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ESP: PubMed Auto Bibliography 13 Aug 2026 at 01:52 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: 2026-04-30
CmpDate: 2026-04-30
Gut microbial community of patients with Parkinson's disease analyzed using metagenome-assembled genomes.
Neural regeneration research, 21(8):3815-3823.
Previous investigations into gut microbiota dysbiosis in patients with Parkinson’s disease have relied on 16S rRNA amplicon sequencing and assembly-free metagenomic approaches. However, there is an urgent need to study the function of the gut microbiome at the genome level using metagenome-assembled genomes. Here, we conducted single-sample metagenomic binning analysis using shotgun metagenomic sequencing data and retrieved 2837 metagenome-assembled genomes to explore the gut microbiota profile at the genome level. Reconstructing microbial genomes from metagenomic sequences greatly enriched the diversity and number of microbial genomes, especially those of uncultivable strains. By integrating the analysis of metagenome-assembled genomes with clinical parameters, we observed higher α-diversity indexes and a very different composition of microbial communities in patients with Parkinson’s disease. We also identified microbial species and metagenome-assembled genomes that were significantly associated with clinical characteristics, including disease severity, medication, motor complications, and non-motor symptoms. The genes of Parkinson’s disease severity-associated metagenome-assembled genomes were distributed across multiple pathways, such as carbon metabolism, phosphonate metabolism, carbohydrate metabolism, amino acid metabolism, fatty acid metabolism, bile acid metabolism, metabolism of cofactors and vitamins, neuroprotective molecules, immunogenic components, toxic metabolites, translation, and bacterial secretion. Our work provides a comprehensive resource for investigating the gut microbiota–Parkinson’s disease relationship at the genome level, which may enhance our comprehension of the underlying mechanisms of this disease.
Additional Links: PMID-41017724
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@article {pmid41017724,
year = {2026},
author = {Zhang, Y and Mo, C and He, X and Xiao, Q and Yang, X},
title = {Gut microbial community of patients with Parkinson's disease analyzed using metagenome-assembled genomes.},
journal = {Neural regeneration research},
volume = {21},
number = {8},
pages = {3815-3823},
pmid = {41017724},
issn = {1673-5374},
abstract = {Previous investigations into gut microbiota dysbiosis in patients with Parkinson’s disease have relied on 16S rRNA amplicon sequencing and assembly-free metagenomic approaches. However, there is an urgent need to study the function of the gut microbiome at the genome level using metagenome-assembled genomes. Here, we conducted single-sample metagenomic binning analysis using shotgun metagenomic sequencing data and retrieved 2837 metagenome-assembled genomes to explore the gut microbiota profile at the genome level. Reconstructing microbial genomes from metagenomic sequences greatly enriched the diversity and number of microbial genomes, especially those of uncultivable strains. By integrating the analysis of metagenome-assembled genomes with clinical parameters, we observed higher α-diversity indexes and a very different composition of microbial communities in patients with Parkinson’s disease. We also identified microbial species and metagenome-assembled genomes that were significantly associated with clinical characteristics, including disease severity, medication, motor complications, and non-motor symptoms. The genes of Parkinson’s disease severity-associated metagenome-assembled genomes were distributed across multiple pathways, such as carbon metabolism, phosphonate metabolism, carbohydrate metabolism, amino acid metabolism, fatty acid metabolism, bile acid metabolism, metabolism of cofactors and vitamins, neuroprotective molecules, immunogenic components, toxic metabolites, translation, and bacterial secretion. Our work provides a comprehensive resource for investigating the gut microbiota–Parkinson’s disease relationship at the genome level, which may enhance our comprehension of the underlying mechanisms of this disease.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Streamlining the isolation of fungal hyphae: a semi-automated approach for soil substrates.
Journal of experimental botany, 77(15):4857-4873.
Extracting fungal hyphae with their naturally associated microbiota from soil samples presents a significant challenge due to their small size, typically in the micrometer range, and the formation of dynamic fungal networks. We combined elements of previous protocols and automated the wet-sieving steps of the methodology to efficiently extract fungal hyphae from various soil types, including natural loamy soils. This approach reduces manual handling, minimizes operator-dependent variability, and shortens processing time by up to 2.5-fold. Unlike earlier methods that require sand or glass bead supplementation, which can introduce artificial conditions and limit large-scale field applications, our sieving and sucrose centrifugation (SSC) method avoids these drawbacks. The SSC technique both enables quantification of hyphal length density (HLD) and, importantly, preserves surface-associated microbes for downstream analyses. Among the tested methods, SSC yielded the highest HLD. Using a combination of microscopy, molecular techniques, and next-generation sequencing (NGS), we demonstrate that this method allows targeted study of bacteria tightly attached to fungal hyphae. Furthermore, the SSC approach effectively enriched fungal hyphae from a highly diverse soil community, establishing a dependable tool for advancing research on fungal hyphae as microbial hotspots in soil ecosystems.
Additional Links: PMID-41400283
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@article {pmid41400283,
year = {2026},
author = {Metzen, IE and Bucher, M},
title = {Streamlining the isolation of fungal hyphae: a semi-automated approach for soil substrates.},
journal = {Journal of experimental botany},
volume = {77},
number = {15},
pages = {4857-4873},
pmid = {41400283},
issn = {1460-2431},
support = {//Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)/ ; },
mesh = {*Hyphae/isolation & purification ; *Soil Microbiology ; *Fungi/isolation & purification ; Soil/chemistry ; Centrifugation/methods ; },
abstract = {Extracting fungal hyphae with their naturally associated microbiota from soil samples presents a significant challenge due to their small size, typically in the micrometer range, and the formation of dynamic fungal networks. We combined elements of previous protocols and automated the wet-sieving steps of the methodology to efficiently extract fungal hyphae from various soil types, including natural loamy soils. This approach reduces manual handling, minimizes operator-dependent variability, and shortens processing time by up to 2.5-fold. Unlike earlier methods that require sand or glass bead supplementation, which can introduce artificial conditions and limit large-scale field applications, our sieving and sucrose centrifugation (SSC) method avoids these drawbacks. The SSC technique both enables quantification of hyphal length density (HLD) and, importantly, preserves surface-associated microbes for downstream analyses. Among the tested methods, SSC yielded the highest HLD. Using a combination of microscopy, molecular techniques, and next-generation sequencing (NGS), we demonstrate that this method allows targeted study of bacteria tightly attached to fungal hyphae. Furthermore, the SSC approach effectively enriched fungal hyphae from a highly diverse soil community, establishing a dependable tool for advancing research on fungal hyphae as microbial hotspots in soil ecosystems.},
}
MeSH Terms:
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*Hyphae/isolation & purification
*Soil Microbiology
*Fungi/isolation & purification
Soil/chemistry
Centrifugation/methods
RevDate: 2026-08-11
Physical, mental and biochemical effects of probiotics in multiple sclerosis: A systematic review and meta-analysis.
Clinical nutrition (Edinburgh, Scotland), 64:106747 pii:S0261-5614(26)00174-3 [Epub ahead of print].
BACKGROUND AND AIMS: This systematic review and meta-analysis aimed to evaluate the effects of probiotic supplementation on physical, mental, and biochemical outcomes in adults with multiple sclerosis (MS).
METHODS: A comprehensive search of major databases (PubMed, Embase, Scopus, Cochrane Library, and Web of Science) following PRISMA guidelines for studies published up to December 2025.
RESULTS: Six randomized placebo-controlled trials (RCTs) involving 282 participants met the inclusion criteria. Interventions varied in probiotic strains, doses, and duration. Quantitative synthesis showed that probiotic supplementation produced significant beneficial effects on motor outcomes, particularly fatigue and pain. No significant improvements were observed in disability status measured by the Expanded Disability Status Scale. Mental health outcomes, including depression and general psychological well-being, did not demonstrate statistically significant changes following probiotic use. In addition, biochemical analyses revealed a moderate overall benefit, driven primarily by reductions in systemic inflammatory markers, including high-sensitivity C-reactive protein. Effects on oxidative stress parameters were inconsistent, though some studies reported decreased malondialdehyde levels and improved antioxidant capacity.
CONCLUSION: Overall, findings suggest that probiotics may offer moderate benefits for symptom management in MS, particularly for fatigue, pain, and inflammation, while evidence for effects on mental health remains limited. Further well-designed, multi-ethnic RCTs integrating microbiome and immunological assessments are needed to confirm these results and clarify underlying mechanisms. PROSPERO registration number: CRD42024511183.
Additional Links: PMID-42580083
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PubMed:
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@article {pmid42580083,
year = {2026},
author = {Blanca-Serrano, T and Agredano-Sánchez, M and López Gigosos, RM and Jiménez Navarro, MF and González-Domenech, CM and Gutiérrez-Bedmar, M},
title = {Physical, mental and biochemical effects of probiotics in multiple sclerosis: A systematic review and meta-analysis.},
journal = {Clinical nutrition (Edinburgh, Scotland)},
volume = {64},
number = {},
pages = {106747},
doi = {10.1016/j.clnu.2026.106747},
pmid = {42580083},
issn = {1532-1983},
abstract = {BACKGROUND AND AIMS: This systematic review and meta-analysis aimed to evaluate the effects of probiotic supplementation on physical, mental, and biochemical outcomes in adults with multiple sclerosis (MS).
METHODS: A comprehensive search of major databases (PubMed, Embase, Scopus, Cochrane Library, and Web of Science) following PRISMA guidelines for studies published up to December 2025.
RESULTS: Six randomized placebo-controlled trials (RCTs) involving 282 participants met the inclusion criteria. Interventions varied in probiotic strains, doses, and duration. Quantitative synthesis showed that probiotic supplementation produced significant beneficial effects on motor outcomes, particularly fatigue and pain. No significant improvements were observed in disability status measured by the Expanded Disability Status Scale. Mental health outcomes, including depression and general psychological well-being, did not demonstrate statistically significant changes following probiotic use. In addition, biochemical analyses revealed a moderate overall benefit, driven primarily by reductions in systemic inflammatory markers, including high-sensitivity C-reactive protein. Effects on oxidative stress parameters were inconsistent, though some studies reported decreased malondialdehyde levels and improved antioxidant capacity.
CONCLUSION: Overall, findings suggest that probiotics may offer moderate benefits for symptom management in MS, particularly for fatigue, pain, and inflammation, while evidence for effects on mental health remains limited. Further well-designed, multi-ethnic RCTs integrating microbiome and immunological assessments are needed to confirm these results and clarify underlying mechanisms. PROSPERO registration number: CRD42024511183.},
}
RevDate: 2026-08-11
Investigating Gut Homeostasis in Stray Animals Across Different Air Pollution Zones.
Environmental research pii:S0013-9351(26)01793-7 [Epub ahead of print].
Areas previously fulfilling air quality targets may face increased pressure to reevaluate due to stricter criteria. The gut homeostasis of stray animals may serve as a sensitive indicator of air pollution levels, yet previous research has primarily focused on model organisms. This cross-sectional study employed 16S rRNA sequencing and non-targeted metabolomics to assess changes in gut microbiota and metabolites across stray cat fecal samples from three air pollution zones in a coal-based industrial region in northern China-Polluted Zone 1 (DS), Polluted Zone 2 (WC), and Clean Zone (ZB). Air quality data confirmed significantly higher PM2.5, SO2, CO, and NO2 concentrations in polluted zones. The clean zone exhibited the highest gut microbial α-diversity, while polluted zones showed significantly lower diversity. Fecal metabolomic profiling identified a high-confidence subset of differentially abundant metabolites (DAMs). The transition from clean to polluted zones was associated with more pronounced biological remodeling than between polluted sites, suggesting a potential metabolic threshold effect. Lipids and lipid-like molecules represented the most disrupted superclass, with polluted cohorts showing altered bile acid profiles and accumulation of exogenous chemical remnants. Key neuroactive pathways-specifically retrograde endocannabinoid signaling and glutamatergic synapse-were consistently enriched among DAMs in polluted environments, reflecting localized remodeling of the host metabolic network. These findings suggest that air pollution exposure is associated with potential systemic health effects extending from the gut to the neuroendocrine level. This study provides evidence that environmental pollution gradients are independently associated with alterations in the feline gut microbiome-metabolome axis, highlighting the translational potential of urban stray cats as sentinel species within the One Health framework. Given the observational design, reported associations do not imply causation.
Additional Links: PMID-42580383
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PubMed:
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@article {pmid42580383,
year = {2026},
author = {Wang, S and Cui, L and Yue, H},
title = {Investigating Gut Homeostasis in Stray Animals Across Different Air Pollution Zones.},
journal = {Environmental research},
volume = {},
number = {},
pages = {125462},
doi = {10.1016/j.envres.2026.125462},
pmid = {42580383},
issn = {1096-0953},
abstract = {Areas previously fulfilling air quality targets may face increased pressure to reevaluate due to stricter criteria. The gut homeostasis of stray animals may serve as a sensitive indicator of air pollution levels, yet previous research has primarily focused on model organisms. This cross-sectional study employed 16S rRNA sequencing and non-targeted metabolomics to assess changes in gut microbiota and metabolites across stray cat fecal samples from three air pollution zones in a coal-based industrial region in northern China-Polluted Zone 1 (DS), Polluted Zone 2 (WC), and Clean Zone (ZB). Air quality data confirmed significantly higher PM2.5, SO2, CO, and NO2 concentrations in polluted zones. The clean zone exhibited the highest gut microbial α-diversity, while polluted zones showed significantly lower diversity. Fecal metabolomic profiling identified a high-confidence subset of differentially abundant metabolites (DAMs). The transition from clean to polluted zones was associated with more pronounced biological remodeling than between polluted sites, suggesting a potential metabolic threshold effect. Lipids and lipid-like molecules represented the most disrupted superclass, with polluted cohorts showing altered bile acid profiles and accumulation of exogenous chemical remnants. Key neuroactive pathways-specifically retrograde endocannabinoid signaling and glutamatergic synapse-were consistently enriched among DAMs in polluted environments, reflecting localized remodeling of the host metabolic network. These findings suggest that air pollution exposure is associated with potential systemic health effects extending from the gut to the neuroendocrine level. This study provides evidence that environmental pollution gradients are independently associated with alterations in the feline gut microbiome-metabolome axis, highlighting the translational potential of urban stray cats as sentinel species within the One Health framework. Given the observational design, reported associations do not imply causation.},
}
RevDate: 2026-08-11
Melatonin system integrity shapes gut-brain interaction in schizophrenia-derived microbiota transplant phenotype in mice.
Life sciences pii:S0024-3205(26)00442-X [Epub ahead of print].
AIMS: This study investigates whether the melatonin (MLT) system modulates the behavioral, neurophysiological and neurochemical effects of fecal microbiota transplantation (FMT) from individuals with schizophrenia (SCZ), highlighting the role of the tryptophan (Trp) to MLT and kynurenine (Kyn) pathways.
MATERIALS AND METHODS: FMT was performed using fecal samples from individuals with SCZ, characterized by distinct clinical, cognitive and metabolic profiles (severe vs mild SCZ), into antibiotic-treated MLT-deficient (C57BL/6) and MLT-proficient (C3H/HeJ) mice. Post-FMT evaluations included locomotor activity assessment (open field test), working memory testing (T-maze), in-vivo electrophysiological recordings from ventral tegmental area (VTA) dopamine (DA) neurons, and quantification of peripheral cytokines and central and peripheral Trp metabolites.
KEY FINDINGS: In MLT-deficient mice, FMT from severe SCZ induced hyperlocomotion and altered peripheral inflammatory markers (decreased IL-1β, increased keratinocyte-derived cytokine) compared to FMT from mild SCZ. Conversely, in MLT-proficient mice, severe SCZ FMT induced persistent spatial working memory deficits and a significant reduction in overall VTA DA neuronal firing, specifically driven by the high-firing subpopulation. Furthermore, MLT-proficient mice receiving severe SCZ FMT selectively exhibited increased brain Trp levels alongside a decreased Kyn/Trp ratio.
SIGNIFICANCE: Our findings identify the MLT system as a key biological switch that gates the impact of SCZ-associated microbiota on brain and behavior, dissociating behavioral from cognitive, neurophysiological and neurochemical outcomes. This work links circadian biology to microbiota-driven effects and points to the Trp-Kyn-MLT axis as a critical interface. This work provides a conceptual framework for targeting circadian-microbiome interactions, as a novel strategy to modulate disease-relevant phenotypes in SCZ.
Additional Links: PMID-42580395
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PubMed:
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@article {pmid42580395,
year = {2026},
author = {Barzon, B and Shkodra, A and D'Incalci, M and Sapienza, J and Paribello, P and Nasini, S and Dall'Acqua, S and Bertazzo, A and Pitsikas, N and De Gregorio, D and Valtorta, F and Manchia, M and Squassina, A and Fadda, P and Cavallaro, R and Pisanu, C and Bosia, M and Comai, S},
title = {Melatonin system integrity shapes gut-brain interaction in schizophrenia-derived microbiota transplant phenotype in mice.},
journal = {Life sciences},
volume = {},
number = {},
pages = {124633},
doi = {10.1016/j.lfs.2026.124633},
pmid = {42580395},
issn = {1879-0631},
abstract = {AIMS: This study investigates whether the melatonin (MLT) system modulates the behavioral, neurophysiological and neurochemical effects of fecal microbiota transplantation (FMT) from individuals with schizophrenia (SCZ), highlighting the role of the tryptophan (Trp) to MLT and kynurenine (Kyn) pathways.
MATERIALS AND METHODS: FMT was performed using fecal samples from individuals with SCZ, characterized by distinct clinical, cognitive and metabolic profiles (severe vs mild SCZ), into antibiotic-treated MLT-deficient (C57BL/6) and MLT-proficient (C3H/HeJ) mice. Post-FMT evaluations included locomotor activity assessment (open field test), working memory testing (T-maze), in-vivo electrophysiological recordings from ventral tegmental area (VTA) dopamine (DA) neurons, and quantification of peripheral cytokines and central and peripheral Trp metabolites.
KEY FINDINGS: In MLT-deficient mice, FMT from severe SCZ induced hyperlocomotion and altered peripheral inflammatory markers (decreased IL-1β, increased keratinocyte-derived cytokine) compared to FMT from mild SCZ. Conversely, in MLT-proficient mice, severe SCZ FMT induced persistent spatial working memory deficits and a significant reduction in overall VTA DA neuronal firing, specifically driven by the high-firing subpopulation. Furthermore, MLT-proficient mice receiving severe SCZ FMT selectively exhibited increased brain Trp levels alongside a decreased Kyn/Trp ratio.
SIGNIFICANCE: Our findings identify the MLT system as a key biological switch that gates the impact of SCZ-associated microbiota on brain and behavior, dissociating behavioral from cognitive, neurophysiological and neurochemical outcomes. This work links circadian biology to microbiota-driven effects and points to the Trp-Kyn-MLT axis as a critical interface. This work provides a conceptual framework for targeting circadian-microbiome interactions, as a novel strategy to modulate disease-relevant phenotypes in SCZ.},
}
RevDate: 2026-08-11
Clostridium saudiense bacteremia: case report and literature review of C.celatum group infections.
