. However, metatranscriptomic analysis revealed pronounced phase-specific transcriptional reprogramming. During the pre-ovulatory phase, pathways involved in DNA replication, biosynthesis, and central carbon metabolism were upregulated. On the first day after ovulation, pathways associated with carbohydrate utilization, quorum sensing, and redox homeostasis were selectively upregulated. During the mid-to-late luteal phase, pathways related to cell proliferation and growth were generally downregulated, whereas pathways involved in cofactor biosynthesis, the pentose phosphate pathway, and D-amino acid metabolism showed increased expression. Mfuzz clustering further revealed distinct phase-specific functional transitions in L. crispatus that were absent in non-L. crispatus lactobacilli.
CONCLUSION: The ecological dominance of Lactobacillus crispatus is maintained not solely through numerical abundance, but also through rhythmic and phase-specific transcriptional regulation. Dynamic functional remodeling and metabolic plasticity may represent important mechanisms underlying its long-term persistence and ecological dominance within healthy CST-I vaginal communities.},
}
MeSH Terms:
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*Lactobacillus crispatus/genetics/metabolism
Female
RNA, Ribosomal, 16S/genetics
*Vagina/microbiology
Humans
Longitudinal Studies
Microbiota/genetics
*Transcription, Genetic
Gene Expression Profiling
Transcriptome
Gene Expression Regulation, Bacterial
RevDate: 2026-07-30
Viruses help shape microbiome response to polyphenol rewiring of methane-suppressed peat microcosms.
PLoS biology, 24(7):e3003925 pii:PBIOLOGY-D-26-00309 [Epub ahead of print].
Human activities are accelerating permafrost thaw and subsequent methane emissions from increased microbial activity, prompting microbiome engineering efforts as an emissions mitigation strategy. We recently demonstrated that catechin amendment could drastically reduce methane emissions (>80%) in peat microcosms by enriching catechin-degrading prokaryotes that outcompeted methanogens for hydrogen. However, viral contributions to such microbiome-level responses remain unexplored and we hypothesized that viral dynamics could help shape the microbiome response as nutrient amendments may alter cellular physiology in ways that could induce lytic viral activity. Here, we performed virus eco-genomics analyses of the previously-studied time-resolved multi-omics data collected from catechin-amended peat microcosms. We conservatively identified 900 putatively lytic viral operational taxonomic units (vOTUs), with 41% predicted to infect active host genomes including the most transcriptionally active vOTUs predicted to infect key catechin-degrading genera (Clostridium and undescribed Bacillota JAGFXR01). Notably, a single JAGFXR01-targeting vOTU dominating the viral response (>40% of community viral transcription; 20-156-fold more abundant than its host), which we interpreted as induction resulting in intense lytic activity that could release catechin degradation intermediates to other community members. Consistent with this, gene expression analysis revealed elevated catechin-intermediate degradation and hydrogenase signals in 34 additional polyphenol-degrading metagenome-assembled genomes. These findings support a model consistent with a viral shunt-like process that extends our previous prokaryote-centric model: viral lysis of fast-growing catechin degraders redistributes phenolic intermediates to diverse phenol-degrading taxa that sustain methane suppression via hydrogen consumption. Beyond carbon cycling importance in this system, elucidating unintended virus-mediated responses to nutrient and prebiotic interventions will enable more predictable and effective microbiome engineering strategies across soil, ocean, and human ecosystems.
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@article {pmid42531353,
year = {2026},
author = {Riddell V, J and Shatadru, RN and Smith, GJ and McGivern, BB and Ellenbogen, JB and Jurgensen, SK and Fofana, A and Tfaily, MM and Wrighton, KC and Sullivan, MB},
title = {Viruses help shape microbiome response to polyphenol rewiring of methane-suppressed peat microcosms.},
journal = {PLoS biology},
volume = {24},
number = {7},
pages = {e3003925},
doi = {10.1371/journal.pbio.3003925},
pmid = {42531353},
issn = {1545-7885},
abstract = {Human activities are accelerating permafrost thaw and subsequent methane emissions from increased microbial activity, prompting microbiome engineering efforts as an emissions mitigation strategy. We recently demonstrated that catechin amendment could drastically reduce methane emissions (>80%) in peat microcosms by enriching catechin-degrading prokaryotes that outcompeted methanogens for hydrogen. However, viral contributions to such microbiome-level responses remain unexplored and we hypothesized that viral dynamics could help shape the microbiome response as nutrient amendments may alter cellular physiology in ways that could induce lytic viral activity. Here, we performed virus eco-genomics analyses of the previously-studied time-resolved multi-omics data collected from catechin-amended peat microcosms. We conservatively identified 900 putatively lytic viral operational taxonomic units (vOTUs), with 41% predicted to infect active host genomes including the most transcriptionally active vOTUs predicted to infect key catechin-degrading genera (Clostridium and undescribed Bacillota JAGFXR01). Notably, a single JAGFXR01-targeting vOTU dominating the viral response (>40% of community viral transcription; 20-156-fold more abundant than its host), which we interpreted as induction resulting in intense lytic activity that could release catechin degradation intermediates to other community members. Consistent with this, gene expression analysis revealed elevated catechin-intermediate degradation and hydrogenase signals in 34 additional polyphenol-degrading metagenome-assembled genomes. These findings support a model consistent with a viral shunt-like process that extends our previous prokaryote-centric model: viral lysis of fast-growing catechin degraders redistributes phenolic intermediates to diverse phenol-degrading taxa that sustain methane suppression via hydrogen consumption. Beyond carbon cycling importance in this system, elucidating unintended virus-mediated responses to nutrient and prebiotic interventions will enable more predictable and effective microbiome engineering strategies across soil, ocean, and human ecosystems.},
}
RevDate: 2026-07-30
Association Characteristics and Potential Mechanisms of Aging, Gut Microbiota, and Hearing Loss.
Integrative zoology [Epub ahead of print].
Age-related hearing loss (ARHL) is the leading sensory disability among the global elderly, yet its pathogenesis remains unclear. The "gut-ear axis" hypothesis offers a novel perspective. Using young, middle-aged, and aging C57BL/6 mice, we systematically investigated the interplay between aging, gut microbiota, and hearing loss through auditory function tests, cochlear histology, microbiome, and metabolome profiling. Results showed that aging induced a gradient hearing decline starting at high frequencies, progressing to severe pan-frequency loss in old age. Histology confirmed the degeneration of inner hair cells and synaptic connections, alongside hair cell loss in the basal cochlea. While gut microbiota α-diversity remained stable, β-diversity shifted significantly, marked by increased Bacteroidota and decreased Bacillota. Furthermore, 22 genera, 67 species, and 207 functional pathways were identified as being commonly associated with both aging and hearing loss. Metabolomic profiling further screened out 285 metabolites significantly associated with aging, 16 of which were also correlated with hearing loss. KEGG enrichment analysis suggested that chronic inflammation mediated by arachidonic acid metabolism, energy metabolic dysfunction regulated by the PPAR signaling pathway, and actin cytoskeleton homeostasis imbalance may represent a potential axis linking systemic metabolic dysregulation to cochlear‑specific damage. Moreover, these metabolites exhibited significant correlations with gut microbiota abundance. In conclusion, aging is associated with ARHL progression alongside gut microbiota remodeling and metabolic dysregulation. These findings supported a potential relationship between gut microbial-metabolic alterations and ARHL, which suggested that the gut microbiota may represent a candidate target for future mechanistic investigation.
Additional Links: PMID-42531517
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@article {pmid42531517,
year = {2026},
author = {Cheng, C and Wang, L and Li, R and Lai, W and Sun, C and Cui, J and Zhu, B and Zhang, J},
title = {Association Characteristics and Potential Mechanisms of Aging, Gut Microbiota, and Hearing Loss.},
journal = {Integrative zoology},
volume = {},
number = {},
pages = {},
doi = {10.1111/1749-4877.70156},
pmid = {42531517},
issn = {1749-4877},
support = {32370536//National Natural Science Foundation of China/ ; QNTS202304//CIB Youth Exploration Project/ ; //Tianchi Talents Fund of Xinjiang/ ; },
abstract = {Age-related hearing loss (ARHL) is the leading sensory disability among the global elderly, yet its pathogenesis remains unclear. The "gut-ear axis" hypothesis offers a novel perspective. Using young, middle-aged, and aging C57BL/6 mice, we systematically investigated the interplay between aging, gut microbiota, and hearing loss through auditory function tests, cochlear histology, microbiome, and metabolome profiling. Results showed that aging induced a gradient hearing decline starting at high frequencies, progressing to severe pan-frequency loss in old age. Histology confirmed the degeneration of inner hair cells and synaptic connections, alongside hair cell loss in the basal cochlea. While gut microbiota α-diversity remained stable, β-diversity shifted significantly, marked by increased Bacteroidota and decreased Bacillota. Furthermore, 22 genera, 67 species, and 207 functional pathways were identified as being commonly associated with both aging and hearing loss. Metabolomic profiling further screened out 285 metabolites significantly associated with aging, 16 of which were also correlated with hearing loss. KEGG enrichment analysis suggested that chronic inflammation mediated by arachidonic acid metabolism, energy metabolic dysfunction regulated by the PPAR signaling pathway, and actin cytoskeleton homeostasis imbalance may represent a potential axis linking systemic metabolic dysregulation to cochlear‑specific damage. Moreover, these metabolites exhibited significant correlations with gut microbiota abundance. In conclusion, aging is associated with ARHL progression alongside gut microbiota remodeling and metabolic dysregulation. These findings supported a potential relationship between gut microbial-metabolic alterations and ARHL, which suggested that the gut microbiota may represent a candidate target for future mechanistic investigation.},
}
RevDate: 2026-07-30
Polycystic ovary syndrome and insulin resistance: A focus on pathogenesis, risk factors, and therapeutic strategies.
Journal of reproductive immunology, 176:104943 pii:S0165-0378(26)00112-9 [Epub ahead of print].
Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder characterized by significant reproductive and metabolic complications. Insulin resistance (IR) plays a central role in the pathophysiology of PCOS and contributes to several associated metabolic abnormalities. This review highlights the key mechanisms underlying PCOS, including IR, hyperandrogenism, cardiovascular disease, gut microbiota dysbiosis, and the increased risk of type 2 diabetes mellitus (T2DM), along with current and emerging therapeutic strategies for improving disease outcomes. Accumulating evidence suggests that genetic predisposition contributes to PCOS susceptibility. Polymorphisms in genes such as the androgen receptor (AR), cytochrome P450 17A1 (CYP17), and follicle-stimulating hormone receptor (FSHR) have been associated with altered steroidogenesis and ovarian dysfunction, thereby influencing disease severity. In addition to genetic factors, environmental influences, including exposure to endocrine-disrupting chemicals (EDCs) and air pollution, may exacerbate metabolic disturbances and increase the risk of developing PCOS. Conventional therapeutic approaches focus on improving insulin sensitivity and correcting hormonal imbalances. These include pharmacological treatments such as metformin, oral contraceptives, and lifestyle modifications involving diet and physical activity. Recently, novel therapeutic strategies have emerged, including glucagon-like peptide-1 receptor agonists (GLP-1RAs), microRNA-based therapies, and interleukin-22 (IL-22)-mediated interventions, which show potential in targeting IR and metabolic dysfunction in PCOS. Furthermore, modulation of gut microbiota through probiotics, prebiotics, and fecal microbiota transplantation (FMT) represents an emerging strategy for restoring metabolic homeostasis. Overall, a comprehensive and personalized therapeutic approach integrating pharmacological, lifestyle, and microbiome-targeted interventions may significantly improve PCOS management and reduce long-term metabolic and reproductive complications.
Additional Links: PMID-42531755
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@article {pmid42531755,
year = {2026},
author = {Singla, J and Yadav, S and Gayen, JR},
title = {Polycystic ovary syndrome and insulin resistance: A focus on pathogenesis, risk factors, and therapeutic strategies.},
journal = {Journal of reproductive immunology},
volume = {176},
number = {},
pages = {104943},
doi = {10.1016/j.jri.2026.104943},
pmid = {42531755},
issn = {1872-7603},
abstract = {Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder characterized by significant reproductive and metabolic complications. Insulin resistance (IR) plays a central role in the pathophysiology of PCOS and contributes to several associated metabolic abnormalities. This review highlights the key mechanisms underlying PCOS, including IR, hyperandrogenism, cardiovascular disease, gut microbiota dysbiosis, and the increased risk of type 2 diabetes mellitus (T2DM), along with current and emerging therapeutic strategies for improving disease outcomes. Accumulating evidence suggests that genetic predisposition contributes to PCOS susceptibility. Polymorphisms in genes such as the androgen receptor (AR), cytochrome P450 17A1 (CYP17), and follicle-stimulating hormone receptor (FSHR) have been associated with altered steroidogenesis and ovarian dysfunction, thereby influencing disease severity. In addition to genetic factors, environmental influences, including exposure to endocrine-disrupting chemicals (EDCs) and air pollution, may exacerbate metabolic disturbances and increase the risk of developing PCOS. Conventional therapeutic approaches focus on improving insulin sensitivity and correcting hormonal imbalances. These include pharmacological treatments such as metformin, oral contraceptives, and lifestyle modifications involving diet and physical activity. Recently, novel therapeutic strategies have emerged, including glucagon-like peptide-1 receptor agonists (GLP-1RAs), microRNA-based therapies, and interleukin-22 (IL-22)-mediated interventions, which show potential in targeting IR and metabolic dysfunction in PCOS. Furthermore, modulation of gut microbiota through probiotics, prebiotics, and fecal microbiota transplantation (FMT) represents an emerging strategy for restoring metabolic homeostasis. Overall, a comprehensive and personalized therapeutic approach integrating pharmacological, lifestyle, and microbiome-targeted interventions may significantly improve PCOS management and reduce long-term metabolic and reproductive complications.},
}
RevDate: 2026-07-30
Poricoic acid a ameliorates ulcerative colitis via AMPK/PPARγ pathway-dependent cellular senescence inhibition and concomitant gut microbiota-metabolome modulation.
Phytomedicine : international journal of phytotherapy and phytopharmacology, 160:158628 pii:S0944-7113(26)00859-7 [Epub ahead of print].
BACKGROUND: Ulcerative colitis (UC) is an intractable inflammatory bowel disorder characterized by persistent intestinal inflammation and impaired gut barrier integrity. Its pathogenesis is multifactorial, involving gut microbiota dysbiosis, metabolic dysfunction, and cellular senescence. Current therapeutic regimens remain limited, underscoring an urgent need for innovative agents that target these interrelated pathological cascades.
PURPOSE: This study aimed to evaluate the pharmacological effects of poricoic acid A (PAA) on DSS-induced senescence in intestinal epithelial cells and in a murine model of ulcerative colitis (UC), as well as the underlying molecular mechanisms.
METHODS: We established a DSS-stimulated senescent intestinal epithelial cell model and a DSS-induced UC mouse model. Multi-omics and bioinformatics strategies, including network pharmacology, transcriptome profiling, gut metagenomics, and intestinal targeted metabolomics, were combined with molecular docking to predict candidate signaling axes. Subsequent pharmacological inhibition and siRNA-mediated silencing assays were performed to validate core pathways functionally.
RESULTS: PAA robustly suppressed DSS-induced senescence and inflammatory responses in intestinal epithelial cells. In vivo assays verified that PAA alleviated UC-related manifestations, including body weight loss, rectal hemorrhage, and colonic histological injury. Joint network pharmacology and transcriptomic screening identified the AMPK/PPARγ as the core pathway mediating PAA's bioactivity. Mechanistic experiments confirmed that PAA directly bound and activated PPAR, further functionally triggering downstream AMPK/SirT1/PGC1α signaling. Blockade of AMPK via pharmaceutical antagonists or siRNA largely abolished PAA's anti-senescence and anti-inflammatory capacities; PPARγ suppression, in turn, secondary deactivated the AMPK and its downstream functional effectors. In mouse models, AMPK inhibition drastically compromised PAA's protective effects against UC. Moreover, PAA treatment of UC is closely associated with remodeling of the gut microbiome-metabolome axis and restoration of intestinal homeostasis.
CONCLUSION: PAA exerts potent anti-senescence, anti-inflammatory, and colon-protective effects in UC via activating the AMPK/PPARγ signaling pathway. Such beneficial activity may be associated with the normalization of gut microbiota-metabolome homeostasis. This work identifies novel molecular targets and a promising lead compound for the intervention of ulcerative colitis.
Additional Links: PMID-42531833
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PubMed:
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@article {pmid42531833,
year = {2026},
author = {Wang, Y and Liu, Z and Hou, Q and Xu, Y and Chen, W and Chen, M and Liu, J and Tang, J and Wang, Y and Zhou, M and Wu, X and Wang, X},
title = {Poricoic acid a ameliorates ulcerative colitis via AMPK/PPARγ pathway-dependent cellular senescence inhibition and concomitant gut microbiota-metabolome modulation.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {160},
number = {},
pages = {158628},
doi = {10.1016/j.phymed.2026.158628},
pmid = {42531833},
issn = {1618-095X},
abstract = {BACKGROUND: Ulcerative colitis (UC) is an intractable inflammatory bowel disorder characterized by persistent intestinal inflammation and impaired gut barrier integrity. Its pathogenesis is multifactorial, involving gut microbiota dysbiosis, metabolic dysfunction, and cellular senescence. Current therapeutic regimens remain limited, underscoring an urgent need for innovative agents that target these interrelated pathological cascades.
PURPOSE: This study aimed to evaluate the pharmacological effects of poricoic acid A (PAA) on DSS-induced senescence in intestinal epithelial cells and in a murine model of ulcerative colitis (UC), as well as the underlying molecular mechanisms.
METHODS: We established a DSS-stimulated senescent intestinal epithelial cell model and a DSS-induced UC mouse model. Multi-omics and bioinformatics strategies, including network pharmacology, transcriptome profiling, gut metagenomics, and intestinal targeted metabolomics, were combined with molecular docking to predict candidate signaling axes. Subsequent pharmacological inhibition and siRNA-mediated silencing assays were performed to validate core pathways functionally.
RESULTS: PAA robustly suppressed DSS-induced senescence and inflammatory responses in intestinal epithelial cells. In vivo assays verified that PAA alleviated UC-related manifestations, including body weight loss, rectal hemorrhage, and colonic histological injury. Joint network pharmacology and transcriptomic screening identified the AMPK/PPARγ as the core pathway mediating PAA's bioactivity. Mechanistic experiments confirmed that PAA directly bound and activated PPAR, further functionally triggering downstream AMPK/SirT1/PGC1α signaling. Blockade of AMPK via pharmaceutical antagonists or siRNA largely abolished PAA's anti-senescence and anti-inflammatory capacities; PPARγ suppression, in turn, secondary deactivated the AMPK and its downstream functional effectors. In mouse models, AMPK inhibition drastically compromised PAA's protective effects against UC. Moreover, PAA treatment of UC is closely associated with remodeling of the gut microbiome-metabolome axis and restoration of intestinal homeostasis.
CONCLUSION: PAA exerts potent anti-senescence, anti-inflammatory, and colon-protective effects in UC via activating the AMPK/PPARγ signaling pathway. Such beneficial activity may be associated with the normalization of gut microbiota-metabolome homeostasis. This work identifies novel molecular targets and a promising lead compound for the intervention of ulcerative colitis.},
}
RevDate: 2026-07-30
Root exudates recruit microbial allies to override their own mobilization effects for cadmium immobilization in intercropped rice.
Journal of hazardous materials, 515:143010 pii:S0304-3894(26)01990-4 [Epub ahead of print].
Challenging the conventional view that root exudates inevitably exacerbate cadmium (Cd) bioavailability in paddy soils, this study revealed that intercropping high- and low-Cd-accumulating rice cultivars creates a distinct rhizosphere microenvironment wherein specifically enriched metabolites exert a dual function, ultimately driving net Cd immobilization. Through field experiments coupled with metabolomic and microbiome analyses, we showed that intercropping significantly reduces grain Cd concentrations by 18.45% in the high-Cd cultivar and 8.13% in the low-Cd cultivar, accompanied by substantial decreases in acid-extractable and oxidizable Cd fractions in rhizosphere soils. Mechanistic analyses revealed that intercropping reshaped the rhizosphere metabolome, enriching organic acids that exert dual functions: transient mobilization of oxidizable Cd and, more critically, recruitment of functional microorganisms, including sulfate-reducing bacteria (Candidatus Sulfobium mesophilum) and nitrifiers (Nitrospira), that promote Cd immobilization. Structural equation modeling confirmed that microbe-driven immobilization (path coefficient = -0.31) outweighs metabolite-mediated mobilization (path coefficient = 0.25), thereby reducing bioavailable Cd in the rice rhizosphere and suppressing its translocation to grains. A pot validation experiment substantiated this causal pathway: exogenous application of organic acids (citric acid) increased the abundance of the target sulfate-reducing bacterium by over 200% and induced a dose-dependent reduction in grain Cd content ranging from 32.29% to 56.25%. Collectively, our findings uncover a microbial-mediated Cd immobilization strategy triggered by intercropping-induced metabolite shifts, offering a streamlined framework that translates mechanistic insights into the efficient screening of green and cost-effective root metabolites as potential remediation agents for sustainable agriculture.
Additional Links: PMID-42531933
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@article {pmid42531933,
year = {2026},
author = {Li, Y and Hou, J and Liu, M and Chen, H and Wang, X and Sun, P and Zhao, L and Yao, Y and Du, Z and An, Y},
title = {Root exudates recruit microbial allies to override their own mobilization effects for cadmium immobilization in intercropped rice.},
journal = {Journal of hazardous materials},
volume = {515},
number = {},
pages = {143010},
doi = {10.1016/j.jhazmat.2026.143010},
pmid = {42531933},
issn = {1873-3336},
abstract = {Challenging the conventional view that root exudates inevitably exacerbate cadmium (Cd) bioavailability in paddy soils, this study revealed that intercropping high- and low-Cd-accumulating rice cultivars creates a distinct rhizosphere microenvironment wherein specifically enriched metabolites exert a dual function, ultimately driving net Cd immobilization. Through field experiments coupled with metabolomic and microbiome analyses, we showed that intercropping significantly reduces grain Cd concentrations by 18.45% in the high-Cd cultivar and 8.13% in the low-Cd cultivar, accompanied by substantial decreases in acid-extractable and oxidizable Cd fractions in rhizosphere soils. Mechanistic analyses revealed that intercropping reshaped the rhizosphere metabolome, enriching organic acids that exert dual functions: transient mobilization of oxidizable Cd and, more critically, recruitment of functional microorganisms, including sulfate-reducing bacteria (Candidatus Sulfobium mesophilum) and nitrifiers (Nitrospira), that promote Cd immobilization. Structural equation modeling confirmed that microbe-driven immobilization (path coefficient = -0.31) outweighs metabolite-mediated mobilization (path coefficient = 0.25), thereby reducing bioavailable Cd in the rice rhizosphere and suppressing its translocation to grains. A pot validation experiment substantiated this causal pathway: exogenous application of organic acids (citric acid) increased the abundance of the target sulfate-reducing bacterium by over 200% and induced a dose-dependent reduction in grain Cd content ranging from 32.29% to 56.25%. Collectively, our findings uncover a microbial-mediated Cd immobilization strategy triggered by intercropping-induced metabolite shifts, offering a streamlined framework that translates mechanistic insights into the efficient screening of green and cost-effective root metabolites as potential remediation agents for sustainable agriculture.},
}
RevDate: 2026-07-30
Synergistic integration of forensic transcriptome and microbiome: A robust multi-marker strategy combined with machine learning for accurate body fluid identification.
Forensic science international. Genetics, 86:103583 pii:S1872-4973(26)00164-X [Epub ahead of print].
In recent years, the development of microbiome and transcriptome analyses has significantly improved the efficiency of forensic body fluid identification. However, challenging or limited biological samples in forensic practice demand highly efficient utilization of biological samples to minimize sample loss. In this study, we developed two independent assays based on a capillary electrophoresis (CE) approach: a 21-mRNA assay and a 10-bacteria system. The co-extracted RNA and DNA were amplified independently to identify five body fluids using mRNA profiling, and to specifically identify saliva (SA) and vaginal secretion (VS) using bacterial markers. Validation experiments of the two detection systems evaluated specificity, sensitivity, and performance on mixtures, aged, and degraded samples. In order to achieve accurate and intelligent identification of body fluid types, four machine learning (ML) models (Random Forest, K-Nearest Neighbors, Support Vector Machine, and Naive Bayes) were constructed and evaluated. Validation experiments demonstrated that both systems exhibited high overall specificity of body fluids, although certain markers showed cross-reactivity in some non-target samples. The two different assays yielded robust profiles from the samples as low as 1 ng of RNA or 0.1 ng of DNA, as well as most low-volume samples down to 1 μL or a 1/16 swab. Furthermore, the 21-mRNA and 10-bacteria systems effectively analyzed most aged or degraded samples, and mixtures. Despite suboptimal profiles from challenging samples (e.g. 1 μL semen, and aged or degraded semen samples), the SVM classifier overall outperformed other ML models, achieving a 100% classification accuracy for both single-source body fluids and pairwise mixtures on independent test sets. Overall, this study combining multi-omics biomarkers with ML models for precise body fluid identification provides strong technical support for practical forensic application.
Additional Links: PMID-42531989
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PubMed:
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@article {pmid42531989,
year = {2026},
author = {Wang, X and Liang, Q and Yuan, X and Cai, M and Zhu, B},
title = {Synergistic integration of forensic transcriptome and microbiome: A robust multi-marker strategy combined with machine learning for accurate body fluid identification.},
journal = {Forensic science international. Genetics},
volume = {86},
number = {},
pages = {103583},
doi = {10.1016/j.fsigen.2026.103583},
pmid = {42531989},
issn = {1878-0326},
abstract = {In recent years, the development of microbiome and transcriptome analyses has significantly improved the efficiency of forensic body fluid identification. However, challenging or limited biological samples in forensic practice demand highly efficient utilization of biological samples to minimize sample loss. In this study, we developed two independent assays based on a capillary electrophoresis (CE) approach: a 21-mRNA assay and a 10-bacteria system. The co-extracted RNA and DNA were amplified independently to identify five body fluids using mRNA profiling, and to specifically identify saliva (SA) and vaginal secretion (VS) using bacterial markers. Validation experiments of the two detection systems evaluated specificity, sensitivity, and performance on mixtures, aged, and degraded samples. In order to achieve accurate and intelligent identification of body fluid types, four machine learning (ML) models (Random Forest, K-Nearest Neighbors, Support Vector Machine, and Naive Bayes) were constructed and evaluated. Validation experiments demonstrated that both systems exhibited high overall specificity of body fluids, although certain markers showed cross-reactivity in some non-target samples. The two different assays yielded robust profiles from the samples as low as 1 ng of RNA or 0.1 ng of DNA, as well as most low-volume samples down to 1 μL or a 1/16 swab. Furthermore, the 21-mRNA and 10-bacteria systems effectively analyzed most aged or degraded samples, and mixtures. Despite suboptimal profiles from challenging samples (e.g. 1 μL semen, and aged or degraded semen samples), the SVM classifier overall outperformed other ML models, achieving a 100% classification accuracy for both single-source body fluids and pairwise mixtures on independent test sets. Overall, this study combining multi-omics biomarkers with ML models for precise body fluid identification provides strong technical support for practical forensic application.},
}
RevDate: 2026-07-30
The human gut microbiome: still more questions than answers.
Additional Links: PMID-42532085
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PubMed:
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@article {pmid42532085,
year = {2026},
author = {The Lancet Microbe, },
title = {The human gut microbiome: still more questions than answers.},
journal = {The Lancet. Microbe},
volume = {},
number = {},
pages = {101513},
doi = {10.1016/j.lanmic.2026.101513},
pmid = {42532085},
issn = {2666-5247},
}
RevDate: 2026-07-30
Bivalent gambogic acid-functionalized curcumin nanoparticles with insulin modulate the gut-liver-kidney network in type 2 diabetes.
Journal of controlled release : official journal of the Controlled Release Society pii:S0168-3659(26)00628-0 [Epub ahead of print].