Anaerobe pii:S1075-9964(26)00055-7 [Epub ahead of print].
BACKGROUND: Clostridium saudiense is a commensal bacterium of the human gut, recently included in the Clostridium celatum group. Infections caused by these pathogens are rarely reported, and their pathogenic mechanisms are not yet well understood.
CASE PRESENTATION/RESULTS: We describe the case of an 82-year-old woman with bacteremia and an iliopsoas abscess due to C. saudiense. Blood cultures and abscess fluid sample confirmed the presence of C. saudiense through 16S rDNA gene sequencing. The patient underwent a three-week course of teicoplanin, guided by therapeutic drug monitoring, for a total duration of three months. A literature review identified six additional cases of C. celatum group infections, emphasizing the rarity of the condition, the variability of clinical manifestations and the therapeutic approaches followed. All cases had a favorable outcome.
CONCLUSION: C. celatum group infections are rare and require a multidisciplinary approach for optimal management. 16S rDNA sequencing has proven essential for accurate identification. Further research is needed to better understand the pathogenic role of these bacteria and to establish optimal therapeutic strategies.
Additional Links: PMID-42580435
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PubMed:
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@article {pmid42580435,
year = {2026},
author = {Visicaro, M and Franceschi, G and Calandra Buonaura, F and Venturelli, I and Venturelli, C and Sarti, M and Fregni Serpini, G and Grottola, A and Monica, P and Mussini, C and Puzzolante, C},
title = {Clostridium saudiense bacteremia: case report and literature review of C.celatum group infections.},
journal = {Anaerobe},
volume = {},
number = {},
pages = {103075},
doi = {10.1016/j.anaerobe.2026.103075},
pmid = {42580435},
issn = {1095-8274},
abstract = {BACKGROUND: Clostridium saudiense is a commensal bacterium of the human gut, recently included in the Clostridium celatum group. Infections caused by these pathogens are rarely reported, and their pathogenic mechanisms are not yet well understood.
CASE PRESENTATION/RESULTS: We describe the case of an 82-year-old woman with bacteremia and an iliopsoas abscess due to C. saudiense. Blood cultures and abscess fluid sample confirmed the presence of C. saudiense through 16S rDNA gene sequencing. The patient underwent a three-week course of teicoplanin, guided by therapeutic drug monitoring, for a total duration of three months. A literature review identified six additional cases of C. celatum group infections, emphasizing the rarity of the condition, the variability of clinical manifestations and the therapeutic approaches followed. All cases had a favorable outcome.
CONCLUSION: C. celatum group infections are rare and require a multidisciplinary approach for optimal management. 16S rDNA sequencing has proven essential for accurate identification. Further research is needed to better understand the pathogenic role of these bacteria and to establish optimal therapeutic strategies.},
}
RevDate: 2026-08-11
Probiotic Bacillus strains enhance cellulose digestibility and silkworms growth via gut microbiota modulation.
Journal of insect physiology pii:S0022-1910(26)00120-4 [Epub ahead of print].
Dietary supplementation with probiotics has been demonstrated to enhance nutritional efficiency and economic traits in the silkworms (Bombyx mori), with mechanistic insights indicating that these benefits are associated with gut microbiota activity and mucosal immune modulation through the regulation of enzymatic functions. This study investigated the effects of probiotic Bacillus species on intestinal microbiome diversity in fifth-instar silkworms. Two native isolates, Bacillus subtilis Y11 and Bacillus velezensis Z55, were administered either individually or in combination to experimental groups (CK, Y11, Z55, and Y11/Z55) on the first day of the fifth instar. Intestinal contents were collected at days 1, 3, and 5 after treatment for 16S rRNA gene sequencing, and cellulose content in silkworm excrement was measured on a daily basis. Experimental groups exhibited significantly elevated body weight, digestive capacity, and cocoon weight compared to controls. The cellulose content in silkworm excrement decreased by 24.7% and 31.8% on days 2 and 3, respectively, compared to the control (CK) group at the corresponding time points. Tax4Fun2 analysis further predicted a rapid increase in the potential abundance of cellulose degradation-related genes within the gut microbiome, an inference based on taxonomic composition. These findings support the hypothesis that probiotic treatment may enhance the net efficiency of cellulose degradation in silkworms by modulating the gut microbial community and structure, thereby offering new insights into improving their growth performance.
Additional Links: PMID-42580513
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PubMed:
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@article {pmid42580513,
year = {2026},
author = {Jin, Y and Zhao, Y and Chen, C and Jiang, X and Chen, S and Zhang, R and Li, H and Gui, Z},
title = {Probiotic Bacillus strains enhance cellulose digestibility and silkworms growth via gut microbiota modulation.},
journal = {Journal of insect physiology},
volume = {},
number = {},
pages = {105047},
doi = {10.1016/j.jinsphys.2026.105047},
pmid = {42580513},
issn = {1879-1611},
abstract = {Dietary supplementation with probiotics has been demonstrated to enhance nutritional efficiency and economic traits in the silkworms (Bombyx mori), with mechanistic insights indicating that these benefits are associated with gut microbiota activity and mucosal immune modulation through the regulation of enzymatic functions. This study investigated the effects of probiotic Bacillus species on intestinal microbiome diversity in fifth-instar silkworms. Two native isolates, Bacillus subtilis Y11 and Bacillus velezensis Z55, were administered either individually or in combination to experimental groups (CK, Y11, Z55, and Y11/Z55) on the first day of the fifth instar. Intestinal contents were collected at days 1, 3, and 5 after treatment for 16S rRNA gene sequencing, and cellulose content in silkworm excrement was measured on a daily basis. Experimental groups exhibited significantly elevated body weight, digestive capacity, and cocoon weight compared to controls. The cellulose content in silkworm excrement decreased by 24.7% and 31.8% on days 2 and 3, respectively, compared to the control (CK) group at the corresponding time points. Tax4Fun2 analysis further predicted a rapid increase in the potential abundance of cellulose degradation-related genes within the gut microbiome, an inference based on taxonomic composition. These findings support the hypothesis that probiotic treatment may enhance the net efficiency of cellulose degradation in silkworms by modulating the gut microbial community and structure, thereby offering new insights into improving their growth performance.},
}
RevDate: 2026-08-11
Antibiotic Mixture Exposure in Meconium Affects Child Neurodevelopment via Altering Early-Life Gut Microbiome and Metabolome.
Environmental pollution (Barking, Essex : 1987) pii:S0269-7491(26)01312-6 [Epub ahead of print].
Previous evidence has established associations of antibiotic exposure in early life with neurodevelopmental disorders. However, previous studies have often relied on self-reported or record-based exposure measures that may not accurately reflect internal fetal exposure, and few have integrated prenatal exposure biomarkers with infant microbiome, metabolome, and longitudinal neurodevelopmental data. This study included 300 mother-infant pairs from the Shanghai Maternal-Child Pairs Cohort. Meconium samples were used to quantify concentrations of 18 antibiotics using high-performance liquid chromatography (HPLC). Neurodevelopmental outcomes were assessed using Ages and Stages Questionnaires (ASQ) at 2, 6, 12, and 24 months of age. Multi-omics profiling of 6-month fecal samples was conducted, employing 16S rRNA gene amplicon sequencing and HPLC-based metabolomics. Linear and logistic regression models, negative binomial regression, interpretable machine learning algorithms, metabolome-wide association/pathway analyses and high-dimensional mediation modeling were used. Our study population demonstrated predominant exposure to three antibiotics: chlortetracycline, penicillin, and chloramphenicol. Each interquartile range (IQR) increase in meconium-measured antibiotic burden was associated with a lower total ASQ score at 6 months (β = -4.49, 95% CI: -7.14 to -1.86) and lower scores across all five developmental domains (βs ranging from -0.53 to -1.11; all P < 0.05). Each IQR increment of antibiotic burden was also associated with greater odds of belonging to the lower-score group of total ASQ trajectory (OR = 1.20, 95% CI: 1.04, 1.42) and the lower-score group of personal-social trajectory (OR = 1.13, 95% CI: 1.01, 1.28). Exploratory high-dimensional mediation analyses identified Lactobacillus and 2-(14,15-epoxyeicosatrienoyl) glycerol (2-14,15-EG) as candidate intermediates in the association between meconium-measured antibiotic burden and neurodevelopment. Our study suggested that higher meconium-based biomarkers of intrauterine antibiotic burden were significantly associated with lower neurodevelopmental outcomes in early childhood, with the strongest inverse associations observed at 6 months. Lactobacillus and 2-14,15-EG were identified as potential mediator biomarkers. These hypothesis-generating findings require independent replication, longitudinal temporal validation, and experimental studies before causal mechanisms or microbiota-targeted interventions can be inferred.
Additional Links: PMID-42580549
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PubMed:
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@article {pmid42580549,
year = {2026},
author = {Zhou, Y and Wang, F and Zhao, Y and Wang, H and Ma, W and Shi, H and Zhang, Y},
title = {Antibiotic Mixture Exposure in Meconium Affects Child Neurodevelopment via Altering Early-Life Gut Microbiome and Metabolome.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {128942},
doi = {10.1016/j.envpol.2026.128942},
pmid = {42580549},
issn = {1873-6424},
abstract = {Previous evidence has established associations of antibiotic exposure in early life with neurodevelopmental disorders. However, previous studies have often relied on self-reported or record-based exposure measures that may not accurately reflect internal fetal exposure, and few have integrated prenatal exposure biomarkers with infant microbiome, metabolome, and longitudinal neurodevelopmental data. This study included 300 mother-infant pairs from the Shanghai Maternal-Child Pairs Cohort. Meconium samples were used to quantify concentrations of 18 antibiotics using high-performance liquid chromatography (HPLC). Neurodevelopmental outcomes were assessed using Ages and Stages Questionnaires (ASQ) at 2, 6, 12, and 24 months of age. Multi-omics profiling of 6-month fecal samples was conducted, employing 16S rRNA gene amplicon sequencing and HPLC-based metabolomics. Linear and logistic regression models, negative binomial regression, interpretable machine learning algorithms, metabolome-wide association/pathway analyses and high-dimensional mediation modeling were used. Our study population demonstrated predominant exposure to three antibiotics: chlortetracycline, penicillin, and chloramphenicol. Each interquartile range (IQR) increase in meconium-measured antibiotic burden was associated with a lower total ASQ score at 6 months (β = -4.49, 95% CI: -7.14 to -1.86) and lower scores across all five developmental domains (βs ranging from -0.53 to -1.11; all P < 0.05). Each IQR increment of antibiotic burden was also associated with greater odds of belonging to the lower-score group of total ASQ trajectory (OR = 1.20, 95% CI: 1.04, 1.42) and the lower-score group of personal-social trajectory (OR = 1.13, 95% CI: 1.01, 1.28). Exploratory high-dimensional mediation analyses identified Lactobacillus and 2-(14,15-epoxyeicosatrienoyl) glycerol (2-14,15-EG) as candidate intermediates in the association between meconium-measured antibiotic burden and neurodevelopment. Our study suggested that higher meconium-based biomarkers of intrauterine antibiotic burden were significantly associated with lower neurodevelopmental outcomes in early childhood, with the strongest inverse associations observed at 6 months. Lactobacillus and 2-14,15-EG were identified as potential mediator biomarkers. These hypothesis-generating findings require independent replication, longitudinal temporal validation, and experimental studies before causal mechanisms or microbiota-targeted interventions can be inferred.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
TRECing down the source: naive and memory T cell generation in dirty mice and men.
Journal of immunology (Baltimore, Md. : 1950), 215(8):.
Healthy aging relies on the maintenance of a diverse T cell pool. This diversity is ensured by balancing thymic output, differentiation of naive into memory T cells, T cell proliferation and cell death. For naive T cells, the balance of these processes differs between standard laboratory mice and humans. This may be a true species difference or, alternatively, result from the vastly different amounts of antigens to which standard laboratory mice and humans are exposed. Using wildlings, that is, laboratory mice born to wild mice, we studied the impact of antigen-exposure through a natural microbiome on naive and memory T cell maintenance. We found that standard laboratory mice and wildlings maintain their naive T cell pools similarly: naive T cells rarely divide and are replaced by thymic emigrants at similar rates. The daily replacement rate of memory T cells, on the other hand, is about 50% faster in wildlings than in standard laboratory mice. In both types of mice, about 20% of newly produced memory T cells originate from recruitment of naive T cells, while the remaining cells are produced by their clonal expansion and by self-renewal. In older mice, this drops to 5%. In humans, a similarly large fraction of memory cells originate from recruitment of naive T cells. Unlike in mice, most naive T cells in human adults are formed by naive T cell proliferation. Thus, while both types of mice mimic the maintenance mechanisms of the memory T cell pool in humans, even wildlings fall short as a model for human naive T cell maintenance.
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@article {pmid42580672,
year = {2026},
author = {Derksen, LY and de Dios Panal, ES and Brouwers, TMJ and Sanal, E and Schuren, AB and Westera, L and van den Berg, SPH and van Baarle, D and de Boer, RJ and Rosshart, SP and Tesselaar, K and Borghans, JAM},
title = {TRECing down the source: naive and memory T cell generation in dirty mice and men.},
journal = {Journal of immunology (Baltimore, Md. : 1950)},
volume = {215},
number = {8},
pages = {},
doi = {10.1093/jimmun/vkag216},
pmid = {42580672},
issn = {1550-6606},
support = {/NWO_/Dutch Research Council/Netherlands ; //Science domain NWO-ENW/ ; //European Union's Horizon 2020 Research and Innovation Programme/ ; 764698//Marie Skłodowska-Curie Grant Agreement/ ; },
mesh = {Animals ; *Memory T Cells/immunology ; Humans ; Mice ; *Immunologic Memory ; Cell Differentiation/immunology ; Cell Proliferation ; Aging/immunology ; Thymus Gland/immunology ; *T-Lymphocytes/immunology ; Male ; },
abstract = {Healthy aging relies on the maintenance of a diverse T cell pool. This diversity is ensured by balancing thymic output, differentiation of naive into memory T cells, T cell proliferation and cell death. For naive T cells, the balance of these processes differs between standard laboratory mice and humans. This may be a true species difference or, alternatively, result from the vastly different amounts of antigens to which standard laboratory mice and humans are exposed. Using wildlings, that is, laboratory mice born to wild mice, we studied the impact of antigen-exposure through a natural microbiome on naive and memory T cell maintenance. We found that standard laboratory mice and wildlings maintain their naive T cell pools similarly: naive T cells rarely divide and are replaced by thymic emigrants at similar rates. The daily replacement rate of memory T cells, on the other hand, is about 50% faster in wildlings than in standard laboratory mice. In both types of mice, about 20% of newly produced memory T cells originate from recruitment of naive T cells, while the remaining cells are produced by their clonal expansion and by self-renewal. In older mice, this drops to 5%. In humans, a similarly large fraction of memory cells originate from recruitment of naive T cells. Unlike in mice, most naive T cells in human adults are formed by naive T cell proliferation. Thus, while both types of mice mimic the maintenance mechanisms of the memory T cell pool in humans, even wildlings fall short as a model for human naive T cell maintenance.},
}
MeSH Terms:
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Animals
*Memory T Cells/immunology
Humans
Mice
*Immunologic Memory
Cell Differentiation/immunology
Cell Proliferation
Aging/immunology
Thymus Gland/immunology
*T-Lymphocytes/immunology
Male
RevDate: 2026-08-11
The Giardia secretome disrupts gut microbiota biofilms.
Trends in parasitology pii:S1471-4922(26)00207-2 [Epub ahead of print].
This review provides a state-of-the-art update on Giardia intestinalis pathogenesis and its immunomodulatory effects during enteric coinfections. We examine mechanisms underlying abnormalities in mucus structure and glycosylation, alongside parasite-induced alterations in host immunity. Recent evidence reveals a protective role for gut microbiota biofilms and demonstrates how the Giardia secretome disrupts these communities. In particular, trophozoite-derived cysteine proteases and extracellular vesicles, along with their small RNA cargo, remodel microbiota biofilms and drive the conversion of commensal bacteria into invasive pathobionts. Collectively, these findings establish Giardia as a central regulator of gut microbial ecology and intestinal barrier function, highlighting its value as a model for developing novel therapeutic strategies against enteric disease.
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@article {pmid42580912,
year = {2026},
author = {Buret, AG and Allain, T},
title = {The Giardia secretome disrupts gut microbiota biofilms.},
journal = {Trends in parasitology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.pt.2026.07.011},
pmid = {42580912},
issn = {1471-5007},
abstract = {This review provides a state-of-the-art update on Giardia intestinalis pathogenesis and its immunomodulatory effects during enteric coinfections. We examine mechanisms underlying abnormalities in mucus structure and glycosylation, alongside parasite-induced alterations in host immunity. Recent evidence reveals a protective role for gut microbiota biofilms and demonstrates how the Giardia secretome disrupts these communities. In particular, trophozoite-derived cysteine proteases and extracellular vesicles, along with their small RNA cargo, remodel microbiota biofilms and drive the conversion of commensal bacteria into invasive pathobionts. Collectively, these findings establish Giardia as a central regulator of gut microbial ecology and intestinal barrier function, highlighting its value as a model for developing novel therapeutic strategies against enteric disease.},
}
RevDate: 2026-08-11
Pediatric appendicitis: Incidence, trends and pathophysiology.
Seminars in pediatric surgery pii:S1055-8586(26)00101-0 [Epub ahead of print].
Appendicitis remains the most common surgical emergency in children and adolescents, yet its epidemiology and pathophysiology remain incompletely understood. Studies have demonstrated substantial geographic, racial, temporal, and socioeconomic variation in appendicitis incidence and severity. Advances in population-based investigation, imaging, and microbiome analysis have further challenged the traditional concept of appendicitis as a uniform disease process caused solely by luminal obstruction. Increasing evidence instead supports a multifactorial process influenced by environmental exposures, host susceptibility, microbial factors, and healthcare access. Epidemiologic observations additionally suggest important differences between uncomplicated and perforated appendicitis. Improved understanding of these relationships has important implications for disease classification, risk stratification, and future treatment strategies. This review summarizes the current understanding of the incidence, epidemiologic trends, and pathophysiology of pediatric appendicitis.
Additional Links: PMID-42580959
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@article {pmid42580959,
year = {2026},
author = {Alturki, N and St Peter, SD},
title = {Pediatric appendicitis: Incidence, trends and pathophysiology.},
journal = {Seminars in pediatric surgery},
volume = {},
number = {},
pages = {151685},
doi = {10.1016/j.sempedsurg.2026.151685},
pmid = {42580959},
issn = {1532-9453},
abstract = {Appendicitis remains the most common surgical emergency in children and adolescents, yet its epidemiology and pathophysiology remain incompletely understood. Studies have demonstrated substantial geographic, racial, temporal, and socioeconomic variation in appendicitis incidence and severity. Advances in population-based investigation, imaging, and microbiome analysis have further challenged the traditional concept of appendicitis as a uniform disease process caused solely by luminal obstruction. Increasing evidence instead supports a multifactorial process influenced by environmental exposures, host susceptibility, microbial factors, and healthcare access. Epidemiologic observations additionally suggest important differences between uncomplicated and perforated appendicitis. Improved understanding of these relationships has important implications for disease classification, risk stratification, and future treatment strategies. This review summarizes the current understanding of the incidence, epidemiologic trends, and pathophysiology of pediatric appendicitis.},
}
RevDate: 2026-08-11
From association to mechanism: AA:DHA supplementation, the preterm gut microbiome, and retinopathy of prematurity.
Pediatric research [Epub ahead of print].
AA:DHA supplementation may be associated with selected taxonomic and inferred functional features of the gut microbiome in extremely preterm infants, but current evidence does not establish the microbiome as a mediator of reduced severe retinopathy of prematurity. Denser longitudinal sampling and detailed information on antibiotics, feeding, microbial function, and clinical events are needed to move from microbial associations towards causal mechanisms.
Additional Links: PMID-42581136
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@article {pmid42581136,
year = {2026},
author = {Lamadrid-Figueroa, H},
title = {From association to mechanism: AA:DHA supplementation, the preterm gut microbiome, and retinopathy of prematurity.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42581136},
issn = {1530-0447},
abstract = {AA:DHA supplementation may be associated with selected taxonomic and inferred functional features of the gut microbiome in extremely preterm infants, but current evidence does not establish the microbiome as a mediator of reduced severe retinopathy of prematurity. Denser longitudinal sampling and detailed information on antibiotics, feeding, microbial function, and clinical events are needed to move from microbial associations towards causal mechanisms.},
}
RevDate: 2026-08-11
When 'vape-free' should mean 'smoke-free': third-hand e-cigarette residues and the developing lung.
Pediatric research [Epub ahead of print].
E-cigarettes are widely perceived as a safer alternative to tobacco, and that perception often extends to their use around infants and children. Yet exhaled aerosol deposits onto indoor surfaces, leaving a residue, known as third-hand e-cigarette aerosol, that can be re-emitted, ingested, or absorbed through the skin. The developmental consequences of such exposure have been almost entirely unexplored. In this issue of Pediatric Research, Zaman et al. begin to address that gap, exposing neonatal mice to third-hand e-cigarette aerosol-contaminated terrycloth and carpet in early-life. The authors report sex-divergent outcomes: transient neutrophilic inflammation in females, and broader transcriptional disturbance, delayed alveolar maturation, gut microbiome shifts, and persistent adult obstructive lung dysfunction in males, with tobacco flavouring amplifying the male response. This commentary considers the study's strengths, outlines future research priorities, and argues that the findings strengthen the case for extending 'smoke-free' protections to vaping.
Additional Links: PMID-42581137
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@article {pmid42581137,
year = {2026},
author = {Larcombe, AN},
title = {When 'vape-free' should mean 'smoke-free': third-hand e-cigarette residues and the developing lung.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42581137},
issn = {1530-0447},
abstract = {E-cigarettes are widely perceived as a safer alternative to tobacco, and that perception often extends to their use around infants and children. Yet exhaled aerosol deposits onto indoor surfaces, leaving a residue, known as third-hand e-cigarette aerosol, that can be re-emitted, ingested, or absorbed through the skin. The developmental consequences of such exposure have been almost entirely unexplored. In this issue of Pediatric Research, Zaman et al. begin to address that gap, exposing neonatal mice to third-hand e-cigarette aerosol-contaminated terrycloth and carpet in early-life. The authors report sex-divergent outcomes: transient neutrophilic inflammation in females, and broader transcriptional disturbance, delayed alveolar maturation, gut microbiome shifts, and persistent adult obstructive lung dysfunction in males, with tobacco flavouring amplifying the male response. This commentary considers the study's strengths, outlines future research priorities, and argues that the findings strengthen the case for extending 'smoke-free' protections to vaping.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-12
Gut microbiota modulation of systemic immunity and cancer immunotherapy: mechanisms, evidence, and therapeutic implications.
Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 34(4):.
The gut microbiota plays a critical role in regulating systemic immune responses and has emerged as a key determinant of therapeutic efficacy and toxicity in cancer immunotherapy. Accumulating evidence indicates that specific microbial taxa and microbiota-derived metabolites modulate antitumor immunity by shaping immune cell maturation, cytokine signaling, and the tumor microenvironment. In particular, gut microbial metabolites such as short-chain fatty acids, bile acids, and inosine influence immune checkpoint inhibitor responses by regulating T-cell activation, dendritic cell function, and immune homeostasis beyond the intestinal compartment. Preclinical and clinical studies have demonstrated that alterations in gut microbiota composition are associated with variability in immunotherapy outcomes, including treatment resistance and immune-related adverse events. Importantly, microbiota-targeted interventions such as dietary modulation, probiotics, prebiotics, antibiotics, and fecal microbiota transplantation have shown promise in enhancing immunotherapy efficacy and reducing toxicity. This review synthesizes current mechanistic insights and clinical evidence linking the gut microbiota to systemic immunity and cancer immunotherapy outcomes, highlighting microbiome modulation as a potential therapeutic adjuvant to optimize immunotherapy response and support precision oncology.
Additional Links: PMID-42581182
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@article {pmid42581182,
year = {2026},
author = {Alotaibi, BS},
title = {Gut microbiota modulation of systemic immunity and cancer immunotherapy: mechanisms, evidence, and therapeutic implications.},
journal = {Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society},
volume = {34},
number = {4},
pages = {},
pmid = {42581182},
issn = {1319-0164},
abstract = {The gut microbiota plays a critical role in regulating systemic immune responses and has emerged as a key determinant of therapeutic efficacy and toxicity in cancer immunotherapy. Accumulating evidence indicates that specific microbial taxa and microbiota-derived metabolites modulate antitumor immunity by shaping immune cell maturation, cytokine signaling, and the tumor microenvironment. In particular, gut microbial metabolites such as short-chain fatty acids, bile acids, and inosine influence immune checkpoint inhibitor responses by regulating T-cell activation, dendritic cell function, and immune homeostasis beyond the intestinal compartment. Preclinical and clinical studies have demonstrated that alterations in gut microbiota composition are associated with variability in immunotherapy outcomes, including treatment resistance and immune-related adverse events. Importantly, microbiota-targeted interventions such as dietary modulation, probiotics, prebiotics, antibiotics, and fecal microbiota transplantation have shown promise in enhancing immunotherapy efficacy and reducing toxicity. This review synthesizes current mechanistic insights and clinical evidence linking the gut microbiota to systemic immunity and cancer immunotherapy outcomes, highlighting microbiome modulation as a potential therapeutic adjuvant to optimize immunotherapy response and support precision oncology.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-12
Microbiome-Inflammation-Mitochondria Coupling in Neurodegeneration and Depression: An Integrative Opinion.
Molecular neurobiology, 63(1):.
There is increasing evidence that gut microbiome dysbiosis, systemic inflammation, and mitochondrial dysfunction interact in ways that influence psychiatric and neurodegenerative disease vulnerability. Recent findings indicate that microbial signaling, inflammatory activation, and mitochondrial stress responses form dynamic bidirectional networks that may influence neurotransmission, neuroplasticity, metabolism, and behavior. This integrative opinion article distinguishes major depressive disorder (MDD), Parkinson's disease (PD), and Alzheimer's disease (AD) as mechanistically distinct disorders while proposing that they may share overlapping upstream modulatory pathways involving inflammation, microbial dysregulation, and mitochondrial dysfunction. Importantly, the microbiome-inflammation-mitochondria axis is presented as a disease-modifying and vulnerability-associated framework rather than a singular unifying etiology. Current limitations including reverse causation, microbiome heterogeneity, and differences in treatment responsiveness are also discussed.
Additional Links: PMID-42581224
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@article {pmid42581224,
year = {2026},
author = {Stefano, GB and Esch, T},
title = {Microbiome-Inflammation-Mitochondria Coupling in Neurodegeneration and Depression: An Integrative Opinion.},
journal = {Molecular neurobiology},
volume = {63},
number = {1},
pages = {},
pmid = {42581224},
issn = {1559-1182},
mesh = {Humans ; *Mitochondria/metabolism/pathology ; Animals ; *Inflammation/pathology/microbiology/metabolism ; *Depression/microbiology/metabolism/pathology ; *Neurodegenerative Diseases/microbiology/pathology/metabolism ; *Microbiota ; *Gastrointestinal Microbiome/physiology ; *Nerve Degeneration/pathology ; },
abstract = {There is increasing evidence that gut microbiome dysbiosis, systemic inflammation, and mitochondrial dysfunction interact in ways that influence psychiatric and neurodegenerative disease vulnerability. Recent findings indicate that microbial signaling, inflammatory activation, and mitochondrial stress responses form dynamic bidirectional networks that may influence neurotransmission, neuroplasticity, metabolism, and behavior. This integrative opinion article distinguishes major depressive disorder (MDD), Parkinson's disease (PD), and Alzheimer's disease (AD) as mechanistically distinct disorders while proposing that they may share overlapping upstream modulatory pathways involving inflammation, microbial dysregulation, and mitochondrial dysfunction. Importantly, the microbiome-inflammation-mitochondria axis is presented as a disease-modifying and vulnerability-associated framework rather than a singular unifying etiology. Current limitations including reverse causation, microbiome heterogeneity, and differences in treatment responsiveness are also discussed.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Mitochondria/metabolism/pathology
Animals
*Inflammation/pathology/microbiology/metabolism
*Depression/microbiology/metabolism/pathology
*Neurodegenerative Diseases/microbiology/pathology/metabolism
*Microbiota
*Gastrointestinal Microbiome/physiology
*Nerve Degeneration/pathology
RevDate: 2026-08-11
CmpDate: 2026-08-12
Associations between the oral microbiome, age, and cumulative dental caries experience: a cross-sectional study.
Clinical oral investigations, 30(9):.
OBJECTIVES: Age is consistently associated with higher cumulative caries experience, but whether age-related oral microbiome shifts contribute to this association remains unclear. This study characterized age-related oral microbiome alterations, developed a microbial health index, and explored the interplay between the microbiome, age, and caries experience in adults.
MATERIALS AND METHODS: Among 4,763 participants aged ≥ 14 years from the National Health and Nutrition Examination Survey (NHANES), caries experience was quantified using the Decayed, Missing, and Filled Surfaces (DMFS) index. Oral microbiomes were profiled by 16 S rRNA sequencing. Restricted cubic splines, diversity and network analyses, random forest modeling for an Oral Microbial Health Index (OMHI), and mediation analysis were used to examine relationships among age, microbiome, and caries.
RESULTS: Age explained 40.5% of DMFS variance with a non-linear positive correlation (P < 0.001). Microbial α-diversity declined non-linearly with age and DMFS (P < 0.001). Community structure and networks differed across age groups and caries experience levels. OMHI discriminated caries-free from high-burden individuals (AUC = 0.789), and the OMHI-based mediation accounted for 23.8% (95% CI: 21.3%-26.2%) of the age-DMFS association.
CONCLUSIONS: The microbiome mediates a substantial portion of the age-caries association. Age-related shifts in diversity, taxonomy, and network structure are associated with greater caries burden. The OMHI shows promise as a non-invasive tool for caries risk stratification and age-specific prevention.
CLINICAL RELEVANCE: These findings support microbiome-informed, age-stratified caries prevention and offer a non-invasive indicator for identifying adults at elevated risk in clinical and public health settings.
Additional Links: PMID-42581286
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@article {pmid42581286,
year = {2026},
author = {Tang, H and Huang, J and Li, J and Zhang, X and Tang, Z and An, H and Zhou, Q and Niu, Z and Wang, Y},
title = {Associations between the oral microbiome, age, and cumulative dental caries experience: a cross-sectional study.},
journal = {Clinical oral investigations},
volume = {30},
number = {9},
pages = {},
pmid = {42581286},
issn = {1436-3771},
support = {42507570//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Microbiota ; *Dental Caries/microbiology/epidemiology ; Cross-Sectional Studies ; Female ; Age Factors ; Male ; Adult ; Middle Aged ; DMF Index ; Nutrition Surveys ; *Mouth/microbiology ; Adolescent ; Aged ; },
abstract = {OBJECTIVES: Age is consistently associated with higher cumulative caries experience, but whether age-related oral microbiome shifts contribute to this association remains unclear. This study characterized age-related oral microbiome alterations, developed a microbial health index, and explored the interplay between the microbiome, age, and caries experience in adults.
MATERIALS AND METHODS: Among 4,763 participants aged ≥ 14 years from the National Health and Nutrition Examination Survey (NHANES), caries experience was quantified using the Decayed, Missing, and Filled Surfaces (DMFS) index. Oral microbiomes were profiled by 16 S rRNA sequencing. Restricted cubic splines, diversity and network analyses, random forest modeling for an Oral Microbial Health Index (OMHI), and mediation analysis were used to examine relationships among age, microbiome, and caries.
RESULTS: Age explained 40.5% of DMFS variance with a non-linear positive correlation (P < 0.001). Microbial α-diversity declined non-linearly with age and DMFS (P < 0.001). Community structure and networks differed across age groups and caries experience levels. OMHI discriminated caries-free from high-burden individuals (AUC = 0.789), and the OMHI-based mediation accounted for 23.8% (95% CI: 21.3%-26.2%) of the age-DMFS association.
CONCLUSIONS: The microbiome mediates a substantial portion of the age-caries association. Age-related shifts in diversity, taxonomy, and network structure are associated with greater caries burden. The OMHI shows promise as a non-invasive tool for caries risk stratification and age-specific prevention.
CLINICAL RELEVANCE: These findings support microbiome-informed, age-stratified caries prevention and offer a non-invasive indicator for identifying adults at elevated risk in clinical and public health settings.},
}
MeSH Terms:
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Humans
*Microbiota
*Dental Caries/microbiology/epidemiology
Cross-Sectional Studies
Female
Age Factors
Male
Adult
Middle Aged
DMF Index
Nutrition Surveys
*Mouth/microbiology
Adolescent
Aged
RevDate: 2026-08-12
CmpDate: 2026-08-12
Longitudinal profiling of upper respiratory tract microbiota and metabolome in hospitalized COVID-19 convalescents: a 3-year prospective cohort study.
Journal of translational medicine, 24(1):.
BACKGROUND: Long COVID is characterized by persistent, far-reaching effects in convalescent individuals, with pulmonary diffusion impairment emerging as a clinically impactful sequela affecting more than one-third of this population. The salivary microbiome and metabolome, reflecting the oral-lung axis, offer a window into the mechanisms underlying this condition. However, systematic longitudinal evidence on their long-term dynamics after infection and their predictive value for persistent pulmonary diffusion impairment remains scarce.
METHODS: In this prospective cohort, we profiled the salivary bacterial microbiome (16S rRNA sequencing) and metabolome (untargeted LC-MS/MS) in 424 COVID-19 convalescents at 2 (T1) and 3 (T2) years post-discharge, alongside 106 demographically matched healthy controls. To explore whether 2-year salivary multiomics signatures were associated with 3-year pulmonary diffusion status, microbial and metabolic features were ranked using random forest mean decrease in accuracy and used to train 10 machine-learning classifiers after stratified training/internal validation splitting. Because this modeling strategy was exploratory, we further performed a repeated stability-selection analysis across 100 stratified resampling iterations to identify reproducibly selected salivary multiomics features.
RESULTS: COVID-19 convalescents exhibited sustained, interrelated salivary microbiome dysbiosis and metabolic reprogramming at 3 years post-infection. The microbial perturbations were characterized by reduced alpha diversity, a shift in phylogenetic dominance from Bacteroidota to Actinobacteriota, and a marked expansion of Proteobacteria at the 2-year follow-up. The microbial co-occurrence networks also became sparser, suggesting diminished stability. Metabolomic profiling revealed upregulation of the TCA cycle, purine/pyrimidine metabolism, arginine biosynthesis, and other pathways at the 2-year follow-up, with a discernible trend toward recovery by year 3. Notably, 36.6% of patients presented with persistent pulmonary diffusion dysfunction at the 3-year follow-up. Leveraging 2-year salivary multiomics signatures, we developed an exploratory proof-of-concept model for predicting 3-year pulmonary diffusion dysfunction. The CatBoost classifier achieved the best overall performance, achieving an area under the curve of 0.808 in the internal validation set; key predictive features included genera Catonella and Actinomyces, and metabolites adenosine 3',5'-diphosphate, triiodothyronine sulfate and betaine. In an exploratory stability-selected analysis, a conservatively tuned CatBoost model based on repeatedly selected features achieved an internal validation AUC of 0.798.
CONCLUSIONS: This research provides the first longitudinal characterization of the salivary bacterial microbiome and metabolome in COVID-19 convalescents up to 3 years post infection. Furthermore, we developed a novel predictive model for post-SARS-CoV-2 pulmonary diffusion impairment based on salivary multiomics features, which may represent a promising screening tool for identifying high-risk individuals.
Additional Links: PMID-42581368
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@article {pmid42581368,
year = {2026},
author = {Zhang, Z and Gao, L and Guan, L and Qian, Z and Li, J and Tong, Z},
title = {Longitudinal profiling of upper respiratory tract microbiota and metabolome in hospitalized COVID-19 convalescents: a 3-year prospective cohort study.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
pmid = {42581368},
issn = {1479-5876},
support = {2023YFC0872500//the Ministry of Science and Technology of the People's Republic of China/ ; BJRID2024-008//Beijing Research Center for Respiratory Infectious Diseases Project/ ; 062//Beijing Scholars Program/ ; Laboratory for Clinical Medicine, Capital Medical University//Laboratory for Clinical Medicine, Capital Medical University/ ; },
mesh = {Humans ; *COVID-19/microbiology/metabolism ; Prospective Studies ; *Microbiota ; *Metabolome ; Saliva/microbiology ; SARS-CoV-2 ; Female ; Longitudinal Studies ; Male ; Multiomics ; Post-Acute COVID-19 Syndrome ; RNA, Ribosomal, 16S/genetics ; Hospitalization ; *Convalescence ; },
abstract = {BACKGROUND: Long COVID is characterized by persistent, far-reaching effects in convalescent individuals, with pulmonary diffusion impairment emerging as a clinically impactful sequela affecting more than one-third of this population. The salivary microbiome and metabolome, reflecting the oral-lung axis, offer a window into the mechanisms underlying this condition. However, systematic longitudinal evidence on their long-term dynamics after infection and their predictive value for persistent pulmonary diffusion impairment remains scarce.
METHODS: In this prospective cohort, we profiled the salivary bacterial microbiome (16S rRNA sequencing) and metabolome (untargeted LC-MS/MS) in 424 COVID-19 convalescents at 2 (T1) and 3 (T2) years post-discharge, alongside 106 demographically matched healthy controls. To explore whether 2-year salivary multiomics signatures were associated with 3-year pulmonary diffusion status, microbial and metabolic features were ranked using random forest mean decrease in accuracy and used to train 10 machine-learning classifiers after stratified training/internal validation splitting. Because this modeling strategy was exploratory, we further performed a repeated stability-selection analysis across 100 stratified resampling iterations to identify reproducibly selected salivary multiomics features.