The gut-liver-kidney (GLK) network is a critical driver of type 2 diabetes mellitus (T2DM) complications, where gut dysbiosis triggers cycle of hepatic metabolic stress and subsequent renal dysfunction through a complex, bidirectional signaling crosstalk. Despite its importance, therapeutic strategies capable of addressing this multi-organ crosstalk remain elusive. Here, we demonstrate that bivalent functionalized curcumin-encapsulating PLGA nanoparticles (nGA2-CUR) combined with subcutaneous insulin beneficially modulate the GLK network in obese T2DM mice. This combination therapy successfully stabilized systemic glucose homeostasis and restored essential endocrine signaling (insulin, GLP-1, and GIP) while significantly suppressing pro-inflammatory markers (MCP-1, haptoglobin). Microbiome profiling revealed a suppression of pathobionts alongside distinct sex-specific restorative responses, where males exhibited Muribaculaceae enrichment while females showed Bifidobacterium expansion. Integrated liver metabolomics associated these microbial shifts with unique organ-specific repair responses in each sex. Males showed elevated levels of purine salvage pathway intermediates alongside suppression of a specific pathobiont cluster (including Lautropia and Porphyromonas) correlated with oxidative stress, whereas females replenished aromatic amino acids, consistent with reduced predicted microbial proteolytic potential and lower markers of nephrotoxic uremic toxin production. Molecular analysis confirmed the downregulation of glucose-sensitive pathways (Chrebp/Srebp-1c). These systemic improvements were accompanied by an anti-inflammatory M2 macrophage profile shift, alongside suppression of renal fibrosis via the TGFβ/SMAD network and reduced injury markers (Cystatin C and Osteopontin). Our findings suggest that by reshaping the gut microbiome to alleviate upstream hepatic metabolic burden, this nanoparticle-enhanced therapy provides a sex-specific framework for attenuating irreversible diabetic renal injury.
Additional Links: PMID-42532147
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PubMed:
Citation:
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@article {pmid42532147,
year = {2026},
author = {Allamreddy, SR and Ganugula, R and Gonzalez, A and Arora, M and Friend, R and Kumar, MNVR},
title = {Bivalent gambogic acid-functionalized curcumin nanoparticles with insulin modulate the gut-liver-kidney network in type 2 diabetes.},
journal = {Journal of controlled release : official journal of the Controlled Release Society},
volume = {},
number = {},
pages = {115224},
doi = {10.1016/j.jconrel.2026.115224},
pmid = {42532147},
issn = {1873-4995},
abstract = {The gut-liver-kidney (GLK) network is a critical driver of type 2 diabetes mellitus (T2DM) complications, where gut dysbiosis triggers cycle of hepatic metabolic stress and subsequent renal dysfunction through a complex, bidirectional signaling crosstalk. Despite its importance, therapeutic strategies capable of addressing this multi-organ crosstalk remain elusive. Here, we demonstrate that bivalent functionalized curcumin-encapsulating PLGA nanoparticles (nGA2-CUR) combined with subcutaneous insulin beneficially modulate the GLK network in obese T2DM mice. This combination therapy successfully stabilized systemic glucose homeostasis and restored essential endocrine signaling (insulin, GLP-1, and GIP) while significantly suppressing pro-inflammatory markers (MCP-1, haptoglobin). Microbiome profiling revealed a suppression of pathobionts alongside distinct sex-specific restorative responses, where males exhibited Muribaculaceae enrichment while females showed Bifidobacterium expansion. Integrated liver metabolomics associated these microbial shifts with unique organ-specific repair responses in each sex. Males showed elevated levels of purine salvage pathway intermediates alongside suppression of a specific pathobiont cluster (including Lautropia and Porphyromonas) correlated with oxidative stress, whereas females replenished aromatic amino acids, consistent with reduced predicted microbial proteolytic potential and lower markers of nephrotoxic uremic toxin production. Molecular analysis confirmed the downregulation of glucose-sensitive pathways (Chrebp/Srebp-1c). These systemic improvements were accompanied by an anti-inflammatory M2 macrophage profile shift, alongside suppression of renal fibrosis via the TGFβ/SMAD network and reduced injury markers (Cystatin C and Osteopontin). Our findings suggest that by reshaping the gut microbiome to alleviate upstream hepatic metabolic burden, this nanoparticle-enhanced therapy provides a sex-specific framework for attenuating irreversible diabetic renal injury.},
}
RevDate: 2026-07-28
THE EFFECT OF ENDODONTIC DISINFECTION ON MICROBIAL REDUCTION AND BIODIVERSITY OF ROOT CANAL SYSTEMS WITH NECROTIC PULPS.
Journal of endodontics pii:S0099-2399(26)00383-3 [Epub ahead of print].
AIM: To analyze microbial reduction and diversity changes after cleaning and shaping procedures, and calcium hydroxide interappointment medication. The influence of clinical and radiographic factors was assessed as well.
METHODOLOGY: Thirty-two teeth diagnosed with pulp necrosis and evidence of apical periodontitis were included. Five samples were collected on each tooth: surface sample before access (C1), before treatment (S1), after cleaning and shaping with ultrasonic irrigant activation (S2), at the second visit after removal of the temporary restoration (C2), and after removal of calcium hydroxide (S3). All samples were processed using quantitative real-time polymerase chain reaction (qPCR) and 16S rRNA next generation sequencing. The Shannon and Chao1 indices were used to measure alpha diversity. Differences in abundances of genera were evaluated using the Kruskal-Wallis test. Differences in community composition (beta diversity) were evaluated using analysis of similarity (ANOSIM) with Bray-Curtis dissimilarity matrices.
RESULTS: The qPCR analysis revealed significant differences between S1 and S2 as well as between S1 and S3 (P =0.0001). No significant differences between S2 and S3 were observed for qPCR (P =0.458) as well as for Chao1 alpha diversity. ANOSIM revealed differences between S1 and S3 (P < 0.001, R = 0.59), and between S1 and S2 (P < 0.001, R = 0.40). The presence of percussion sensitivity (ANOSIM R = 0.07, p < 0.023) and sinus tracts (ANOSIM R = 0.06, p < 0.03) had significant interactions with the results. Most of preoperative taxa (top 20) found before treatment were significantly impacted by root canal procedures except Peptostreptococcus and Clostridiales (P > 0.05). The relative abundance of Schaalia (P = 0.004) and Enterococcus (P = 0.001) increased significantly after treatment.
CONCLUSION: A significant reduction in microbial load after instrumentation (S2) and after calcium hydroxide medication (S3) was observed. The effect on root canal composition (beta diversity) was impacted after the cleaning and shaping. No additional changes were observed after the use of calcium hydroxide. The effects produced by clinical factors although significant were low, the results reinforce the value of robust chemical and mechanical disinfection procedures.
Additional Links: PMID-42521142
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PubMed:
Citation:
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@article {pmid42521142,
year = {2026},
author = {Chen, A and Ordinola-Zapata, R and Noblett, WC and Clarke, BC and Baumgardner, KR and Gould, M and Staley, C},
title = {THE EFFECT OF ENDODONTIC DISINFECTION ON MICROBIAL REDUCTION AND BIODIVERSITY OF ROOT CANAL SYSTEMS WITH NECROTIC PULPS.},
journal = {Journal of endodontics},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.joen.2026.07.016},
pmid = {42521142},
issn = {1878-3554},
abstract = {AIM: To analyze microbial reduction and diversity changes after cleaning and shaping procedures, and calcium hydroxide interappointment medication. The influence of clinical and radiographic factors was assessed as well.
METHODOLOGY: Thirty-two teeth diagnosed with pulp necrosis and evidence of apical periodontitis were included. Five samples were collected on each tooth: surface sample before access (C1), before treatment (S1), after cleaning and shaping with ultrasonic irrigant activation (S2), at the second visit after removal of the temporary restoration (C2), and after removal of calcium hydroxide (S3). All samples were processed using quantitative real-time polymerase chain reaction (qPCR) and 16S rRNA next generation sequencing. The Shannon and Chao1 indices were used to measure alpha diversity. Differences in abundances of genera were evaluated using the Kruskal-Wallis test. Differences in community composition (beta diversity) were evaluated using analysis of similarity (ANOSIM) with Bray-Curtis dissimilarity matrices.
RESULTS: The qPCR analysis revealed significant differences between S1 and S2 as well as between S1 and S3 (P =0.0001). No significant differences between S2 and S3 were observed for qPCR (P =0.458) as well as for Chao1 alpha diversity. ANOSIM revealed differences between S1 and S3 (P < 0.001, R = 0.59), and between S1 and S2 (P < 0.001, R = 0.40). The presence of percussion sensitivity (ANOSIM R = 0.07, p < 0.023) and sinus tracts (ANOSIM R = 0.06, p < 0.03) had significant interactions with the results. Most of preoperative taxa (top 20) found before treatment were significantly impacted by root canal procedures except Peptostreptococcus and Clostridiales (P > 0.05). The relative abundance of Schaalia (P = 0.004) and Enterococcus (P = 0.001) increased significantly after treatment.
CONCLUSION: A significant reduction in microbial load after instrumentation (S2) and after calcium hydroxide medication (S3) was observed. The effect on root canal composition (beta diversity) was impacted after the cleaning and shaping. No additional changes were observed after the use of calcium hydroxide. The effects produced by clinical factors although significant were low, the results reinforce the value of robust chemical and mechanical disinfection procedures.},
}
RevDate: 2026-07-28
Controlled incubation, leachate, and pot assays of shrimp shell-based compost for suppressing Verticillium dahliae in olive.
Pest management science [Epub ahead of print].
BACKGROUND: Verticillium wilt of olive (Olea europaea L.), caused by Verticillium dahliae Kleb., is difficult to manage because long-lived microsclerotia persist in soil, and disease risk is influenced by inoculum distribution, irrigation and cultivar susceptibility. This study evaluated mature shrimp shell-based compost (SSC), a chitin-containing circular-economy amendment, for suppressing V. dahliae in naturally infested olive-orchard soil, inhibiting fungal growth in vitro, and reducing disease in a controlled pot assay. Green-waste compost (GWC) was included as a reference amendment.
RESULTS: After 60 days, SSC 5% reduced microsclerotia density by 39.6% and viable microsclerotia by 42.8% relative to unamended soil. Nonsterile SSC leachate inhibited radial growth by 83.7% at 50% (v/v), whereas filter-sterilized leachate retained 58.3% inhibition. In the controlled pot assay, SSC 5% lowered model-estimated final disease incidence from 85% to 30%, and reduced disease severity by 46.5% relative to the infected control. SSC 5% also increased plant height, shoot and root dry weight, leaf area, SPAD index, and rhizosphere chitinase and beta-glucosidase activities.
CONCLUSION: SSC suppressed V. dahliae survival and improved olive plant performance under controlled incubation, in vitro and pot conditions. The results identify SSC as a candidate amendment for further testing, but the proposed inhibitory, chitinolytic, microbiome-mediated, and plant-vigor mechanisms remain hypotheses pending microbiome, pathogen-DNA, metabolite, plant-defense and field validation studies. © 2026 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
Additional Links: PMID-42521216
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PubMed:
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@article {pmid42521216,
year = {2026},
author = {Yaakoub, G and Emna, B and Hfayeth, H and Mohamed Ali, T},
title = {Controlled incubation, leachate, and pot assays of shrimp shell-based compost for suppressing Verticillium dahliae in olive.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.71158},
pmid = {42521216},
issn = {1526-4998},
abstract = {BACKGROUND: Verticillium wilt of olive (Olea europaea L.), caused by Verticillium dahliae Kleb., is difficult to manage because long-lived microsclerotia persist in soil, and disease risk is influenced by inoculum distribution, irrigation and cultivar susceptibility. This study evaluated mature shrimp shell-based compost (SSC), a chitin-containing circular-economy amendment, for suppressing V. dahliae in naturally infested olive-orchard soil, inhibiting fungal growth in vitro, and reducing disease in a controlled pot assay. Green-waste compost (GWC) was included as a reference amendment.
RESULTS: After 60 days, SSC 5% reduced microsclerotia density by 39.6% and viable microsclerotia by 42.8% relative to unamended soil. Nonsterile SSC leachate inhibited radial growth by 83.7% at 50% (v/v), whereas filter-sterilized leachate retained 58.3% inhibition. In the controlled pot assay, SSC 5% lowered model-estimated final disease incidence from 85% to 30%, and reduced disease severity by 46.5% relative to the infected control. SSC 5% also increased plant height, shoot and root dry weight, leaf area, SPAD index, and rhizosphere chitinase and beta-glucosidase activities.
CONCLUSION: SSC suppressed V. dahliae survival and improved olive plant performance under controlled incubation, in vitro and pot conditions. The results identify SSC as a candidate amendment for further testing, but the proposed inhibitory, chitinolytic, microbiome-mediated, and plant-vigor mechanisms remain hypotheses pending microbiome, pathogen-DNA, metabolite, plant-defense and field validation studies. © 2026 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.},
}
RevDate: 2026-07-28
Clinical improvement and scalp microbiome restructuring following a 28-day piroctone olamine shampoo intervention.
International journal of cosmetic science [Epub ahead of print].
OBJECTIVE: To evaluate the clinical efficacy of a piroctone olamine-containing shampoo in individuals with oily dandruff and to characterize associated temporal changes in bacterial and fungal scalp microbiota.
METHODS: An open-label, single-arm, longitudinal study was conducted in 41 volunteers with oily dandruff over 28 days. Participants applied the test shampoo three times weekly. Clinical assessments (erythema, pruritus, desquamation index and sebum levels) were performed at baseline, Day 14, and Day 28. Scalp microbiome samples were collected by standardized swabbing and analyzed using full-length 16S rRNA gene and ITS amplicon sequencing. Microbial community dynamics were evaluated using compositional data analysis, including centred log-ratio transformation, robust Aitchison distance, compositional tensor factorization and linear mixed-effects modelling.
RESULTS: Significant clinical improvement was observed by Day 28, with marked reductions in erythema and pruritus. Sebum levels increased during the study period (p < 0.01), indicating that symptom improvement occurred independently of reduced sebum production. Bacterial community analysis revealed progressive restructuring of the scalp microbiome, becoming most evident by Day 28. This shift was characterized by a descriptive increase in the relative abundance of Cutibacterium acnes together with a numerical decline in Staphylococcus capitis, resulting in an increase in the C. acnes/Staphylococcus ratio from 2.83 to 4.51. Longitudinal compositional analyses further identified several bacterial genera associated with the temporal shift, including Streptococcus, Flavobacterium and Sphingomonas. The fungal community responded earlier to treatment, showing directional reduction of Malassezia-associated dominance together with enrichment of several non-Malassezia genera. Fungal richness increased significantly by Day 14 and remained elevated at Day 28, while beta-diversity analyses confirmed significant temporal restructuring of both bacterial and fungal communities.
CONCLUSION: Use of a piroctone olamine shampoo was associated with significant clinical improvement and measurable shifts in both bacterial and fungal scalp microbiota. These findings suggest that dandruff improvement may coincide with ecological restructuring of the scalp microbiome rather than broad microbial suppression.
Additional Links: PMID-42521217
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PubMed:
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@article {pmid42521217,
year = {2026},
author = {Markos, S and Praefke, L and Kapetanstatakis, Y and Tsanakas, M and Beletsiotis, E},
title = {Clinical improvement and scalp microbiome restructuring following a 28-day piroctone olamine shampoo intervention.},
journal = {International journal of cosmetic science},
volume = {},
number = {},
pages = {},
doi = {10.1111/ics.70128},
pmid = {42521217},
issn = {1468-2494},
abstract = {OBJECTIVE: To evaluate the clinical efficacy of a piroctone olamine-containing shampoo in individuals with oily dandruff and to characterize associated temporal changes in bacterial and fungal scalp microbiota.
METHODS: An open-label, single-arm, longitudinal study was conducted in 41 volunteers with oily dandruff over 28 days. Participants applied the test shampoo three times weekly. Clinical assessments (erythema, pruritus, desquamation index and sebum levels) were performed at baseline, Day 14, and Day 28. Scalp microbiome samples were collected by standardized swabbing and analyzed using full-length 16S rRNA gene and ITS amplicon sequencing. Microbial community dynamics were evaluated using compositional data analysis, including centred log-ratio transformation, robust Aitchison distance, compositional tensor factorization and linear mixed-effects modelling.
RESULTS: Significant clinical improvement was observed by Day 28, with marked reductions in erythema and pruritus. Sebum levels increased during the study period (p < 0.01), indicating that symptom improvement occurred independently of reduced sebum production. Bacterial community analysis revealed progressive restructuring of the scalp microbiome, becoming most evident by Day 28. This shift was characterized by a descriptive increase in the relative abundance of Cutibacterium acnes together with a numerical decline in Staphylococcus capitis, resulting in an increase in the C. acnes/Staphylococcus ratio from 2.83 to 4.51. Longitudinal compositional analyses further identified several bacterial genera associated with the temporal shift, including Streptococcus, Flavobacterium and Sphingomonas. The fungal community responded earlier to treatment, showing directional reduction of Malassezia-associated dominance together with enrichment of several non-Malassezia genera. Fungal richness increased significantly by Day 14 and remained elevated at Day 28, while beta-diversity analyses confirmed significant temporal restructuring of both bacterial and fungal communities.
CONCLUSION: Use of a piroctone olamine shampoo was associated with significant clinical improvement and measurable shifts in both bacterial and fungal scalp microbiota. These findings suggest that dandruff improvement may coincide with ecological restructuring of the scalp microbiome rather than broad microbial suppression.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Resistant starch as a dietary strategy for metabolic and gut health: Implications for Asia-Pacific populations.
Asia Pacific journal of clinical nutrition, 35(4):577-588.
BACKGROUND AND OBJECTIVES: Metabolic diseases are rising rapidly across the Asia-Pacific region as traditional diets are displaced by refined, low-fibre foods. Resistant starch (RS) is a fermentable dietary component that modulates gut microbial activity and short-chain fatty acid (SCFA) production, representing a promising strategy for metabolic and gut health. However, responses to RS vary according to dose, RS type, and individual context.
METHODS AND STUDY DESIGN: This narrative review synthesised evidence from animal and human studies on RS classification, food sources, microbial interactions, and metabolic regulation. We evaluated how responses differ by dose, RS type, baseline microbiome composition, metabolic phenotype, and habitual diet, with particular attention to traditional Asia-Pacific staple foods and ongoing dietary transitions.
RESULTS: Across studies, RS supplementation at moderate-to-high doses improves insulin sensitivity, hepatic lipid accumulation, and markers of gut barrier function, primarily through SCFA-mediated and gut hormone pathways. However, responses are highly context-dependent, varying with baseline metabolic status, micro-biome composition, habitual fibre intake and RS type. Individuals with metabolic disturbances or low fibre intake tend to show greater metabolic and microbial shifts.
CONCLUSIONS: RS is a promising strategy for supporting metabolic and gut health in Asia-Pacific populations undergoing rapid nutritional transition. Culturally familiar RS-rich foods offer practical, regionally tailored intervention opportunities. Standardised characterisation, microbiome-stratified analyses and long-term human studies are needed to clarify who benefits most, under which conditions and through which mechanisms.
Additional Links: PMID-42521223
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PubMed:
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@article {pmid42521223,
year = {2026},
author = {Phuong-Nguyen, K and Rivera, LR and Biesiekierski, JR},
title = {Resistant starch as a dietary strategy for metabolic and gut health: Implications for Asia-Pacific populations.},
journal = {Asia Pacific journal of clinical nutrition},
volume = {35},
number = {4},
pages = {577-588},
doi = {10.6133/apjcn.202608_35(4).0003},
pmid = {42521223},
issn = {1440-6047},
mesh = {Humans ; *Gastrointestinal Microbiome ; Animals ; Asia ; *Diet ; *Starch/administration & dosage ; },
abstract = {BACKGROUND AND OBJECTIVES: Metabolic diseases are rising rapidly across the Asia-Pacific region as traditional diets are displaced by refined, low-fibre foods. Resistant starch (RS) is a fermentable dietary component that modulates gut microbial activity and short-chain fatty acid (SCFA) production, representing a promising strategy for metabolic and gut health. However, responses to RS vary according to dose, RS type, and individual context.
METHODS AND STUDY DESIGN: This narrative review synthesised evidence from animal and human studies on RS classification, food sources, microbial interactions, and metabolic regulation. We evaluated how responses differ by dose, RS type, baseline microbiome composition, metabolic phenotype, and habitual diet, with particular attention to traditional Asia-Pacific staple foods and ongoing dietary transitions.
RESULTS: Across studies, RS supplementation at moderate-to-high doses improves insulin sensitivity, hepatic lipid accumulation, and markers of gut barrier function, primarily through SCFA-mediated and gut hormone pathways. However, responses are highly context-dependent, varying with baseline metabolic status, micro-biome composition, habitual fibre intake and RS type. Individuals with metabolic disturbances or low fibre intake tend to show greater metabolic and microbial shifts.
CONCLUSIONS: RS is a promising strategy for supporting metabolic and gut health in Asia-Pacific populations undergoing rapid nutritional transition. Culturally familiar RS-rich foods offer practical, regionally tailored intervention opportunities. Standardised characterisation, microbiome-stratified analyses and long-term human studies are needed to clarify who benefits most, under which conditions and through which mechanisms.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome
Animals
Asia
*Diet
*Starch/administration & dosage
RevDate: 2026-07-29
CmpDate: 2026-07-29
Causal associations between gut microbiota and inflammatory factors in neonatal jaundice: a Mendelian randomization study.
The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians, 39(1):2709189.
BACKGROUND: Neonatal jaundice is a common clinical condition, affecting approximately 60% of full-term infants and 80% of preterm infants. The majority of neonatal jaundice represents benign physiological hyperbilirubinemia that resolves spontaneously, yet a subset progresses to clinically significant hyperbilirubinemia (CSH), defined as elevated serum bilirubin requiring phototherapy or exchange transfusion to prevent permanent neurotoxic injury. The gut microbiota plays a crucial role in human health and disease, with inflammatory mediators frequently contributing to the body's response to illness or injury, often through their modulation of immune system function. As a result, the interplay between gut microbiota, inflammatory factors, and neonatal jaundice has garnered considerable research interest. Investigating the involvement of gut microbiota and inflammatory factors in neonatal jaundice holds the potential to inform the development of novel therapeutic strategies.
METHODS: This study employed Mendelian Randomization (MR) to investigate the causal relationships between 418 gut microbiota taxa, 91 inflammatory factors, and clinically significant neonatal hyperbilirubinemia. Instrumental variables (IVs) genetic variants used as proxies for the exposure were selected from genome-wide association study (GWAS) summary statistics according to stringent criteria. Five well-established MR methods-namely, inverse variance weighting (IVW), MR-Egger, weighted median, simple mode, and weighted mode-were applied to evaluate the causal associations between gut microbiota composition and susceptibility to neonatal jaundice. Sensitivity analyses and tests for pleiotropy were performed on the MR results to assess the robustness and reliability of the findings.
RESULTS: Mendelian Randomization analysis identified ten bacterial taxa associated with neonatal jaundice. The consistency in the direction of beta values across nine microbial taxa further substantiates the robustness of these associations. Notably, the genus Slackia (id.825) exhibited a protective effect against neonatal jaundice, while the genus Adlercreutzia (id.812) was linked to an increased risk of this condition. Additionally, significant correlations were observed between Adlercreutzia and three inflammatory markers: β-nerve growth factor (NGF), C-X-C motif chemokine 1 (CXCL1), and interleukin-6 (IL-6).
CONCLUSION: This study provides evidence supporting associations between specific gut microbiota taxa and neonatal jaundice, as well as potential links with inflammatory markers. These findings are hypothesis-generating and should be interpreted cautiously, especially because the gut microbiome instruments were derived from adult cohorts rather than neonatal cohorts. They do not support immediate clinical recommendations regarding probiotics or antibiotics in newborns, but may help guide future mechanistic and pediatric validation studies.
Additional Links: PMID-42521607
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@article {pmid42521607,
year = {2026},
author = {Li, Y and Chen, Y and Huang, X and Yang, J and Zhou, Z and Ma, X and Zeng, L},
title = {Causal associations between gut microbiota and inflammatory factors in neonatal jaundice: a Mendelian randomization study.},
journal = {The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians},
volume = {39},
number = {1},
pages = {2709189},
doi = {10.1080/14767058.2026.2709189},
pmid = {42521607},
issn = {1476-4954},
mesh = {Humans ; Mendelian Randomization Analysis ; Infant, Newborn ; *Gastrointestinal Microbiome/genetics ; *Jaundice, Neonatal/microbiology/genetics ; Genome-Wide Association Study ; Inflammation/genetics ; },
abstract = {BACKGROUND: Neonatal jaundice is a common clinical condition, affecting approximately 60% of full-term infants and 80% of preterm infants. The majority of neonatal jaundice represents benign physiological hyperbilirubinemia that resolves spontaneously, yet a subset progresses to clinically significant hyperbilirubinemia (CSH), defined as elevated serum bilirubin requiring phototherapy or exchange transfusion to prevent permanent neurotoxic injury. The gut microbiota plays a crucial role in human health and disease, with inflammatory mediators frequently contributing to the body's response to illness or injury, often through their modulation of immune system function. As a result, the interplay between gut microbiota, inflammatory factors, and neonatal jaundice has garnered considerable research interest. Investigating the involvement of gut microbiota and inflammatory factors in neonatal jaundice holds the potential to inform the development of novel therapeutic strategies.
METHODS: This study employed Mendelian Randomization (MR) to investigate the causal relationships between 418 gut microbiota taxa, 91 inflammatory factors, and clinically significant neonatal hyperbilirubinemia. Instrumental variables (IVs) genetic variants used as proxies for the exposure were selected from genome-wide association study (GWAS) summary statistics according to stringent criteria. Five well-established MR methods-namely, inverse variance weighting (IVW), MR-Egger, weighted median, simple mode, and weighted mode-were applied to evaluate the causal associations between gut microbiota composition and susceptibility to neonatal jaundice. Sensitivity analyses and tests for pleiotropy were performed on the MR results to assess the robustness and reliability of the findings.
RESULTS: Mendelian Randomization analysis identified ten bacterial taxa associated with neonatal jaundice. The consistency in the direction of beta values across nine microbial taxa further substantiates the robustness of these associations. Notably, the genus Slackia (id.825) exhibited a protective effect against neonatal jaundice, while the genus Adlercreutzia (id.812) was linked to an increased risk of this condition. Additionally, significant correlations were observed between Adlercreutzia and three inflammatory markers: β-nerve growth factor (NGF), C-X-C motif chemokine 1 (CXCL1), and interleukin-6 (IL-6).
CONCLUSION: This study provides evidence supporting associations between specific gut microbiota taxa and neonatal jaundice, as well as potential links with inflammatory markers. These findings are hypothesis-generating and should be interpreted cautiously, especially because the gut microbiome instruments were derived from adult cohorts rather than neonatal cohorts. They do not support immediate clinical recommendations regarding probiotics or antibiotics in newborns, but may help guide future mechanistic and pediatric validation studies.},
}
MeSH Terms:
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Humans
Mendelian Randomization Analysis
Infant, Newborn
*Gastrointestinal Microbiome/genetics
*Jaundice, Neonatal/microbiology/genetics
Genome-Wide Association Study
Inflammation/genetics
RevDate: 2026-07-29
CmpDate: 2026-07-29
Machine learning reveals biocontrol agents shaping disease outcome in natural Arabidopsis populations.
Nature communications, 17(1):.
Plants recruit antagonistic microbes to defend against phytopathogens, offering a route to rational biocontrol beyond empirical screening. Here, using six generations of leaf-microbiome data from natural Arabidopsis populations infected by the oomycete Albugo laibachii, we show that microbial diversity is driven by infection, site, and host genotype, and that infected plants form modular networks with increased inter-kingdom antagonism. We train four machine-learning models to discriminate infected from uninfected plants by microbiota composition and identify microbes enriched in diseased (disease-associated) or healthy (health-associated) plants. Testing the most predictive bacteria, fungi, and cercozoa in planta, we find all confer varying protection against Albugo, with health-associated microbes outperforming disease-associated taxa. The best candidate, a Cystofilobasidium fungus, is validated in a synthetic community, where genomic and community assays indicate biocontrol acts mainly through microbe-microbe interactions rather than plant immune activation. This work shows that pairing microbiome data with machine learning identifies effective biocontrol agents.