RESULTS: COVID-19 convalescents exhibited sustained, interrelated salivary microbiome dysbiosis and metabolic reprogramming at 3 years post-infection. The microbial perturbations were characterized by reduced alpha diversity, a shift in phylogenetic dominance from Bacteroidota to Actinobacteriota, and a marked expansion of Proteobacteria at the 2-year follow-up. The microbial co-occurrence networks also became sparser, suggesting diminished stability. Metabolomic profiling revealed upregulation of the TCA cycle, purine/pyrimidine metabolism, arginine biosynthesis, and other pathways at the 2-year follow-up, with a discernible trend toward recovery by year 3. Notably, 36.6% of patients presented with persistent pulmonary diffusion dysfunction at the 3-year follow-up. Leveraging 2-year salivary multiomics signatures, we developed an exploratory proof-of-concept model for predicting 3-year pulmonary diffusion dysfunction. The CatBoost classifier achieved the best overall performance, achieving an area under the curve of 0.808 in the internal validation set; key predictive features included genera Catonella and Actinomyces, and metabolites adenosine 3',5'-diphosphate, triiodothyronine sulfate and betaine. In an exploratory stability-selected analysis, a conservatively tuned CatBoost model based on repeatedly selected features achieved an internal validation AUC of 0.798.
CONCLUSIONS: This research provides the first longitudinal characterization of the salivary bacterial microbiome and metabolome in COVID-19 convalescents up to 3 years post infection. Furthermore, we developed a novel predictive model for post-SARS-CoV-2 pulmonary diffusion impairment based on salivary multiomics features, which may represent a promising screening tool for identifying high-risk individuals.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*COVID-19/microbiology/metabolism
Prospective Studies
*Microbiota
*Metabolome
Saliva/microbiology
SARS-CoV-2
Female
Longitudinal Studies
Male
Multiomics
Post-Acute COVID-19 Syndrome
RNA, Ribosomal, 16S/genetics
Hospitalization
*Convalescence
RevDate: 2026-08-12
Increasing gut short-chain fatty acids protects intestinal barrier function but does not spare muscle glycogen or impact aerobic performance.
The Journal of physiology [Epub ahead of print].
Animal studies suggest gut microbiota-derived short-chain fatty acids (SCFA) provide an intestinal barrier-protecting, glycogen-sparing energy source that increases aerobic endurance performance, but confirmation in humans is needed. This study aimed to determine whether increasing colonic SCFA availability impacts intestinal barrier function, substrate metabolism, muscle glycogen and aerobic performance in healthy adults. Using a randomized, double-blind, crossover design 12 active men (age 18-30 years; V . O 2 peak 40.0 ± 7.1 mL/kg/min) performed prescribed exercise and consumed a provided diet supplemented with acetylated and butyrylated high-amylose maize starch engineered to deliver SCFA to the colon (HAMS-A/B) or low-amylose maize starch (LAMS) for 7 days, separated by a 2 week washout. Indirect calorimetry, stable isotopes and blood, muscle and urine biomarkers were measured on intervention day 8 while participants completed 90 min of steady-state cycle ergometry (ExSS; 60 ± 5% V . O 2 peak) followed by a 5 km treadmill time trial. HAMS-A/B, relative to LAMS, increased faecal and serum SCFA. Multiple markers of intestinal barrier damage and permeability were lower, and the respiratory exchange ratio during ExSS was higher (0.02 [95% confidence interval (CI): 0.01, 0.03], Ptreatment < 0.001) following HAMS-A/B versus LAMS. However no between-treatment difference in glucose turnover, muscle glycogen depletion (14 µmol/kg/g dry wt. [95% CI: -116, 143], Pinteractio n = 0.613) or TT performance (5 s [95%CI: -44, 54], Ptreatment = 0.816) was observed. Increasing colonic and circulating SCFA modestly altered substrate oxidation and preserved intestinal barrier function during endurance exercise. However effects were not sufficient to spare muscle glycogen or increase aerobic endurance performance, leaving the practical relevance unclear and underscoring challenges inherent in translating promising preclinical findings to humans. KEY POINTS: Animal studies suggest gut microbiota-derived short-chain fatty acids (SCFA) provide an intestinal barrier-protecting, glycogen-sparing energy source that increases aerobic endurance performance, but confirmation in humans is lacking. A gut microbiota-targeted dietary supplementation strategy was used to deliver SCFA to the colon and successfully increased colonic and systemic SCFA concentrations in healthy, physically active adults before and during an endurance exercise bout and aerobic performance test. Increasing colonic and systemic SCFA availability preserved intestinal barrier function but did not impact glucose turnover, alter protein expression in muscle or spare muscle glycogen during endurance exercise. Increasing colonic and systemic SCFA availability did not impact aerobic endurance performance.
Additional Links: PMID-42581384
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@article {pmid42581384,
year = {2026},
author = {Karl, JP and Fagnant, HS and Carrigan, CT and Margolis, LM},
title = {Increasing gut short-chain fatty acids protects intestinal barrier function but does not spare muscle glycogen or impact aerobic performance.},
journal = {The Journal of physiology},
volume = {},
number = {},
pages = {},
doi = {10.1113/JP291470},
pmid = {42581384},
issn = {1469-7793},
support = {MO220066//U.S. Army Medical Research and Development Command/ ; },
abstract = {Animal studies suggest gut microbiota-derived short-chain fatty acids (SCFA) provide an intestinal barrier-protecting, glycogen-sparing energy source that increases aerobic endurance performance, but confirmation in humans is needed. This study aimed to determine whether increasing colonic SCFA availability impacts intestinal barrier function, substrate metabolism, muscle glycogen and aerobic performance in healthy adults. Using a randomized, double-blind, crossover design 12 active men (age 18-30 years; V . O 2 peak 40.0 ± 7.1 mL/kg/min) performed prescribed exercise and consumed a provided diet supplemented with acetylated and butyrylated high-amylose maize starch engineered to deliver SCFA to the colon (HAMS-A/B) or low-amylose maize starch (LAMS) for 7 days, separated by a 2 week washout. Indirect calorimetry, stable isotopes and blood, muscle and urine biomarkers were measured on intervention day 8 while participants completed 90 min of steady-state cycle ergometry (ExSS; 60 ± 5% V . O 2 peak) followed by a 5 km treadmill time trial. HAMS-A/B, relative to LAMS, increased faecal and serum SCFA. Multiple markers of intestinal barrier damage and permeability were lower, and the respiratory exchange ratio during ExSS was higher (0.02 [95% confidence interval (CI): 0.01, 0.03], Ptreatment < 0.001) following HAMS-A/B versus LAMS. However no between-treatment difference in glucose turnover, muscle glycogen depletion (14 µmol/kg/g dry wt. [95% CI: -116, 143], Pinteractio n = 0.613) or TT performance (5 s [95%CI: -44, 54], Ptreatment = 0.816) was observed. Increasing colonic and circulating SCFA modestly altered substrate oxidation and preserved intestinal barrier function during endurance exercise. However effects were not sufficient to spare muscle glycogen or increase aerobic endurance performance, leaving the practical relevance unclear and underscoring challenges inherent in translating promising preclinical findings to humans. KEY POINTS: Animal studies suggest gut microbiota-derived short-chain fatty acids (SCFA) provide an intestinal barrier-protecting, glycogen-sparing energy source that increases aerobic endurance performance, but confirmation in humans is lacking. A gut microbiota-targeted dietary supplementation strategy was used to deliver SCFA to the colon and successfully increased colonic and systemic SCFA concentrations in healthy, physically active adults before and during an endurance exercise bout and aerobic performance test. Increasing colonic and systemic SCFA availability preserved intestinal barrier function but did not impact glucose turnover, alter protein expression in muscle or spare muscle glycogen during endurance exercise. Increasing colonic and systemic SCFA availability did not impact aerobic endurance performance.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Spatial Partitioning of Microbial Functional Potential Suggests Complex Nitrogen Cycling in a Subterranean Estuary.
Environmental microbiology, 28(8):e70400.
Subterranean estuaries (STEs) are key bioreactors regulating the quantity and chemical composition of groundwater-derived nitrogen (N) reaching coastal ecosystems. Yet, the microbial controls on N-cycling within these groundwater-seawater mixing zones remain poorly understood. We investigated the spatio-temporal variations in microbial communities and their N-cycling potential within an alluvial Mediterranean STE with high N concentration. We explored changes in microbial abundance, heterotrophic activity, taxonomic composition, and the abundance of N-cycling genes across groundwater samples collected at several depths and distances from the shoreline in winter and summer. Microbial abundance, activity, and diversity varied strongly across hydrochemical zones according to physicochemistry and aquifer depth but showed limited seasonality. Functional predictions suggested a complex, spatially structured suite of N pathways encoded by diverse taxa occupying different STE zones, and quantitative-PCR revealed niche partitioning between ammonia-oxidizing archaea, prevalent in fresh-groundwater, and bacterial denitrifiers enriched in deep-saline layers. Multiple linear model predictions showed a stronger fit for NO2 [-] and NH4 [+] concentrations when using microbial properties than when using environmental variables, highlighting their importance for understanding N cycling in STEs. Our results suggest that the functional potential of the STE microbiome is complex and spatially structured across hydrochemical zones, explaining spatial variations in STE N-cycling.
Additional Links: PMID-42581800
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@article {pmid42581800,
year = {2026},
author = {Romano-Gude, D and Arandia-Gorostidi, N and Mena, C and Diego-Feliu, M and Almillategui, B and Székely, AJ and Bertilsson, S and Bravo, AG and Carrera, J and Romera-Castillo, C and Folch, A and Garcia-Orellana, J and Rodellas, V and Ruiz-González, C},
title = {Spatial Partitioning of Microbial Functional Potential Suggests Complex Nitrogen Cycling in a Subterranean Estuary.},
journal = {Environmental microbiology},
volume = {28},
number = {8},
pages = {e70400},
pmid = {42581800},
issn = {1462-2920},
support = {PRE2020-095468//FPI grant/ ; CEX2024-001494-S//'Severo Ochoa Centre of Excellence' accreditation/ ; PID2022-142480NB-I00//MINIOM/ ; CNS2023-144233//PATCHI/ ; PID2019-111722RJ-I00//MerTerMar/ ; 20213AT018//Mer_ICM/ ; PID2022-140862OB-C21//MUCHOGUSTO/ ; PID2022-140862OB-C22//MUCHOGUSTO/ ; //Spanish Ministry of Science Innovation and Universities (MICINN)/ ; JDC2022-050316-I//MCIN/AEI/ ; //European Union - NextGenerationEU/PRTR/ ; //Grup d'Hidrologia Subterrània - GHS (Universitat Politècnica de Catalunya)/ ; 2021-SGR 00609//Direcció General de Recerca from Generalitat de Catalunya/ ; FJC2021-047745-I//Juan de la Cierva-formación fellowship, the Spanish Ministry of Science and Innovation (MCIN/AEI)/ ; //EU ("NextGenerationEU"/PRTR)/ ; BIDP-I-2020-016//SENACYT doctoral scholarship from the Government of Panama/ ; },
mesh = {*Estuaries ; *Nitrogen Cycle ; *Archaea/metabolism/genetics/classification/isolation & purification ; *Bacteria/metabolism/classification/genetics/isolation & purification ; Nitrogen/metabolism ; *Groundwater/microbiology/chemistry ; Seawater/microbiology ; *Microbiota ; Ammonia/metabolism ; Ecosystem ; Seasons ; },
abstract = {Subterranean estuaries (STEs) are key bioreactors regulating the quantity and chemical composition of groundwater-derived nitrogen (N) reaching coastal ecosystems. Yet, the microbial controls on N-cycling within these groundwater-seawater mixing zones remain poorly understood. We investigated the spatio-temporal variations in microbial communities and their N-cycling potential within an alluvial Mediterranean STE with high N concentration. We explored changes in microbial abundance, heterotrophic activity, taxonomic composition, and the abundance of N-cycling genes across groundwater samples collected at several depths and distances from the shoreline in winter and summer. Microbial abundance, activity, and diversity varied strongly across hydrochemical zones according to physicochemistry and aquifer depth but showed limited seasonality. Functional predictions suggested a complex, spatially structured suite of N pathways encoded by diverse taxa occupying different STE zones, and quantitative-PCR revealed niche partitioning between ammonia-oxidizing archaea, prevalent in fresh-groundwater, and bacterial denitrifiers enriched in deep-saline layers. Multiple linear model predictions showed a stronger fit for NO2 [-] and NH4 [+] concentrations when using microbial properties than when using environmental variables, highlighting their importance for understanding N cycling in STEs. Our results suggest that the functional potential of the STE microbiome is complex and spatially structured across hydrochemical zones, explaining spatial variations in STE N-cycling.},
}
MeSH Terms:
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*Estuaries
*Nitrogen Cycle
*Archaea/metabolism/genetics/classification/isolation & purification
*Bacteria/metabolism/classification/genetics/isolation & purification
Nitrogen/metabolism
*Groundwater/microbiology/chemistry
Seawater/microbiology
*Microbiota
Ammonia/metabolism
Ecosystem
Seasons
RevDate: 2026-08-12
CmpDate: 2026-08-12
Intestinal pooling of taurine conjugated bile acids is associated with tissue aging and senescent immune evasion.
Frontiers in immunology, 17:1845117.
BACKGROUND: Aging drives metabolic decline and the accumulation of senescent cells that evade immune clearance. The mechanisms linking host-microbiome co-metabolism to peripheral tissue deterioration remain unclear. We hypothesized that age-dysregulated enterohepatic bile acid (BA) signaling directly promotes systemic aging and immune senescence.
METHODS: We conducted targeted BA metabolomics in the intestinal and peripheral compartments of young and middle-aged mice. To establish causality, 12-month-old mice underwent systemic BA depletion via a cholestyramine diet, followed by assessments of Farnesoid X Receptor (FXR) and Retinoic Acid Receptor alpha (RARα) signaling, cellular senescence, PD-L1/PD-L2 expression, and multi-organ transcriptomics.
RESULTS: Advancing age sequesters potent endogenous FXR antagonists (T-α-MCA, T-ω-MCA) within the gut lumen. However, peripheral tissues (lungs, skin, lymph nodes) progressively decrease in the levels of these regulatory molecules. This spatial disconnect triggers chronic peripheral FXR hyperactivation, disrupting local RARα signaling. which accelerates the accumulation of senescent cells and actively shields them from immune clearance by upregulating PD-L1 and PD-L2 surface checkpoints. Crucially, systemic BA sequestration reversed this phenotype. Depleting the pathological BA pool suppressed peripheral FXR overreaction. Further cleared the senescent burden, stripped senescent cells of their immune-evasive checkpoints, and drove a multi-organ of age-associated transcriptional changes.
CONCLUSION: The age-altered BA metabolome may contribute to systemic aging and to upregulation of PD-L1 and PD-L2. Rebalancing the enterohepatic BA network to relieve peripheral FXR hyperactivation represents a potent, broad-spectrum geroprotective strategy to restore immune surveillance and multi-organ homeostasis.
Additional Links: PMID-42581953
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@article {pmid42581953,
year = {2026},
author = {Tan, J and Xiong, W and Feng, Y and Li, X and Jiang, H and Zhang, Z},
title = {Intestinal pooling of taurine conjugated bile acids is associated with tissue aging and senescent immune evasion.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1845117},
pmid = {42581953},
issn = {1664-3224},
mesh = {Animals ; *Aging/immunology/metabolism ; *Bile Acids and Salts/metabolism/immunology ; Mice ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptor, Farnesoid X-Activated ; *Cellular Senescence/immunology ; *Intestinal Mucosa/metabolism/immunology ; Signal Transduction ; *Taurine/metabolism ; B7-H1 Antigen/metabolism ; Mice, Inbred C57BL ; Male ; *Intestines/immunology ; },
abstract = {BACKGROUND: Aging drives metabolic decline and the accumulation of senescent cells that evade immune clearance. The mechanisms linking host-microbiome co-metabolism to peripheral tissue deterioration remain unclear. We hypothesized that age-dysregulated enterohepatic bile acid (BA) signaling directly promotes systemic aging and immune senescence.
METHODS: We conducted targeted BA metabolomics in the intestinal and peripheral compartments of young and middle-aged mice. To establish causality, 12-month-old mice underwent systemic BA depletion via a cholestyramine diet, followed by assessments of Farnesoid X Receptor (FXR) and Retinoic Acid Receptor alpha (RARα) signaling, cellular senescence, PD-L1/PD-L2 expression, and multi-organ transcriptomics.
RESULTS: Advancing age sequesters potent endogenous FXR antagonists (T-α-MCA, T-ω-MCA) within the gut lumen. However, peripheral tissues (lungs, skin, lymph nodes) progressively decrease in the levels of these regulatory molecules. This spatial disconnect triggers chronic peripheral FXR hyperactivation, disrupting local RARα signaling. which accelerates the accumulation of senescent cells and actively shields them from immune clearance by upregulating PD-L1 and PD-L2 surface checkpoints. Crucially, systemic BA sequestration reversed this phenotype. Depleting the pathological BA pool suppressed peripheral FXR overreaction. Further cleared the senescent burden, stripped senescent cells of their immune-evasive checkpoints, and drove a multi-organ of age-associated transcriptional changes.
CONCLUSION: The age-altered BA metabolome may contribute to systemic aging and to upregulation of PD-L1 and PD-L2. Rebalancing the enterohepatic BA network to relieve peripheral FXR hyperactivation represents a potent, broad-spectrum geroprotective strategy to restore immune surveillance and multi-organ homeostasis.},
}
MeSH Terms:
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Animals
*Aging/immunology/metabolism
*Bile Acids and Salts/metabolism/immunology
Mice
Receptors, Cytoplasmic and Nuclear/metabolism
Receptor, Farnesoid X-Activated
*Cellular Senescence/immunology
*Intestinal Mucosa/metabolism/immunology
Signal Transduction
*Taurine/metabolism
B7-H1 Antigen/metabolism
Mice, Inbred C57BL
Male
*Intestines/immunology
RevDate: 2026-08-12
CmpDate: 2026-08-12
Bacteriophage-mediated biofilm control: a novel targeted strategy for the management of dental caries.
Frontiers in cellular and infection microbiology, 16:1880231.