Additional Links: PMID-42521687
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Citation:
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@article {pmid42521687,
year = {2026},
author = {Mahmoudi, M and Hu, Y and Almario, J and Stincone, P and Tenzer, LM and Chaudhry, V and Braun, L and Quinzer, S and Nieselt, K and Kemen, E},
title = {Machine learning reveals biocontrol agents shaping disease outcome in natural Arabidopsis populations.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42521687},
issn = {2041-1723},
support = {DeCoCt ERC-2018-COG 820124//EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council)/ ; SPP 2125 DECRyPT//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; TRR 356 PlantMicrobe//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; Germany's excellence strategy-EXC 2124-390838134//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; },
mesh = {*Arabidopsis/microbiology/genetics ; *Plant Diseases/microbiology/prevention & control ; *Machine Learning ; Microbiota/genetics ; *Oomycetes/physiology/pathogenicity ; Plant Leaves/microbiology ; Host-Pathogen Interactions ; },
abstract = {Plants recruit antagonistic microbes to defend against phytopathogens, offering a route to rational biocontrol beyond empirical screening. Here, using six generations of leaf-microbiome data from natural Arabidopsis populations infected by the oomycete Albugo laibachii, we show that microbial diversity is driven by infection, site, and host genotype, and that infected plants form modular networks with increased inter-kingdom antagonism. We train four machine-learning models to discriminate infected from uninfected plants by microbiota composition and identify microbes enriched in diseased (disease-associated) or healthy (health-associated) plants. Testing the most predictive bacteria, fungi, and cercozoa in planta, we find all confer varying protection against Albugo, with health-associated microbes outperforming disease-associated taxa. The best candidate, a Cystofilobasidium fungus, is validated in a synthetic community, where genomic and community assays indicate biocontrol acts mainly through microbe-microbe interactions rather than plant immune activation. This work shows that pairing microbiome data with machine learning identifies effective biocontrol agents.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Arabidopsis/microbiology/genetics
*Plant Diseases/microbiology/prevention & control
*Machine Learning
Microbiota/genetics
*Oomycetes/physiology/pathogenicity
Plant Leaves/microbiology
Host-Pathogen Interactions
RevDate: 2026-07-29
CmpDate: 2026-07-29
Inhalation of cadmium oxide nanoparticles alters intestinal and pulmonary microbiomes in mice.
Applied microbiology and biotechnology, 110(1):.
Exposure to cadmium (Cd), a toxic heavy metal, is a severe threat to organismal health, causing a wide range of pathological alterations in various tissues and organs. Alterations in the composition and function of the gut microbiome have been indicated across numerous animals exposed to Cd. However, the impact of Cd inhalation exposure on the pulmonary microbiome has not been well investigated yet. Therefore, in this study, we investigated the effects of exposure to CdONPs and its clearance on both colonic and pulmonary microbiomes in mice. The diversity of both colonic and pulmonary microbiomes of exposed mice was significantly affected after 9 weeks of CdONPs inhalation. The effects of CdONPs exposure on bacterial composition and function were more pronounced in the colonic microbiome than in the pulmonary microbiome. The clearance was more efficient in the restoration of gut microbiome composition in comparison to the lung microbiome. Moreover, we evaluated a bidirectional interaction between Cd exposure and gut microbiota. Duncaniella, Odoribacter, and Pontibacter were the prominent biomarkers that significantly positively correlated with dysregulated functions in the colonic microbiome of exposed mice. Based on the PICRUSt2 prediction analysis, our results suggested that perturbations in the gut microbiota balance due to Cd exposure were associated with the increase in the proportion level of bacteria with excessive membrane transporters, which may potentially augment the absorption of this metal by intestinal microbiota thereby leading to the accumulation of Cd in intestinal bacteria and the potential alleviation of the Cd toxicity effect. Furthermore, genes related to metal chelators were consistent with the colonic microbiome of exposed mice, suggesting possible promotion of Cd excretion and its eventual fecal elimination. However, these observations derived from 16S rRNA profiling and PICRUSt2 predictions would need to be verified experimentally to establish any functional or mechanistic implications. This could be considered a key factor in determining the intestinal bacterial species able to minimize the toxicity of heavy metals in future therapeutic approaches. KEY POINTS: • Inhalation of CdO nanoparticles significantly alters both gut and pulmonary microbiome composition and diversity in mice. • Microbiome changes are more pronounced in the gut than in the lungs following inhalation exposure. • Partial recovery of microbiome composition occurs after the clearance period, with greater restoration in the gut than in the lung. • Predicted functional profiles indicate shifts in microbial metabolic potential associated with Cd exposure. • The findings support a potential interaction between inhaled Cd exposure and the gut microbiome, highlighting the relevance of the gut-lung axis.
Additional Links: PMID-42521792
PubMed:
Citation:
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@article {pmid42521792,
year = {2026},
author = {Mekadim, C and Kristeková, D and Mikuška, P and Buchtová, M and Mrázek, J},
title = {Inhalation of cadmium oxide nanoparticles alters intestinal and pulmonary microbiomes in mice.},
journal = {Applied microbiology and biotechnology},
volume = {110},
number = {1},
pages = {},
pmid = {42521792},
issn = {1432-0614},
support = {24-10051S//Czech Science Foundation/ ; },
mesh = {Animals ; *Lung/microbiology/drug effects ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Oxides/administration & dosage/toxicity ; *Cadmium Compounds/administration & dosage/toxicity ; *Microbiota/drug effects ; Bacteria/classification/drug effects/genetics ; Male ; Colon/microbiology ; *Nanoparticles/administration & dosage ; *Inhalation Exposure ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Exposure to cadmium (Cd), a toxic heavy metal, is a severe threat to organismal health, causing a wide range of pathological alterations in various tissues and organs. Alterations in the composition and function of the gut microbiome have been indicated across numerous animals exposed to Cd. However, the impact of Cd inhalation exposure on the pulmonary microbiome has not been well investigated yet. Therefore, in this study, we investigated the effects of exposure to CdONPs and its clearance on both colonic and pulmonary microbiomes in mice. The diversity of both colonic and pulmonary microbiomes of exposed mice was significantly affected after 9 weeks of CdONPs inhalation. The effects of CdONPs exposure on bacterial composition and function were more pronounced in the colonic microbiome than in the pulmonary microbiome. The clearance was more efficient in the restoration of gut microbiome composition in comparison to the lung microbiome. Moreover, we evaluated a bidirectional interaction between Cd exposure and gut microbiota. Duncaniella, Odoribacter, and Pontibacter were the prominent biomarkers that significantly positively correlated with dysregulated functions in the colonic microbiome of exposed mice. Based on the PICRUSt2 prediction analysis, our results suggested that perturbations in the gut microbiota balance due to Cd exposure were associated with the increase in the proportion level of bacteria with excessive membrane transporters, which may potentially augment the absorption of this metal by intestinal microbiota thereby leading to the accumulation of Cd in intestinal bacteria and the potential alleviation of the Cd toxicity effect. Furthermore, genes related to metal chelators were consistent with the colonic microbiome of exposed mice, suggesting possible promotion of Cd excretion and its eventual fecal elimination. However, these observations derived from 16S rRNA profiling and PICRUSt2 predictions would need to be verified experimentally to establish any functional or mechanistic implications. This could be considered a key factor in determining the intestinal bacterial species able to minimize the toxicity of heavy metals in future therapeutic approaches. KEY POINTS: • Inhalation of CdO nanoparticles significantly alters both gut and pulmonary microbiome composition and diversity in mice. • Microbiome changes are more pronounced in the gut than in the lungs following inhalation exposure. • Partial recovery of microbiome composition occurs after the clearance period, with greater restoration in the gut than in the lung. • Predicted functional profiles indicate shifts in microbial metabolic potential associated with Cd exposure. • The findings support a potential interaction between inhaled Cd exposure and the gut microbiome, highlighting the relevance of the gut-lung axis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Lung/microbiology/drug effects
*Gastrointestinal Microbiome/drug effects
Mice
*Oxides/administration & dosage/toxicity
*Cadmium Compounds/administration & dosage/toxicity
*Microbiota/drug effects
Bacteria/classification/drug effects/genetics
Male
Colon/microbiology
*Nanoparticles/administration & dosage
*Inhalation Exposure
RNA, Ribosomal, 16S/genetics
RevDate: 2026-07-29
CmpDate: 2026-07-29
Earthworm Gut Microbiota as a Biological Driver of Plastic Degradation: Implications for Microplastic Mitigation.
Environmental microbiology, 28(8):e70387.
Microplastic pollution in terrestrial environments has emerged as a growing threat to agricultural sustainability. Earthworms and their gut microbiota have recently attracted attention as potential nature-based agents for microplastic mitigation. This study systematically synthesizes empirical evidence on the role of earthworm intestinal microorganisms in the transformation and potential biodegradation of microplastics. A literature synthesis was conducted using Scopus-indexed, peer-reviewed publications published between 2018 and 2025 that examined interactions among microplastics, earthworms, and gut microbiota. The synthesis indicates that microplastic degradation within the earthworm digestive system is a multifactorial process involving mechanical fragmentation, selective microbial enrichment, and biological and metabolic activity. Across different earthworm species and polymer types, the phyla Actinobacteria, Proteobacteria, and Firmicutes consistently dominated the gut microbiome. Several genera, including Bacillus, Paenibacillus, Rhodococcus and Streptomyces, were repeatedly associated with microplastic transformation. Earthworm activity may also improve nutrient availability, stabilize soil microbial communities and enhance plant tolerance to microplastic-induced stress. However, major gaps remain in quantifying biodegradation rates, determining microbial removal efficiency and identifying enzymes directly involved in plastic degradation. Overall, this synthesis positions vermiremediation as a promising strategy for managing terrestrial microplastic contamination, while underscoring the need for stronger mechanistic evidence to support practical application.
Additional Links: PMID-42522116
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PubMed:
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@article {pmid42522116,
year = {2026},
author = {Rahayu, ID and Iswahyudi, I and Sutanto, A and Garfansa, MP and Meylanzharie, Z and Nurfadilah, LR and Amani, SA and Hidayati, A and Ekalaturrahmah, YAC and Gafur, MAA and Chanan, M and Budiyono, A},
title = {Earthworm Gut Microbiota as a Biological Driver of Plastic Degradation: Implications for Microplastic Mitigation.},
journal = {Environmental microbiology},
volume = {28},
number = {8},
pages = {e70387},
doi = {10.1111/1462-2920.70387},
pmid = {42522116},
issn = {1462-2920},
support = {E.2.a/275.10/RPK/UMM/2025//Universitas Muhammadiyah Malang/ ; },
mesh = {Animals ; *Oligochaeta/microbiology/metabolism ; *Biodegradation, Environmental ; *Microplastics/metabolism ; *Gastrointestinal Microbiome ; Bacteria/metabolism/classification/genetics/isolation & purification ; *Soil Pollutants/metabolism ; Soil Microbiology ; },
abstract = {Microplastic pollution in terrestrial environments has emerged as a growing threat to agricultural sustainability. Earthworms and their gut microbiota have recently attracted attention as potential nature-based agents for microplastic mitigation. This study systematically synthesizes empirical evidence on the role of earthworm intestinal microorganisms in the transformation and potential biodegradation of microplastics. A literature synthesis was conducted using Scopus-indexed, peer-reviewed publications published between 2018 and 2025 that examined interactions among microplastics, earthworms, and gut microbiota. The synthesis indicates that microplastic degradation within the earthworm digestive system is a multifactorial process involving mechanical fragmentation, selective microbial enrichment, and biological and metabolic activity. Across different earthworm species and polymer types, the phyla Actinobacteria, Proteobacteria, and Firmicutes consistently dominated the gut microbiome. Several genera, including Bacillus, Paenibacillus, Rhodococcus and Streptomyces, were repeatedly associated with microplastic transformation. Earthworm activity may also improve nutrient availability, stabilize soil microbial communities and enhance plant tolerance to microplastic-induced stress. However, major gaps remain in quantifying biodegradation rates, determining microbial removal efficiency and identifying enzymes directly involved in plastic degradation. Overall, this synthesis positions vermiremediation as a promising strategy for managing terrestrial microplastic contamination, while underscoring the need for stronger mechanistic evidence to support practical application.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Oligochaeta/microbiology/metabolism
*Biodegradation, Environmental
*Microplastics/metabolism
*Gastrointestinal Microbiome
Bacteria/metabolism/classification/genetics/isolation & purification
*Soil Pollutants/metabolism
Soil Microbiology
RevDate: 2026-07-29
CmpDate: 2026-07-29
The microbiome of the wood-dwelling Cossus cossus (Lepidoptera: Cossidae): a functional approach.
Environmental entomology, 55(4):.
Microorganisms associated with insects can offer diverse benefits to their host, but the degree to which hosts rely on them varies across insect groups. Although research has increasingly focused on Lepidoptera, many of which are important pest species, key aspects of their microbiome's stability and functional importance remain ambiguous and seem context-dependent. The caterpillars of the goat moth, Cossus cossus (Linnaeus), which develop over 2 to 5 years within trunks of deciduous trees and consume a wood-based diet rich in recalcitrant lignin, provide an intriguing model to examine potential microbial contributions to lignocellulose degradation. Full-length 16S rRNA gene sequencing revealed a gut microbiome dominated by Enterococcus spp. and a high Leuconostoc spp. presence in the mandibular glands. Concurrent culturomics approaches recovered 64 taxa identified by sequencing and uncovered additional diversity, such as Brevibacterium spp. and Streptomyces spp. Notably, several isolates, including strains of Acinetobacter johnsonii, Citrobacter gillenii, Leucobacter sp., and Pseudomonas sp., demonstrated growth on minimal media supplemented with wood, lignin, or lignin-derived aromatics as the sole carbon and energy sources. These findings provide the first evidence that specific bacterial members of the goat moth caterpillar's microbiome may contribute to wood digestion, suggesting a functional symbiosis suited to a challenging dietary niche.
Additional Links: PMID-42522258
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PubMed:
Citation:
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@article {pmid42522258,
year = {2026},
author = {Curias, C and Wieme, AD and Joossens, M and Vandamme, P},
title = {The microbiome of the wood-dwelling Cossus cossus (Lepidoptera: Cossidae): a functional approach.},
journal = {Environmental entomology},
volume = {55},
number = {4},
pages = {},
doi = {10.1093/ee/nvag081},
pmid = {42522258},
issn = {1938-2936},
mesh = {Animals ; *Moths/microbiology/growth & development ; *Bacteria/classification/isolation & purification/genetics ; RNA, Ribosomal, 16S/analysis/genetics ; Wood ; Larva/microbiology/growth & development ; *Microbiota ; *Gastrointestinal Microbiome ; Lignin/metabolism ; },
abstract = {Microorganisms associated with insects can offer diverse benefits to their host, but the degree to which hosts rely on them varies across insect groups. Although research has increasingly focused on Lepidoptera, many of which are important pest species, key aspects of their microbiome's stability and functional importance remain ambiguous and seem context-dependent. The caterpillars of the goat moth, Cossus cossus (Linnaeus), which develop over 2 to 5 years within trunks of deciduous trees and consume a wood-based diet rich in recalcitrant lignin, provide an intriguing model to examine potential microbial contributions to lignocellulose degradation. Full-length 16S rRNA gene sequencing revealed a gut microbiome dominated by Enterococcus spp. and a high Leuconostoc spp. presence in the mandibular glands. Concurrent culturomics approaches recovered 64 taxa identified by sequencing and uncovered additional diversity, such as Brevibacterium spp. and Streptomyces spp. Notably, several isolates, including strains of Acinetobacter johnsonii, Citrobacter gillenii, Leucobacter sp., and Pseudomonas sp., demonstrated growth on minimal media supplemented with wood, lignin, or lignin-derived aromatics as the sole carbon and energy sources. These findings provide the first evidence that specific bacterial members of the goat moth caterpillar's microbiome may contribute to wood digestion, suggesting a functional symbiosis suited to a challenging dietary niche.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Moths/microbiology/growth & development
*Bacteria/classification/isolation & purification/genetics
RNA, Ribosomal, 16S/analysis/genetics
Wood
Larva/microbiology/growth & development
*Microbiota
*Gastrointestinal Microbiome
Lignin/metabolism
RevDate: 2026-07-29
CmpDate: 2026-07-29
Microbiome dysbiosis in psoriatic skin among Asian populations: Insights from a systematic review and meta-analysis.
Dermatology online journal, 32(3):.
BACKGROUND: Psoriasis is a chronic immune-mediated skin disease increasingly associated with microbial dysbiosis.
OBJECTIVE: To clarify patterns of skin microbiome alteration in psoriasis.
METHODS: We conducted a systematic review and meta-analysis of Asian cohort studies. Eleven studies were included.
RESULTS: Results for α-diversity were inconsistent, with Shannon and Simpson indices showing heterogeneous outcomes. In contrast, genus-level analysis revealed consistent taxonomic trends: psoriatic lesions demonstrated enrichment of Staphylococcus and Streptococcus with concurrent depletion of Cutibacterium. Fungal analyses showed redistribution of Malassezia species, with increased burden reported in Japanese, Chinese, and Iranian cohorts. Funnel plots indicated limited publication bias, and sensitivity analyses confirmed that exclusion of therapeutic cohorts did not alter results. Importantly, IL-17A inhibitor studies demonstrated partial restoration of microbial balance following treatment. These findings provide reproducible evidence of microbiome shifts in psoriatic skin across Asian populations. The results suggest that specific bacterial and fungal taxa may serve as biomarkers of disease activity and therapeutic response.
CONCLUSION: Future mechanistic work should integrate microbiome and host immune pathways to advance development of microbiome-targeted interventions in psoriasis.
Additional Links: PMID-42522515
PubMed:
Citation:
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@article {pmid42522515,
year = {2026},
author = {Khan, S and Hussain, D and Ahmad, H and Ahmed, S},
title = {Microbiome dysbiosis in psoriatic skin among Asian populations: Insights from a systematic review and meta-analysis.},
journal = {Dermatology online journal},
volume = {32},
number = {3},
pages = {},
pmid = {42522515},
issn = {1087-2108},
mesh = {Humans ; *Psoriasis/microbiology/drug therapy ; *Skin Microbiome ; Asian People ; *Dysbiosis/microbiology ; Malassezia/isolation & purification ; *Skin/microbiology ; },
abstract = {BACKGROUND: Psoriasis is a chronic immune-mediated skin disease increasingly associated with microbial dysbiosis.
OBJECTIVE: To clarify patterns of skin microbiome alteration in psoriasis.
METHODS: We conducted a systematic review and meta-analysis of Asian cohort studies. Eleven studies were included.
RESULTS: Results for α-diversity were inconsistent, with Shannon and Simpson indices showing heterogeneous outcomes. In contrast, genus-level analysis revealed consistent taxonomic trends: psoriatic lesions demonstrated enrichment of Staphylococcus and Streptococcus with concurrent depletion of Cutibacterium. Fungal analyses showed redistribution of Malassezia species, with increased burden reported in Japanese, Chinese, and Iranian cohorts. Funnel plots indicated limited publication bias, and sensitivity analyses confirmed that exclusion of therapeutic cohorts did not alter results. Importantly, IL-17A inhibitor studies demonstrated partial restoration of microbial balance following treatment. These findings provide reproducible evidence of microbiome shifts in psoriatic skin across Asian populations. The results suggest that specific bacterial and fungal taxa may serve as biomarkers of disease activity and therapeutic response.
CONCLUSION: Future mechanistic work should integrate microbiome and host immune pathways to advance development of microbiome-targeted interventions in psoriasis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Psoriasis/microbiology/drug therapy
*Skin Microbiome
Asian People
*Dysbiosis/microbiology
Malassezia/isolation & purification
*Skin/microbiology
RevDate: 2026-07-29
CmpDate: 2026-07-29
[Artificial intelligence-based mining of antimicrobial peptides in the microbiome].
Sheng wu gong cheng xue bao = Chinese journal of biotechnology, 42(7):2881-2901.
Antimicrobial peptides (AMPs) are small-molecule polypeptides with broad-spectrum antimicrobial activity that are induced by the innate immune system of organisms and constitute a crucial component of the innate immune defense. With the misuse of antibiotics and other antimicrobial agents, the problem of bacterial resistance has become increasingly severe. Naturally occurring AMPs derived from the microbiome, owing to their broad availability, stable physicochemical properties, relatively low propensity to induce resistance, and capacity to contribute to the maintenance of commensal microbiota homeostasis, are regarded as beneficial supplements and adjuvant therapeutic strategies to traditional antibiotics. In recent years, the rapid advancement of artificial intelligence (AI) technologies has facilitated their application in the field of drug discovery, thereby opening new avenues for the large-scale screening of AMPs and substantially accelerating the overall research progress. This review summarizes the developmental trajectory of AMP research methodologies from early approaches to the present day and provides a comparative overview of AI-based AMP screening tools and databases. In addition, the criteria for AMP screening and the recent progress in AI-assisted AMP development, both domestically and internationally, are systematically compiled. The aim of this review is to provide a systematic synthesis of the methodological framework for AI-based mining of microbiome-derived AMPs, thereby offering theoretical references and technical guidance for the efficient identification of novel AMPs. It is anticipated that this review will stimulate further consideration regarding AMP screening and design, and will promote advancements in the field of human health in the era of AI.
Additional Links: PMID-42522607
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PubMed:
Citation:
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@article {pmid42522607,
year = {2026},
author = {Guo, X and Mo, N and Fu, T and Lai, Y and Hou, X and Zhou, Y},
title = {[Artificial intelligence-based mining of antimicrobial peptides in the microbiome].},
journal = {Sheng wu gong cheng xue bao = Chinese journal of biotechnology},
volume = {42},
number = {7},
pages = {2881-2901},
doi = {10.13345/j.cjb.250842},
pmid = {42522607},
issn = {1872-2075},
support = {32402702//the National Natural Science Foundation of China/ ; LMS25C170002//the Natural Science Foundation of Zhejiang Province/ ; 2024-2026QNRC001//the Young Elite Scientists Sponsorship Program by CAST/ ; },
mesh = {*Artificial Intelligence ; *Antimicrobial Peptides ; *Microbiota ; Humans ; Drug Discovery ; *Data Mining ; },
abstract = {Antimicrobial peptides (AMPs) are small-molecule polypeptides with broad-spectrum antimicrobial activity that are induced by the innate immune system of organisms and constitute a crucial component of the innate immune defense. With the misuse of antibiotics and other antimicrobial agents, the problem of bacterial resistance has become increasingly severe. Naturally occurring AMPs derived from the microbiome, owing to their broad availability, stable physicochemical properties, relatively low propensity to induce resistance, and capacity to contribute to the maintenance of commensal microbiota homeostasis, are regarded as beneficial supplements and adjuvant therapeutic strategies to traditional antibiotics. In recent years, the rapid advancement of artificial intelligence (AI) technologies has facilitated their application in the field of drug discovery, thereby opening new avenues for the large-scale screening of AMPs and substantially accelerating the overall research progress. This review summarizes the developmental trajectory of AMP research methodologies from early approaches to the present day and provides a comparative overview of AI-based AMP screening tools and databases. In addition, the criteria for AMP screening and the recent progress in AI-assisted AMP development, both domestically and internationally, are systematically compiled. The aim of this review is to provide a systematic synthesis of the methodological framework for AI-based mining of microbiome-derived AMPs, thereby offering theoretical references and technical guidance for the efficient identification of novel AMPs. It is anticipated that this review will stimulate further consideration regarding AMP screening and design, and will promote advancements in the field of human health in the era of AI.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Artificial Intelligence
*Antimicrobial Peptides
*Microbiota
Humans
Drug Discovery
*Data Mining
RevDate: 2026-07-29
CmpDate: 2026-07-29
Microbial Composition Study in Cholangiocarcinoma: Stage-Specific Diversity Analysis in Bile and Tumor Microbiome.
Asian Pacific journal of cancer prevention : APJCP, 27(7):2509-2518 pii:92271.
OBJECTIVE: Cholangiocarcinoma (CCA) is an aggressive malignancy of the biliary tract with poor prognosis and limited early diagnostic tools. Microbial dysbiosis has been implicated in carcinogenesis, yet microbial signatures across disease stages and anatomical sites in CCA remain poorly defined. This study aimed to characterize the microbial diversity in bile and tumor tissue of CCA patients and evaluate association with disease stage.
METHODS: Microbiome profiles were analyzed from 36 subjects using 16Sr RNA gene sequencing data from the Sequence Read Archive (SRA). Alpha diversity (Chao1 index) and beta diversity (Bray-Curtis dissimilarity) were assessed across bile and intratumoral samples. Linear discriminant analysis effect size (LEfSe) was employed to identify stage-specific microbial taxa.
RESULT: Alpha diversity did not differ significantly between disease stages (ANOVA, F = 0.385, p = 0.816), suggesting stable microbial richness throughout progression. However, beta diversity analysis (PERMANOVA, R² = 0.279, p = 0.013) revealed distinct clustering by sample type and tumor stage. LEfSe identified enrichment of Fusobacterium, Escherichia-Shigella, and Enterococcus in advanced-stage tumor samples, while Lactobacillus and Streptococcus were more abundant in early-stage bile samples.
CONCLUSION: This study demonstrates distinct microbial composition patterns across disease stages and anatomical sites in CCA. Enrichment of specific pathogenic taxa in advanced stages supports a role for microbiome alterations in CCA pathogenesis. Microbial markers may serve as potential tools for staging and prognosis, warranting further functional and prospective validation studies.
Additional Links: PMID-42522811
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PubMed:
Citation:
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@article {pmid42522811,
year = {2026},
author = {Sindhughosa, DA and Mariadi, IK and Lesmana Dewi, PIS and Pamungkas, KMN and Yunia Dewi, NLP and Dewi, NNGK and Alamsyah, AZ and Widiada, PA},
title = {Microbial Composition Study in Cholangiocarcinoma: Stage-Specific Diversity Analysis in Bile and Tumor Microbiome.},
journal = {Asian Pacific journal of cancer prevention : APJCP},
volume = {27},
number = {7},
pages = {2509-2518},
doi = {10.31557/APJCP.2026.27.7.2509},
pmid = {42522811},
issn = {2476-762X},
mesh = {Humans ; *Cholangiocarcinoma/microbiology/pathology ; *Bile Duct Neoplasms/microbiology/pathology/genetics ; *Microbiota ; Female ; Male ; *Bile/microbiology ; Prognosis ; RNA, Ribosomal, 16S/genetics ; Middle Aged ; Neoplasm Staging ; *Bacteria/genetics/classification/isolation & purification ; Follow-Up Studies ; Aged ; },
abstract = {OBJECTIVE: Cholangiocarcinoma (CCA) is an aggressive malignancy of the biliary tract with poor prognosis and limited early diagnostic tools. Microbial dysbiosis has been implicated in carcinogenesis, yet microbial signatures across disease stages and anatomical sites in CCA remain poorly defined. This study aimed to characterize the microbial diversity in bile and tumor tissue of CCA patients and evaluate association with disease stage.
METHODS: Microbiome profiles were analyzed from 36 subjects using 16Sr RNA gene sequencing data from the Sequence Read Archive (SRA). Alpha diversity (Chao1 index) and beta diversity (Bray-Curtis dissimilarity) were assessed across bile and intratumoral samples. Linear discriminant analysis effect size (LEfSe) was employed to identify stage-specific microbial taxa.
RESULT: Alpha diversity did not differ significantly between disease stages (ANOVA, F = 0.385, p = 0.816), suggesting stable microbial richness throughout progression. However, beta diversity analysis (PERMANOVA, R² = 0.279, p = 0.013) revealed distinct clustering by sample type and tumor stage. LEfSe identified enrichment of Fusobacterium, Escherichia-Shigella, and Enterococcus in advanced-stage tumor samples, while Lactobacillus and Streptococcus were more abundant in early-stage bile samples.
CONCLUSION: This study demonstrates distinct microbial composition patterns across disease stages and anatomical sites in CCA. Enrichment of specific pathogenic taxa in advanced stages supports a role for microbiome alterations in CCA pathogenesis. Microbial markers may serve as potential tools for staging and prognosis, warranting further functional and prospective validation studies.},
}
MeSH Terms:
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Humans
*Cholangiocarcinoma/microbiology/pathology
*Bile Duct Neoplasms/microbiology/pathology/genetics
*Microbiota
Female
Male
*Bile/microbiology
Prognosis
RNA, Ribosomal, 16S/genetics
Middle Aged
Neoplasm Staging
*Bacteria/genetics/classification/isolation & purification
Follow-Up Studies
Aged
RevDate: 2026-07-29
Spatial microbiome and synthetic community analyses reveal Trinickia sclerotiorum sp. nov. promotes sclerotia mortality of Sclerotinia sclerotiorum.
The ISME journal pii:8746741 [Epub ahead of print].