Dental caries, a globally prevalent chronic infectious disease, is driven by microbial dysbiosis of dental biofilm, involving multiple caries-associated colonizers. Conventional broad-spectrum antimicrobials and fluoride-based formulations often disrupt the commensal oral microbiota, contributing to antimicrobial resistance and imbalance of the oral ecosystem. In contrast, bacteriophage (phage) therapy has emerged as a promising precision strategy for caries control due to its high specificity, minimal off-target effects, and biofilm-disrupting capacity. Our review systematically summarizes recent advances in phage-based interventions for caries prevention and treatment. It describes the diversity and distribution of the oral phageome and its role in regulating oral microbial homeostasis. The review further details phages targeting key cariogenic bacteria, including S. mutans (e.g., φAPCM01, SMHBZ8), Actinomyces spp. (e.g., Av-1), and related phage enzymes. Core anti-bacterial and anti-biofilm mechanisms of oral phage are elucidated, such as direct bacterial lysis mediated by endolysins and holins, and inhibition and disassembly of biofilms through multiple mechanisms. Strategies for applying phages in caries management are also discussed, encompassing phage cocktails, combination therapies with conventional antimicrobials, and development of advanced delivery systems. Finally, current challenges and future directions of phage therapy are addressed. Overall, this review provides a comprehensive theoretical foundation for developing targeted, oral microbiome-friendly phage-based strategies against dental caries.
Additional Links: PMID-42582037
PubMed:
Citation:
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@article {pmid42582037,
year = {2026},
author = {Sun, H and Zhang, K and Chu, F and Dong, J and Chen, S and Ren, B and Guo, Q},
title = {Bacteriophage-mediated biofilm control: a novel targeted strategy for the management of dental caries.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1880231},
pmid = {42582037},
issn = {2235-2988},
mesh = {*Biofilms/growth & development ; *Dental Caries/therapy/microbiology/prevention & control ; *Bacteriophages/physiology ; Humans ; *Phage Therapy/methods ; Microbiota ; Bacteria/virology ; Streptococcus mutans/virology ; Mouth/microbiology ; },
abstract = {Dental caries, a globally prevalent chronic infectious disease, is driven by microbial dysbiosis of dental biofilm, involving multiple caries-associated colonizers. Conventional broad-spectrum antimicrobials and fluoride-based formulations often disrupt the commensal oral microbiota, contributing to antimicrobial resistance and imbalance of the oral ecosystem. In contrast, bacteriophage (phage) therapy has emerged as a promising precision strategy for caries control due to its high specificity, minimal off-target effects, and biofilm-disrupting capacity. Our review systematically summarizes recent advances in phage-based interventions for caries prevention and treatment. It describes the diversity and distribution of the oral phageome and its role in regulating oral microbial homeostasis. The review further details phages targeting key cariogenic bacteria, including S. mutans (e.g., φAPCM01, SMHBZ8), Actinomyces spp. (e.g., Av-1), and related phage enzymes. Core anti-bacterial and anti-biofilm mechanisms of oral phage are elucidated, such as direct bacterial lysis mediated by endolysins and holins, and inhibition and disassembly of biofilms through multiple mechanisms. Strategies for applying phages in caries management are also discussed, encompassing phage cocktails, combination therapies with conventional antimicrobials, and development of advanced delivery systems. Finally, current challenges and future directions of phage therapy are addressed. Overall, this review provides a comprehensive theoretical foundation for developing targeted, oral microbiome-friendly phage-based strategies against dental caries.},
}
MeSH Terms:
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*Biofilms/growth & development
*Dental Caries/therapy/microbiology/prevention & control
*Bacteriophages/physiology
Humans
*Phage Therapy/methods
Microbiota
Bacteria/virology
Streptococcus mutans/virology
Mouth/microbiology
RevDate: 2026-08-12
Editorial: Community series in epigenetics in the microbiome-host crosstalk: from mechanisms to therapeutics, volume II.
Frontiers in immunology, 17:1929447.
Additional Links: PMID-42582040
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Citation:
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@article {pmid42582040,
year = {2026},
author = {Liu, HY and Liu, C and Ramos-Lopez, O},
title = {Editorial: Community series in epigenetics in the microbiome-host crosstalk: from mechanisms to therapeutics, volume II.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1929447},
pmid = {42582040},
issn = {1664-3224},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Childhood type 1 diabetes mellitus and gut microbiota: from microbiome characteristics to prevention and treatment strategies.
Frontiers in cellular and infection microbiology, 16:1873700.
Type 1 diabetes mellitus (T1DM) in children is a chronic metabolic disease mediated by autoimmune abnormalities, characterized by extensive destruction and impairment of pancreatic islet β-cells, and represents a common chronic endocrine disorder in childhood. The occurrence and progression of T1DM are closely associated with genetic susceptibility and environmental factors. Compared with healthy children, children with T1DM exhibit a disrupted gut microecological balance, characterized by a marked reduction in microbial diversity, structural disturbances in dominant microbiota, and concomitant abnormalities in multiple metabolic pathways. Recent studies have indicated that the gut microbiota, as a key environmental factor, is associated with the pathophysiological processes of pediatric T1DM through mechanisms including altered intestinal permeability and modulation of immune homeostasis. This article provides a comprehensive narrative review of the characteristics of the gut microbiota in children with T1DM, summarizes current evidence regarding microbiome alterations and their underlying mechanisms, and discusses emerging microbiota-targeted interventions. The aim is to provide new insights for the early prevention, control, and clinical management of T1DM in children.
Additional Links: PMID-42582052
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@article {pmid42582052,
year = {2026},
author = {Yang, C},
title = {Childhood type 1 diabetes mellitus and gut microbiota: from microbiome characteristics to prevention and treatment strategies.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1873700},
pmid = {42582052},
issn = {2235-2988},
mesh = {Humans ; *Diabetes Mellitus, Type 1/therapy/prevention & control/microbiology ; *Gastrointestinal Microbiome ; Child ; Probiotics/therapeutic use ; Dysbiosis ; },
abstract = {Type 1 diabetes mellitus (T1DM) in children is a chronic metabolic disease mediated by autoimmune abnormalities, characterized by extensive destruction and impairment of pancreatic islet β-cells, and represents a common chronic endocrine disorder in childhood. The occurrence and progression of T1DM are closely associated with genetic susceptibility and environmental factors. Compared with healthy children, children with T1DM exhibit a disrupted gut microecological balance, characterized by a marked reduction in microbial diversity, structural disturbances in dominant microbiota, and concomitant abnormalities in multiple metabolic pathways. Recent studies have indicated that the gut microbiota, as a key environmental factor, is associated with the pathophysiological processes of pediatric T1DM through mechanisms including altered intestinal permeability and modulation of immune homeostasis. This article provides a comprehensive narrative review of the characteristics of the gut microbiota in children with T1DM, summarizes current evidence regarding microbiome alterations and their underlying mechanisms, and discusses emerging microbiota-targeted interventions. The aim is to provide new insights for the early prevention, control, and clinical management of T1DM in children.},
}
MeSH Terms:
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Humans
*Diabetes Mellitus, Type 1/therapy/prevention & control/microbiology
*Gastrointestinal Microbiome
Child
Probiotics/therapeutic use
Dysbiosis
RevDate: 2026-08-12
CmpDate: 2026-08-12
Host systemic metabolism and cancer metabolic vulnerabilities: mechanisms and therapeutic opportunities.
Frontiers in oncology, 16:1897564.
BACKGROUND: Central molecular mediators-including hypoxia-inducible factors (HIF-1α/HIF-2α), MYC, wild-type and mutant p53, NF-κB, STAT3, SREBPs, NRF2, and KRAS-orchestrate these pathways by linking nutrient availability to oncogenic signalling, epigenetic reprogramming, and immune-metabolic crosstalk within the tumour microenvironment. Key metabolic enzymes including HK2, PKM2, LDH-A, IDH1/2, GLS1, and FASN serve as direct effectors and therapeutic targets. Mitochondrial dynamics-biogenesis (PGC-1α), fission (DRP1), fusion (MFN1/2, OPA1), and mitophagy (PINK1-Parkin)-constitute a critical regulatory layer. The bidirectional epigenetic-metabolic axis, mediated by acetyl-CoA, SAM, α-ketoglutarate, 2-hydroxyglutarate, and lysine lactylation, amplifies oncogenic transcriptional programs and locks cells into malignant states. Central to this review is the thesis that metabolic plasticity-the capacity of cancer cells to dynamically switch between and co-opt multiple metabolic programs-is the primary driver of tumour progression, immune evasion, and resistance to therapy. Understanding and targeting this plasticity represents the central translational challenge of cancer metabolic oncology.
METHODS: A comprehensive narrative literature review was conducted across PubMed, Scopus, and Web of Science (2015-2025) using terms including metabolic reprogramming, Warburg effect, oncometabolites, mitochondrial dynamics, epigenetic metabolism, immunometabolism, and metabolic therapeutics. Peer-reviewed primary research and comprehensive reviews were evaluated. Limitations include restriction to English-language literature (2015-2025), potential publication bias toward high-impact journals, and the rapidly evolving nature of the field.
CONCLUSION: Metabolic reprogramming is governed by an interconnected network of transcription factors, signalling cascades, epigenetic regulators, mitochondrial dynamics, and TME-immune crosstalk. FDA-validated targets include IDH1/2 (ivosidenib, enasidenib, vorasidenib-August 2024), HIF-2α (belzutifan), and mTOR (everolimus). An expanding clinical pipeline encompasses GLS1, MCT1, OXPHOS Complex I, FASN, and metabolic immune checkpoints. Future advances require single-cell/spatial metabolomics, AI-driven patient stratification, and rational combination strategies that preempt adaptive metabolic escape. Future advances require AI-driven genome-scale metabolic modelling for patient stratification, single-cell and spatial metabolomics to resolve intra-tumoral metabolic heterogeneity, and rational combination strategies targeting multiple metabolic nodes simultaneously to preempt adaptive resistance. Integration of circadian pharmacology, host metabolic comorbidity management (obesity, diabetes, gut microbiome modulation), and TME metabolic normalisation into cancer treatment frameworks will drive the next generation of precision metabolic oncology.
Additional Links: PMID-42582071
PubMed:
Citation:
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@article {pmid42582071,
year = {2026},
author = {Mir, R and Barnawi, J and Algehainy, NA and M Jalal, M and Altayar, MA and Almotairi, RM and Tayeb, FJ and Moawadh, MS and Bedaiwi, RI and Almasoudi, KS and Albalawi, IA and Alasmari, A and Mir, MM},
title = {Host systemic metabolism and cancer metabolic vulnerabilities: mechanisms and therapeutic opportunities.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1897564},
pmid = {42582071},
issn = {2234-943X},
abstract = {BACKGROUND: Central molecular mediators-including hypoxia-inducible factors (HIF-1α/HIF-2α), MYC, wild-type and mutant p53, NF-κB, STAT3, SREBPs, NRF2, and KRAS-orchestrate these pathways by linking nutrient availability to oncogenic signalling, epigenetic reprogramming, and immune-metabolic crosstalk within the tumour microenvironment. Key metabolic enzymes including HK2, PKM2, LDH-A, IDH1/2, GLS1, and FASN serve as direct effectors and therapeutic targets. Mitochondrial dynamics-biogenesis (PGC-1α), fission (DRP1), fusion (MFN1/2, OPA1), and mitophagy (PINK1-Parkin)-constitute a critical regulatory layer. The bidirectional epigenetic-metabolic axis, mediated by acetyl-CoA, SAM, α-ketoglutarate, 2-hydroxyglutarate, and lysine lactylation, amplifies oncogenic transcriptional programs and locks cells into malignant states. Central to this review is the thesis that metabolic plasticity-the capacity of cancer cells to dynamically switch between and co-opt multiple metabolic programs-is the primary driver of tumour progression, immune evasion, and resistance to therapy. Understanding and targeting this plasticity represents the central translational challenge of cancer metabolic oncology.
METHODS: A comprehensive narrative literature review was conducted across PubMed, Scopus, and Web of Science (2015-2025) using terms including metabolic reprogramming, Warburg effect, oncometabolites, mitochondrial dynamics, epigenetic metabolism, immunometabolism, and metabolic therapeutics. Peer-reviewed primary research and comprehensive reviews were evaluated. Limitations include restriction to English-language literature (2015-2025), potential publication bias toward high-impact journals, and the rapidly evolving nature of the field.
CONCLUSION: Metabolic reprogramming is governed by an interconnected network of transcription factors, signalling cascades, epigenetic regulators, mitochondrial dynamics, and TME-immune crosstalk. FDA-validated targets include IDH1/2 (ivosidenib, enasidenib, vorasidenib-August 2024), HIF-2α (belzutifan), and mTOR (everolimus). An expanding clinical pipeline encompasses GLS1, MCT1, OXPHOS Complex I, FASN, and metabolic immune checkpoints. Future advances require single-cell/spatial metabolomics, AI-driven patient stratification, and rational combination strategies that preempt adaptive metabolic escape. Future advances require AI-driven genome-scale metabolic modelling for patient stratification, single-cell and spatial metabolomics to resolve intra-tumoral metabolic heterogeneity, and rational combination strategies targeting multiple metabolic nodes simultaneously to preempt adaptive resistance. Integration of circadian pharmacology, host metabolic comorbidity management (obesity, diabetes, gut microbiome modulation), and TME metabolic normalisation into cancer treatment frameworks will drive the next generation of precision metabolic oncology.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Immune cells harbor their own microbiome-derived metabolome: a new layer of immunometabolic regulation.
Frontiers in immunology, 17:1852583.
Current models of microbiome, immune crosstalk center on extracellular receptor-mediated signaling, yet a critical observation challenges this paradigm: intracellular concentrations of gut-derived bacterial metabolites (GDBMs) in CD4[+] T cells do not correlate with paired plasma levels, and it is intracellular, not circulating, GDBM burden that associates with metabolic pathway disruption and immune senescence. Here we propose the concept of an intracellular microbiome metabolome: a pool of aromatic GDBMs actively accumulated through carrier-mediated transport, retained through transcriptional suppression of efflux transporters, and integrated into host metabolic networks where metabolites directly engage intracellular senescence pathways. Using p-cresol sulfate (PCS) as a mechanistic prototype, we provide transcriptomic, proteomic, and metabolomic evidence implicating SLCO4A1/OATP4A1 as the primary entry transporter, whose suppression following PCS exposure creates a feed-forward intracellular retention loop. Once accumulated, PCS functions as a direct agonist of the aryl hydrocarbon receptor (AhR), engaging five downstream effector programs, TGF-β/SMAD signaling, Wnt/β-catenin reprogramming, Foxp3-dependent Treg induction, Notch dysregulation, and PTGS2/COX-2 induction with coordinate HPGD suppression driving PGE2 excess via EP2/EP4/cAMP/CREM, that converge on mTOR suppression, glycolytic collapse, and mitochondrial dysfunction. This metabolic collapse in turn activates the integrated stress response (ISR) as a downstream consequence, driving p16/CDKN2A and p21/CDKN1A induction and the full immunometabolic signature of accelerated CD4[+] T cell aging. The plasma intracellular dissociation explains why circulating GDBM levels have failed to predict immune outcomes in HIV-1 infection, chronic kidney disease, and aging, and positions intracellular GDBM quantification as the biologically relevant exposure metric. We discuss three therapeutic intervention layers: reduction of microbial metabolite production, blockade of SLCO4A1-mediated entry and efflux suppression, and targeting the AhR signaling axis with downstream metabolic and ISR consequences.
Additional Links: PMID-42582102
PubMed:
Citation:
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@article {pmid42582102,
year = {2026},
author = {Daley-Bauer, L and Flantzer, L and Kyu, S and Godoy, A and Weinberg, J and Marconi, VC and Jones, DP and Younes, SA},
title = {Immune cells harbor their own microbiome-derived metabolome: a new layer of immunometabolic regulation.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1852583},
pmid = {42582102},
issn = {1664-3224},
mesh = {*Metabolome/immunology ; Humans ; Cresols/metabolism ; Receptors, Aryl Hydrocarbon/metabolism ; Animals ; Organic Anion Transporters/metabolism ; *Gastrointestinal Microbiome/immunology ; Signal Transduction ; Sulfuric Acid Esters/metabolism ; },
abstract = {Current models of microbiome, immune crosstalk center on extracellular receptor-mediated signaling, yet a critical observation challenges this paradigm: intracellular concentrations of gut-derived bacterial metabolites (GDBMs) in CD4[+] T cells do not correlate with paired plasma levels, and it is intracellular, not circulating, GDBM burden that associates with metabolic pathway disruption and immune senescence. Here we propose the concept of an intracellular microbiome metabolome: a pool of aromatic GDBMs actively accumulated through carrier-mediated transport, retained through transcriptional suppression of efflux transporters, and integrated into host metabolic networks where metabolites directly engage intracellular senescence pathways. Using p-cresol sulfate (PCS) as a mechanistic prototype, we provide transcriptomic, proteomic, and metabolomic evidence implicating SLCO4A1/OATP4A1 as the primary entry transporter, whose suppression following PCS exposure creates a feed-forward intracellular retention loop. Once accumulated, PCS functions as a direct agonist of the aryl hydrocarbon receptor (AhR), engaging five downstream effector programs, TGF-β/SMAD signaling, Wnt/β-catenin reprogramming, Foxp3-dependent Treg induction, Notch dysregulation, and PTGS2/COX-2 induction with coordinate HPGD suppression driving PGE2 excess via EP2/EP4/cAMP/CREM, that converge on mTOR suppression, glycolytic collapse, and mitochondrial dysfunction. This metabolic collapse in turn activates the integrated stress response (ISR) as a downstream consequence, driving p16/CDKN2A and p21/CDKN1A induction and the full immunometabolic signature of accelerated CD4[+] T cell aging. The plasma intracellular dissociation explains why circulating GDBM levels have failed to predict immune outcomes in HIV-1 infection, chronic kidney disease, and aging, and positions intracellular GDBM quantification as the biologically relevant exposure metric. We discuss three therapeutic intervention layers: reduction of microbial metabolite production, blockade of SLCO4A1-mediated entry and efflux suppression, and targeting the AhR signaling axis with downstream metabolic and ISR consequences.},
}
MeSH Terms:
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*Metabolome/immunology
Humans
Cresols/metabolism
Receptors, Aryl Hydrocarbon/metabolism
Animals
Organic Anion Transporters/metabolism
*Gastrointestinal Microbiome/immunology
Signal Transduction
Sulfuric Acid Esters/metabolism
RevDate: 2026-08-12
CmpDate: 2026-08-12
Oral microbiome contribution in colorectal carcinogenesis: polymicrobial interactions and virulence determinants.
Frontiers in cellular and infection microbiology, 16:1887826.