Bulk microbiome analysis obscures the spatial heterogeneity of microbial communities, limiting the understanding of bacterial distribution inside fungal sclerotia, which are the survival structures of the plant pathogen Sclerotinia sclerotiorum. Although studies have profiled microbiomes of different fungal structures, sclerotia microbiome remains largely unexplored. We applied bulk microbiome using PacBio full-length 16S rRNA sequencing, synthetic community (SynCom), and 10x Genomics Xenium platform to resolve the spatiotemporal contribution of soil bacteria to sclerotia mortality. In the bulk microbiome, the relative abundance of soil bacteria such as Massilia and Trinickia were enriched when sclerotia mortality increased under flooding conditions. Twelve enriched sclerotia-associated bacteria were assembled into a SynCom to study their causality for sclerotia mortality. Spatial microbiome analysis revealed the temporal dynamics and distribution pattern of each SynCom member. Among them, Trinickia sclerotiorum sp. nov. type strain MC (TsMC) was found to reach the most interior sclerotia and its relative abundance coincided with sclerotia mortality. TsMC exhibits the highest importance in four antagonistic assays and SynCom drop-out test. Whole genome sequencing confirmed TsMC as a novel species with antifungal potentials. Collectively, we document a novel bacterium for sclerotia mortality and demonstrate the advantage of spatiotemporal distribution in microbiome research.
Additional Links: PMID-42523014
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PubMed:
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@article {pmid42523014,
year = {2026},
author = {Shie, ZH and Chang, HX},
title = {Spatial microbiome and synthetic community analyses reveal Trinickia sclerotiorum sp. nov. promotes sclerotia mortality of Sclerotinia sclerotiorum.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag201},
pmid = {42523014},
issn = {1751-7370},
abstract = {Bulk microbiome analysis obscures the spatial heterogeneity of microbial communities, limiting the understanding of bacterial distribution inside fungal sclerotia, which are the survival structures of the plant pathogen Sclerotinia sclerotiorum. Although studies have profiled microbiomes of different fungal structures, sclerotia microbiome remains largely unexplored. We applied bulk microbiome using PacBio full-length 16S rRNA sequencing, synthetic community (SynCom), and 10x Genomics Xenium platform to resolve the spatiotemporal contribution of soil bacteria to sclerotia mortality. In the bulk microbiome, the relative abundance of soil bacteria such as Massilia and Trinickia were enriched when sclerotia mortality increased under flooding conditions. Twelve enriched sclerotia-associated bacteria were assembled into a SynCom to study their causality for sclerotia mortality. Spatial microbiome analysis revealed the temporal dynamics and distribution pattern of each SynCom member. Among them, Trinickia sclerotiorum sp. nov. type strain MC (TsMC) was found to reach the most interior sclerotia and its relative abundance coincided with sclerotia mortality. TsMC exhibits the highest importance in four antagonistic assays and SynCom drop-out test. Whole genome sequencing confirmed TsMC as a novel species with antifungal potentials. Collectively, we document a novel bacterium for sclerotia mortality and demonstrate the advantage of spatiotemporal distribution in microbiome research.},
}
RevDate: 2026-07-29
The faecal microbiome and carriage of Salmonella in Australian captive pythons.
FEMS microbiology ecology pii:8746770 [Epub ahead of print].
There is a growing interest in keeping exotic pets such as pythons in Australia. Reptiles are known asymptomatic carriers of Salmonella in their digestive tract. This study investigated the microbiome and carriage of Salmonella in faeces from captive Australian pythons (n=28). This study also aimed to determine the effect of temperature and nutrient availability on monospecies biofilm formation of python-associated Salmonella isolated in this study (n=10) as a possible indicator of persistence. A total of 23 Salmonella strains were identified from 28 captive Australian pythons, representing diverse serovars of subspecies enterica, namely S. Bergedorf, S. Havana, S. Jangwani, S. Java, S. Kottbus, S. Muenchen, and S. Umbadah, as well as subspecies S. diarizonae and S. salamae. The composition of the microbial communities differed according to sampling location, diet and Salmonella serovars or subspecies. Bacillota, Bacteroidota, and Pseudomonadota were the most abundant taxa across the faecal microbiome. Strains belonging to subspecies enterica were generally poorer biofilm formers than strains belonging to subspecies salamae and diarizonae. This study shows that microbial communities are variable depending on the environmental factors, which could increase the risk of acquiring reptile-associated salmonellosis whilst handling captive pythons.
Additional Links: PMID-42523065
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@article {pmid42523065,
year = {2026},
author = {Sarjit, A and Hall, AM and Sellapperumage, N and Makings, C and Dykes, GA},
title = {The faecal microbiome and carriage of Salmonella in Australian captive pythons.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag084},
pmid = {42523065},
issn = {1574-6941},
abstract = {There is a growing interest in keeping exotic pets such as pythons in Australia. Reptiles are known asymptomatic carriers of Salmonella in their digestive tract. This study investigated the microbiome and carriage of Salmonella in faeces from captive Australian pythons (n=28). This study also aimed to determine the effect of temperature and nutrient availability on monospecies biofilm formation of python-associated Salmonella isolated in this study (n=10) as a possible indicator of persistence. A total of 23 Salmonella strains were identified from 28 captive Australian pythons, representing diverse serovars of subspecies enterica, namely S. Bergedorf, S. Havana, S. Jangwani, S. Java, S. Kottbus, S. Muenchen, and S. Umbadah, as well as subspecies S. diarizonae and S. salamae. The composition of the microbial communities differed according to sampling location, diet and Salmonella serovars or subspecies. Bacillota, Bacteroidota, and Pseudomonadota were the most abundant taxa across the faecal microbiome. Strains belonging to subspecies enterica were generally poorer biofilm formers than strains belonging to subspecies salamae and diarizonae. This study shows that microbial communities are variable depending on the environmental factors, which could increase the risk of acquiring reptile-associated salmonellosis whilst handling captive pythons.},
}
RevDate: 2026-07-29
The associations of human genetic variations with airway microbiome, environmental exposures, and respiratory health.
mSystems [Epub ahead of print].
UNLABELLED: The intricate interactions between environmental exposures, the respiratory microbiome, and host genetic variations remain inadequately understood in the context of respiratory health. This study utilized sputum metagenomic data from 1,651 individuals in our previous cohort to elucidate these associations. Mendelian randomization indicated that air pollutants (e.g., SO2, CO, and PM2.5) were associated with lung function, which is potentially mediated by microbes, such as Actinomyces, Haemophilus influenzae, and Veillonella spp. Several genetic loci associated with respiratory microbiome variation were found to be linked to genotype-dependent associations between environmental exposures and lung function. For bacteria, the MEOX1 locus (rs1973191819) was associated with lower Filifactor alocis abundance under air pollutant exposure. The FAM110D (1:26157175) and USP36 (rs1343834070) loci showed associations with higher levels of certain pathogenic taxa (e.g., Ralstonia pickettii, Neisseria) and lower levels of the commensal Oribacterium, increasing chronic obstructive pulmonary disease (COPD) risk. For fungi, DNAJC18 and CCDC57 loci exhibited associations with Candida and Penicillium abundance, respectively. These genotype-dependent associations between the microbiome and environmental exposures provide insights into airway dysbiosis and susceptibility to respiratory diseases.
IMPORTANCE: This study reveals why individuals exposed to identical air pollution exhibit varying degrees of respiratory severity, pointing to a critical missing link: our genetics. While pollution is a known disease trigger, our findings demonstrate that host genetic variation actively regulates and shapes the respiratory microbiome under environmental stress. By mapping specific genetic loci to pollutant-driven bacterial shifts, this work elucidates how host genetics filters environmental risks to govern microbial homeostasis. These results underscore the necessity of incorporating host-microbiome genetic regulation into environmental health research. Ultimately, this study shifts the paradigm toward personalized medicine, enabling the early identification of at-risk individuals and the development of targeted, microbiome-informed interventions.
Additional Links: PMID-42523106
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PubMed:
Citation:
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@article {pmid42523106,
year = {2026},
author = {Xu, S and Yang, L and Gao, J and Shi, Y and Tang, X and Cai, H and Yang, L and Han, Y and Lin, L and Meng, R and Sun, J and Guan, W-j and Tang, T and Shu, W and Cao, C and Zheng, X-y and Wang, Z and Yi, X},
title = {The associations of human genetic variations with airway microbiome, environmental exposures, and respiratory health.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0044226},
doi = {10.1128/msystems.00442-26},
pmid = {42523106},
issn = {2379-5077},
abstract = {UNLABELLED: The intricate interactions between environmental exposures, the respiratory microbiome, and host genetic variations remain inadequately understood in the context of respiratory health. This study utilized sputum metagenomic data from 1,651 individuals in our previous cohort to elucidate these associations. Mendelian randomization indicated that air pollutants (e.g., SO2, CO, and PM2.5) were associated with lung function, which is potentially mediated by microbes, such as Actinomyces, Haemophilus influenzae, and Veillonella spp. Several genetic loci associated with respiratory microbiome variation were found to be linked to genotype-dependent associations between environmental exposures and lung function. For bacteria, the MEOX1 locus (rs1973191819) was associated with lower Filifactor alocis abundance under air pollutant exposure. The FAM110D (1:26157175) and USP36 (rs1343834070) loci showed associations with higher levels of certain pathogenic taxa (e.g., Ralstonia pickettii, Neisseria) and lower levels of the commensal Oribacterium, increasing chronic obstructive pulmonary disease (COPD) risk. For fungi, DNAJC18 and CCDC57 loci exhibited associations with Candida and Penicillium abundance, respectively. These genotype-dependent associations between the microbiome and environmental exposures provide insights into airway dysbiosis and susceptibility to respiratory diseases.
IMPORTANCE: This study reveals why individuals exposed to identical air pollution exhibit varying degrees of respiratory severity, pointing to a critical missing link: our genetics. While pollution is a known disease trigger, our findings demonstrate that host genetic variation actively regulates and shapes the respiratory microbiome under environmental stress. By mapping specific genetic loci to pollutant-driven bacterial shifts, this work elucidates how host genetics filters environmental risks to govern microbial homeostasis. These results underscore the necessity of incorporating host-microbiome genetic regulation into environmental health research. Ultimately, this study shifts the paradigm toward personalized medicine, enabling the early identification of at-risk individuals and the development of targeted, microbiome-informed interventions.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Phylogenize2: robust phylogenetic methods link genes to phenotypes across host-associated and environmental microbiomes.
bioRxiv : the preprint server for biology pii:2026.07.15.738685.
UNLABELLED: In microbiome studies, associations between microbial functions and the environment are often confounded by phylogeny. While some methods explicitly account for this confounder, they require information about genome content, limiting their use in biomes where few genomes have been available. To make these methods more universally accessible, we have developed Phylogenize2, a redesigned phylogeny-aware tool for linking microbial gene families to abundance phenotypes. Phylogenize2 integrates large metagenome-assembled genome collections, including both biome-specific collections from MGnify and a broadly sampled general purpose database, GlobDB, to substantially expand species coverage, allowing its application in environments like the mouse gut and ocean. In addition, by default, Phylogenize2 uses a new robust phylogenetic testing framework that has been optimized for microbial abundance data, while also allowing the use of other comparative methods such as POMS. In an experimental mouse study, Phylogenize2 identifies that Muribaculaceae with higher abundance on a high-fat diet are enriched for proteins in the thioredoxin family, with likely roles in oxidative stress. When we apply Phylogenize2 to a polar ocean study, we find that a molybdenum-dependent PaoABC/YagTSR-like aldehyde oxidoreductase system differentiates mesopelagic from surface-dwelling Flavobacteriaceae , suggesting that aldehyde detoxification may be important for organisms that degrade marine snow. Together, these results show that Phylogenize2 expands phylogeny-aware microbiome analysis beyond the human gut and can provide insight into the genetic basis of microbiome-encoded traits in diverse environments.
IMPORTANCE: Microbiome studies often set out to identify which microbes are more or less abundant across environments, but these patterns can be difficult to interpret. Phylogenize2 is an open-source software package that allows researchers to ask whether individual microbial gene families are associated with the environment across independent branches of the microbial tree of life. By incorporating large collections of genomes from uncultivated microbes, as well as modern statistical methods designed for microbial abundance data, Phylogenize2 makes this approach practical for microbiomes beyond the human gut, including in model organisms like lab mice and free-living environments like the ocean. We also provide a pipeline that allows the use of new genome collections. In two case studies, we demonstrate that Phylogenize2 effectively prioritizes specific genes and pathways from metagenomic data, thereby leading researchers from changes in microbial abundance to more biologically interpretable explanations.
Additional Links: PMID-42523201
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@article {pmid42523201,
year = {2026},
author = {Kananen, K and Tran, N and Bradley, PH},
title = {Phylogenize2: robust phylogenetic methods link genes to phenotypes across host-associated and environmental microbiomes.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.15.738685},
pmid = {42523201},
issn = {2692-8205},
abstract = {UNLABELLED: In microbiome studies, associations between microbial functions and the environment are often confounded by phylogeny. While some methods explicitly account for this confounder, they require information about genome content, limiting their use in biomes where few genomes have been available. To make these methods more universally accessible, we have developed Phylogenize2, a redesigned phylogeny-aware tool for linking microbial gene families to abundance phenotypes. Phylogenize2 integrates large metagenome-assembled genome collections, including both biome-specific collections from MGnify and a broadly sampled general purpose database, GlobDB, to substantially expand species coverage, allowing its application in environments like the mouse gut and ocean. In addition, by default, Phylogenize2 uses a new robust phylogenetic testing framework that has been optimized for microbial abundance data, while also allowing the use of other comparative methods such as POMS. In an experimental mouse study, Phylogenize2 identifies that Muribaculaceae with higher abundance on a high-fat diet are enriched for proteins in the thioredoxin family, with likely roles in oxidative stress. When we apply Phylogenize2 to a polar ocean study, we find that a molybdenum-dependent PaoABC/YagTSR-like aldehyde oxidoreductase system differentiates mesopelagic from surface-dwelling Flavobacteriaceae , suggesting that aldehyde detoxification may be important for organisms that degrade marine snow. Together, these results show that Phylogenize2 expands phylogeny-aware microbiome analysis beyond the human gut and can provide insight into the genetic basis of microbiome-encoded traits in diverse environments.
IMPORTANCE: Microbiome studies often set out to identify which microbes are more or less abundant across environments, but these patterns can be difficult to interpret. Phylogenize2 is an open-source software package that allows researchers to ask whether individual microbial gene families are associated with the environment across independent branches of the microbial tree of life. By incorporating large collections of genomes from uncultivated microbes, as well as modern statistical methods designed for microbial abundance data, Phylogenize2 makes this approach practical for microbiomes beyond the human gut, including in model organisms like lab mice and free-living environments like the ocean. We also provide a pipeline that allows the use of new genome collections. In two case studies, we demonstrate that Phylogenize2 effectively prioritizes specific genes and pathways from metagenomic data, thereby leading researchers from changes in microbial abundance to more biologically interpretable explanations.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Study of microbe-microbe interactions between the sexually transmitted parasite Trichomonas vaginalis with the cervicovaginal bacteria Lactobacillus iners.
bioRxiv : the preprint server for biology pii:2026.07.14.738301.
Trichomonas vaginalis is the leading cause of non-viral sexually transmitted infections and it is associated with comorbidities that affect female health. Lactobacillus iners is one of the most predominant bacteria in the cervicovaginal microbiome. As so, both microbes are likely to encounter one another upon T. vaginalis infection. To our knowledge, the interaction of both microbes has not been previously investigated. Here, we report that T. vaginalis and L. iners bind to one another at early time points of co-incubation. Using imaging flow cytometry and scanning electron microscopy, we capture the dynamics of this microbe-microbe association. We observed active remodeling of the T. vaginalis cell surface leading to thin-membrane protrusions that make contact with L. iners . Larger T. vaginalis membrane extensions that surround and engulf L. iners were also visible. These T. vaginalis - L. iners interactions ultimately lead to a reduction of L. iners viability while T. vaginalis viability was unaffected by exposure to L. iners . Inhibition of actin polymerization blocked T. vaginalis antibacterial activity against L. iners . Together our findings reveal novel insight about T. vaginalis - L. iners interactions and highlight a new T. vaginalis pathogenic effect.
Additional Links: PMID-42523245
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@article {pmid42523245,
year = {2026},
author = {Smedshammer, S and Baxter, B and Briceno, GJ and Morales, KE and Lizcano, A and Clark, T and Willard, D and Riestra, AM},
title = {Study of microbe-microbe interactions between the sexually transmitted parasite Trichomonas vaginalis with the cervicovaginal bacteria Lactobacillus iners.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.14.738301},
pmid = {42523245},
issn = {2692-8205},
abstract = {Trichomonas vaginalis is the leading cause of non-viral sexually transmitted infections and it is associated with comorbidities that affect female health. Lactobacillus iners is one of the most predominant bacteria in the cervicovaginal microbiome. As so, both microbes are likely to encounter one another upon T. vaginalis infection. To our knowledge, the interaction of both microbes has not been previously investigated. Here, we report that T. vaginalis and L. iners bind to one another at early time points of co-incubation. Using imaging flow cytometry and scanning electron microscopy, we capture the dynamics of this microbe-microbe association. We observed active remodeling of the T. vaginalis cell surface leading to thin-membrane protrusions that make contact with L. iners . Larger T. vaginalis membrane extensions that surround and engulf L. iners were also visible. These T. vaginalis - L. iners interactions ultimately lead to a reduction of L. iners viability while T. vaginalis viability was unaffected by exposure to L. iners . Inhibition of actin polymerization blocked T. vaginalis antibacterial activity against L. iners . Together our findings reveal novel insight about T. vaginalis - L. iners interactions and highlight a new T. vaginalis pathogenic effect.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Deciphering the Streptococcus mutans essentialome: multi-omic resolution of hypothetical genes and identification of a functional RocS equivalent.
bioRxiv : the preprint server for biology pii:2026.07.15.738700.
UNLABELLED: Genome-wide viability catalogs produced by transposon sequencing (Tn-seq) and CRISPR interference (CRISPRi) have successfully mapped the essential genome of Streptococcus mutans . However, particularly for genes annotated as "hypothetical" or uncharacterized, translating these findings into mechanistic biological functions remains a significant bottleneck. In this study, we developed an integrated functional genomics pipeline combining predictive bioinformatics, tunable CRISPRi transcriptional silencing, transmission electron microscopy, transcriptomics, and genetic suppressor screens to characterize nine legacy hypothetical essential genes in S. mutans . Comparative transcriptomics and proteomics revealed a conserved baseline stress signature across diverse essential pathways, marked by the coordinated downregulation of the citZ - citB - idh metabolic locus and insoluble matrix synthesis enzymes (gtfBC), paired with the robust activation of the integrative and conjugative element Tn Smu1 . Against this backdrop of systemic stress, we successfully resolved the function of SMU_393, defining it as a functional equivalent of the pneumococcal regulator of chromosome segregation, RocS. Depletion of SMU_393 resulted in abnormal cell widening, hypersensitivity to DNA damage, and a significant subpopulation of anucleate cells. Remarkably, these phenotypes were bypassed by a spontaneous surface-exposed missense mutation (dnaA [Q197E]) within the AAA+ ATPase domain of the replication initiator. Together, this work uncovers an important cell cycle regulator and provides a framework for exploring uncharacterized essential genes of the oral microbiome.
IMPORTANCE: Although genome sequencing has identified thousands of genes required for bacterial survival, the precise biological roles for many of them remain completely unknown. This study implements an integrated functional genomics pipeline to resolve the molecular functions of legacy uncharacterized essential genes in the oral pathogen Streptococcus mutans . We discovered a critical molecular checkpoint that acts as a physical anchor, linking the bacterial chromosome to the cell envelope to ensure that chromosome replication is synchronized with cell division. Remarkably, a single mutation in the replication machinery can fully bypass the loss of this anchor, maintaining proper genetic inheritance even during severe cellular stress. Ultimately, this study provides a pipeline for uncovering highly specific physiological vulnerabilities that can be exploited for targeted therapeutics against oral pathogens.
Additional Links: PMID-42523308
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@article {pmid42523308,
year = {2026},
author = {Dover, CE and Tamrakar, K and Dwivedi, B and Roberts, ER and Chudal, S and King, S and Chavez, ES and de Crécy-Lagard, V and Shields, RC},
title = {Deciphering the Streptococcus mutans essentialome: multi-omic resolution of hypothetical genes and identification of a functional RocS equivalent.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.15.738700},
pmid = {42523308},
issn = {2692-8205},
abstract = {UNLABELLED: Genome-wide viability catalogs produced by transposon sequencing (Tn-seq) and CRISPR interference (CRISPRi) have successfully mapped the essential genome of Streptococcus mutans . However, particularly for genes annotated as "hypothetical" or uncharacterized, translating these findings into mechanistic biological functions remains a significant bottleneck. In this study, we developed an integrated functional genomics pipeline combining predictive bioinformatics, tunable CRISPRi transcriptional silencing, transmission electron microscopy, transcriptomics, and genetic suppressor screens to characterize nine legacy hypothetical essential genes in S. mutans . Comparative transcriptomics and proteomics revealed a conserved baseline stress signature across diverse essential pathways, marked by the coordinated downregulation of the citZ - citB - idh metabolic locus and insoluble matrix synthesis enzymes (gtfBC), paired with the robust activation of the integrative and conjugative element Tn Smu1 . Against this backdrop of systemic stress, we successfully resolved the function of SMU_393, defining it as a functional equivalent of the pneumococcal regulator of chromosome segregation, RocS. Depletion of SMU_393 resulted in abnormal cell widening, hypersensitivity to DNA damage, and a significant subpopulation of anucleate cells. Remarkably, these phenotypes were bypassed by a spontaneous surface-exposed missense mutation (dnaA [Q197E]) within the AAA+ ATPase domain of the replication initiator. Together, this work uncovers an important cell cycle regulator and provides a framework for exploring uncharacterized essential genes of the oral microbiome.
IMPORTANCE: Although genome sequencing has identified thousands of genes required for bacterial survival, the precise biological roles for many of them remain completely unknown. This study implements an integrated functional genomics pipeline to resolve the molecular functions of legacy uncharacterized essential genes in the oral pathogen Streptococcus mutans . We discovered a critical molecular checkpoint that acts as a physical anchor, linking the bacterial chromosome to the cell envelope to ensure that chromosome replication is synchronized with cell division. Remarkably, a single mutation in the replication machinery can fully bypass the loss of this anchor, maintaining proper genetic inheritance even during severe cellular stress. Ultimately, this study provides a pipeline for uncovering highly specific physiological vulnerabilities that can be exploited for targeted therapeutics against oral pathogens.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Perinatal exposures and upper respiratory tract microbiome composition are associated with age at first acute otitis media episode.
bioRxiv : the preprint server for biology pii:2026.07.13.738158.
UNLABELLED: Acute otitis media (AOM) is the most common bacterial infection of childhood and the leading indication for antibiotic prescriptions and healthcare consultations globally. Colonization of the upper respiratory tract (URT) microbiome by bacterial respiratory pathogens precedes AOM episodes; however, the factors that influence colonization susceptibility and subsequent AOM are not well understood. We hypothesized that perinatal exposures, including mode of delivery, intrapartum antibiotic exposure, and infant feeding influence the composition of the URT microbiome at birth, modifying risk of AOM in infancy. We characterized the URT microbiome in nasopharyngeal swabs collected from 163 infants at birth. Swabs were generally collected within two days of delivery (median [IQR] collection time: 25 [17, 45] hours) and microbiome composition was evaluated with 16S rRNA V4 sequencing. Exposures evaluated included birth mode, intrapartum antibiotic exposures, and feeding type at hospital discharge. AOM episodes were identified through electronic health records data. We built Cox proportional hazards models to determine if perinatal exposures and/or microbiome characteristics at birth were associated with the time to first AOM episode in the first two years of life. URT microbiome diversity and composition were associated with feeding type at hospital discharge, wherein exclusive formula feeding was associated with increased diversity and the presence of Staphylococcus and Haemophilus spp. Increased URT microbiome diversity was associated with younger age at first AOM episode. Our findings suggest that perinatal exposures may influence the composition of the birth URT microbiome, and that this early composition may be related to AOM susceptibility in infancy.
IMPORTANCE: Ear infections are the most common bacterial infection of childhood and the leading indication for healthcare consultation and antibiotic receipt. Previous studies have demonstrated that the microbes that inhabit the upper respiratory tract, known as the microbiome, influence risk of ear infection. This study sought to understand how exposures around the time of birth, including delivery type, maternal antibiotic exposures, and infant feeding, influence the development of the infant microbiome, and in turn, how the microbiome is related to ear infections. An analysis of nasal swabs collected from infants shortly after birth demonstrated that increased microbial diversity is associated with earlier age at first ear infection episode. Overall, this study demonstrates that exposures in early life influence respiratory microbiome development, which contributes to infection susceptibility.
Additional Links: PMID-42523323
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@article {pmid42523323,
year = {2026},
author = {Hite, CR and Zhao, C and Hoffman, K and Hurst, JH},
title = {Perinatal exposures and upper respiratory tract microbiome composition are associated with age at first acute otitis media episode.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.13.738158},
pmid = {42523323},
issn = {2692-8205},
abstract = {UNLABELLED: Acute otitis media (AOM) is the most common bacterial infection of childhood and the leading indication for antibiotic prescriptions and healthcare consultations globally. Colonization of the upper respiratory tract (URT) microbiome by bacterial respiratory pathogens precedes AOM episodes; however, the factors that influence colonization susceptibility and subsequent AOM are not well understood. We hypothesized that perinatal exposures, including mode of delivery, intrapartum antibiotic exposure, and infant feeding influence the composition of the URT microbiome at birth, modifying risk of AOM in infancy. We characterized the URT microbiome in nasopharyngeal swabs collected from 163 infants at birth. Swabs were generally collected within two days of delivery (median [IQR] collection time: 25 [17, 45] hours) and microbiome composition was evaluated with 16S rRNA V4 sequencing. Exposures evaluated included birth mode, intrapartum antibiotic exposures, and feeding type at hospital discharge. AOM episodes were identified through electronic health records data. We built Cox proportional hazards models to determine if perinatal exposures and/or microbiome characteristics at birth were associated with the time to first AOM episode in the first two years of life. URT microbiome diversity and composition were associated with feeding type at hospital discharge, wherein exclusive formula feeding was associated with increased diversity and the presence of Staphylococcus and Haemophilus spp. Increased URT microbiome diversity was associated with younger age at first AOM episode. Our findings suggest that perinatal exposures may influence the composition of the birth URT microbiome, and that this early composition may be related to AOM susceptibility in infancy.
IMPORTANCE: Ear infections are the most common bacterial infection of childhood and the leading indication for healthcare consultation and antibiotic receipt. Previous studies have demonstrated that the microbes that inhabit the upper respiratory tract, known as the microbiome, influence risk of ear infection. This study sought to understand how exposures around the time of birth, including delivery type, maternal antibiotic exposures, and infant feeding, influence the development of the infant microbiome, and in turn, how the microbiome is related to ear infections. An analysis of nasal swabs collected from infants shortly after birth demonstrated that increased microbial diversity is associated with earlier age at first ear infection episode. Overall, this study demonstrates that exposures in early life influence respiratory microbiome development, which contributes to infection susceptibility.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
A robust, sensitive phylogenetic method enables gene-level metagenomic analyses.
bioRxiv : the preprint server for biology pii:2026.07.15.738679.
UNLABELLED: A key goal in the microbiome field is to move from taxonomic associations towards mechanistic hypotheses about microbial gene function. However, most methods for linking microbiome changes to specific genes are biased towards finding marker genes, with weak evidence for functional relevance. Phylogenetic regression can address this issue and has been previously applied to changes in microbial prevalence, but many environments (such as the gut in health vs. disease) are characterized more by changes in abundance, which presents unique statistical challenges. We show that when applied to real differential abundances from metagenomes, phylogenetic regression has an anti-conservative bias, indicating inflated false positives. We develop an alternative non-parametric method called "robust permutration," designed specifically for differential abundance data, and evaluate its performance against phylogenetic regression as well as several other phylogenetic comparative methods in realistic simulations of metagenomic data. These results show that robust permutration is the most powerful method that appropriately controls the false positive rate. We further apply robust permutration to a human case-control study of liver cirrhosis, revealing that Lachnospiraceae abundance in disease is linked to a previously uncharacterized iron- sulfur transcription factor encoded near homologs of the butyryl-CoA oxygen oxidoreductase system, a recently discovered system for oxygen detoxification. This illustrates how robust, sensitive phylogenetic methods can enable the generation of new molecular hypotheses directly from metagenomic case-control data.
IMPORTANCE: Previously, we showed that phylogenetic regression can effectively detect genes associated with microbial presence or absence while correcting for evolutionary relationships. Unexpectedly, however, we here observe that this method can lead to high false positive rates when applied to microbial abundance data. In realistic simulations, other methods we test either have similar problems with false positives, or display very low power. We outline a new statistical test that better accounts for measurement uncertainty, outliers, and model violations, achieving more balanced sensitivity and accuracy than competing methods. Applying this test to a cirrhosis study reveals an uncharacterized transcription factor enriched in disease, with an apparent role in oxidative stress based on its sequence and gene neighborhood. This suggests a functional explanation for the observed taxonomic shifts, and demonstrates how improved phylogenetic methods could help inform future microbiome-targeted treatments.
Additional Links: PMID-42523339
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@article {pmid42523339,
year = {2026},
author = {Tran, N and Kananen, K and Bradley, PH},
title = {A robust, sensitive phylogenetic method enables gene-level metagenomic analyses.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.15.738679},
pmid = {42523339},
issn = {2692-8205},
abstract = {UNLABELLED: A key goal in the microbiome field is to move from taxonomic associations towards mechanistic hypotheses about microbial gene function. However, most methods for linking microbiome changes to specific genes are biased towards finding marker genes, with weak evidence for functional relevance. Phylogenetic regression can address this issue and has been previously applied to changes in microbial prevalence, but many environments (such as the gut in health vs. disease) are characterized more by changes in abundance, which presents unique statistical challenges. We show that when applied to real differential abundances from metagenomes, phylogenetic regression has an anti-conservative bias, indicating inflated false positives. We develop an alternative non-parametric method called "robust permutration," designed specifically for differential abundance data, and evaluate its performance against phylogenetic regression as well as several other phylogenetic comparative methods in realistic simulations of metagenomic data. These results show that robust permutration is the most powerful method that appropriately controls the false positive rate. We further apply robust permutration to a human case-control study of liver cirrhosis, revealing that Lachnospiraceae abundance in disease is linked to a previously uncharacterized iron- sulfur transcription factor encoded near homologs of the butyryl-CoA oxygen oxidoreductase system, a recently discovered system for oxygen detoxification. This illustrates how robust, sensitive phylogenetic methods can enable the generation of new molecular hypotheses directly from metagenomic case-control data.
IMPORTANCE: Previously, we showed that phylogenetic regression can effectively detect genes associated with microbial presence or absence while correcting for evolutionary relationships. Unexpectedly, however, we here observe that this method can lead to high false positive rates when applied to microbial abundance data. In realistic simulations, other methods we test either have similar problems with false positives, or display very low power. We outline a new statistical test that better accounts for measurement uncertainty, outliers, and model violations, achieving more balanced sensitivity and accuracy than competing methods. Applying this test to a cirrhosis study reveals an uncharacterized transcription factor enriched in disease, with an apparent role in oxidative stress based on its sequence and gene neighborhood. This suggests a functional explanation for the observed taxonomic shifts, and demonstrates how improved phylogenetic methods could help inform future microbiome-targeted treatments.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Ocular community state types reveal distinct microbial compositions among microbiomes with implications for trachoma control.
bioRxiv : the preprint server for biology.
Trachoma, a chronic ocular disease caused by Chlamydia trachomatis (Ct), is the leading infectious cause of blindness worldwide. Despite WHO's SAFE (Surgery, Antibiotics, Facial cleanliness, Environmental improvement) strategy, ~100M are at risk of blindness. Using metagenomic shotgun sequencing, we characterized the ocular microbiome of 680 villagers in Amhara Ethiopia, identifying 10 Community State Types (CSTs) associated with different population characteristics. Children with the highest prevalence of inflammatory trachoma and Ct were in CST10, dominated by Haemophilus influenzae and four other Haemophilus spp. Adults with the highest prevalence of scarring trachoma were in CST3 and CST6, dominated by Corynebacterium macginleyi. CST5, dominated by Mesomycoplasma hyorhinis and Staphylococcus aureus, had the lowest prevalence of Ct and trachoma, and was the only CST without zoonotic Chlamydia spp. Both M. hyorhinis, a zoonotic porcine bacterium, and S. aureus are capable of forming biofilms, which may competitively prevent/down-regulate chlamydial infections. Other CSTs were dominated by environmental species like Vibrio. This is the first microbiome study to develop CSTs for trachoma. Pathogenic and potentially protective microbes showed distinct associations with demographic, clinical, and chlamydial characteristics, which will guide the design of microbial therapeutics as alternatives to antibiotics and strategies for WHO's global elimination of blinding trachoma.
Additional Links: PMID-42523359
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Citation:
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@article {pmid42523359,
year = {2026},
author = {Uwamanzu-Nna, A and Olagoke, O and Shi, CX and Mengistie, HD and Asfaha, K and Read, TD and Dean, D},
title = {Ocular community state types reveal distinct microbial compositions among microbiomes with implications for trachoma control.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42523359},
issn = {2692-8205},
abstract = {Trachoma, a chronic ocular disease caused by Chlamydia trachomatis (Ct), is the leading infectious cause of blindness worldwide. Despite WHO's SAFE (Surgery, Antibiotics, Facial cleanliness, Environmental improvement) strategy, ~100M are at risk of blindness. Using metagenomic shotgun sequencing, we characterized the ocular microbiome of 680 villagers in Amhara Ethiopia, identifying 10 Community State Types (CSTs) associated with different population characteristics. Children with the highest prevalence of inflammatory trachoma and Ct were in CST10, dominated by Haemophilus influenzae and four other Haemophilus spp. Adults with the highest prevalence of scarring trachoma were in CST3 and CST6, dominated by Corynebacterium macginleyi. CST5, dominated by Mesomycoplasma hyorhinis and Staphylococcus aureus, had the lowest prevalence of Ct and trachoma, and was the only CST without zoonotic Chlamydia spp. Both M. hyorhinis, a zoonotic porcine bacterium, and S. aureus are capable of forming biofilms, which may competitively prevent/down-regulate chlamydial infections. Other CSTs were dominated by environmental species like Vibrio. This is the first microbiome study to develop CSTs for trachoma. Pathogenic and potentially protective microbes showed distinct associations with demographic, clinical, and chlamydial characteristics, which will guide the design of microbial therapeutics as alternatives to antibiotics and strategies for WHO's global elimination of blinding trachoma.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Non-invasive Vagal Nerve Stimulation as a Potential Treatment for Repetitive Blast Trauma.
bioRxiv : the preprint server for biology pii:2026.07.13.737563.
BACKGROUND: Polytrauma caused by exposure to high explosives (blast) is increasingly common among military personnel and civilians yet treatment for related post-concussive symptoms and chronic behavioral dysfunction is limited. Therapeutic targets following these injuries are typically focused on the central nervous system, with less attention placed on potentially more accessible peripheral targets. Vagus nerve stimulation (VNS) has recently gained traction as a potential therapeutic modality but has yet to be examined in a blast trauma setting.
METHODS: Our well-established blast overpressure model was utilized to induce repetitive (3x) blast trauma, followed by treatment with non-invasive transcutaneous VNS one hour following each blast exposure in male mice. Acutely following repetitive blast exposure, we measured serum and brain cytokine levels, fecal microbial abundance, and locomotion and anxiety-like behavior in the open field assay. Chronically (1-3 months post blast), mice were assessed for behavioral outcomes related to mild traumatic brain injury (mTBI) and posttraumatic stress disorder (PTSD), including acoustic startle (hyperreactivity), probabilistic discounting (risky decision making), and two-bottle choice test (voluntary alcohol consumption).
RESULTS: VNS treatment following blast exposure decreased acute blast-induced inflammatory response in the blood and brain, especially serum IL-9 and IP-10, and brain MPC-1. Chronic behavior tests demonstrated a VNS-dependent reduction in blast-induced risky decision-making and a decreased intake and preference for ethanol. Conversely, VNS was not effective in preventing acute blast effects on the microbiome or chronic hyperreactivity behaviors measured with acoustic startle.
DISCUSSION: This study identifies the vagus nerve as a novel peripheral target for treating acute and chronic blast-induced dysfunction.
Additional Links: PMID-42523378
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@article {pmid42523378,
year = {2026},
author = {Baskin, BM and Easton, A and Tschang, M and Lee, SJ and Skillen, E and Wong, K and Schuessler, B and Meabon, J and Wolden-Hanson, T and Cook, DG and Gibbons, SM and Schindler, AG},
title = {Non-invasive Vagal Nerve Stimulation as a Potential Treatment for Repetitive Blast Trauma.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.13.737563},
pmid = {42523378},
issn = {2692-8205},
abstract = {BACKGROUND: Polytrauma caused by exposure to high explosives (blast) is increasingly common among military personnel and civilians yet treatment for related post-concussive symptoms and chronic behavioral dysfunction is limited. Therapeutic targets following these injuries are typically focused on the central nervous system, with less attention placed on potentially more accessible peripheral targets. Vagus nerve stimulation (VNS) has recently gained traction as a potential therapeutic modality but has yet to be examined in a blast trauma setting.
METHODS: Our well-established blast overpressure model was utilized to induce repetitive (3x) blast trauma, followed by treatment with non-invasive transcutaneous VNS one hour following each blast exposure in male mice. Acutely following repetitive blast exposure, we measured serum and brain cytokine levels, fecal microbial abundance, and locomotion and anxiety-like behavior in the open field assay. Chronically (1-3 months post blast), mice were assessed for behavioral outcomes related to mild traumatic brain injury (mTBI) and posttraumatic stress disorder (PTSD), including acoustic startle (hyperreactivity), probabilistic discounting (risky decision making), and two-bottle choice test (voluntary alcohol consumption).
RESULTS: VNS treatment following blast exposure decreased acute blast-induced inflammatory response in the blood and brain, especially serum IL-9 and IP-10, and brain MPC-1. Chronic behavior tests demonstrated a VNS-dependent reduction in blast-induced risky decision-making and a decreased intake and preference for ethanol. Conversely, VNS was not effective in preventing acute blast effects on the microbiome or chronic hyperreactivity behaviors measured with acoustic startle.
DISCUSSION: This study identifies the vagus nerve as a novel peripheral target for treating acute and chronic blast-induced dysfunction.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Gut microbiome derived folate metabolite suppresses colorectal cancer progression.
bioRxiv : the preprint server for biology pii:2026.07.14.738490.
The gut microbiota influences colorectal cancer (CRC) progression, primarily through the secretion of small molecule metabolites. While numerous microbial products are known to drive CRC, endogenous protective mechanisms remain largely uncharacterized. Utilizing a folate metabolomics platform, we demonstrate that the healthy gut microbiota produces folinic acid (FA), a known chemotherapeutic adjuvant also known as leucovorin. This microbially derived folinic acid is progressively depleted in mouse models of colitis-associated CRC and in human clinical metagenomic cohorts with advancing disease severity. Mechanistically, folinic acid acts as a signaling molecule that directly binds and inhibits the intracellular protease calpain-2. This interaction stabilizes epithelial E-cadherin protein expression and suppresses CRC epithelial-to-mesenchymal transition driving metastasis. Genetically manipulating gut microbial production of FA is sufficient to modulate CRC in vivo , even in the presence of chronic inflammation. This study reframes folinic acid from a chemotherapeutic enhancer to an endogenous microbial metabolite that actively suppresses CRC progression.
Additional Links: PMID-42523540
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@article {pmid42523540,
year = {2026},
author = {Danner, R and Cho, J and Detwiler, Z and Williams, J and Han, JA and Yang, C and Diebold, X and Maeder, K and Van Vranken, JG and Walker, AS and Lesser, C and Chaudhari, SN},
title = {Gut microbiome derived folate metabolite suppresses colorectal cancer progression.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.07.14.738490},
pmid = {42523540},
issn = {2692-8205},
abstract = {The gut microbiota influences colorectal cancer (CRC) progression, primarily through the secretion of small molecule metabolites. While numerous microbial products are known to drive CRC, endogenous protective mechanisms remain largely uncharacterized. Utilizing a folate metabolomics platform, we demonstrate that the healthy gut microbiota produces folinic acid (FA), a known chemotherapeutic adjuvant also known as leucovorin. This microbially derived folinic acid is progressively depleted in mouse models of colitis-associated CRC and in human clinical metagenomic cohorts with advancing disease severity. Mechanistically, folinic acid acts as a signaling molecule that directly binds and inhibits the intracellular protease calpain-2. This interaction stabilizes epithelial E-cadherin protein expression and suppresses CRC epithelial-to-mesenchymal transition driving metastasis. Genetically manipulating gut microbial production of FA is sufficient to modulate CRC in vivo , even in the presence of chronic inflammation. This study reframes folinic acid from a chemotherapeutic enhancer to an endogenous microbial metabolite that actively suppresses CRC progression.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Optimized protocol for profiling mucosa-associated microbiota from formalin-fixed paraffin-embedded gut tissues from treatment-naïve pediatric patients with Crohn's disease.
Frontiers in cellular and infection microbiology, 16:1885816.
BACKGROUND: Formalin-fixed, paraffin-embedded (FFPE) tissues are yet underutilized resources for microbiome studies. Data on the mucosa-associated microbiota (MAM) of patients with Crohn's disease (CD) are scarce, due to several methodological limitations. In this study, we aimed to develop and validate a new optimized amplicon-based workflow to profile MAM from FFPE gut biopsies of pediatric CD patients.
METHODS: We examined 68 FFPE samples, including 34 biopsies from treatment-naïve patients with CD and 34 from healthy controls (HC). V3-V7 regions of the 16S rRNA gene were amplified and sequenced on the Oxford Nanopore platform. Two protocols were tested: Protocol 1 (P1), consisting of a single PCR amplification and purification step, and Protocol 2 (P2), including two sequential PCR amplifications with purification after each round. The second amplification and purification steps were introduced to increase sequencing yield and improve microbiota detection.
RESULTS: P2 consistently outperformed P1, yielding significantly higher DNA concentration and purity, reducing human DNA contamination and sustaining pore performance. P2 also generated more microbial reads and recovered a richer, more taxonomically diverse community, including increased detection of species with low abundance. More taxa were enriched in P2 across all levels, enhancing species-level resolution. P2 enabled comprehensive detection of pathogenic genera, such as Escherichia, Mycobacterium, and Klebsiella, which were significantly enriched in the P2 samples compared to the P1 samples. Alpha diversity analysis showed increased richness and reduced evenness in P2 compared to P1, with a significant difference in beta diversity, while maintaining community structure in both CD and HC.
CONCLUSIONS: The optimized workflow with a two-step strategy improved sequencing performance and enhanced microbiota detection in FFPE tissues. This approach enabled successful profiling of MAM, providing a novel method for retrospective characterization of the microbiome from archival tissues and providing a scalable platform for clinical biomarker discovery.
Additional Links: PMID-42523620
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Citation:
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@article {pmid42523620,
year = {2026},
author = {Al-Ali, N and Al-Awadhi, H and Hassane, M and Al-Salam, S and Al-Marzooq, F},
title = {Optimized protocol for profiling mucosa-associated microbiota from formalin-fixed paraffin-embedded gut tissues from treatment-naïve pediatric patients with Crohn's disease.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1885816},
pmid = {42523620},
issn = {2235-2988},
mesh = {Humans ; *Crohn Disease/microbiology/pathology ; Paraffin Embedding ; RNA, Ribosomal, 16S/genetics ; Child ; Formaldehyde ; *Intestinal Mucosa/microbiology ; DNA, Bacterial/genetics ; *Gastrointestinal Microbiome/genetics ; Female ; Tissue Fixation ; Sequence Analysis, DNA ; Polymerase Chain Reaction ; Bacteria/classification/genetics/isolation & purification ; Male ; Adolescent ; Biopsy ; },
abstract = {BACKGROUND: Formalin-fixed, paraffin-embedded (FFPE) tissues are yet underutilized resources for microbiome studies. Data on the mucosa-associated microbiota (MAM) of patients with Crohn's disease (CD) are scarce, due to several methodological limitations. In this study, we aimed to develop and validate a new optimized amplicon-based workflow to profile MAM from FFPE gut biopsies of pediatric CD patients.
METHODS: We examined 68 FFPE samples, including 34 biopsies from treatment-naïve patients with CD and 34 from healthy controls (HC). V3-V7 regions of the 16S rRNA gene were amplified and sequenced on the Oxford Nanopore platform. Two protocols were tested: Protocol 1 (P1), consisting of a single PCR amplification and purification step, and Protocol 2 (P2), including two sequential PCR amplifications with purification after each round. The second amplification and purification steps were introduced to increase sequencing yield and improve microbiota detection.
RESULTS: P2 consistently outperformed P1, yielding significantly higher DNA concentration and purity, reducing human DNA contamination and sustaining pore performance. P2 also generated more microbial reads and recovered a richer, more taxonomically diverse community, including increased detection of species with low abundance. More taxa were enriched in P2 across all levels, enhancing species-level resolution. P2 enabled comprehensive detection of pathogenic genera, such as Escherichia, Mycobacterium, and Klebsiella, which were significantly enriched in the P2 samples compared to the P1 samples. Alpha diversity analysis showed increased richness and reduced evenness in P2 compared to P1, with a significant difference in beta diversity, while maintaining community structure in both CD and HC.
CONCLUSIONS: The optimized workflow with a two-step strategy improved sequencing performance and enhanced microbiota detection in FFPE tissues. This approach enabled successful profiling of MAM, providing a novel method for retrospective characterization of the microbiome from archival tissues and providing a scalable platform for clinical biomarker discovery.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Crohn Disease/microbiology/pathology
Paraffin Embedding
RNA, Ribosomal, 16S/genetics
Child
Formaldehyde
*Intestinal Mucosa/microbiology
DNA, Bacterial/genetics
*Gastrointestinal Microbiome/genetics
Female
Tissue Fixation
Sequence Analysis, DNA
Polymerase Chain Reaction
Bacteria/classification/genetics/isolation & purification
Male
Adolescent
Biopsy
RevDate: 2026-07-29
CmpDate: 2026-07-29
Virulome over taxonomy: refining the driver-passenger model in colorectal carcinogenesis.
Frontiers in cellular and infection microbiology, 16:1858868.
Colorectal carcinogenesis is increasingly viewed as a predominantly microbiome-driven process, yet it extends well beyond simple taxonomic associations. The taxon-based classical driver-passenger model, while conceptually useful, may benefit from incorporating the underlying mechanisms of microbial participation and the functional complexity of taxa contributions across CRC stages. In particular, the same taxa may exert distinct effects across carcinogenesis, and individual metabolic pathways frequently mediate multiple and divergent host responses. To address these limitations, we re-examine the roles of CRC-associated microbiota through the lens of individual virulence factor effects on the host, demonstrating their functional pleiotropy, and propose an expanded driver-passenger model. This approach highlights the central role of the virulome in CRC initiation, promotion and progression. By shifting the analytical focus from taxonomy to function, the proposed framework enables improved causality assessment and supports the development of stage-specific diagnostic and prognostic markers, as well as more targeted microbiome-directed therapeutic strategies.
Additional Links: PMID-42523711
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@article {pmid42523711,
year = {2026},
author = {Glazunova, E and Kurnosov, A and Bogacheva, A and Makarov, V and Zlobovskaya, O},
title = {Virulome over taxonomy: refining the driver-passenger model in colorectal carcinogenesis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1858868},
pmid = {42523711},
issn = {2235-2988},
mesh = {*Colorectal Neoplasms/microbiology/pathology/diagnosis ; Humans ; *Carcinogenesis ; *Gastrointestinal Microbiome ; *Virulence Factors ; Microbiota ; Animals ; },
abstract = {Colorectal carcinogenesis is increasingly viewed as a predominantly microbiome-driven process, yet it extends well beyond simple taxonomic associations. The taxon-based classical driver-passenger model, while conceptually useful, may benefit from incorporating the underlying mechanisms of microbial participation and the functional complexity of taxa contributions across CRC stages. In particular, the same taxa may exert distinct effects across carcinogenesis, and individual metabolic pathways frequently mediate multiple and divergent host responses. To address these limitations, we re-examine the roles of CRC-associated microbiota through the lens of individual virulence factor effects on the host, demonstrating their functional pleiotropy, and propose an expanded driver-passenger model. This approach highlights the central role of the virulome in CRC initiation, promotion and progression. By shifting the analytical focus from taxonomy to function, the proposed framework enables improved causality assessment and supports the development of stage-specific diagnostic and prognostic markers, as well as more targeted microbiome-directed therapeutic strategies.},
}
MeSH Terms:
show MeSH Terms
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*Colorectal Neoplasms/microbiology/pathology/diagnosis
Humans
*Carcinogenesis
*Gastrointestinal Microbiome
*Virulence Factors
Microbiota
Animals
RevDate: 2026-07-29
CmpDate: 2026-07-29
Comparative metagenomic analysis of gut microbiota in Anacanthotermes turkestanicus and A. ahngerianus reveals diet- and habitat-driven functional divergence.
Frontiers in insect science, 6:1807673.
The gut microbiome of termites plays a crucial role in lignocellulose degradation and nutrient recycling. This study presents the first metagenomic characterization of the gut microbiota in two lower termite species, Anacanthotermes ahngerianus and Anacanthotermes turkestanicus, collected from distinct ecological habitats. In Uzbekistan, the first lives in building a mound in nature in the West part while the second mainly lives in contact with human constructions in the East part without building a proper mound. Both species showed similar bacterial dominance (~53%) in their guts but A. ahngerianus exhibited higher overall microbial diversity (Shannon index: 4.046 vs. 3.363; Simpson's index: 0.927 vs. 0.776). Moreover, both termite species showed differences in microbial profiles, including bacterial taxa and eukaryotic groups relevant to lower-termite gut symbiosis. Protist-associated eukaryotic reads were retained because flagellated protists are essential symbionts of lower termites, whereas unexpected non-protist eukaryotic assignments were interpreted cautiously and were not used as evidence of functional gut symbionts or host adaptation. Functional profiling revealed enrichment of pathways related to carbohydrate metabolism, amino acid transport, and energy production in both species. However, A. turkestanicus exhibited stronger bacterial dominance associated with lignocellulose degradation and nitrogen cycling, while A. ahngerianus maintained a more balanced representation of bacteria, fungi, and viruses. These findings suggest that species identity and ecological habits may be associated with differences in gut microbiome structure and predicted functional potential.
Additional Links: PMID-42523736
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Citation:
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@article {pmid42523736,
year = {2026},
author = {Togaev, U and Mathur, V and Rakhmonkulova, A and Agarwal, S and Mathur, A and Turageldiyev, S and Ruzmetov, R and Turaev, AS and Tillyabaev, Z and Matchanov, A and Sillam-Dussès, D},
title = {Comparative metagenomic analysis of gut microbiota in Anacanthotermes turkestanicus and A. ahngerianus reveals diet- and habitat-driven functional divergence.},
journal = {Frontiers in insect science},
volume = {6},
number = {},
pages = {1807673},
pmid = {42523736},
issn = {2673-8600},
abstract = {The gut microbiome of termites plays a crucial role in lignocellulose degradation and nutrient recycling. This study presents the first metagenomic characterization of the gut microbiota in two lower termite species, Anacanthotermes ahngerianus and Anacanthotermes turkestanicus, collected from distinct ecological habitats. In Uzbekistan, the first lives in building a mound in nature in the West part while the second mainly lives in contact with human constructions in the East part without building a proper mound. Both species showed similar bacterial dominance (~53%) in their guts but A. ahngerianus exhibited higher overall microbial diversity (Shannon index: 4.046 vs. 3.363; Simpson's index: 0.927 vs. 0.776). Moreover, both termite species showed differences in microbial profiles, including bacterial taxa and eukaryotic groups relevant to lower-termite gut symbiosis. Protist-associated eukaryotic reads were retained because flagellated protists are essential symbionts of lower termites, whereas unexpected non-protist eukaryotic assignments were interpreted cautiously and were not used as evidence of functional gut symbionts or host adaptation. Functional profiling revealed enrichment of pathways related to carbohydrate metabolism, amino acid transport, and energy production in both species. However, A. turkestanicus exhibited stronger bacterial dominance associated with lignocellulose degradation and nitrogen cycling, while A. ahngerianus maintained a more balanced representation of bacteria, fungi, and viruses. These findings suggest that species identity and ecological habits may be associated with differences in gut microbiome structure and predicted functional potential.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Tri-kingdom interactions in bamboo microbiomes: mechanisms of pathogen cooperation and implications for disease management.
Frontiers in microbiology, 17:1865230.
Multi-kingdom disease complexes, where fungi, bacteria, and viruses interact synergistically, are increasingly recognized as a threat to bamboo, a fast-growing Poaceae lineage of high ecological and economic value. However, the mechanisms regulating tri-kingdom disease synergy in bamboo remain poorly understood. This review addresses a central question: Through which molecular and ecological pathways do pathogens from three kingdoms cooperatively enhance bamboo disease severity? We synthesize four key synergy mechanisms: (1) Facilitation of infection: Fusarium proliferatum hyphae build physical entry points as well as transport channels that assist Erwinia sp. to colonize vascular tissues. (2) Immunosuppression: Bamboo mosaic virus (BaMV; genus Potexvirus, family Alphaflexiviridae) inhibits host RNA silencing through viral-encoded proteins TGBp1 and CP, which bind small RNA's and inhibit amplification by RDR6, thereby establishing a permissive environment for secondary invaders, a mechanism inferred from other Potexvirus systems, as direct co-infection evidence in bamboo is currently unavailable. (3) Metabolic cross-feeding: fungal virulence enhanced by bacterial metabolites (e.g., lipopeptides, siderophores), although metabolic synergy in bamboo has not been demonstrated. (4) Biofilm protection: scanning electron microscopy reveals bacterial biofilm on the fungal hyphae surfaces that protect pathogens against host defenses. Quantitatively, the Fusarium-Erwinia co-infection synergy coefficient of bamboo culm rot is S ≈ 1.8, indicating approximately 80% disease severity. Assuming multiplicative independence among mechanisms, tri-kingdom synergy could exceed S > 3.0, a testable hypothesis. This review identifies the following knowledge gaps: (1) no mycovirus isolated from a bamboo-infecting fungus; (2) no bacteriophage characterized against bamboo bacterial pathogen; (3) no quantified studies involving BaMV; and (4) no genome-wide association studies identifying genetic determinants of synergy. This review proposes that effective biocontrol means disrupting the interfaces of pathogen cooperation - disrupting infection courts, interfering with immunosuppression, chelating iron, and degrading biofilm-rather than introducing beneficial microbes. This review proposes a conceptual framework for cross-kingdom microbial interactions in bamboo-associated microbiomes.
Additional Links: PMID-42523806
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@article {pmid42523806,
year = {2026},
author = {Zafar, M and Wang, Y and Wajid, K and Zhao, B and Cao, Y and Hu, S and Xu, G},
title = {Tri-kingdom interactions in bamboo microbiomes: mechanisms of pathogen cooperation and implications for disease management.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1865230},
pmid = {42523806},
issn = {1664-302X},
abstract = {Multi-kingdom disease complexes, where fungi, bacteria, and viruses interact synergistically, are increasingly recognized as a threat to bamboo, a fast-growing Poaceae lineage of high ecological and economic value. However, the mechanisms regulating tri-kingdom disease synergy in bamboo remain poorly understood. This review addresses a central question: Through which molecular and ecological pathways do pathogens from three kingdoms cooperatively enhance bamboo disease severity? We synthesize four key synergy mechanisms: (1) Facilitation of infection: Fusarium proliferatum hyphae build physical entry points as well as transport channels that assist Erwinia sp. to colonize vascular tissues. (2) Immunosuppression: Bamboo mosaic virus (BaMV; genus Potexvirus, family Alphaflexiviridae) inhibits host RNA silencing through viral-encoded proteins TGBp1 and CP, which bind small RNA's and inhibit amplification by RDR6, thereby establishing a permissive environment for secondary invaders, a mechanism inferred from other Potexvirus systems, as direct co-infection evidence in bamboo is currently unavailable. (3) Metabolic cross-feeding: fungal virulence enhanced by bacterial metabolites (e.g., lipopeptides, siderophores), although metabolic synergy in bamboo has not been demonstrated. (4) Biofilm protection: scanning electron microscopy reveals bacterial biofilm on the fungal hyphae surfaces that protect pathogens against host defenses. Quantitatively, the Fusarium-Erwinia co-infection synergy coefficient of bamboo culm rot is S ≈ 1.8, indicating approximately 80% disease severity. Assuming multiplicative independence among mechanisms, tri-kingdom synergy could exceed S > 3.0, a testable hypothesis. This review identifies the following knowledge gaps: (1) no mycovirus isolated from a bamboo-infecting fungus; (2) no bacteriophage characterized against bamboo bacterial pathogen; (3) no quantified studies involving BaMV; and (4) no genome-wide association studies identifying genetic determinants of synergy. This review proposes that effective biocontrol means disrupting the interfaces of pathogen cooperation - disrupting infection courts, interfering with immunosuppression, chelating iron, and degrading biofilm-rather than introducing beneficial microbes. This review proposes a conceptual framework for cross-kingdom microbial interactions in bamboo-associated microbiomes.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
From diversity to function: microbiome-mediated plant growth promotion, secondary metabolism, and antimicrobial resistance in Rauwolfia serpentina.