The contribution of the microbiome to sporadic colorectal cancer (CRC) has traditionally been interpreted through the detection of individual tumor-enriched taxa or isolated virulence factors. However, accumulating evidence indicates that CRC-associated microorganisms often act as structured polymicrobial consortia rather than as independent agents. This review proposes an expanded ecological framework for understanding the role of oral taxa in colorectal carcinogenesis. Oral bacteria, including genera Fusobacterium, Parvimonas, Peptostreptococcus, Porphyromonas, Prevotella, Streptococcus, and related taxa, may translocate to the colorectal niche through enteral or hematogenous routes and establish tumor-associated communities that partially recapitulate the structural organization and succession patterns of oral biofilms. Within these communities, Fusobacterium nucleatum serves as the primary bridging organism, facilitating interspecies adhesion and spatial organization. Parvimonas micra, Porphyromonas gingivalis, and Candida albicans display potential bridging structural and functional properties, with their roles in cooperative pathogenicity and tumor progression supported by substantial experimental evidence. We integrate three complementary conceptual frameworks: oral microbial complexes (gut co-abundance groups), bridging organisms and the extended driver-passenger model of CRC. This synthesis supports a shift from taxonomy-centered interpretation toward a functional virulome-based view, in which the role of a taxon is defined by its ecological position, interaction network, and virulence determinants. Key oral virulence factors contribute to biofilm formation, epithelial adhesion and invasion, barrier disruption, immune evasion, inflammatory modulation, metabolic remodeling of the tumor microenvironment, and metastatic potential. Because the composition of translocated oral consortia changes gradually within the colorectal niche, successive consortium members and their associated virulence determinants may serve as indirect microbial signatures of CRC progression. Recognizing CRC-associated oral communities as structured, interactive ecosystems has important diagnostic and therapeutic implications. Simultaneous detection of pathobionts, their cooperative clusters, and functionally relevant virulence determinants may improve microbiome-based risk stratification. Moreover, targeted disruption of bridging functions, interspecies interactions, or virulence factor activity may offer a precision strategy to weaken carcinogenic consortia without broad, dysbiosis-promoting antimicrobial pressure.
Additional Links: PMID-42582119
PubMed:
Citation:
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@article {pmid42582119,
year = {2026},
author = {Glazunova, E and Astakhova, L and Kurnosov, A and Doludin, Y and Lyundup, A and Kostin, A and Makarov, V and Yudin, S and Zlobovskaya, O},
title = {Oral microbiome contribution in colorectal carcinogenesis: polymicrobial interactions and virulence determinants.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1887826},
pmid = {42582119},
issn = {2235-2988},
mesh = {Humans ; *Colorectal Neoplasms/microbiology/pathology ; *Microbiota ; *Mouth/microbiology ; Virulence Factors ; *Microbial Interactions ; *Carcinogenesis ; Virulence ; Biofilms/growth & development ; Bacteria/pathogenicity/classification ; Coinfection/microbiology ; Animals ; },
abstract = {The contribution of the microbiome to sporadic colorectal cancer (CRC) has traditionally been interpreted through the detection of individual tumor-enriched taxa or isolated virulence factors. However, accumulating evidence indicates that CRC-associated microorganisms often act as structured polymicrobial consortia rather than as independent agents. This review proposes an expanded ecological framework for understanding the role of oral taxa in colorectal carcinogenesis. Oral bacteria, including genera Fusobacterium, Parvimonas, Peptostreptococcus, Porphyromonas, Prevotella, Streptococcus, and related taxa, may translocate to the colorectal niche through enteral or hematogenous routes and establish tumor-associated communities that partially recapitulate the structural organization and succession patterns of oral biofilms. Within these communities, Fusobacterium nucleatum serves as the primary bridging organism, facilitating interspecies adhesion and spatial organization. Parvimonas micra, Porphyromonas gingivalis, and Candida albicans display potential bridging structural and functional properties, with their roles in cooperative pathogenicity and tumor progression supported by substantial experimental evidence. We integrate three complementary conceptual frameworks: oral microbial complexes (gut co-abundance groups), bridging organisms and the extended driver-passenger model of CRC. This synthesis supports a shift from taxonomy-centered interpretation toward a functional virulome-based view, in which the role of a taxon is defined by its ecological position, interaction network, and virulence determinants. Key oral virulence factors contribute to biofilm formation, epithelial adhesion and invasion, barrier disruption, immune evasion, inflammatory modulation, metabolic remodeling of the tumor microenvironment, and metastatic potential. Because the composition of translocated oral consortia changes gradually within the colorectal niche, successive consortium members and their associated virulence determinants may serve as indirect microbial signatures of CRC progression. Recognizing CRC-associated oral communities as structured, interactive ecosystems has important diagnostic and therapeutic implications. Simultaneous detection of pathobionts, their cooperative clusters, and functionally relevant virulence determinants may improve microbiome-based risk stratification. Moreover, targeted disruption of bridging functions, interspecies interactions, or virulence factor activity may offer a precision strategy to weaken carcinogenic consortia without broad, dysbiosis-promoting antimicrobial pressure.},
}
MeSH Terms:
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Humans
*Colorectal Neoplasms/microbiology/pathology
*Microbiota
*Mouth/microbiology
Virulence Factors
*Microbial Interactions
*Carcinogenesis
Virulence
Biofilms/growth & development
Bacteria/pathogenicity/classification
Coinfection/microbiology
Animals
RevDate: 2026-08-12
CmpDate: 2026-08-12
Potential plastic biodegradation in lakes worldwide.
Innovation (Cambridge (Mass.)), 7(8):101338.
Plastic pollution is ubiquitous, yet the biodegradation of plastic waste remains poorly understood due to limited knowledge of microbial plastic degradation potential. Here, we demonstrate that plastic waste shapes the global distribution of plastic-degrading potential across 182,661 lakes worldwide using integrated metagenomic and machine learning analyses and identify a tipping point (≥7.44 particles/m[3]) for effective in situ bioremediation. We constructed, for the first time, a catalog of candidate plastic-degrading bacteria, including 15,715 nonredundant enzyme homologs and 4,856 metagenome-assembled genomes. To facilitate future applications, we developed a computational approach to categorizing candidate plastic-degrading bacteria according to their degradation potential, ecological risk, environmental adaptation, and competition capacity. Furthermore, we customized eight template culture media based on the growth factor biosynthesis profiles of high-priority candidate plastic-degrading bacteria. Using these media, we successfully enriched the plastic-degrading microbial communities and isolated a high-priority strain, Serratia ficaria HfyG-1, from Xiazhu Lake, which harbors a wide variety of previously uncharacterized putative degrading enzymes that effectively degrade polylactic acid and polyethylene terephthalate. Our study provides a molecular resource for the bioremediation of plastic-polluted environments worldwide and highlights a proof-of-concept framework for identifying, investigating, and exploiting unknown functional microorganisms for practical applications.
Additional Links: PMID-42582222
PubMed:
Citation:
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@article {pmid42582222,
year = {2026},
author = {Zhang, Q and Zhang, Z and Zhang, Z and Qin, G and Jin, M and Chen, B and Yu, Y and Wang, T and Wang, M and Lu, T and Zhu, D and Cui, L and Qian, H and Rillig, MC and Zhu, YG},
title = {Potential plastic biodegradation in lakes worldwide.},
journal = {Innovation (Cambridge (Mass.))},
volume = {7},
number = {8},
pages = {101338},
pmid = {42582222},
issn = {2666-6758},
abstract = {Plastic pollution is ubiquitous, yet the biodegradation of plastic waste remains poorly understood due to limited knowledge of microbial plastic degradation potential. Here, we demonstrate that plastic waste shapes the global distribution of plastic-degrading potential across 182,661 lakes worldwide using integrated metagenomic and machine learning analyses and identify a tipping point (≥7.44 particles/m[3]) for effective in situ bioremediation. We constructed, for the first time, a catalog of candidate plastic-degrading bacteria, including 15,715 nonredundant enzyme homologs and 4,856 metagenome-assembled genomes. To facilitate future applications, we developed a computational approach to categorizing candidate plastic-degrading bacteria according to their degradation potential, ecological risk, environmental adaptation, and competition capacity. Furthermore, we customized eight template culture media based on the growth factor biosynthesis profiles of high-priority candidate plastic-degrading bacteria. Using these media, we successfully enriched the plastic-degrading microbial communities and isolated a high-priority strain, Serratia ficaria HfyG-1, from Xiazhu Lake, which harbors a wide variety of previously uncharacterized putative degrading enzymes that effectively degrade polylactic acid and polyethylene terephthalate. Our study provides a molecular resource for the bioremediation of plastic-polluted environments worldwide and highlights a proof-of-concept framework for identifying, investigating, and exploiting unknown functional microorganisms for practical applications.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Deep phenotyping of infants and toddlers undergoing food oral immunotherapy (DINOSAUR): design and baseline characteristics of a prospective multi-omics cohort.
Frontiers in allergy, 7:1919415.
BACKGROUND: The mechanisms influencing successful outcomes of oral Immunotherapy (OIT) are poorly understood. This study investigates the role of environmental, microbial, genetic, and immunological factors on the effectiveness of OIT in infants.
OBJECTIVES: To identify biological and environmental mechanisms associated with successful OIT in infants by characterizing longitudinal changes in the microbiome and other multi-omic markers and relating these changes to clinical treatment outcomes.
METHODS: The Deep phenotypINg Of infantS And toddlers Undergoing food oral immunotheRapy (DINOSAUR) study is a prospective cohort study with two groups: infants (<18 months) undergoing OIT, and a comparison group (18-36 months) on the OIT waitlist. In the OIT group, biomaterial (blood, stool, urine, throat and skin swabs, skin tape strips, saliva, and nasal lining samples) and extensive information on environmental exposures has been collected at baseline immediately before initiation of OIT and ongoingly at the end of OIT (exit time-point), and has been collected once in the comparison group (age-matched to the exit time-point). Participant recruitment and sample collection were completed at BC Children's Hospital, Vancouver, Canada. Multi-omics analyses of the collected samples are ongoing and will be reported separately.The primary outcome is changes in the composition and functional profile of the oral- and gut microbiome during infant OIT.
RESULTS: A total of 81 participants with suspicion of food allergy attending the BC Children's Hospital Allergy Clinic between March 2023 and November 2023 were included; 58 infants in the OIT group and 23 children in the age-matched comparison group awaiting OIT. Of the 58 infants, 5 turned out not to have an IgE-mediated allergy. Their samples were archived and regarded as "non-food allergic controls". In the infant group (n = 53), 66% were male, 85% had atopic dermatitis, and 42% were born by cesarean section. The majority (70%) were of Asian descent and lived in an urban environment (90%). The most common allergies were against peanut (51%), egg (40%) and cow's milk (26%).
CONCLUSIONS: This prospective cohort study is the first of its kind to employ a systems biology approach to investigate how extensive biological and environmental factors influence OIT outcomes.
Additional Links: PMID-42582270
PubMed:
Citation:
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@article {pmid42582270,
year = {2026},
author = {Schoos, AM and Skov, FR and Borge, SV and Mak, R and Wong, T and Erdle, SC and Sham, HP and Vallance, BA and Soller, L and Chan, ES},
title = {Deep phenotyping of infants and toddlers undergoing food oral immunotherapy (DINOSAUR): design and baseline characteristics of a prospective multi-omics cohort.},
journal = {Frontiers in allergy},
volume = {7},
number = {},
pages = {1919415},
pmid = {42582270},
issn = {2673-6101},
abstract = {BACKGROUND: The mechanisms influencing successful outcomes of oral Immunotherapy (OIT) are poorly understood. This study investigates the role of environmental, microbial, genetic, and immunological factors on the effectiveness of OIT in infants.
OBJECTIVES: To identify biological and environmental mechanisms associated with successful OIT in infants by characterizing longitudinal changes in the microbiome and other multi-omic markers and relating these changes to clinical treatment outcomes.
METHODS: The Deep phenotypINg Of infantS And toddlers Undergoing food oral immunotheRapy (DINOSAUR) study is a prospective cohort study with two groups: infants (<18 months) undergoing OIT, and a comparison group (18-36 months) on the OIT waitlist. In the OIT group, biomaterial (blood, stool, urine, throat and skin swabs, skin tape strips, saliva, and nasal lining samples) and extensive information on environmental exposures has been collected at baseline immediately before initiation of OIT and ongoingly at the end of OIT (exit time-point), and has been collected once in the comparison group (age-matched to the exit time-point). Participant recruitment and sample collection were completed at BC Children's Hospital, Vancouver, Canada. Multi-omics analyses of the collected samples are ongoing and will be reported separately.The primary outcome is changes in the composition and functional profile of the oral- and gut microbiome during infant OIT.
RESULTS: A total of 81 participants with suspicion of food allergy attending the BC Children's Hospital Allergy Clinic between March 2023 and November 2023 were included; 58 infants in the OIT group and 23 children in the age-matched comparison group awaiting OIT. Of the 58 infants, 5 turned out not to have an IgE-mediated allergy. Their samples were archived and regarded as "non-food allergic controls". In the infant group (n = 53), 66% were male, 85% had atopic dermatitis, and 42% were born by cesarean section. The majority (70%) were of Asian descent and lived in an urban environment (90%). The most common allergies were against peanut (51%), egg (40%) and cow's milk (26%).
CONCLUSIONS: This prospective cohort study is the first of its kind to employ a systems biology approach to investigate how extensive biological and environmental factors influence OIT outcomes.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Gut microbiota dysbiosis in autism spectrum disorder: 10 years of progress on compositional alterations, metabolic/immune mechanisms, and therapeutic strategies.
Frontiers in neuroscience, 20:1873864.
Autism spectrum disorder (ASD) is a common neurodevelopmental condition frequently accompanied by gastrointestinal symptoms, pointing to a potential role of the gut microbiota-brain axis. To explore this connection, the present review synthesizes findings from studies published between 2016 and 2026, including observational studies, meta-analyses, animal experiments, and clinical trials, with the aim of characterizing gut microbiota alterations in ASD, elucidating underlying mechanisms, and evaluating emerging therapeutic strategies. Across diverse populations, the most consistent microbial signatures in ASD include reduced abundances of Bifidobacterium and Akkermansia muciniphila, together with increased abundances of Clostridium, Bacteroides, and Escherichia-Shigella; however, geographic, age-, and sex-specific variations exist. In addition to bacterial changes, the gut virome and mycobiome are also perturbed, as evidenced by enrichment of Candida albicans and Clostridium phages. Mechanistically, these alterations are linked to reduced short-chain fatty acids (especially butyrate), disrupted tryptophan-serotonin metabolism, and elevated neuroinflammatory cytokines (e.g., TNF-α, IL-6). Causal evidence from animal models using fecal microbiota transplantation further demonstrates that ASD microbiota can directly induce autistic-like behaviors. Building on this causal link, early-phase clinical trials indicate that fecal microbiota transplantation, probiotics, prebiotics, and dietary interventions (e.g., ketogenic diet) can improve both gastrointestinal and behavioral symptoms, although larger double-blind, placebo-controlled trials are needed to confirm efficacy. Furthermore, multi-omics integration and host epigenetic signatures show promise for developing non-invasive diagnostic biomarkers. In conclusion, gut dysbiosis plays a causal role in ASD pathophysiology, and microbiome-based interventions represent a rational and potentially transformative therapeutic avenue.
Additional Links: PMID-42582282
PubMed:
Citation:
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@article {pmid42582282,
year = {2026},
author = {Zeng, Y and Wang, F and Li, S and Liu, Q and Liu, L and Song, B},
title = {Gut microbiota dysbiosis in autism spectrum disorder: 10 years of progress on compositional alterations, metabolic/immune mechanisms, and therapeutic strategies.},
journal = {Frontiers in neuroscience},
volume = {20},
number = {},
pages = {1873864},
pmid = {42582282},
issn = {1662-4548},
abstract = {Autism spectrum disorder (ASD) is a common neurodevelopmental condition frequently accompanied by gastrointestinal symptoms, pointing to a potential role of the gut microbiota-brain axis. To explore this connection, the present review synthesizes findings from studies published between 2016 and 2026, including observational studies, meta-analyses, animal experiments, and clinical trials, with the aim of characterizing gut microbiota alterations in ASD, elucidating underlying mechanisms, and evaluating emerging therapeutic strategies. Across diverse populations, the most consistent microbial signatures in ASD include reduced abundances of Bifidobacterium and Akkermansia muciniphila, together with increased abundances of Clostridium, Bacteroides, and Escherichia-Shigella; however, geographic, age-, and sex-specific variations exist. In addition to bacterial changes, the gut virome and mycobiome are also perturbed, as evidenced by enrichment of Candida albicans and Clostridium phages. Mechanistically, these alterations are linked to reduced short-chain fatty acids (especially butyrate), disrupted tryptophan-serotonin metabolism, and elevated neuroinflammatory cytokines (e.g., TNF-α, IL-6). Causal evidence from animal models using fecal microbiota transplantation further demonstrates that ASD microbiota can directly induce autistic-like behaviors. Building on this causal link, early-phase clinical trials indicate that fecal microbiota transplantation, probiotics, prebiotics, and dietary interventions (e.g., ketogenic diet) can improve both gastrointestinal and behavioral symptoms, although larger double-blind, placebo-controlled trials are needed to confirm efficacy. Furthermore, multi-omics integration and host epigenetic signatures show promise for developing non-invasive diagnostic biomarkers. In conclusion, gut dysbiosis plays a causal role in ASD pathophysiology, and microbiome-based interventions represent a rational and potentially transformative therapeutic avenue.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
The impact of human milk oligosaccharides and galacto-oligosaccharides on the growth of early life pathogenic gut bacteria.
Frontiers in microbiology, 17:1854651.
Antibiotics are widely used to prevent and treat early life gut infections, but their aberrant use has raised global concerns about antibiotic resistance. As breastfed infants have fewer intestinal infections than formula-fed infants, this stimulated scientific interest in the anti-pathogenic properties of breastmilk, specifically human milk oligosaccharides (HMOs). HMOs are non-digestible sugars that support infant gut microbiome development, immune maturation, and protection against pathogens. However, to determine how specific HMO structures differentially affect microbial growth and pathogen susceptibility investigating individual HMOs is essential. This study therefore evaluates the effects of single-structure HMOs and galacto-oligosaccharides (GOS) on the growth of key early-life gut pathogens, Escherichia coli, Salmonella enterica, Yersinia enterocolitica, and Clostridium perfringens. The strongest pathogen inhibitory effects of HMOs were further assessed by colony forming unit enumeration and tested across variable media to confirm oligosaccharide-specific efficacy. Oligosaccharide screening revealed clear differences in bacterial growth, with S. enterica most strongly inhibited and C. perfringens exhibiting growth stimulation. Among the tested oligosaccharides, 3'-galactosyllactose and GOS showed the most pronounced growth-inhibitory effects against Escherichia coli, Salmonella enterica, Yersinia enterocolitica. Salt concentration and nutrient richness further modulated oligosaccharide activity, highlighting the multifactorial nature of their antibacterial potential. Overall, our findings show that oligosaccharides display structure-specific and environment-dependent effects on bacterial growth, indicating that their antimicrobial activity is shaped by oligosaccharide structure, bacterial species, and growth environment.