Frontiers in bioinformatics, 6:1796770.
INTRODUCTION: This study presents the first metagenomic analysis of the root and rhizosphere microbiomes of Rauvolfia serpentina, an endangered medicinal plant. Metagenomic sequencing and bioinformatics analysis were used to characterize the diverse microbial communities and their functional attributes to assess the ecological and biotechnological potential of this plant-associated microbiome.
METHODS: High-throughput Illumina sequencing and bioinformatics analysis were used to profile the microbial communities. Functional annotation was performed to identify plant growth-promoting traits using PLABASE, to predict pathways for the biosynthesis of novel bioactive compounds using antiSMASH, and to identify antimicrobial resistance genes using ResFinder.
RESULTS: The analysis revealed highly diverse microbial communities in both habitats, predominantly composed of Pseudomonadota, Bacillota, and Actinomycetota, with minor but consistent contributions from archaea and eukaryotes. Functional annotation identified extensive PGPTs, including genes associated with phosphate solubilization, nitrogen fixation, siderophore-mediated iron acquisition, and stress tolerance. The rhizosphere microbiome exhibited greater metabolic versatility and stress tolerance, characterized by a higher copy number of heavy metal efflux pumps, whereas the root microbiome was enriched in genes involved in plant hormone regulation and plant-microbe interactions. A diverse array of non-ribosomal peptide synthase, polyketide synthase, and lasso peptide pathways were predicted, underscoring the potential to produce novel bioactive compounds. These distinct functional profiles demonstrates that the protected root endomicrobiome specializes in plant signalling and nutrient assimilation, while the rhizosphere microbiome, facing higher competition, specializes in nutrient acquisition and stress resilience.
CONCLUSION: These findings provide novel insights into the ecological specialization and biotechnological potential of the R. serpentina microbiome, offering significant implications for the sustainable utilization and conservation of this endangered medicinal plant.
Additional Links: PMID-42523840
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Citation:
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@article {pmid42523840,
year = {2026},
author = {Bankar, VR and Chapadgaonkar, SS and Bhattacharyya, K and K, P},
title = {From diversity to function: microbiome-mediated plant growth promotion, secondary metabolism, and antimicrobial resistance in Rauwolfia serpentina.},
journal = {Frontiers in bioinformatics},
volume = {6},
number = {},
pages = {1796770},
pmid = {42523840},
issn = {2673-7647},
abstract = {INTRODUCTION: This study presents the first metagenomic analysis of the root and rhizosphere microbiomes of Rauvolfia serpentina, an endangered medicinal plant. Metagenomic sequencing and bioinformatics analysis were used to characterize the diverse microbial communities and their functional attributes to assess the ecological and biotechnological potential of this plant-associated microbiome.
METHODS: High-throughput Illumina sequencing and bioinformatics analysis were used to profile the microbial communities. Functional annotation was performed to identify plant growth-promoting traits using PLABASE, to predict pathways for the biosynthesis of novel bioactive compounds using antiSMASH, and to identify antimicrobial resistance genes using ResFinder.
RESULTS: The analysis revealed highly diverse microbial communities in both habitats, predominantly composed of Pseudomonadota, Bacillota, and Actinomycetota, with minor but consistent contributions from archaea and eukaryotes. Functional annotation identified extensive PGPTs, including genes associated with phosphate solubilization, nitrogen fixation, siderophore-mediated iron acquisition, and stress tolerance. The rhizosphere microbiome exhibited greater metabolic versatility and stress tolerance, characterized by a higher copy number of heavy metal efflux pumps, whereas the root microbiome was enriched in genes involved in plant hormone regulation and plant-microbe interactions. A diverse array of non-ribosomal peptide synthase, polyketide synthase, and lasso peptide pathways were predicted, underscoring the potential to produce novel bioactive compounds. These distinct functional profiles demonstrates that the protected root endomicrobiome specializes in plant signalling and nutrient assimilation, while the rhizosphere microbiome, facing higher competition, specializes in nutrient acquisition and stress resilience.
CONCLUSION: These findings provide novel insights into the ecological specialization and biotechnological potential of the R. serpentina microbiome, offering significant implications for the sustainable utilization and conservation of this endangered medicinal plant.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Gut microbial metabolites in cutaneous inflammation: shared mechanisms and therapeutic opportunities.
Frontiers in immunology, 17:1850282.
Cutaneous inflammation is influenced by systemic signals beyond the skin, and gut microbial metabolites contribute to skin homeostasis and inflammatory responses. Major classes of gut-derived metabolites, including short-chain fatty acids, tryptophan-derived compounds, and secondary bile acids, may shape cutaneous inflammation through immune, neural, and endocrine pathways. However, current research remains fragmented across metabolite classes and pathways, and cross-pathway interactions remain unclear. As a result, the relationship between metabolite disturbances and distinct inflammatory phenotypes remains incompletely understood. Atopic dermatitis and chronic spontaneous urticaria are used as representative examples of this variability. This review summarizes major metabolite classes, the pathways linking them to cutaneous inflammation, and current therapeutic strategies targeting these pathways. Therapeutic strategies targeting gut microbial metabolites include direct metabolite supplementation, microbiome-targeted strategies that modify metabolite output, and indirect host-directed interventions. Available evidence suggests that gut microbial metabolites may serve as potential therapeutic targets in cutaneous inflammation. However, current limitations include context-dependent effects, limited causal evidence, variable treatment response, and unresolved issues in delivery and tissue specificity.
Additional Links: PMID-42523841
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Citation:
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@article {pmid42523841,
year = {2026},
author = {Hu, B and Du, L and Chu, D and Kou, E and Zhao, H and Dong, B and Wang, B and Zhu, Y},
title = {Gut microbial metabolites in cutaneous inflammation: shared mechanisms and therapeutic opportunities.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1850282},
pmid = {42523841},
issn = {1664-3224},
mesh = {Humans ; Animals ; *Gastrointestinal Microbiome/immunology ; *Skin/metabolism/immunology ; *Dermatitis, Atopic/metabolism/therapy ; Inflammation/metabolism ; },
abstract = {Cutaneous inflammation is influenced by systemic signals beyond the skin, and gut microbial metabolites contribute to skin homeostasis and inflammatory responses. Major classes of gut-derived metabolites, including short-chain fatty acids, tryptophan-derived compounds, and secondary bile acids, may shape cutaneous inflammation through immune, neural, and endocrine pathways. However, current research remains fragmented across metabolite classes and pathways, and cross-pathway interactions remain unclear. As a result, the relationship between metabolite disturbances and distinct inflammatory phenotypes remains incompletely understood. Atopic dermatitis and chronic spontaneous urticaria are used as representative examples of this variability. This review summarizes major metabolite classes, the pathways linking them to cutaneous inflammation, and current therapeutic strategies targeting these pathways. Therapeutic strategies targeting gut microbial metabolites include direct metabolite supplementation, microbiome-targeted strategies that modify metabolite output, and indirect host-directed interventions. Available evidence suggests that gut microbial metabolites may serve as potential therapeutic targets in cutaneous inflammation. However, current limitations include context-dependent effects, limited causal evidence, variable treatment response, and unresolved issues in delivery and tissue specificity.},
}
MeSH Terms:
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Humans
Animals
*Gastrointestinal Microbiome/immunology
*Skin/metabolism/immunology
*Dermatitis, Atopic/metabolism/therapy
Inflammation/metabolism
RevDate: 2026-07-29
CmpDate: 2026-07-29
Gut feelings and sweet teeth: nutritional solutions to the gut damage in inflammatory bowel disease and HIV infection.
Frontiers in nutrition, 13:1878885.
Damage to the mucosal layer of the gut is a central feature of chronic inflammatory diseases, often resulting in gut dysbiosis, microbial imbalances, and dysregulated immunometabolism. Gut dysfunction significantly impacts human health, disrupting metabolic, cardiovascular, and neurological systems, and leading to metabolic syndrome. Here, we discuss two clinical entities that are apparently unrelated but actually share similar alterations to gut mucosal barrier integrity: inflammatory bowel disease (IBD) and human immunodeficiency virus (HIV). We use the particular cases of pediatric IBD and nonhuman primate models of HIV infection to compare and contrast the impact of these diseases on gut integrity and microbiome composition. We also explore potential therapies, focusing on dietary interventions. Both HIV infection and IBD cause gut barrier disruption, but via different mechanisms. HIV rapidly depletes mucosal CD4[+] T cells (especially Th17 cells), weakening epithelial defenses, leading to a loss of tight junctions ("leaky gut"), microbial translocation, and systemic inflammation. In IBD (Crohn's disease and ulcerative colitis), chronic immune attacks on the gut lining produce ulcers and tight-junction defects. These ulcerations trigger immune-cell infiltration and markedly increase permeability. In both conditions, impaired mucus and epithelial integrity result in higher circulating lipopolysaccharides (LPS), macrophage activation, and systemic inflammation. HIV and IBD also induce distinct yet overlapping dysbioses. HIV infection is associated with markedly reduced bacterial diversity and an overgrowth of potentially inflammatory taxa (e.g., Proteobacteria, Prevotella). Similarly, IBD patients have low diversity and loss of beneficial Firmicutes (notably Faecalibacterium prausnitzii) with relative Proteobacteria overabundance. In both diseases, the gut flora shifts away from fiber-fermenting commensals to "pathobionts," fueling local inflammation. While the therapeutic potential of targeting metabolic products is widely explored, there is also a push towards discovering nondrug solutions, particularly through diet and nutrition. We present the effects of micronutrient intake, feeding mechanisms (exclusive enteral nutrition), and different diets (high fiber, Mediterranean, high fat) on disease progression and cellular metabolism. As a low-intervention approach, nutrition has enormous potential to improve human health by reducing inflammation and associated metabolic disturbances. Finally, we emphasize the capabilities of using animal models to elucidate the complexities of disease mechanics in IBD and HIV.
Additional Links: PMID-42523904
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Citation:
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@article {pmid42523904,
year = {2026},
author = {Labiner, A and Spoiala, EL and Apetrei, C and Trandafir, LM and Pandrea, I},
title = {Gut feelings and sweet teeth: nutritional solutions to the gut damage in inflammatory bowel disease and HIV infection.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1878885},
pmid = {42523904},
issn = {2296-861X},
abstract = {Damage to the mucosal layer of the gut is a central feature of chronic inflammatory diseases, often resulting in gut dysbiosis, microbial imbalances, and dysregulated immunometabolism. Gut dysfunction significantly impacts human health, disrupting metabolic, cardiovascular, and neurological systems, and leading to metabolic syndrome. Here, we discuss two clinical entities that are apparently unrelated but actually share similar alterations to gut mucosal barrier integrity: inflammatory bowel disease (IBD) and human immunodeficiency virus (HIV). We use the particular cases of pediatric IBD and nonhuman primate models of HIV infection to compare and contrast the impact of these diseases on gut integrity and microbiome composition. We also explore potential therapies, focusing on dietary interventions. Both HIV infection and IBD cause gut barrier disruption, but via different mechanisms. HIV rapidly depletes mucosal CD4[+] T cells (especially Th17 cells), weakening epithelial defenses, leading to a loss of tight junctions ("leaky gut"), microbial translocation, and systemic inflammation. In IBD (Crohn's disease and ulcerative colitis), chronic immune attacks on the gut lining produce ulcers and tight-junction defects. These ulcerations trigger immune-cell infiltration and markedly increase permeability. In both conditions, impaired mucus and epithelial integrity result in higher circulating lipopolysaccharides (LPS), macrophage activation, and systemic inflammation. HIV and IBD also induce distinct yet overlapping dysbioses. HIV infection is associated with markedly reduced bacterial diversity and an overgrowth of potentially inflammatory taxa (e.g., Proteobacteria, Prevotella). Similarly, IBD patients have low diversity and loss of beneficial Firmicutes (notably Faecalibacterium prausnitzii) with relative Proteobacteria overabundance. In both diseases, the gut flora shifts away from fiber-fermenting commensals to "pathobionts," fueling local inflammation. While the therapeutic potential of targeting metabolic products is widely explored, there is also a push towards discovering nondrug solutions, particularly through diet and nutrition. We present the effects of micronutrient intake, feeding mechanisms (exclusive enteral nutrition), and different diets (high fiber, Mediterranean, high fat) on disease progression and cellular metabolism. As a low-intervention approach, nutrition has enormous potential to improve human health by reducing inflammation and associated metabolic disturbances. Finally, we emphasize the capabilities of using animal models to elucidate the complexities of disease mechanics in IBD and HIV.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Functional convergence amid taxonomic variability in gut microbiome-immune checkpoint inhibitor research: a bibliometric and mechanistic synthesis.
Frontiers in immunology, 17:1883259.
Immune checkpoint inhibitors (ICIs) have transformed cancer therapy, yet clinical responses remain highly variable, and microbiome-associated findings lack reproducibility across studies. Increasing evidence implicates the gut microbiome in modulating ICI efficacy; however, findings remain inconsistent at the taxonomic level, raising the possibility that functionally convergent immunological mechanisms may underlie this apparent variability. To address this, a critical synthesis was conducted, integrating bibliometric mapping of publications indexed in the Web of Science Core Collection (2013-2025; n = 2,195) with a secondary analysis of ClinicalTrials.gov to evaluate interventional activity. Bibliometric approaches assessed scientific production, thematic evolution, and co-citation structure, complemented by a cross-cohort functional integration of representative clinical and preclinical studies to evaluate whether microbiome-ICI interactions converge on shared immunological pathways despite divergent taxonomic signatures. Publication output increased steadily, with a marked translational surge following landmark clinical studies in 2018 and a peak in trial initiation in 2021. Thematic analyses revealed a shift from mechanistic and tumor-centered research toward clinically oriented and intervention-driven themes, including microbiome modulation, microbial metabolites, and the tumor microenvironment. Although individual response-associated taxa differed substantially across independent cohorts, qualitative functional integration supported a model of convergence in immunomodulatory pathways involving short-chain fatty acid production, dendritic cell activation, and CD8[+] T-cell priming. Collectively, these findings suggest that apparent taxonomic inconsistencies across microbiome-ICI studies may reflect underlying functional convergence rather than biological contradiction, supporting a shift toward function-based frameworks for biomarker discovery and microbiome-directed immunomodulation.
Additional Links: PMID-42524136
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Citation:
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@article {pmid42524136,
year = {2026},
author = {Alanazi, YN},
title = {Functional convergence amid taxonomic variability in gut microbiome-immune checkpoint inhibitor research: a bibliometric and mechanistic synthesis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1883259},
pmid = {42524136},
issn = {1664-3224},
mesh = {Humans ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; *Gastrointestinal Microbiome/immunology/drug effects ; Bibliometrics ; Animals ; Tumor Microenvironment/immunology/drug effects ; *Neoplasms/immunology/drug therapy/microbiology ; },
abstract = {Immune checkpoint inhibitors (ICIs) have transformed cancer therapy, yet clinical responses remain highly variable, and microbiome-associated findings lack reproducibility across studies. Increasing evidence implicates the gut microbiome in modulating ICI efficacy; however, findings remain inconsistent at the taxonomic level, raising the possibility that functionally convergent immunological mechanisms may underlie this apparent variability. To address this, a critical synthesis was conducted, integrating bibliometric mapping of publications indexed in the Web of Science Core Collection (2013-2025; n = 2,195) with a secondary analysis of ClinicalTrials.gov to evaluate interventional activity. Bibliometric approaches assessed scientific production, thematic evolution, and co-citation structure, complemented by a cross-cohort functional integration of representative clinical and preclinical studies to evaluate whether microbiome-ICI interactions converge on shared immunological pathways despite divergent taxonomic signatures. Publication output increased steadily, with a marked translational surge following landmark clinical studies in 2018 and a peak in trial initiation in 2021. Thematic analyses revealed a shift from mechanistic and tumor-centered research toward clinically oriented and intervention-driven themes, including microbiome modulation, microbial metabolites, and the tumor microenvironment. Although individual response-associated taxa differed substantially across independent cohorts, qualitative functional integration supported a model of convergence in immunomodulatory pathways involving short-chain fatty acid production, dendritic cell activation, and CD8[+] T-cell priming. Collectively, these findings suggest that apparent taxonomic inconsistencies across microbiome-ICI studies may reflect underlying functional convergence rather than biological contradiction, supporting a shift toward function-based frameworks for biomarker discovery and microbiome-directed immunomodulation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
*Gastrointestinal Microbiome/immunology/drug effects
Bibliometrics
Animals
Tumor Microenvironment/immunology/drug effects
*Neoplasms/immunology/drug therapy/microbiology
RevDate: 2026-07-29
Melting Mountains, Shifting Microbiomes: Reconsidering Microbial Roles in Post-Glacial Ecosystem Services.
Current opinion in environmental sustainability, 83:.
The coldest biomes on Earth are mountains with permanent glaciers and permafrost, vulnerable to climate change. These biomes have experienced marked changes and are projected to undergo accelerated transformation due to elevation-dependent warming. While the physical and vegetative responses to glacial retreat are well documented, associated microbial and biochemical shifts remain poorly understood. During deglaciation, newly exposed forefields undergo rapid physical, chemical, and ecological transitions, selecting for specialised microbial communities that mediate ecosystem development through nutrient cycling, soil formation, carbon storage, and early plant establishment. These early-stage microbiomes should not be viewed as passive responders but as active ecosystem engineers shaping post-glacial landscapes and influencing water quality, biodiversity, and downstream ecosystem services. Ignoring microbial contributions in climate assessments risks underestimating ecosystem trajectories and weakening adaptation strategies. This review highlights the need to integrate microbial processes into mountain sustainability frameworks to support informed management, conservation, and long-term ecosystem resilience.
Additional Links: PMID-42524160
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Citation:
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@article {pmid42524160,
year = {2026},
author = {Kumar, A and Dahal, N and Lamichhaney, S and Kumar, R},
title = {Melting Mountains, Shifting Microbiomes: Reconsidering Microbial Roles in Post-Glacial Ecosystem Services.},
journal = {Current opinion in environmental sustainability},
volume = {83},
number = {},
pages = {},
pmid = {42524160},
issn = {1877-3435},
abstract = {The coldest biomes on Earth are mountains with permanent glaciers and permafrost, vulnerable to climate change. These biomes have experienced marked changes and are projected to undergo accelerated transformation due to elevation-dependent warming. While the physical and vegetative responses to glacial retreat are well documented, associated microbial and biochemical shifts remain poorly understood. During deglaciation, newly exposed forefields undergo rapid physical, chemical, and ecological transitions, selecting for specialised microbial communities that mediate ecosystem development through nutrient cycling, soil formation, carbon storage, and early plant establishment. These early-stage microbiomes should not be viewed as passive responders but as active ecosystem engineers shaping post-glacial landscapes and influencing water quality, biodiversity, and downstream ecosystem services. Ignoring microbial contributions in climate assessments risks underestimating ecosystem trajectories and weakening adaptation strategies. This review highlights the need to integrate microbial processes into mountain sustainability frameworks to support informed management, conservation, and long-term ecosystem resilience.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Psychobiotic Effects of Postbiotics in Depression, Psychosis and Mania.
Health promotion perspectives, 16(1):27-47.
BACKGROUND: The gut microbiota significantly influences mental health through the gut-brain axis, modulating mood, cognition, and emotional regulation. While probiotics and prebiotics have been widely studied for their psychobiotic effects, postbiotics-metabolic byproducts of probiotics-represent an underexplored area with potential therapeutic applications. Understanding the role of postbiotics in mental health disorders, such as depression, psychosis, and mania, could lead to novel treatment strategies. This review examines the psychobiotic potential of postbiotics and their mechanisms of action.
METHODS: A systematic literature review was conducted to evaluate the effects of postbiotics on mental health conditions. We searched PubMed, Medline, EMBASE, and the Cochrane Library for English-language articles published between January 1, 2015, and January 1, 2025, using keywords such as "postbiotic," "paraprobiotic," "depression," "anxiety," and "psychosis." A manual search supplemented the electronic search to ensure comprehensive coverage. Studies focusing on postbiotic effects on mood regulation, neuroinflammation, and neurotransmitter modulation were included.
RESULTS: Postbiotics demonstrate promising psychobiotic effects in depression, psychosis, and mania. They modulate neurotransmitter levels, including serotonin and gamma-aminobutyric acid (GABA), and reduce neuroinflammation, contributing to improved mood and cognitive function. Additionally, postbiotics influence the hypothalamic-pituitary-adrenal (HPA) axis, enhancing stress response and emotional regulation. These findings suggest that postbiotics may serve as effective therapeutic agents for mental health disorders.
CONCLUSION: Postbiotics offer significant potential as novel interventions for mental health conditions, with mechanisms involving neurotransmitter modulation and neuroinflammation reduction. Further empirical research is needed to elucidate their clinical applications and optimize therapeutic protocols. This review highlights the importance of postbiotics in advancing innovative strategies to improve mental health outcomes and well-being.
Additional Links: PMID-42524177
PubMed:
Citation:
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@article {pmid42524177,
year = {2026},
author = {Homayouni-Rad, A and Houshyar, J and Alikhah, H and Kamalledin Moghadam, S and Osouli, Z and Asgharzadeh, A and Sarabi-Aghdam, V and Asghari, A},
title = {Psychobiotic Effects of Postbiotics in Depression, Psychosis and Mania.},
journal = {Health promotion perspectives},
volume = {16},
number = {1},
pages = {27-47},
pmid = {42524177},
issn = {2228-6497},
abstract = {BACKGROUND: The gut microbiota significantly influences mental health through the gut-brain axis, modulating mood, cognition, and emotional regulation. While probiotics and prebiotics have been widely studied for their psychobiotic effects, postbiotics-metabolic byproducts of probiotics-represent an underexplored area with potential therapeutic applications. Understanding the role of postbiotics in mental health disorders, such as depression, psychosis, and mania, could lead to novel treatment strategies. This review examines the psychobiotic potential of postbiotics and their mechanisms of action.
METHODS: A systematic literature review was conducted to evaluate the effects of postbiotics on mental health conditions. We searched PubMed, Medline, EMBASE, and the Cochrane Library for English-language articles published between January 1, 2015, and January 1, 2025, using keywords such as "postbiotic," "paraprobiotic," "depression," "anxiety," and "psychosis." A manual search supplemented the electronic search to ensure comprehensive coverage. Studies focusing on postbiotic effects on mood regulation, neuroinflammation, and neurotransmitter modulation were included.
RESULTS: Postbiotics demonstrate promising psychobiotic effects in depression, psychosis, and mania. They modulate neurotransmitter levels, including serotonin and gamma-aminobutyric acid (GABA), and reduce neuroinflammation, contributing to improved mood and cognitive function. Additionally, postbiotics influence the hypothalamic-pituitary-adrenal (HPA) axis, enhancing stress response and emotional regulation. These findings suggest that postbiotics may serve as effective therapeutic agents for mental health disorders.
CONCLUSION: Postbiotics offer significant potential as novel interventions for mental health conditions, with mechanisms involving neurotransmitter modulation and neuroinflammation reduction. Further empirical research is needed to elucidate their clinical applications and optimize therapeutic protocols. This review highlights the importance of postbiotics in advancing innovative strategies to improve mental health outcomes and well-being.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Post-diagnostic ultra-processed food exposure in gastrointestinal cancers: scoping review with narrative synthesis and clinical implications.
Frontiers in nutrition, 13:1884359.
BACKGROUND: Modifiable lifestyle factors, including diet quality, are strongly associated with the incidence of gastrointestinal cancers. However, the impact of ultra-processed food (UPF) consumption after cancer diagnosis remains poorly understood, with scarce and fragmented evidence. In particular, the role of post-diagnostic UPF exposure in shaping survival outcomes and disease progression has not been systematically explored.
METHODS: We conducted a scoping review with narrative synthesis of the available literature on post-diagnostic UPF consumption and clinical outcomes in gastrointestinal cancers. Eligible studies included adult patients with gastrointestinal malignancies, assessment of dietary exposure after diagnosis, and outcomes such as overall survival, cancer-specific mortality, recurrence, progression, and treatment-related outcomes.
RESULTS: Direct evidence was extremely limited. The only available prospective study in colorectal cancer survivors showed that higher post-diagnostic UPF intake was not associated with overall or cancer-specific mortality but was associated with increased cardiovascular mortality, highlighting the relevance of competing risks in cancer survivorship. Furthermore, specific UPF subgroups showed adverse associations with colorectal cancer-specific mortality. Supportive studies suggested that dietary quality may deteriorate after treatment, with increasing UPF consumption over time. Mechanistic evidence supports a biologically plausible link between UPF exposure, metabolic dysfunction, chronic inflammation, microbiota alterations, and survivorship outcomes.
CONCLUSIONS: Despite the increasing burden of gastrointestinal cancers and the widespread consumption of ultra-processed foods, post-diagnostic UPF exposure remains largely overlooked in oncologic research. Direct evidence is currently limited and mainly restricted to colorectal cancer survivors, where higher UPF intake has been associated with cardiovascular mortality but not consistently with cancer-specific outcomes. These findings, together with biological plausibility from mechanistic studies, support the need for prospective post-diagnostic cohorts and intervention trials integrating standardized dietary assessment into gastrointestinal cancer survivorship research.
Additional Links: PMID-42524374
PubMed:
Citation:
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@article {pmid42524374,
year = {2026},
author = {Oneda, E and Noventa, S and Libertini, M and Cherri, S and Manno, A and Meriggi, F and Petrelli, F and Zaniboni, A},
title = {Post-diagnostic ultra-processed food exposure in gastrointestinal cancers: scoping review with narrative synthesis and clinical implications.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1884359},
pmid = {42524374},
issn = {2296-861X},
abstract = {BACKGROUND: Modifiable lifestyle factors, including diet quality, are strongly associated with the incidence of gastrointestinal cancers. However, the impact of ultra-processed food (UPF) consumption after cancer diagnosis remains poorly understood, with scarce and fragmented evidence. In particular, the role of post-diagnostic UPF exposure in shaping survival outcomes and disease progression has not been systematically explored.
METHODS: We conducted a scoping review with narrative synthesis of the available literature on post-diagnostic UPF consumption and clinical outcomes in gastrointestinal cancers. Eligible studies included adult patients with gastrointestinal malignancies, assessment of dietary exposure after diagnosis, and outcomes such as overall survival, cancer-specific mortality, recurrence, progression, and treatment-related outcomes.
RESULTS: Direct evidence was extremely limited. The only available prospective study in colorectal cancer survivors showed that higher post-diagnostic UPF intake was not associated with overall or cancer-specific mortality but was associated with increased cardiovascular mortality, highlighting the relevance of competing risks in cancer survivorship. Furthermore, specific UPF subgroups showed adverse associations with colorectal cancer-specific mortality. Supportive studies suggested that dietary quality may deteriorate after treatment, with increasing UPF consumption over time. Mechanistic evidence supports a biologically plausible link between UPF exposure, metabolic dysfunction, chronic inflammation, microbiota alterations, and survivorship outcomes.
CONCLUSIONS: Despite the increasing burden of gastrointestinal cancers and the widespread consumption of ultra-processed foods, post-diagnostic UPF exposure remains largely overlooked in oncologic research. Direct evidence is currently limited and mainly restricted to colorectal cancer survivors, where higher UPF intake has been associated with cardiovascular mortality but not consistently with cancer-specific outcomes. These findings, together with biological plausibility from mechanistic studies, support the need for prospective post-diagnostic cohorts and intervention trials integrating standardized dietary assessment into gastrointestinal cancer survivorship research.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
From Host-Microbiome Symbiosis to Clinical Translation: A Gut Microbiome Perspective on Radiation Enteritis.
International journal of biological sciences, 22(12):6709-6734.
Radiotherapy is an essential component of multimodal treatment for solid tumors, and more than half of patients with cancer receive radiation during their disease course. Because of the unique anatomical and physiological features of the intestine, radiation enteritis (RE) remains a common and clinically challenging complication of abdominal and pelvic irradiation, with limited effective treatment options. In this review, we re-examine RE from a host-microbiome perspective. We summarize classical pathophysiological mechanisms and discuss how radiotherapy reshapes gut microbial composition and metabolism. We also highlight the roles of microbial metabolites, including short-chain fatty acids, bile acids and tryptophan derivatives, in barrier repair, immune homeostasis and stem-cell regeneration. Finally, we discuss microbiome heterogeneity across disease phases, tumor types and host factors, as well as microbiota-mediated gut-brain, gut-cardiopulmonary, gut-skin and gut-bone-marrow axes involved in systemic radiation injury. We further outline microbiome-based strategies for individualized risk stratification and early prediction, and recent advances and limitations of probiotics and synbiotics, fecal microbiota transplantation, dietary and lifestyle interventions, drugs and natural products, engineered microbes and novel delivery systems, highlighting the gut microbiome as a promising entry point to improve prevention and treatment of RE and systemic radiation toxicity.
Additional Links: PMID-42524477
PubMed:
Citation:
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@article {pmid42524477,
year = {2026},
author = {Zhuang, J and Zhong, Y and Lin, Z and Lu, Y and Wang, H and Chen, L and Yang, K and Tan, D and Qiu, Y and Zhang, Y and Wang, H and Ge, Z},
title = {From Host-Microbiome Symbiosis to Clinical Translation: A Gut Microbiome Perspective on Radiation Enteritis.},
journal = {International journal of biological sciences},
volume = {22},
number = {12},
pages = {6709-6734},
pmid = {42524477},
issn = {1449-2288},
mesh = {Humans ; *Enteritis/microbiology/etiology ; *Gastrointestinal Microbiome/physiology/radiation effects ; *Symbiosis ; *Radiation Injuries/microbiology ; Animals ; },
abstract = {Radiotherapy is an essential component of multimodal treatment for solid tumors, and more than half of patients with cancer receive radiation during their disease course. Because of the unique anatomical and physiological features of the intestine, radiation enteritis (RE) remains a common and clinically challenging complication of abdominal and pelvic irradiation, with limited effective treatment options. In this review, we re-examine RE from a host-microbiome perspective. We summarize classical pathophysiological mechanisms and discuss how radiotherapy reshapes gut microbial composition and metabolism. We also highlight the roles of microbial metabolites, including short-chain fatty acids, bile acids and tryptophan derivatives, in barrier repair, immune homeostasis and stem-cell regeneration. Finally, we discuss microbiome heterogeneity across disease phases, tumor types and host factors, as well as microbiota-mediated gut-brain, gut-cardiopulmonary, gut-skin and gut-bone-marrow axes involved in systemic radiation injury. We further outline microbiome-based strategies for individualized risk stratification and early prediction, and recent advances and limitations of probiotics and synbiotics, fecal microbiota transplantation, dietary and lifestyle interventions, drugs and natural products, engineered microbes and novel delivery systems, highlighting the gut microbiome as a promising entry point to improve prevention and treatment of RE and systemic radiation toxicity.},
}
MeSH Terms:
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Humans
*Enteritis/microbiology/etiology
*Gastrointestinal Microbiome/physiology/radiation effects
*Symbiosis
*Radiation Injuries/microbiology
Animals
RevDate: 2026-07-29
CmpDate: 2026-07-29
Faecal immunoglobulin A as a non-invasive biomarker of mucosal immunity and health in zoo and wild mammals.
Conservation physiology, 14(1):coag054.
Non-invasive biomarkers of immune function are increasingly important for assessing health, welfare and disease risk in zoo and wild mammals, particularly because they support repeated monitoring while minimizing handling-related disturbance. Secretory immunoglobulin A (IgA), a key component of mucosal immunity, can be quantified from faecal samples and provides a practical measure of gut-associated immune activity without invasive sampling. We conducted a systematic literature review of 21 peer-reviewed studies that quantified faecal IgA across diverse mammalian taxa and ecological contexts. Across species, faecal IgA was technically measurable and biologically responsive, but its interpretation was strongly context dependent. Reported patterns reflected interactions among pathogen exposure, physiological stress, nutritional state, life-history stage and management conditions. In captive settings, faecal IgA frequently varied with individual heterogeneity and management factors and showed inconsistent alignment with endocrine stress markers. In free-ranging populations, faecal IgA more commonly tracked parasite burden, reproductive investment, seasonal variation and host-microbiome dynamics. However, most ecological and welfare-associated patterns were derived from observational designs, which limit causal inference. Additionally, methodological heterogeneity in assay validation, sample processing and preservation limited direct quantitative comparison among studies. Overall, faecal IgA does not function as a unidimensional indicator of stress or welfare, but rather as a context-sensitive marker of mucosal immune allocation. We integrate these findings into a conceptual framework linking external pressures, mucosal immune dynamics, complementary biomarkers and health-related outcomes to guide interpretation across zoo and wild settings. When embedded within longitudinal and multi-marker approaches supported by species-specific validation, faecal IgA has potential to contribute meaningfully to non-invasive health assessment in conservation physiology.
Additional Links: PMID-42524481
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@article {pmid42524481,
year = {2026},
author = {Kosaruk, W and Towiboon, P and Klinhom, S},
title = {Faecal immunoglobulin A as a non-invasive biomarker of mucosal immunity and health in zoo and wild mammals.},
journal = {Conservation physiology},
volume = {14},
number = {1},
pages = {coag054},
pmid = {42524481},
issn = {2051-1434},
abstract = {Non-invasive biomarkers of immune function are increasingly important for assessing health, welfare and disease risk in zoo and wild mammals, particularly because they support repeated monitoring while minimizing handling-related disturbance. Secretory immunoglobulin A (IgA), a key component of mucosal immunity, can be quantified from faecal samples and provides a practical measure of gut-associated immune activity without invasive sampling. We conducted a systematic literature review of 21 peer-reviewed studies that quantified faecal IgA across diverse mammalian taxa and ecological contexts. Across species, faecal IgA was technically measurable and biologically responsive, but its interpretation was strongly context dependent. Reported patterns reflected interactions among pathogen exposure, physiological stress, nutritional state, life-history stage and management conditions. In captive settings, faecal IgA frequently varied with individual heterogeneity and management factors and showed inconsistent alignment with endocrine stress markers. In free-ranging populations, faecal IgA more commonly tracked parasite burden, reproductive investment, seasonal variation and host-microbiome dynamics. However, most ecological and welfare-associated patterns were derived from observational designs, which limit causal inference. Additionally, methodological heterogeneity in assay validation, sample processing and preservation limited direct quantitative comparison among studies. Overall, faecal IgA does not function as a unidimensional indicator of stress or welfare, but rather as a context-sensitive marker of mucosal immune allocation. We integrate these findings into a conceptual framework linking external pressures, mucosal immune dynamics, complementary biomarkers and health-related outcomes to guide interpretation across zoo and wild settings. When embedded within longitudinal and multi-marker approaches supported by species-specific validation, faecal IgA has potential to contribute meaningfully to non-invasive health assessment in conservation physiology.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Progressive Shifts in Oral Plaque Microbiota From Health to Coronary Artery Disease and Acute Myocardial Infarction.
Cardiology research, 17(4):288-299.
BACKGROUND: Growing evidence links oral microbial dysbiosis to atherosclerotic cardiovascular disease (ASCVD), yet its role in acute myocardial infarction (AMI) and the transition from stable coronary artery disease (CAD) to acute events remains unclear. We aimed to characterize taxonomic and functional alterations of the oral plaque microbiome across cardiovascular health states and explore their clinical relevance.
METHODS: We enrolled 60 age- and sex-matched adults, 20 in each group. Supragingival plaque underwent 16S rRNA sequencing and functional inference. Alpha and beta diversity were assessed, and differential features were identified by Linear Discriminant Analysis Effect Size (LEfSe). The metabolic pathway predictions were using Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway.
RESULTS: Alpha and beta diversity showed no significant differences in overall microbial richness, evenness, or global community structure among groups. However, marked taxonomic shifts were observed. AMI patients exhibited enrichment of pro-inflammatory genera (Veillonella, Porphyromonas, Dialister, Megasphaera, and Acidaminococcus) and depletion of commensal taxa (Haemophilus and Lautropia). LEfSe identified disease-specific microbial signatures distinguishing healthy control, CAD, and AMI. Functional prediction revealed enrichment of arachidonic acid, pyrimidine, and D-glutamine/D-glutamate metabolism in CAD, with further increases in necroptosis-, proteasome-, and inflammation-related pathways in AMI, whereas two-component signaling systems were enriched in healthy controls.
CONCLUSIONS: The oral microbiome exhibits progressive taxonomic and functional shifts from health to CAD and AMI, supporting an oral-cardiovascular axis and highlighting oral microbial profiles as potential noninvasive biomarkers for ASCVD risk stratification.
Additional Links: PMID-42524566
PubMed:
Citation:
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@article {pmid42524566,
year = {2026},
author = {Tsai, HL and Chen, YP and Tsai, JY and Yep, CY and Tan, CW and Lee, CP and Wu, CY and Tsai, TH},
title = {Progressive Shifts in Oral Plaque Microbiota From Health to Coronary Artery Disease and Acute Myocardial Infarction.},
journal = {Cardiology research},
volume = {17},
number = {4},
pages = {288-299},
pmid = {42524566},
issn = {1923-2829},
abstract = {BACKGROUND: Growing evidence links oral microbial dysbiosis to atherosclerotic cardiovascular disease (ASCVD), yet its role in acute myocardial infarction (AMI) and the transition from stable coronary artery disease (CAD) to acute events remains unclear. We aimed to characterize taxonomic and functional alterations of the oral plaque microbiome across cardiovascular health states and explore their clinical relevance.
METHODS: We enrolled 60 age- and sex-matched adults, 20 in each group. Supragingival plaque underwent 16S rRNA sequencing and functional inference. Alpha and beta diversity were assessed, and differential features were identified by Linear Discriminant Analysis Effect Size (LEfSe). The metabolic pathway predictions were using Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway.
RESULTS: Alpha and beta diversity showed no significant differences in overall microbial richness, evenness, or global community structure among groups. However, marked taxonomic shifts were observed. AMI patients exhibited enrichment of pro-inflammatory genera (Veillonella, Porphyromonas, Dialister, Megasphaera, and Acidaminococcus) and depletion of commensal taxa (Haemophilus and Lautropia). LEfSe identified disease-specific microbial signatures distinguishing healthy control, CAD, and AMI. Functional prediction revealed enrichment of arachidonic acid, pyrimidine, and D-glutamine/D-glutamate metabolism in CAD, with further increases in necroptosis-, proteasome-, and inflammation-related pathways in AMI, whereas two-component signaling systems were enriched in healthy controls.
CONCLUSIONS: The oral microbiome exhibits progressive taxonomic and functional shifts from health to CAD and AMI, supporting an oral-cardiovascular axis and highlighting oral microbial profiles as potential noninvasive biomarkers for ASCVD risk stratification.},
}
RevDate: 2026-07-29
Evolution of the fecal and oral microbiota after prophylactic antibiotics administered for dental surgeries.
Journal of the American Dental Association (1939) pii:S0002-8177(26)00271-0 [Epub ahead of print].
BACKGROUND: The human oral and gut microbiomes play critical roles in maintaining overall health. Although systemic antibiotics are frequently prescribed perioperatively in dental procedures, their impact on microbiota composition and diversity remains inadequately understood. The authors' objective was to characterize the evolution of the gut and oral microbiomes after a course of antibiotics administered for dental surgeries. The authors hypothesized that the microbiome would experience disruption but eventually recover to baseline levels and that patient-related factors would influence the extent of disruption and recovery.
METHODS: Saliva and stool samples were collected from patients undergoing dental surgeries and receiving prophylactic antibiotics (n = 64) at baseline and then at 3, 10, 30, and 90 days after surgery. Microbial diversity and composition were assessed using 16S ribosomal RNA sequencing. Shotgun metagenomics sequencing was applied to a subset of samples to evaluate changes in antimicrobial resistance genes.
RESULTS: Significant (P < .01) declines in alpha diversity were observed in both oral and fecal microbiomes, most notably at days 3 and 10, with near recovery at day 90. The oral microbiome exhibited greater disruption than the gut microbiome, suggesting higher susceptibility to postoperative disturbance. Patient-level factors including sex, race, gastroesophageal reflux disease, and antibiotic type influenced baseline diversity, disruption, and recovery. Results of taxonomic analyses revealed that key health-associated genera were substantially altered postsurgery. Some antimicrobial resistance genes increased in relative abundance over time, consistent with potential long-term ecological consequences of antibiotic use.
CONCLUSIONS: The findings highlight the dynamic response of the human microbiome to antibiotic exposure and oral surgery and underscore the importance of antibiotic stewardship in practice. Further research on functional outcomes and host-microbiome interactions is warranted to optimize perioperative care in dentistry.
PRACTICAL IMPLICATIONS: Consideration of patient factors is essential to minimize unnecessary disruption of the microbiome and mitigate the risk of developing resistance.
Additional Links: PMID-42524765
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PubMed:
Citation:
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@article {pmid42524765,
year = {2026},
author = {Littlejohn, C and Chang, YC and Teles, F and Korostoff, JM and Redding, LE},
title = {Evolution of the fecal and oral microbiota after prophylactic antibiotics administered for dental surgeries.},
journal = {Journal of the American Dental Association (1939)},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.adaj.2026.04.020},
pmid = {42524765},
issn = {1943-4723},
abstract = {BACKGROUND: The human oral and gut microbiomes play critical roles in maintaining overall health. Although systemic antibiotics are frequently prescribed perioperatively in dental procedures, their impact on microbiota composition and diversity remains inadequately understood. The authors' objective was to characterize the evolution of the gut and oral microbiomes after a course of antibiotics administered for dental surgeries. The authors hypothesized that the microbiome would experience disruption but eventually recover to baseline levels and that patient-related factors would influence the extent of disruption and recovery.
METHODS: Saliva and stool samples were collected from patients undergoing dental surgeries and receiving prophylactic antibiotics (n = 64) at baseline and then at 3, 10, 30, and 90 days after surgery. Microbial diversity and composition were assessed using 16S ribosomal RNA sequencing. Shotgun metagenomics sequencing was applied to a subset of samples to evaluate changes in antimicrobial resistance genes.
RESULTS: Significant (P < .01) declines in alpha diversity were observed in both oral and fecal microbiomes, most notably at days 3 and 10, with near recovery at day 90. The oral microbiome exhibited greater disruption than the gut microbiome, suggesting higher susceptibility to postoperative disturbance. Patient-level factors including sex, race, gastroesophageal reflux disease, and antibiotic type influenced baseline diversity, disruption, and recovery. Results of taxonomic analyses revealed that key health-associated genera were substantially altered postsurgery. Some antimicrobial resistance genes increased in relative abundance over time, consistent with potential long-term ecological consequences of antibiotic use.
CONCLUSIONS: The findings highlight the dynamic response of the human microbiome to antibiotic exposure and oral surgery and underscore the importance of antibiotic stewardship in practice. Further research on functional outcomes and host-microbiome interactions is warranted to optimize perioperative care in dentistry.
PRACTICAL IMPLICATIONS: Consideration of patient factors is essential to minimize unnecessary disruption of the microbiome and mitigate the risk of developing resistance.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
DYSBIOSIS IN ACUTE-ON-CHRONIC LIVER FAILURE - FROM A PATHOPHYSIOLOGICAL COMPONENT TO A THERAPEUTIC TARGET.
Arquivos de gastroenterologia, 63:e25141 pii:S0004-28032026000105006.
BACKGROUND: Acute-on-chronic liver failure (ACLF) affects approximately one-third of patients hospitalized for acute decompensation of cirrhosis. These patients exhibit an extremely high degree of systemic inflammation, and infections as well as severe alcohol-related hepatitis are the most common precipitating factors of ACLF.
OBJECTIVE: This paper aims to discuss the most relevant aspects of ACLF emphasizing the role of gut dysbiosis.
METHODS: This review includes clinical and epidemiological studies, meta-analyses, and other articles published in English and indexed in the following databases: PubMed, Scopus, and Embase. Only full-text articles were selected.
RESULTS: ACLF is the most severe complication in patients with cirrhosis and is associated with high mortality rates. Bacterial translocation is considered responsible for the systemic inflammation leading to acute decompensation of cirrhosis when other precipitating events are not identified. Different microbiome profiles may influence the incidence of decompensation and thus the clinical course of the disease. Dysbiosis causes intestinal inflammation, which contributes to gut barrier dysfunction and pathological bacterial translocation, the main triggering factor of the cascade leading to acute decompensation of cirrhosis and multiple organ failure. Since dysbiosis plays a central role in the pathophysiology of acute decompensation of cirrhosis and ACLF, it is expected that treatments targeting the microbiome could modify the course of the disease. Despite current limitations, the role of probiotics, prebiotics, postbiotics, rifaximin, bacteriophages, and fecal microbiota transplantation is discussed in the present review.
CONCLUSION: ACLF is a highly significant complication of liver disease. Dysbiosis and the gut-liver axis play key roles in its pathophysiology. This knowledge supports the idea that manipulation of the microbiome may be a potential therapeutic strategy.
Additional Links: PMID-42524911
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PubMed:
Citation:
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@article {pmid42524911,
year = {2026},
author = {Mattos, AA and Alves, CA and Acuña, J and Mattos, AZ},
title = {DYSBIOSIS IN ACUTE-ON-CHRONIC LIVER FAILURE - FROM A PATHOPHYSIOLOGICAL COMPONENT TO A THERAPEUTIC TARGET.},
journal = {Arquivos de gastroenterologia},
volume = {63},
number = {},
pages = {e25141},
doi = {10.1590/S0004-2803.24612025-141},
pmid = {42524911},
issn = {1678-4219},
mesh = {Humans ; *Acute-On-Chronic Liver Failure/microbiology/physiopathology/therapy/etiology ; *Dysbiosis/complications/physiopathology/therapy/microbiology ; Gastrointestinal Microbiome/physiology ; Liver Cirrhosis/complications/microbiology ; Bacterial Translocation ; },
abstract = {BACKGROUND: Acute-on-chronic liver failure (ACLF) affects approximately one-third of patients hospitalized for acute decompensation of cirrhosis. These patients exhibit an extremely high degree of systemic inflammation, and infections as well as severe alcohol-related hepatitis are the most common precipitating factors of ACLF.
OBJECTIVE: This paper aims to discuss the most relevant aspects of ACLF emphasizing the role of gut dysbiosis.
METHODS: This review includes clinical and epidemiological studies, meta-analyses, and other articles published in English and indexed in the following databases: PubMed, Scopus, and Embase. Only full-text articles were selected.
RESULTS: ACLF is the most severe complication in patients with cirrhosis and is associated with high mortality rates. Bacterial translocation is considered responsible for the systemic inflammation leading to acute decompensation of cirrhosis when other precipitating events are not identified. Different microbiome profiles may influence the incidence of decompensation and thus the clinical course of the disease. Dysbiosis causes intestinal inflammation, which contributes to gut barrier dysfunction and pathological bacterial translocation, the main triggering factor of the cascade leading to acute decompensation of cirrhosis and multiple organ failure. Since dysbiosis plays a central role in the pathophysiology of acute decompensation of cirrhosis and ACLF, it is expected that treatments targeting the microbiome could modify the course of the disease. Despite current limitations, the role of probiotics, prebiotics, postbiotics, rifaximin, bacteriophages, and fecal microbiota transplantation is discussed in the present review.
CONCLUSION: ACLF is a highly significant complication of liver disease. Dysbiosis and the gut-liver axis play key roles in its pathophysiology. This knowledge supports the idea that manipulation of the microbiome may be a potential therapeutic strategy.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Acute-On-Chronic Liver Failure/microbiology/physiopathology/therapy/etiology
*Dysbiosis/complications/physiopathology/therapy/microbiology
Gastrointestinal Microbiome/physiology
Liver Cirrhosis/complications/microbiology
Bacterial Translocation
RevDate: 2026-07-29
CmpDate: 2026-07-29
GUT MICROBIOTA ALTERATIONS IN RODENT MODELS OF CHOLESTASIS INDUCED BY BILE DUCT LIGATION: A SYSTEMATIC REVIEW.
Arquivos de gastroenterologia, 63:e25159 pii:S0004-28032026000105008.
BACKGROUND AND OBJECTIVE: Cholestatic liver diseases are a major public health issue, marked by impaired bile flow and significant disruptions in liver and systemic physiology. Growing evidence points to the gut microbiota as a key player in cholestasis pathogenesis through gut-liver axis interactions. This systematic review aimed to synthesize and evaluate current findings on intestinal microbiota changes in rodents (rats and mice) subjected to bile duct ligation (BDL)-induced cholestasis, focusing on microbial diversity, taxonomic shifts, and potential pathophysiological implications.
METHODS: A comprehensive literature search was conducted in PubMed, Scopus, and Embase for studies published from January 2020 to February 2025, following PRISMA guidelines. Eligible studies included original research using BDL in rodents without therapeutic intervention and reporting gut microbiota profiles. Data were qualitatively analyzed, emphasizing experimental conditions and microbiome outcomes.
RESULTS: Twenty-two studies met inclusion criteria. Most used 16S rRNA sequencing; two used shotgun metagenomics. BDL consistently induced gut dysbiosis, with reductions in alpha diversity (in most studies), altered beta diversity, and shifts in dominant phyla such as Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria, and Verrucomicrobiota. At finer taxonomic levels, increases in Prevotella, Enterococcus, Escherichia coli, and Alistipes were common, while Lactobacillus and Ruminococcus often decreased. Elevated levels of Akkermansia muciniphila and Bifidobacterium pseudolongum may represent compensatory microbial responses.
CONCLUSION: Bile duct ligation (BDL)-induced cholestasis leads to complex changes in the microbiota that can worsen intestinal barrier integrity, increase bacterial translocation, and intensify liver inflammation. These findings reinforce the central role of the gut-liver axis and corroborate the potential of microbiota-targeted therapies in the management of cholestatic liver diseases. However, as most of the available evidence derives from experimental models, further well-designed clinical studies are needed to validate the safety, efficacy, and translational applicability of these strategies in human diseases.
Additional Links: PMID-42524914
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PubMed:
Citation:
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@article {pmid42524914,
year = {2026},
author = {Calixto, SL and Macedo, ACLP and Aguiar, JAK},
title = {GUT MICROBIOTA ALTERATIONS IN RODENT MODELS OF CHOLESTASIS INDUCED BY BILE DUCT LIGATION: A SYSTEMATIC REVIEW.},
journal = {Arquivos de gastroenterologia},
volume = {63},
number = {},
pages = {e25159},
doi = {10.1590/S0004-2803.24612025-159},
pmid = {42524914},
issn = {1678-4219},
mesh = {Animals ; *Cholestasis/microbiology ; *Gastrointestinal Microbiome/physiology ; Disease Models, Animal ; Ligation ; Bile Ducts/surgery ; Mice ; *Dysbiosis/microbiology ; Rats ; },
abstract = {BACKGROUND AND OBJECTIVE: Cholestatic liver diseases are a major public health issue, marked by impaired bile flow and significant disruptions in liver and systemic physiology. Growing evidence points to the gut microbiota as a key player in cholestasis pathogenesis through gut-liver axis interactions. This systematic review aimed to synthesize and evaluate current findings on intestinal microbiota changes in rodents (rats and mice) subjected to bile duct ligation (BDL)-induced cholestasis, focusing on microbial diversity, taxonomic shifts, and potential pathophysiological implications.
METHODS: A comprehensive literature search was conducted in PubMed, Scopus, and Embase for studies published from January 2020 to February 2025, following PRISMA guidelines. Eligible studies included original research using BDL in rodents without therapeutic intervention and reporting gut microbiota profiles. Data were qualitatively analyzed, emphasizing experimental conditions and microbiome outcomes.
RESULTS: Twenty-two studies met inclusion criteria. Most used 16S rRNA sequencing; two used shotgun metagenomics. BDL consistently induced gut dysbiosis, with reductions in alpha diversity (in most studies), altered beta diversity, and shifts in dominant phyla such as Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria, and Verrucomicrobiota. At finer taxonomic levels, increases in Prevotella, Enterococcus, Escherichia coli, and Alistipes were common, while Lactobacillus and Ruminococcus often decreased. Elevated levels of Akkermansia muciniphila and Bifidobacterium pseudolongum may represent compensatory microbial responses.
CONCLUSION: Bile duct ligation (BDL)-induced cholestasis leads to complex changes in the microbiota that can worsen intestinal barrier integrity, increase bacterial translocation, and intensify liver inflammation. These findings reinforce the central role of the gut-liver axis and corroborate the potential of microbiota-targeted therapies in the management of cholestatic liver diseases. However, as most of the available evidence derives from experimental models, further well-designed clinical studies are needed to validate the safety, efficacy, and translational applicability of these strategies in human diseases.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Cholestasis/microbiology
*Gastrointestinal Microbiome/physiology
Disease Models, Animal
Ligation
Bile Ducts/surgery
Mice
*Dysbiosis/microbiology
Rats
RevDate: 2026-07-29
CmpDate: 2026-07-29
Gut microbiome changes in critically ill adults: a systematic review of longitudinal sequencing studies.
Critical care science, 38:e20260392 pii:S2965-27742026000101027.
OBJECTIVE: Critical illness profoundly alters the gut microbiome, yet its temporal evolution and clinical relevance remain unclear. This systematic review aimed to synthesize evidence from longitudinal sequencing studies describing gut microbiome changes in critically ill adults and their association with clinical outcomes.
METHODS: We systematically searched MEDLINE®, Scopus, and Cochrane CENTRAL from inception to May 2025 for longitudinal observational studies analyzing gastrointestinal samples by sequencing in adult critically ill patients at ≥ 2 times points. Extracted data included study and patient characteristics, as well as microbiome outcomes, including alpha and beta diversity metrics and taxonomic abundance profiles. Due to heterogeneity, we undertook a structured descriptive synthesis: alpha diversity results were grouped by trajectory and compared across intensive care unit populations; beta diversity findings were tabulated and narratively synthesized; and reported associations with mortality and multidrug-resistant organism colonization were summarized narratively. Risk of bias was assessed with RoBANS 2, and certainty of evidence with GRADE.
RESULTS: Thirty-six studies comprising 2,067 critically ill adults were included. Most used 16S rRNA sequencing targeting the V4 region. A decline in alpha diversity was reported in 18 out of 31 studies, while 8 found no change and 4 mixed patterns. Beta diversity shifts over time were reported in 11 studies. Taxonomic analyses consistently revealed the expansion of opportunistic taxa such as Enterococcus, Klebsiella, and other Enterobacteriaceae, alongside the depletion of obligate anaerobes, including Blautia, Coprococcus, and Faecalibacterium. Early low diversity and pathogen-dominated microbiomes were associated with increased mortality. Associations with multidrug-resistant organism colonization were inconsistent. Certainty of evidence (GRADE) for all outcomes was rated very low due to heterogeneity and imprecision.
CONCLUSION: Longitudinal sequencing studies demonstrate progressive loss of microbial diversity and enrichment of pathogenic taxa during critical illness. These shifts, particularly Enterococcus and Klebsiella overgrowth, correlate with adverse outcomes and may reflect the combined effects of antibiotics, disease severity, and critical care interventions. Standardized sampling, sequencing, and reporting protocols are needed to enable meta-analytic synthesis and guide microbiome-targeted interventions in the intensive care unit.
Additional Links: PMID-42524945
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PubMed:
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@article {pmid42524945,
year = {2026},
author = {Theocharidou, CC and Tsinaris, Z and Peristeri, AM and Akritidou, O and Nikopoulou, A},
title = {Gut microbiome changes in critically ill adults: a systematic review of longitudinal sequencing studies.},
journal = {Critical care science},
volume = {38},
number = {},
pages = {e20260392},
doi = {10.62675/2965-2774.20260392},
pmid = {42524945},
issn = {2965-2774},
mesh = {Humans ; *Critical Illness ; *Gastrointestinal Microbiome/physiology ; Longitudinal Studies ; RNA, Ribosomal, 16S ; Adult ; },
abstract = {OBJECTIVE: Critical illness profoundly alters the gut microbiome, yet its temporal evolution and clinical relevance remain unclear. This systematic review aimed to synthesize evidence from longitudinal sequencing studies describing gut microbiome changes in critically ill adults and their association with clinical outcomes.