Additional Links: PMID-42582314
PubMed:
Citation:
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@article {pmid42582314,
year = {2026},
author = {Schlösser, JTS and Unger, WWJ and de Bruijn, ACJM and Delsing, DJ and Groeneveld, A and Nauta, A and Folkerts, G and Wösten, MMSM and Braber, S},
title = {The impact of human milk oligosaccharides and galacto-oligosaccharides on the growth of early life pathogenic gut bacteria.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1854651},
pmid = {42582314},
issn = {1664-302X},
abstract = {Antibiotics are widely used to prevent and treat early life gut infections, but their aberrant use has raised global concerns about antibiotic resistance. As breastfed infants have fewer intestinal infections than formula-fed infants, this stimulated scientific interest in the anti-pathogenic properties of breastmilk, specifically human milk oligosaccharides (HMOs). HMOs are non-digestible sugars that support infant gut microbiome development, immune maturation, and protection against pathogens. However, to determine how specific HMO structures differentially affect microbial growth and pathogen susceptibility investigating individual HMOs is essential. This study therefore evaluates the effects of single-structure HMOs and galacto-oligosaccharides (GOS) on the growth of key early-life gut pathogens, Escherichia coli, Salmonella enterica, Yersinia enterocolitica, and Clostridium perfringens. The strongest pathogen inhibitory effects of HMOs were further assessed by colony forming unit enumeration and tested across variable media to confirm oligosaccharide-specific efficacy. Oligosaccharide screening revealed clear differences in bacterial growth, with S. enterica most strongly inhibited and C. perfringens exhibiting growth stimulation. Among the tested oligosaccharides, 3'-galactosyllactose and GOS showed the most pronounced growth-inhibitory effects against Escherichia coli, Salmonella enterica, Yersinia enterocolitica. Salt concentration and nutrient richness further modulated oligosaccharide activity, highlighting the multifactorial nature of their antibacterial potential. Overall, our findings show that oligosaccharides display structure-specific and environment-dependent effects on bacterial growth, indicating that their antimicrobial activity is shaped by oligosaccharide structure, bacterial species, and growth environment.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Optimal transport analysis of high-dimensional flow cytometry data in immuno-oncology.
Frontiers in immunology, 17:1856896.
INTRODUCTION: Advances in single-cell and spatial profiling have enabled detailed characterization of heterogeneous samples, but analyzing this data remains challenging in settings involving multiple comparisons. While tools like UMAP and t-SNE are valuable for visualization, their stochastic, parameter-sensitive nature limits their use in longitudinal comparisons, treatment group analysis, and multicenter trials. Although OT was first described in the 19th century, the Sinkhorn algorithm makes it computationally tractable for high-dimensional data. By directly comparing distributions of cellular states, OT provides reproducible measures of change in high-dimensional space. This framework is amenable to integration with machine learning, including deep generative models.
METHODS: OT was applied to longitudinal data from a phase I trial of tocilizumab for cavitary malignancies (NCT06016179). The current implementation makes use of expert-guided phenotypic population definitions and their relationships. An OT-based graph representation was created for baseline and follow-up samples. The graph layout was fixed across samples and computed from phenotypic relationships. In this implementation vertex radii are proportional to their relative abundance, allowing for rapid visual assessment of population-level increases and decreases. Graph edge thickness and color encode inter-population similarity based on the optimal transport (Sinkhorn) distance between marker expression distributions.
RESULTS: This representation enabled rapid identification of populations undergoing substantial change, such as the CD8+/IFNɣ+ population, which decreased from 63% to 17% of CD8+ T cells following treatment. Population changes across all fluorescence parameters were encoded in the graph edit distance (GED), which captures changes in population abundance and phenotypic shifts in marker space.
DISCUSSION: Future implementations can combine this expert-guided approach with unbiased clustering algorithms to enhance scalability and cross-platform harmonization. In our recently initiated clinical trials, we will apply OT to identify key shifts in tumor, immune, and stromal cell states, summarizing patient trajectories and quantitatively supporting predictive models of treatment response. Potential applications include quantifying residual disease after chemotherapy, tracking immune activation during immunotherapy, and linking host-microbiome interactions to disease progression. This approach overcomes the limitations of traditional, local-structure-optimized tools (UMAP or t-SNE) to provide a comprehensive, longitudinal view of tumor evolution and treatment response.
Additional Links: PMID-42582472
PubMed:
Citation:
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@article {pmid42582472,
year = {2026},
author = {Sanjana Shemonti, A and Wang, JC and Donnenberg, AD and Rajwa, B and Wagner, PL and Bartlett, DL and Popov, B and Alicuben, ET and Donnenberg, VS},
title = {Optimal transport analysis of high-dimensional flow cytometry data in immuno-oncology.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1856896},
pmid = {42582472},
issn = {1664-3224},
mesh = {Humans ; *Flow Cytometry/methods ; Algorithms ; Machine Learning ; },
abstract = {INTRODUCTION: Advances in single-cell and spatial profiling have enabled detailed characterization of heterogeneous samples, but analyzing this data remains challenging in settings involving multiple comparisons. While tools like UMAP and t-SNE are valuable for visualization, their stochastic, parameter-sensitive nature limits their use in longitudinal comparisons, treatment group analysis, and multicenter trials. Although OT was first described in the 19th century, the Sinkhorn algorithm makes it computationally tractable for high-dimensional data. By directly comparing distributions of cellular states, OT provides reproducible measures of change in high-dimensional space. This framework is amenable to integration with machine learning, including deep generative models.
METHODS: OT was applied to longitudinal data from a phase I trial of tocilizumab for cavitary malignancies (NCT06016179). The current implementation makes use of expert-guided phenotypic population definitions and their relationships. An OT-based graph representation was created for baseline and follow-up samples. The graph layout was fixed across samples and computed from phenotypic relationships. In this implementation vertex radii are proportional to their relative abundance, allowing for rapid visual assessment of population-level increases and decreases. Graph edge thickness and color encode inter-population similarity based on the optimal transport (Sinkhorn) distance between marker expression distributions.
RESULTS: This representation enabled rapid identification of populations undergoing substantial change, such as the CD8+/IFNɣ+ population, which decreased from 63% to 17% of CD8+ T cells following treatment. Population changes across all fluorescence parameters were encoded in the graph edit distance (GED), which captures changes in population abundance and phenotypic shifts in marker space.
DISCUSSION: Future implementations can combine this expert-guided approach with unbiased clustering algorithms to enhance scalability and cross-platform harmonization. In our recently initiated clinical trials, we will apply OT to identify key shifts in tumor, immune, and stromal cell states, summarizing patient trajectories and quantitatively supporting predictive models of treatment response. Potential applications include quantifying residual disease after chemotherapy, tracking immune activation during immunotherapy, and linking host-microbiome interactions to disease progression. This approach overcomes the limitations of traditional, local-structure-optimized tools (UMAP or t-SNE) to provide a comprehensive, longitudinal view of tumor evolution and treatment response.},
}
MeSH Terms:
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Humans
*Flow Cytometry/methods
Algorithms
Machine Learning
RevDate: 2026-08-12
CmpDate: 2026-08-12
Editorial: Plant mineral microbe interactions, vol II.
Frontiers in microbiology, 17:1903162.
Additional Links: PMID-42582592
PubMed:
Citation:
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@article {pmid42582592,
year = {2026},
author = {Mumtaz, MZ and Bouizgarne, B and Castellane, TCL and Tamburini, E},
title = {Editorial: Plant mineral microbe interactions, vol II.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1903162},
pmid = {42582592},
issn = {1664-302X},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Domestication shapes the gut microbial structure and metabolic function in felids: a metagenomic study of wild and domestic cats.
Frontiers in microbiology, 17:1828152.
INTRODUCTION: The domestication process has profoundly altered the dietary patterns and living conditions of cats, with corresponding effects on their gut microbiome.
METHODS: This study compared the gut microbiota composition and metabolic functions between wild felids (Otocolobus manul and Felis bieti) and domestic cats using metagenomic sequencing.
RESULTS: Taxonomic analysis revealed significantly higher microbial alpha diversity and distinct community structure in wild felids compared to domestic cats. The gut microbiota of domestic cats was characterized by a higher relative abundance of Bacteroidota (when compared to F. bieti) and of Pseudomonadota, Uroviricota, and Cyanobacteriota, as well as an enrichment of carbohydrate-associated genera such as Segatella. In contrast, wild felids exhibited enrichment of potential pathogens (e.g., Clostridium perfringens, Escherichia coli) and genera including Clostridium and Fusobacterium, alongside a higher abundance of microbial genes linked to protein degradation and fermentation. Functional metagenomic analysis further identified consistent differences in microbial metabolic potential across both wild species comparisons. Wild felids showed higher abundances of genes involved in butyrate production, lysine degradation, and de novo synthesis of vitamins and cofactors. Domestic cats, in contrast, exhibited enrichment of genes for plant polysaccharide hydrolysis, ketone body formation, aromatic amino acid biosynthesis, and salvage of folate derivatives.
DISCUSSION: These results suggest that domestication is associated with a shift in the gut microbial functional repertoire - from a butyrogenic, protein-catabolic, and de novo-synthesizing profile in wild felids toward a more carbohydrate-hydrolyzing, ketogenic, and salvage-oriented profile in domestic cats, reflecting dietary and environmental adaptations.
Additional Links: PMID-42582600
PubMed:
Citation:
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@article {pmid42582600,
year = {2026},
author = {Chen, J and Fan, W and Chen, X and Zhang, H and Feng, M and He, S and Song, C and Wang, J},
title = {Domestication shapes the gut microbial structure and metabolic function in felids: a metagenomic study of wild and domestic cats.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1828152},
pmid = {42582600},
issn = {1664-302X},
abstract = {INTRODUCTION: The domestication process has profoundly altered the dietary patterns and living conditions of cats, with corresponding effects on their gut microbiome.
METHODS: This study compared the gut microbiota composition and metabolic functions between wild felids (Otocolobus manul and Felis bieti) and domestic cats using metagenomic sequencing.
RESULTS: Taxonomic analysis revealed significantly higher microbial alpha diversity and distinct community structure in wild felids compared to domestic cats. The gut microbiota of domestic cats was characterized by a higher relative abundance of Bacteroidota (when compared to F. bieti) and of Pseudomonadota, Uroviricota, and Cyanobacteriota, as well as an enrichment of carbohydrate-associated genera such as Segatella. In contrast, wild felids exhibited enrichment of potential pathogens (e.g., Clostridium perfringens, Escherichia coli) and genera including Clostridium and Fusobacterium, alongside a higher abundance of microbial genes linked to protein degradation and fermentation. Functional metagenomic analysis further identified consistent differences in microbial metabolic potential across both wild species comparisons. Wild felids showed higher abundances of genes involved in butyrate production, lysine degradation, and de novo synthesis of vitamins and cofactors. Domestic cats, in contrast, exhibited enrichment of genes for plant polysaccharide hydrolysis, ketone body formation, aromatic amino acid biosynthesis, and salvage of folate derivatives.
DISCUSSION: These results suggest that domestication is associated with a shift in the gut microbial functional repertoire - from a butyrogenic, protein-catabolic, and de novo-synthesizing profile in wild felids toward a more carbohydrate-hydrolyzing, ketogenic, and salvage-oriented profile in domestic cats, reflecting dietary and environmental adaptations.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Temporal and Functional Profiling of the Microbiome of High and Low Nitrogen Content Barley Seed in Silo Storage.
Food science & nutrition, 14(8):e72179.
Barley grain quality is influenced by nitrogen content and storage conditions; however, their impact on the composition and function of the grain microbiome is not well understood. This study combined metataxonomic (16S rRNA and ITS) profiling, metagenome sequencing, and metaproteome analyses to characterize the structure and function of the barley grain microbiome. Grains with high (> 1.5%) and low (< 1.5%) nitrogen content from a single barley cultivar (Kadie) were sampled at harvest and after 3, 6, and 9 months of storage. Amplicon sequencing revealed a community dominated by Proteobacteria, Firmicutes, and Ascomycota, while metagenomics confirmed the abundance of genera such as Erwinia, Pantoea, and Pseudomonas, aligning with previous reports of barley endophytes. While a consistent set of core microbial genera was identified, their relative abundances varied throughout storage. Metagenomic analysis revealed the high-nitrogen grain microbiome had potential for rapid metabolic activity that declined post-harvest, whereas the low nitrogen grain community sustained prolonged metabolic potential. Metaproteomics confirmed that these functional shifts revealed a temporal transition from active growth to stress tolerance. Findings from this work contribute to a better understanding of the barley grain microbiome during prolonged storage, offering insights that could help optimize storage for malting and brewing.
Additional Links: PMID-42582632
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@article {pmid42582632,
year = {2026},
author = {Tshisekedi, KA and Van Den Bossche, T and Martens, L and De Maayer, P and Botes, A},
title = {Temporal and Functional Profiling of the Microbiome of High and Low Nitrogen Content Barley Seed in Silo Storage.},
journal = {Food science & nutrition},
volume = {14},
number = {8},
pages = {e72179},
pmid = {42582632},
issn = {2048-7177},
abstract = {Barley grain quality is influenced by nitrogen content and storage conditions; however, their impact on the composition and function of the grain microbiome is not well understood. This study combined metataxonomic (16S rRNA and ITS) profiling, metagenome sequencing, and metaproteome analyses to characterize the structure and function of the barley grain microbiome. Grains with high (> 1.5%) and low (< 1.5%) nitrogen content from a single barley cultivar (Kadie) were sampled at harvest and after 3, 6, and 9 months of storage. Amplicon sequencing revealed a community dominated by Proteobacteria, Firmicutes, and Ascomycota, while metagenomics confirmed the abundance of genera such as Erwinia, Pantoea, and Pseudomonas, aligning with previous reports of barley endophytes. While a consistent set of core microbial genera was identified, their relative abundances varied throughout storage. Metagenomic analysis revealed the high-nitrogen grain microbiome had potential for rapid metabolic activity that declined post-harvest, whereas the low nitrogen grain community sustained prolonged metabolic potential. Metaproteomics confirmed that these functional shifts revealed a temporal transition from active growth to stress tolerance. Findings from this work contribute to a better understanding of the barley grain microbiome during prolonged storage, offering insights that could help optimize storage for malting and brewing.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Molecular mechanisms of bacteria-mediated cancer immunotherapy: from intratumoral microbiota to engineered therapeutics.
Frontiers in immunology, 17:1878878.
Immunotherapy has redefined oncology, yet its efficacy remains constrained by low response rates, primary or acquired resistance, immune-related toxicities, and escalating costs. Bacteria-mediated cancer immunotherapy (BCIT), which exploits the intratumoral microbiota as a programmable immunotherapeutic platform, has therefore emerged as a promising strategy. Although anecdotal links between infection and tumor regression were documented over four millennia ago, the molecular underpinnings of BCIT have only recently become accessible through synthetic biology, single-cell sequencing, and gnotobiotic modeling. Here we synthesize current knowledge on how intratumoral bacteria either enhance or suppress malignancy via genotoxicity, epigenetic reprogramming, metabolic competition, and modulation of the tumor-immune interface. We dissect cutting-edge engineering approaches-quorum-sensing circuits, thermo-inducible switches, molecular mimicry, and biohybrid microrobots, that convert commensal or attenuated pathogenic strains into precision delivery vehicles for cytokines, checkpoint inhibitors, and neoantigens. Finally, we critically evaluate translational bottlenecks (safety, pharmacokinetics, regulatory science, inter-patient heterogeneity) and propose an AI-guided, microbiome-integrated framework to accelerate clinical translation. This Review provides a conceptual framework for harnessing living therapeutics to convert immunologically "cold" tumors into "hot", therapy-sensitive lesions, and discusses key directions for future microbiome-driven oncology trials.
Additional Links: PMID-42582890
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@article {pmid42582890,
year = {2026},
author = {Guo, J and Li, Y and Yang, Y and Wang, B},
title = {Molecular mechanisms of bacteria-mediated cancer immunotherapy: from intratumoral microbiota to engineered therapeutics.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1878878},
pmid = {42582890},
issn = {1664-3224},
mesh = {Humans ; *Immunotherapy/methods ; *Neoplasms/therapy/immunology/microbiology ; Animals ; *Microbiota/immunology ; *Bacteria/immunology ; Tumor Microenvironment/immunology ; },
abstract = {Immunotherapy has redefined oncology, yet its efficacy remains constrained by low response rates, primary or acquired resistance, immune-related toxicities, and escalating costs. Bacteria-mediated cancer immunotherapy (BCIT), which exploits the intratumoral microbiota as a programmable immunotherapeutic platform, has therefore emerged as a promising strategy. Although anecdotal links between infection and tumor regression were documented over four millennia ago, the molecular underpinnings of BCIT have only recently become accessible through synthetic biology, single-cell sequencing, and gnotobiotic modeling. Here we synthesize current knowledge on how intratumoral bacteria either enhance or suppress malignancy via genotoxicity, epigenetic reprogramming, metabolic competition, and modulation of the tumor-immune interface. We dissect cutting-edge engineering approaches-quorum-sensing circuits, thermo-inducible switches, molecular mimicry, and biohybrid microrobots, that convert commensal or attenuated pathogenic strains into precision delivery vehicles for cytokines, checkpoint inhibitors, and neoantigens. Finally, we critically evaluate translational bottlenecks (safety, pharmacokinetics, regulatory science, inter-patient heterogeneity) and propose an AI-guided, microbiome-integrated framework to accelerate clinical translation. This Review provides a conceptual framework for harnessing living therapeutics to convert immunologically "cold" tumors into "hot", therapy-sensitive lesions, and discusses key directions for future microbiome-driven oncology trials.},
}
MeSH Terms:
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Humans
*Immunotherapy/methods
*Neoplasms/therapy/immunology/microbiology
Animals
*Microbiota/immunology
*Bacteria/immunology
Tumor Microenvironment/immunology
RevDate: 2026-08-12
CmpDate: 2026-08-12
Editorial: Women in avian physiology 2025.
Frontiers in physiology, 17:1912029.
Additional Links: PMID-42582907
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@article {pmid42582907,
year = {2026},
author = {Velleman, SG and Pierzchala-Koziec, K},
title = {Editorial: Women in avian physiology 2025.},
journal = {Frontiers in physiology},
volume = {17},
number = {},
pages = {1912029},
doi = {10.3389/fphys.2026.1912029},
pmid = {42582907},
issn = {1664-042X},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Early-life microbiome trajectories as biomarkers to predict health outcomes.
Microbiome research reports, 5(2):15.
The early-life gut microbiome is tightly linked to different aspects of infant development. Microbial colonisation patterns have been repeatedly shown to play a role in a variety of paediatric outcomes, ranging from metabolism and immune function to neurodevelopment. Concomitantly, the identification of early-life biomarkers is crucial, especially considering that for various conditions, reliable diagnostic tools only emerge in early childhood. As such, microbiome data collected in the first two years of life may offer valuable prospects for early detection, prevention, quantification or even correction of adverse health trajectories. With the increasing availability of high-resolution microbiome data, researchers are leveraging both traditional statistical approaches and machine learning (ML) methods to analyse the evolution of these complex microbial communities. While statistical models are well-suited for identifying associations between microbiome features and health states, ML methods allow for predicting health outcomes from those features. This review explores the role of the early-life gut microbiome in infant health and development, with a focus on how data acquisition and analytical methods can shape current knowledge. We contrast statistical approaches with ML methods, summarising key findings on microbial succession and factors influencing it. By addressing current challenges and identifying areas for methodological refinement, we aim to discuss the potential of the microbiome in the assessment of current and future health states of an individual and aid in the development of more robust, clinically-relevant models for paediatric care.