METHODS: We systematically searched MEDLINE®, Scopus, and Cochrane CENTRAL from inception to May 2025 for longitudinal observational studies analyzing gastrointestinal samples by sequencing in adult critically ill patients at ≥ 2 times points. Extracted data included study and patient characteristics, as well as microbiome outcomes, including alpha and beta diversity metrics and taxonomic abundance profiles. Due to heterogeneity, we undertook a structured descriptive synthesis: alpha diversity results were grouped by trajectory and compared across intensive care unit populations; beta diversity findings were tabulated and narratively synthesized; and reported associations with mortality and multidrug-resistant organism colonization were summarized narratively. Risk of bias was assessed with RoBANS 2, and certainty of evidence with GRADE.
RESULTS: Thirty-six studies comprising 2,067 critically ill adults were included. Most used 16S rRNA sequencing targeting the V4 region. A decline in alpha diversity was reported in 18 out of 31 studies, while 8 found no change and 4 mixed patterns. Beta diversity shifts over time were reported in 11 studies. Taxonomic analyses consistently revealed the expansion of opportunistic taxa such as Enterococcus, Klebsiella, and other Enterobacteriaceae, alongside the depletion of obligate anaerobes, including Blautia, Coprococcus, and Faecalibacterium. Early low diversity and pathogen-dominated microbiomes were associated with increased mortality. Associations with multidrug-resistant organism colonization were inconsistent. Certainty of evidence (GRADE) for all outcomes was rated very low due to heterogeneity and imprecision.
CONCLUSION: Longitudinal sequencing studies demonstrate progressive loss of microbial diversity and enrichment of pathogenic taxa during critical illness. These shifts, particularly Enterococcus and Klebsiella overgrowth, correlate with adverse outcomes and may reflect the combined effects of antibiotics, disease severity, and critical care interventions. Standardized sampling, sequencing, and reporting protocols are needed to enable meta-analytic synthesis and guide microbiome-targeted interventions in the intensive care unit.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Critical Illness
*Gastrointestinal Microbiome/physiology
Longitudinal Studies
RNA, Ribosomal, 16S
Adult
RevDate: 2026-07-29
CmpDate: 2026-07-29
The Gut-brain-adipose Axis in Ultra-processed Food and Obesity: A Mechanistic Synthesis and Its Implications for Food Classification.
Current obesity reports, 15(1):.
PURPOSE OF REVIEW: Consumption of ultra-processed food (UPF) tracks closely with obesity across populations, and the Nova classification has become the dominant tool for capturing that exposure. Why UPF promotes weight gain is a separate question, and the biological answer has accumulated in fragments. I draw those strands together and ask whether three mechanisms usually studied in isolation: gut microbial disruption, hypothalamic inflammation, and adipose tissue dysfunction, are better understood as one connected system, and what that would mean for how UPF is classified.
RECENT FINDINGS: Three experimental literatures have converged on a shared pathway. Dietary emulsifiers and non-sugar sweeteners alter microbial composition and weaken the intestinal barrier, raising circulating lipopolysaccharide. In animal models this signal reaches the hypothalamus, where it activates inflammatory pathways, recruits glia, and blunts the leptin response that normally limits intake; though whether the same sequence operates in humans remains unestablished. Visceral fat that expands under this regime secretes its own inflammatory load, which feeds back onto both the gut and the brain. A 2025 UK Biobank analysis added a human imaging dimension, reporting structural differences in feeding-related brain regions that scaled with UPF intake and were only partly explained by adiposity. The evidence coheres best when the three arms are read as a single self-reinforcing loop in which each influences the others. Within that frame, the limitation of the Nova classification becomes specific and tractable: Group 4 mixes products that engage the loop strongly with products that barely touch it. This review sets out where the mechanistic evidence is firm, where it remains thin, and how an attribute-aware refinement of Group 4 might be tested.
Additional Links: PMID-42525211
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@article {pmid42525211,
year = {2026},
author = {Louie, JCY},
title = {The Gut-brain-adipose Axis in Ultra-processed Food and Obesity: A Mechanistic Synthesis and Its Implications for Food Classification.},
journal = {Current obesity reports},
volume = {15},
number = {1},
pages = {},
pmid = {42525211},
issn = {2162-4968},
mesh = {Humans ; *Obesity/etiology/physiopathology/metabolism ; Animals ; *Fast Foods/adverse effects/classification ; *Gastrointestinal Microbiome/physiology ; *Brain/metabolism ; *Adipose Tissue/metabolism/physiopathology ; Inflammation ; },
abstract = {PURPOSE OF REVIEW: Consumption of ultra-processed food (UPF) tracks closely with obesity across populations, and the Nova classification has become the dominant tool for capturing that exposure. Why UPF promotes weight gain is a separate question, and the biological answer has accumulated in fragments. I draw those strands together and ask whether three mechanisms usually studied in isolation: gut microbial disruption, hypothalamic inflammation, and adipose tissue dysfunction, are better understood as one connected system, and what that would mean for how UPF is classified.
RECENT FINDINGS: Three experimental literatures have converged on a shared pathway. Dietary emulsifiers and non-sugar sweeteners alter microbial composition and weaken the intestinal barrier, raising circulating lipopolysaccharide. In animal models this signal reaches the hypothalamus, where it activates inflammatory pathways, recruits glia, and blunts the leptin response that normally limits intake; though whether the same sequence operates in humans remains unestablished. Visceral fat that expands under this regime secretes its own inflammatory load, which feeds back onto both the gut and the brain. A 2025 UK Biobank analysis added a human imaging dimension, reporting structural differences in feeding-related brain regions that scaled with UPF intake and were only partly explained by adiposity. The evidence coheres best when the three arms are read as a single self-reinforcing loop in which each influences the others. Within that frame, the limitation of the Nova classification becomes specific and tractable: Group 4 mixes products that engage the loop strongly with products that barely touch it. This review sets out where the mechanistic evidence is firm, where it remains thin, and how an attribute-aware refinement of Group 4 might be tested.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Obesity/etiology/physiopathology/metabolism
Animals
*Fast Foods/adverse effects/classification
*Gastrointestinal Microbiome/physiology
*Brain/metabolism
*Adipose Tissue/metabolism/physiopathology
Inflammation
RevDate: 2026-07-29
Functional Equivalence and Conserved Sexual Dimorphism in the Gut Microbiome: A Cross-Species Meta-analysis.
Journal of molecular evolution [Epub ahead of print].
The murine model is a standard system in translational microbiome research, yet its functional equivalence to the human microbiome remains debated. To evaluate its translational validity, we conducted a comparative whole-genome shotgun (WGS) metagenomic meta-analysis, integrating an initial retrieval of 520 datasets from 5 independent cohorts (BioProjects) across Homo sapiens (n = 202), Mus musculus (n = 75), and Drosophila melanogaster (n = 243) samples. Taxonomic and functional profiles were evaluated using strict bioinformatic quality control and batch-effect mitigation. Taxonomic profiling revealed pronounced divergence driven by host-specific ecological constraints and filtering. However, metabolic reconstruction demonstrated substantial functional equivalence, supporting the functional redundancy hypothesis for core mammalian metabolic circuits. We also noted a methodological vulnerability in our dataset: a low-depth murine sample clustered with invertebrate profiles, suggesting that technical noise or insufficient depth might artificially compress mammalian functional diversity. Comparative analysis identified sex-biased metabolic pathways conserved across mammalian hosts. Specifically, we observed a consistent enrichment of steroid metabolism in females and mineralocorticoid regulation in males. These findings indicate that functional conservation between humans and mice is modular rather than global. Consequently, the translational value of the murine model lies in domain-specific functional equivalence rather than taxonomic imitation. Moreover, the conservation of sex-specific metabolic signatures suggests that biological sex is a fundamental organising principle of microbiome function. This study highlights the necessity of mapping conserved metabolic modules and rigorously controlling inter-study variance to effectively deploy murine models in biomedical research.
Additional Links: PMID-42525291
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@article {pmid42525291,
year = {2026},
author = {Gutiérrez-Ávila, JL and Gutiérrez-Rebolledo, GA and Avila-Bonilla, RG and Pardo, MES},
title = {Functional Equivalence and Conserved Sexual Dimorphism in the Gut Microbiome: A Cross-Species Meta-analysis.},
journal = {Journal of molecular evolution},
volume = {},
number = {},
pages = {},
pmid = {42525291},
issn = {1432-1432},
abstract = {The murine model is a standard system in translational microbiome research, yet its functional equivalence to the human microbiome remains debated. To evaluate its translational validity, we conducted a comparative whole-genome shotgun (WGS) metagenomic meta-analysis, integrating an initial retrieval of 520 datasets from 5 independent cohorts (BioProjects) across Homo sapiens (n = 202), Mus musculus (n = 75), and Drosophila melanogaster (n = 243) samples. Taxonomic and functional profiles were evaluated using strict bioinformatic quality control and batch-effect mitigation. Taxonomic profiling revealed pronounced divergence driven by host-specific ecological constraints and filtering. However, metabolic reconstruction demonstrated substantial functional equivalence, supporting the functional redundancy hypothesis for core mammalian metabolic circuits. We also noted a methodological vulnerability in our dataset: a low-depth murine sample clustered with invertebrate profiles, suggesting that technical noise or insufficient depth might artificially compress mammalian functional diversity. Comparative analysis identified sex-biased metabolic pathways conserved across mammalian hosts. Specifically, we observed a consistent enrichment of steroid metabolism in females and mineralocorticoid regulation in males. These findings indicate that functional conservation between humans and mice is modular rather than global. Consequently, the translational value of the murine model lies in domain-specific functional equivalence rather than taxonomic imitation. Moreover, the conservation of sex-specific metabolic signatures suggests that biological sex is a fundamental organising principle of microbiome function. This study highlights the necessity of mapping conserved metabolic modules and rigorously controlling inter-study variance to effectively deploy murine models in biomedical research.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
Host-recruited Bacillus and Pseudomonas strains provide potential biocontrol and yield protection against rice bacterial leaf blight.
World journal of microbiology & biotechnology, 42(8):.
Bacterial leaf blight (BLB), caused by Xanthomonas oryzae pv. oryzae (Xoo), threatens global rice production while growing bactericide resistance and environmental concerns necessitate sustainable disease management alternatives. We employed a microbiome-guided, habitat-specific isolation strategy targeting naturally recovered plants from BLB-endemic hotspots across ten districts of Punjab, Pakistan operating on the ecological premise that plants under pathogen pressure selectively enrich protective microbial taxa, making disease-affected hosts the most coherent source of adapted biocontrol agents. Screening of 1,036 bacterial isolates from rice rhizosphere and phyllosphere using dual-culture antagonism assays yielded six elite strains: Bacillus velezensis, B. amyloliquefaciens, B. subtilis, Pseudomonas fluorescens, and two P. aeruginosa isolates, confirmed by 16 S rRNA and rpoD gene sequencing (> 99% sequence identity). Biochemical profiling revealed multifunctional plant growth-promoting traits including siderophore production, biological nitrogen fixation, indole-3-acetic acid biosynthesis, phosphate solubilization, and hydrogen cyanide production, indicating the potential capacity of selected strains for integrated disease suppression and plant growth promotion. Greenhouse trials across six rice varieties with contrasting genetic resistance backgrounds demonstrated significant reductions in BLB incidence (25-67%) and severity (31-55%) relative to uninoculated controls. Field validation under natural pathogen pressure across two consecutive growing seasons confirmed robust performance, with incidence suppression of 33-65% and severity reduction of 46-67% compared to controls. B. velezensis fsdls3 emerged as the most effective individual agent, achieving 114.5% mean yield protection relative to diseased controls and approaching streptomycin sulfate performance with no statistically significant overall yield difference while outperforming the chemical standard on specific variety-strain combinations. Five of six PGPR agents exceeded the 100% yield protection threshold, delivering agronomic co-benefits including enhanced tillering, increased productive panicles, and elevated total biomass unavailable from chemical bactericide treatment alone. Pronounced cultivar × treatment interactions confirmed that PGPR efficacy is modulated by host genetic background, with resistant varieties carrying pyramided Xa resistance genes showing additive responses to biological treatment. These results establish habitat-adapted, host-recruited PGPR as scientifically credible and ecologically coherent alternatives to chemical bactericides for integrated BLB management in rice.
Additional Links: PMID-42525313
PubMed:
Citation:
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@article {pmid42525313,
year = {2026},
author = {Naqvi, SAH and Rehman, AU and Umar, UUD},
title = {Host-recruited Bacillus and Pseudomonas strains provide potential biocontrol and yield protection against rice bacterial leaf blight.},
journal = {World journal of microbiology & biotechnology},
volume = {42},
number = {8},
pages = {},
pmid = {42525313},
issn = {1573-0972},
mesh = {*Oryza/microbiology/growth & development ; *Plant Diseases/microbiology/prevention & control ; *Bacillus/isolation & purification/physiology/genetics/classification ; Rhizosphere ; *Biological Control Agents ; *Xanthomonas/pathogenicity ; Soil Microbiology ; *Pseudomonas/isolation & purification/physiology/genetics/classification ; RNA, Ribosomal, 16S/genetics ; Pakistan ; Plant Leaves/microbiology ; Indoleacetic Acids/metabolism ; Antibiosis ; },
abstract = {Bacterial leaf blight (BLB), caused by Xanthomonas oryzae pv. oryzae (Xoo), threatens global rice production while growing bactericide resistance and environmental concerns necessitate sustainable disease management alternatives. We employed a microbiome-guided, habitat-specific isolation strategy targeting naturally recovered plants from BLB-endemic hotspots across ten districts of Punjab, Pakistan operating on the ecological premise that plants under pathogen pressure selectively enrich protective microbial taxa, making disease-affected hosts the most coherent source of adapted biocontrol agents. Screening of 1,036 bacterial isolates from rice rhizosphere and phyllosphere using dual-culture antagonism assays yielded six elite strains: Bacillus velezensis, B. amyloliquefaciens, B. subtilis, Pseudomonas fluorescens, and two P. aeruginosa isolates, confirmed by 16 S rRNA and rpoD gene sequencing (> 99% sequence identity). Biochemical profiling revealed multifunctional plant growth-promoting traits including siderophore production, biological nitrogen fixation, indole-3-acetic acid biosynthesis, phosphate solubilization, and hydrogen cyanide production, indicating the potential capacity of selected strains for integrated disease suppression and plant growth promotion. Greenhouse trials across six rice varieties with contrasting genetic resistance backgrounds demonstrated significant reductions in BLB incidence (25-67%) and severity (31-55%) relative to uninoculated controls. Field validation under natural pathogen pressure across two consecutive growing seasons confirmed robust performance, with incidence suppression of 33-65% and severity reduction of 46-67% compared to controls. B. velezensis fsdls3 emerged as the most effective individual agent, achieving 114.5% mean yield protection relative to diseased controls and approaching streptomycin sulfate performance with no statistically significant overall yield difference while outperforming the chemical standard on specific variety-strain combinations. Five of six PGPR agents exceeded the 100% yield protection threshold, delivering agronomic co-benefits including enhanced tillering, increased productive panicles, and elevated total biomass unavailable from chemical bactericide treatment alone. Pronounced cultivar × treatment interactions confirmed that PGPR efficacy is modulated by host genetic background, with resistant varieties carrying pyramided Xa resistance genes showing additive responses to biological treatment. These results establish habitat-adapted, host-recruited PGPR as scientifically credible and ecologically coherent alternatives to chemical bactericides for integrated BLB management in rice.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Oryza/microbiology/growth & development
*Plant Diseases/microbiology/prevention & control
*Bacillus/isolation & purification/physiology/genetics/classification
Rhizosphere
*Biological Control Agents
*Xanthomonas/pathogenicity
Soil Microbiology
*Pseudomonas/isolation & purification/physiology/genetics/classification
RNA, Ribosomal, 16S/genetics
Pakistan
Plant Leaves/microbiology
Indoleacetic Acids/metabolism
Antibiosis
RevDate: 2026-07-29
CmpDate: 2026-07-29
Single spore propagation of native arbuscular mycorrhizal fungi associated with Khasi mandarin and their symbiotic efficacy in maize.
Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology], 57(1):.
Arbuscular Mycorrhizal Fungi (AMF) are important members of the soil microbiome that form symbiotic relationships with plant roots, improving nutrient uptake and stress resilience. In the present study, native AMF associated with the rhizosphere of Khasi Mandarin (Citrus reticulata Blanco) were isolated using the wet sieving and decanting method. Trap culture was used to increase the number of native AMF spores. Healthy spores were identified and used for single-spore inoculation to establish single-spore-derived cultures. Molecular identification of the AMF isolates was performed by amplification of the 18 S rDNA region. A controlled pot experiment was conducted to assess the effects of the obtained pure cultures on plant growth. Inoculated maize plants showed significant improvement in root and shoot biomass. This study focuses on evaluating the potential of native AMF isolates associated with Khasi mandarin and their use as cross-inoculants to develop biofertilizer that promote the growth of non-host plants.
Additional Links: PMID-42525325
PubMed:
Citation:
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@article {pmid42525325,
year = {2026},
author = {Mohan, VK and Joshi, SR},
title = {Single spore propagation of native arbuscular mycorrhizal fungi associated with Khasi mandarin and their symbiotic efficacy in maize.},
journal = {Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]},
volume = {57},
number = {1},
pages = {},
pmid = {42525325},
issn = {1678-4405},
support = {(BT/PR40089/NER/951663/2020)//Department of Biotechnology, Ministry of Science and Technology, India/ ; },
mesh = {*Mycorrhizae/physiology/classification/genetics/isolation & purification/growth & development ; *Zea mays/microbiology/growth & development ; *Symbiosis ; *Spores, Fungal/genetics/growth & development/isolation & purification/classification/physiology ; *Citrus/microbiology ; Plant Roots/microbiology/growth & development ; Soil Microbiology ; Phylogeny ; Rhizosphere ; DNA, Fungal/genetics ; },
abstract = {Arbuscular Mycorrhizal Fungi (AMF) are important members of the soil microbiome that form symbiotic relationships with plant roots, improving nutrient uptake and stress resilience. In the present study, native AMF associated with the rhizosphere of Khasi Mandarin (Citrus reticulata Blanco) were isolated using the wet sieving and decanting method. Trap culture was used to increase the number of native AMF spores. Healthy spores were identified and used for single-spore inoculation to establish single-spore-derived cultures. Molecular identification of the AMF isolates was performed by amplification of the 18 S rDNA region. A controlled pot experiment was conducted to assess the effects of the obtained pure cultures on plant growth. Inoculated maize plants showed significant improvement in root and shoot biomass. This study focuses on evaluating the potential of native AMF isolates associated with Khasi mandarin and their use as cross-inoculants to develop biofertilizer that promote the growth of non-host plants.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Mycorrhizae/physiology/classification/genetics/isolation & purification/growth & development
*Zea mays/microbiology/growth & development
*Symbiosis
*Spores, Fungal/genetics/growth & development/isolation & purification/classification/physiology
*Citrus/microbiology
Plant Roots/microbiology/growth & development
Soil Microbiology
Phylogeny
Rhizosphere
DNA, Fungal/genetics
RevDate: 2026-07-29
Functional diversity and ecological consequences of endophytic Bacillus-plant interactions.
Folia microbiologica [Epub ahead of print].
The genus Bacillus, particularly endophytic species, has been widely studied as a source of plant growth-promoting bacteria in agricultural systems. These microorganisms contribute to plant performance through nutrient acquisition, phytohormone production, pathogen suppression, microbiome modulation, and enhanced tolerance to biotic and abiotic stresses. However, their ecological roles, functional plasticity, and genomic diversity remain poorly integrated into conceptual frameworks that extend beyond crop-based applications. Functional plasticity is reflected in their ability to colonize diverse plant hosts and tissues and to promote similar plant responses through distinct molecular mechanisms. Likewise, genomic diversity is evidenced by variation in accessory genomes, biosynthetic gene clusters, and regulatory networks that shape ecological functions and metabolite production. This review examines endophytic Bacillus as a model for understanding how metabolically versatile and genomically plastic bacteria establish functional, but context-dependent, associations with plants. Drawing on evidence from functional genomics, pangenomics, metabolomics, and microbial ecology, we discuss mechanisms associated with plant growth promotion and emphasize their dependence on host identity, environmental conditions, and microbial interactions. We address functional convergence arising from distinct genetic and metabolic routes, the contribution of accessory genomes and regulatory variation, and the ecological consequences of microbial inoculation in resident plant-associated microbiomes. We also highlight the limitations of in vitro screening approaches and the need for experimental validation across multiple biological scales to establish robust genotype-phenotype relationships. Finally, we extend the discussion beyond agricultural systems to consider the use of endophytic Bacillus in wild plant systems and ecological restoration, emphasizing the importance of evaluating both functional outcomes and ecological impacts.
Additional Links: PMID-42525349
PubMed:
Citation:
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@article {pmid42525349,
year = {2026},
author = {Dos Reis, JBA},
title = {Functional diversity and ecological consequences of endophytic Bacillus-plant interactions.},
journal = {Folia microbiologica},
volume = {},
number = {},
pages = {},
pmid = {42525349},
issn = {1874-9356},
abstract = {The genus Bacillus, particularly endophytic species, has been widely studied as a source of plant growth-promoting bacteria in agricultural systems. These microorganisms contribute to plant performance through nutrient acquisition, phytohormone production, pathogen suppression, microbiome modulation, and enhanced tolerance to biotic and abiotic stresses. However, their ecological roles, functional plasticity, and genomic diversity remain poorly integrated into conceptual frameworks that extend beyond crop-based applications. Functional plasticity is reflected in their ability to colonize diverse plant hosts and tissues and to promote similar plant responses through distinct molecular mechanisms. Likewise, genomic diversity is evidenced by variation in accessory genomes, biosynthetic gene clusters, and regulatory networks that shape ecological functions and metabolite production. This review examines endophytic Bacillus as a model for understanding how metabolically versatile and genomically plastic bacteria establish functional, but context-dependent, associations with plants. Drawing on evidence from functional genomics, pangenomics, metabolomics, and microbial ecology, we discuss mechanisms associated with plant growth promotion and emphasize their dependence on host identity, environmental conditions, and microbial interactions. We address functional convergence arising from distinct genetic and metabolic routes, the contribution of accessory genomes and regulatory variation, and the ecological consequences of microbial inoculation in resident plant-associated microbiomes. We also highlight the limitations of in vitro screening approaches and the need for experimental validation across multiple biological scales to establish robust genotype-phenotype relationships. Finally, we extend the discussion beyond agricultural systems to consider the use of endophytic Bacillus in wild plant systems and ecological restoration, emphasizing the importance of evaluating both functional outcomes and ecological impacts.},
}
RevDate: 2026-07-29
CmpDate: 2026-07-29
The role of adhesins of Fusobacterium nucleatum in colorectal cancer - a structural perspective.
Gut microbes, 18(1):2709265.
Fusobacterium nucleatum is frequently found in the colon microbiome of colorectal cancer (CRC) patients. The bacterium is not only a passive bystander of CRC, but is actively involved in disease progression through mediating tumor growth stimulation, metastasis, and immune evasion. These outcomes are achieved through the action of several adhesins that are located on the outer membrane surface of F. nucleatum, which bind to different receptors on tumor or immune cells. Adhesin-receptor interaction as the initial step of host-pathogen interaction then triggers signal transduction pathways responsible for uncontrolled cell growth or downregulation of immune cells. For a number of CRC-relevant adhesins of F. nucleatum (FadA, Fap2, CbpF), the receptors have been known already for several years, but only recently mechanistic details have been elucidated through the determination of high-resolution structures of the complexes. In the case of other adhesins (RadD, Aim1), receptors have only recently been identified, or are as of yet unknown, and the mechanistic details underlying the interaction remain enigmatic. Here, we review the relevance of particular F. nucleatum adhesins in CRC progression, with a focus on recent mechanistic insights derived from structural biology.
Additional Links: PMID-42525450
Publisher:
PubMed:
Citation:
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@article {pmid42525450,
year = {2026},
author = {Schöpf, F and Marongiu, GL and Roderer, D},
title = {The role of adhesins of Fusobacterium nucleatum in colorectal cancer - a structural perspective.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2709265},
doi = {10.1080/19490976.2026.2709265},
pmid = {42525450},
issn = {1949-0984},
mesh = {Humans ; *Fusobacterium nucleatum/metabolism/chemistry/genetics/physiology/pathogenicity ; *Colorectal Neoplasms/microbiology/pathology ; *Adhesins, Bacterial/metabolism/chemistry/genetics ; Host-Pathogen Interactions ; *Fusobacterium Infections/microbiology ; },
abstract = {Fusobacterium nucleatum is frequently found in the colon microbiome of colorectal cancer (CRC) patients. The bacterium is not only a passive bystander of CRC, but is actively involved in disease progression through mediating tumor growth stimulation, metastasis, and immune evasion. These outcomes are achieved through the action of several adhesins that are located on the outer membrane surface of F. nucleatum, which bind to different receptors on tumor or immune cells. Adhesin-receptor interaction as the initial step of host-pathogen interaction then triggers signal transduction pathways responsible for uncontrolled cell growth or downregulation of immune cells. For a number of CRC-relevant adhesins of F. nucleatum (FadA, Fap2, CbpF), the receptors have been known already for several years, but only recently mechanistic details have been elucidated through the determination of high-resolution structures of the complexes. In the case of other adhesins (RadD, Aim1), receptors have only recently been identified, or are as of yet unknown, and the mechanistic details underlying the interaction remain enigmatic. Here, we review the relevance of particular F. nucleatum adhesins in CRC progression, with a focus on recent mechanistic insights derived from structural biology.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Fusobacterium nucleatum/metabolism/chemistry/genetics/physiology/pathogenicity
*Colorectal Neoplasms/microbiology/pathology
*Adhesins, Bacterial/metabolism/chemistry/genetics
Host-Pathogen Interactions
*Fusobacterium Infections/microbiology
RevDate: 2026-07-29
Ceramides and the Defective Barrier in Atopic Dermatitis.
Skin pharmacology and physiology pii:000553705 [Epub ahead of print].
BACKGROUND: Atopic dermatitis (AD) is a common remitting-relapsing inflammatory skin disease characterized by eczematous lesions, xerosis and pruritis. It is associated with a defective permeability barrier and increased susceptibility to Staphylococcus aureus colonization. It has been demonstrated that the abrogated epidermal barrier is related to a decreased mass of ceramides and long-chain fatty acids in the stratum corneum (SC).
SUMMARY: A defective permeability barrier of the SC is the primary defect in AD. This defect reflects a reduction of ceramide and fatty acid mass in the SC due to reduced glucocerebrosidase and acid sphingomyelinase activity and a shift in fatty acid synthesis from long-chain to short-chain fatty acids and the incorporation of these shorter fatty acids into ceramides. Topically applied ceramides can restore epidermal function to a damaged barrier. Ceramide-containing moisturizers have produced partial restoration of the barrier function in AD by influencing lipid organization.
KEY MESSAGE: Correcting the barrier defect by topically supplied ceramides and long-chain fatty acids in sufficient amounts could contribute to restoration of the microbiome and decreasing irritation and pruritis.
Additional Links: PMID-42525582
Publisher:
PubMed:
Citation:
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@article {pmid42525582,
year = {2026},
author = {Wertz, PW and Fluhr, JW},
title = {Ceramides and the Defective Barrier in Atopic Dermatitis.},
journal = {Skin pharmacology and physiology},
volume = {},
number = {},
pages = {1},
doi = {10.1159/spp/aetag001},
pmid = {42525582},
issn = {1660-5535},
abstract = {BACKGROUND: Atopic dermatitis (AD) is a common remitting-relapsing inflammatory skin disease characterized by eczematous lesions, xerosis and pruritis. It is associated with a defective permeability barrier and increased susceptibility to Staphylococcus aureus colonization. It has been demonstrated that the abrogated epidermal barrier is related to a decreased mass of ceramides and long-chain fatty acids in the stratum corneum (SC).
SUMMARY: A defective permeability barrier of the SC is the primary defect in AD. This defect reflects a reduction of ceramide and fatty acid mass in the SC due to reduced glucocerebrosidase and acid sphingomyelinase activity and a shift in fatty acid synthesis from long-chain to short-chain fatty acids and the incorporation of these shorter fatty acids into ceramides. Topically applied ceramides can restore epidermal function to a damaged barrier. Ceramide-containing moisturizers have produced partial restoration of the barrier function in AD by influencing lipid organization.
KEY MESSAGE: Correcting the barrier defect by topically supplied ceramides and long-chain fatty acids in sufficient amounts could contribute to restoration of the microbiome and decreasing irritation and pruritis.},
}
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