Additional Links: PMID-42583000
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@article {pmid42583000,
year = {2026},
author = {Joos, R and Lavelle, A and Dempsey, E and Stanton, C and Ross, RP},
title = {Early-life microbiome trajectories as biomarkers to predict health outcomes.},
journal = {Microbiome research reports},
volume = {5},
number = {2},
pages = {15},
pmid = {42583000},
issn = {2771-5965},
abstract = {The early-life gut microbiome is tightly linked to different aspects of infant development. Microbial colonisation patterns have been repeatedly shown to play a role in a variety of paediatric outcomes, ranging from metabolism and immune function to neurodevelopment. Concomitantly, the identification of early-life biomarkers is crucial, especially considering that for various conditions, reliable diagnostic tools only emerge in early childhood. As such, microbiome data collected in the first two years of life may offer valuable prospects for early detection, prevention, quantification or even correction of adverse health trajectories. With the increasing availability of high-resolution microbiome data, researchers are leveraging both traditional statistical approaches and machine learning (ML) methods to analyse the evolution of these complex microbial communities. While statistical models are well-suited for identifying associations between microbiome features and health states, ML methods allow for predicting health outcomes from those features. This review explores the role of the early-life gut microbiome in infant health and development, with a focus on how data acquisition and analytical methods can shape current knowledge. We contrast statistical approaches with ML methods, summarising key findings on microbial succession and factors influencing it. By addressing current challenges and identifying areas for methodological refinement, we aim to discuss the potential of the microbiome in the assessment of current and future health states of an individual and aid in the development of more robust, clinically-relevant models for paediatric care.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Gut microbiome metabolism of plant phenolic glycosides and its relationship with human health.
Microbiome research reports, 5(3):17.
Additional Links: PMID-42583032
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@article {pmid42583032,
year = {2026},
author = {de Los Reyes-Gavilán, CG and Salazar, N},
title = {Gut microbiome metabolism of plant phenolic glycosides and its relationship with human health.},
journal = {Microbiome research reports},
volume = {5},
number = {3},
pages = {17},
pmid = {42583032},
issn = {2771-5965},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
The gut virome and regulatory T cell axis in health and systemic disease.
Microbiome research reports, 5(2):14.
The gut virome, comprising bacteriophages and eukaryotic viruses, represents a complex and dynamic component of the intestinal microbiome whose functional significance has long been underestimated. Emerging evidence highlights the gut virome as a pivotal modulator of the host immune system, particularly in regulating the balance and function of regulatory T cells (Tregs), which are essential for maintaining immune homeostasis. This review distinguishes two mechanistic axes by which the virome influences Tregs: (i) an indirect 'virome-bacteriome-metabolite-Treg axis', and (ii) a direct 'viral pathogen-associated molecular patterns (PAMPs)-pattern recognition receptors (PRRs)-Treg' signaling axis. This review comprehensively examines the dualistic role of the gut virome in preserving intestinal equilibrium and its involvement in the pathogenesis or amelioration of intestinal inflammatory disorders such as inflammatory bowel disease (IBD). Furthermore, the influence of the gut virome extends beyond the gut, potentially impacting systemic immune-related diseases. By integrating recent advances in metagenomics, viromics, and immunology, we elucidate the molecular mechanisms through which the gut virome orchestrates immune regulation. This synthesis aims to provide a comprehensive understanding of the gut virome as a critical immune regulator and to explore its potential as a biomarker for disease diagnosis and a novel target for therapeutic intervention.
Additional Links: PMID-42583033
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Citation:
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@article {pmid42583033,
year = {2026},
author = {Bi, D and Yu, S and Zhang, M and Huang, Y and Dou, Z and Tian, B and Lu, J},
title = {The gut virome and regulatory T cell axis in health and systemic disease.},
journal = {Microbiome research reports},
volume = {5},
number = {2},
pages = {14},
pmid = {42583033},
issn = {2771-5965},
abstract = {The gut virome, comprising bacteriophages and eukaryotic viruses, represents a complex and dynamic component of the intestinal microbiome whose functional significance has long been underestimated. Emerging evidence highlights the gut virome as a pivotal modulator of the host immune system, particularly in regulating the balance and function of regulatory T cells (Tregs), which are essential for maintaining immune homeostasis. This review distinguishes two mechanistic axes by which the virome influences Tregs: (i) an indirect 'virome-bacteriome-metabolite-Treg axis', and (ii) a direct 'viral pathogen-associated molecular patterns (PAMPs)-pattern recognition receptors (PRRs)-Treg' signaling axis. This review comprehensively examines the dualistic role of the gut virome in preserving intestinal equilibrium and its involvement in the pathogenesis or amelioration of intestinal inflammatory disorders such as inflammatory bowel disease (IBD). Furthermore, the influence of the gut virome extends beyond the gut, potentially impacting systemic immune-related diseases. By integrating recent advances in metagenomics, viromics, and immunology, we elucidate the molecular mechanisms through which the gut virome orchestrates immune regulation. This synthesis aims to provide a comprehensive understanding of the gut virome as a critical immune regulator and to explore its potential as a biomarker for disease diagnosis and a novel target for therapeutic intervention.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Storage-associated shifts in the raw boar seminal microbiome at 17 °C.
Frontiers in veterinary science, 13:1872476.
This study addresses the relevance of the bacterial seminal microbiome in boars, considering that bacterial compositional changes during liquid semen storage may affect sperm quality and limit the efficiency of artificial insemination. The objective was to characterize temporal changes in the seminal microbiota composition of raw boar semen incubated at 17 °C for 12 days. For this purpose, six ejaculates from Landrace boars used as artificial insemination donors were analyzed, with samples evaluated on days 1, 4, 8, and 12 through DNA extraction, amplification of the V3-V4 region of the 16S rRNA gene, and Illumina MiSeq sequencing. The results showed a progressive reduction in bacterial richness and diversity during storage, with a transition from an initially heterogeneous community, mainly represented by Proteobacteria, Firmicutes, Bacteroidota, and Actinobacteriota, toward low-complexity communities relatively dominated by opportunistic taxa such as Pseudomonas, Escherichia-Shigella, Enterococcus, and Bacteroides. Overall, the study concludes that storage at 17 °C is associated with relative compositional shifts in the raw seminal microbiome toward potentially detrimental bacterial profiles, providing a baseline for understanding the dynamics of the seminal microbiota and supporting the development of more targeted and sustainable antimicrobial strategies for porcine semen preservation.
Additional Links: PMID-42583056
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Citation:
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@article {pmid42583056,
year = {2026},
author = {Carrasco-Zambrano, N and Leal, K and Machuca, J and Núñez-Montero, K and Pezo, F and Contreras, MJ},
title = {Storage-associated shifts in the raw boar seminal microbiome at 17 °C.},
journal = {Frontiers in veterinary science},
volume = {13},
number = {},
pages = {1872476},
pmid = {42583056},
issn = {2297-1769},
abstract = {This study addresses the relevance of the bacterial seminal microbiome in boars, considering that bacterial compositional changes during liquid semen storage may affect sperm quality and limit the efficiency of artificial insemination. The objective was to characterize temporal changes in the seminal microbiota composition of raw boar semen incubated at 17 °C for 12 days. For this purpose, six ejaculates from Landrace boars used as artificial insemination donors were analyzed, with samples evaluated on days 1, 4, 8, and 12 through DNA extraction, amplification of the V3-V4 region of the 16S rRNA gene, and Illumina MiSeq sequencing. The results showed a progressive reduction in bacterial richness and diversity during storage, with a transition from an initially heterogeneous community, mainly represented by Proteobacteria, Firmicutes, Bacteroidota, and Actinobacteriota, toward low-complexity communities relatively dominated by opportunistic taxa such as Pseudomonas, Escherichia-Shigella, Enterococcus, and Bacteroides. Overall, the study concludes that storage at 17 °C is associated with relative compositional shifts in the raw seminal microbiome toward potentially detrimental bacterial profiles, providing a baseline for understanding the dynamics of the seminal microbiota and supporting the development of more targeted and sustainable antimicrobial strategies for porcine semen preservation.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Biological features of squamous cell carcinoma of the anus-a deep dive review.
ESMO gastrointestinal oncology, 13(Pt A):100157.
Squamous cell carcinoma of the anus (SCCA) is a human papillomavirus (HPV)-associated cancer with an increasing incidence. Localized disease is treated curatively with chemoradiotherapy (CRT) but has substantial toxicities and impact on quality of life. Despite increasing research over the past decade, much of our biological understanding of SCCA is extrapolated from other HPV-associated cancers. Recently launched initiatives aim to connect clinicians and basic researchers working in SCCA to foster collaboration and knowledge sharing and facilitate access to SCCA materials. To improve outcomes for SCCA patients, a better understanding of SCCA-specific biology is required. This review will discuss areas of SCCA biology that are important to developing targets for drug development and biomarker-based individualized precision treatment. It will discuss the current understanding of radiosensitivity, differences in HPV-positive versus HPV-negative disease, hypoxia, immune environment, molecular characteristics, circulating tumor HPV-DNA, and the microbiome. It will detail when this understanding has been extrapolated from other HPV-associated cancers. Finally, it will discuss our current and upcoming preclinical biological models and discuss future models needed to further our understanding of SCCA biology.
Additional Links: PMID-42583088
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Citation:
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@article {pmid42583088,
year = {2026},
author = {Samuel, RJ and Winder, N and Busk, M and Lycke Wind, K and Guerra, G and Heriot, AG and Gilbert, DC and Macdonald, A and Garm Spindler, KL},
title = {Biological features of squamous cell carcinoma of the anus-a deep dive review.},
journal = {ESMO gastrointestinal oncology},
volume = {13},
number = {Pt A},
pages = {100157},
pmid = {42583088},
issn = {2949-8198},
abstract = {Squamous cell carcinoma of the anus (SCCA) is a human papillomavirus (HPV)-associated cancer with an increasing incidence. Localized disease is treated curatively with chemoradiotherapy (CRT) but has substantial toxicities and impact on quality of life. Despite increasing research over the past decade, much of our biological understanding of SCCA is extrapolated from other HPV-associated cancers. Recently launched initiatives aim to connect clinicians and basic researchers working in SCCA to foster collaboration and knowledge sharing and facilitate access to SCCA materials. To improve outcomes for SCCA patients, a better understanding of SCCA-specific biology is required. This review will discuss areas of SCCA biology that are important to developing targets for drug development and biomarker-based individualized precision treatment. It will discuss the current understanding of radiosensitivity, differences in HPV-positive versus HPV-negative disease, hypoxia, immune environment, molecular characteristics, circulating tumor HPV-DNA, and the microbiome. It will detail when this understanding has been extrapolated from other HPV-associated cancers. Finally, it will discuss our current and upcoming preclinical biological models and discuss future models needed to further our understanding of SCCA biology.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Adolescent Dietary Supplementation of Omega-3 Polyunsaturated Fatty Acids Alleviates PTSD-Like Fear Memory and Affective Dysregulation in Rats.
Smart medicine, 5(4):e70049.
Post-traumatic stress disorder (PTSD) is a debilitating psychiatric disorder affecting approximately 3.9% of individuals worldwide over their lifetimes. Since adolescence is characterized by ongoing brain maturation and increased responsiveness to environmental stressors, this developmental stage may provide an important window for PTSD intervention. Growing evidence supports an association between ω-3 polyunsaturated fatty acids (PUFAs), especially docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), and the restoration of stress-induced neural damage. However, how ω-3 PUFA supplementation during adolescence affects adult susceptibility to PTSD remains poorly understood. Here, we observed significantly reduced DHA and EPA concentrations in the prefrontal cortex (PFC) and serum of PTSD-susceptible rats. Providing 1.2% DHA and EPA in the adolescent diet significantly reduced PTSD-like phenotypes in adulthood, including excessive fear memory retention, depressive-like and anxiety-like behaviors, while also reducing serum levels of proinflammatory cytokines. These phenotypic and inflammatory improvements were associated with changes in the gut microbiome, including its composition and diversity. DHA/EPA supplementation was also linked to alterations in multiple lipid species, with serum phosphatidylcholine levels showing a significant correlation with fear memory expression. Moreover, we observed dysregulation of the PI3K/AKT/mTOR pathway in the PFC of PTSD-like rats, which was less pronounced in DHA/EPA-supplemented animals. Collectively, these findings provide the first evidence relating adolescent ω-3 PUFA status to PTSD-like phenotypes in adulthood. It further identifies that gut microbiota composition, lipid metabolic profiles (notably phosphatidylcholine), and prefrontal PI3K/AKT/mTOR signaling are correlated with these behavioral outcomes, suggesting that these systems may collectively contribute to trauma resilience.
Additional Links: PMID-42583101
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@article {pmid42583101,
year = {2026},
author = {Li, W and Yin, Y and Li, J and Yao, Z and Wang, S and Jin, Y and Bian, L and Guo, J},
title = {Adolescent Dietary Supplementation of Omega-3 Polyunsaturated Fatty Acids Alleviates PTSD-Like Fear Memory and Affective Dysregulation in Rats.},
journal = {Smart medicine},
volume = {5},
number = {4},
pages = {e70049},
pmid = {42583101},
issn = {2751-1871},
abstract = {Post-traumatic stress disorder (PTSD) is a debilitating psychiatric disorder affecting approximately 3.9% of individuals worldwide over their lifetimes. Since adolescence is characterized by ongoing brain maturation and increased responsiveness to environmental stressors, this developmental stage may provide an important window for PTSD intervention. Growing evidence supports an association between ω-3 polyunsaturated fatty acids (PUFAs), especially docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), and the restoration of stress-induced neural damage. However, how ω-3 PUFA supplementation during adolescence affects adult susceptibility to PTSD remains poorly understood. Here, we observed significantly reduced DHA and EPA concentrations in the prefrontal cortex (PFC) and serum of PTSD-susceptible rats. Providing 1.2% DHA and EPA in the adolescent diet significantly reduced PTSD-like phenotypes in adulthood, including excessive fear memory retention, depressive-like and anxiety-like behaviors, while also reducing serum levels of proinflammatory cytokines. These phenotypic and inflammatory improvements were associated with changes in the gut microbiome, including its composition and diversity. DHA/EPA supplementation was also linked to alterations in multiple lipid species, with serum phosphatidylcholine levels showing a significant correlation with fear memory expression. Moreover, we observed dysregulation of the PI3K/AKT/mTOR pathway in the PFC of PTSD-like rats, which was less pronounced in DHA/EPA-supplemented animals. Collectively, these findings provide the first evidence relating adolescent ω-3 PUFA status to PTSD-like phenotypes in adulthood. It further identifies that gut microbiota composition, lipid metabolic profiles (notably phosphatidylcholine), and prefrontal PI3K/AKT/mTOR signaling are correlated with these behavioral outcomes, suggesting that these systems may collectively contribute to trauma resilience.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Gut microbiota and serum metabolome in children with human metapneumovirus infection.
Frontiers in immunology, 17:1855983.
OBJECTIVE: To analyze the alterations in gut microbiota structure and serum metabolic profiles of children with human metapneumovirus (hMPV) infection using 16S rRNA high-throughput sequencing and liquid chromatography-mass spectrometry (LC-MS)-based untargeted metabolomics. Through integrated multi-omics analysis, we aim to explore the correlation between gut microbiota dysbiosis and host metabolic disorder, provide preliminary evidence for potential intervention targets, and offer primary clues for the development of preventive and therapeutic strategies including probiotic supplementation and metabolic pathway regulation.
METHODS: This study enrolled 42 children with hMPV infection and 12 healthy controls. Fecal samples were collected for gut microbiota analysis using 16S rRNA gene sequencing, and serum samples were obtained for metabolomic profiling via LC-MS. Various bioinformatics approaches were applied for independent analysis of microbiome and metabolome data, followed by integrated multi-omics analysis.
RESULTS: The microbial community structure of the hMPV-infected group was clearly separated from that of the healthy control group. Opportunistic pathogens such as Finegoldia, Anaerococcus, and Peptoniphilus were enriched, while beneficial commensals including Bifidobacterium, Blautia, and Faecalibacterium were reduced. Serum metabolic profiles showed global divergence between the two groups, with 558 upregulated and 213 downregulated metabolites identified. Using a VIP threshold >1.5, 24 core differential metabolites were ultimately selected. KEGG enrichment and MetPA topological analyses revealed that these differential metabolites were mainly enriched in pathways including glycerophospholipid metabolism, nucleotide metabolism, alpha-linolenic acid metabolism, and arachidonic acid metabolism. Correlation analysis showed that beneficial commensals with reduced abundance in the infected group, such as Bifidobacterium and Blautia, were positively correlated with anti-inflammatory and barrier-protective metabolites (e.g., alpha-linolenic acid, 11,12-DiHETrE, GPCho(20:4/14:0)), and negatively correlated with pro-inflammatory lipid mediators (e.g., 12,13-DiHOME, 9-OxoODE, vernolic acid).
CONCLUSION: This study indicated that hMPV infection might be associated with intestinal microecological imbalance and serum metabolic disturbances in children. The screened core differential metabolites hold the potential for further evaluation of their diagnostic value. Significant correlations exist between gut microbiota alterations and serum metabolic disorders, providing preliminary clues for the future development of preventive and therapeutic strategies targeting gut microbiota or metabolic pathways.
Additional Links: PMID-42583225
PubMed:
Citation:
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@article {pmid42583225,
year = {2026},
author = {Li, H and Huang, X and Cai, L and Deng, C and Cai, G and Li, L and Zhang, G and Liu, T},
title = {Gut microbiota and serum metabolome in children with human metapneumovirus infection.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1855983},
pmid = {42583225},
issn = {1664-3224},
mesh = {Humans ; *Paramyxoviridae Infections/blood/microbiology/virology/metabolism ; *Metapneumovirus ; Male ; Female ; *Metabolome ; *Gastrointestinal Microbiome ; Child, Preschool ; Multiomics ; Metabolomics/methods ; Child ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; Dysbiosis/blood ; Infant ; Biomarkers/blood ; },
abstract = {OBJECTIVE: To analyze the alterations in gut microbiota structure and serum metabolic profiles of children with human metapneumovirus (hMPV) infection using 16S rRNA high-throughput sequencing and liquid chromatography-mass spectrometry (LC-MS)-based untargeted metabolomics. Through integrated multi-omics analysis, we aim to explore the correlation between gut microbiota dysbiosis and host metabolic disorder, provide preliminary evidence for potential intervention targets, and offer primary clues for the development of preventive and therapeutic strategies including probiotic supplementation and metabolic pathway regulation.
METHODS: This study enrolled 42 children with hMPV infection and 12 healthy controls. Fecal samples were collected for gut microbiota analysis using 16S rRNA gene sequencing, and serum samples were obtained for metabolomic profiling via LC-MS. Various bioinformatics approaches were applied for independent analysis of microbiome and metabolome data, followed by integrated multi-omics analysis.
RESULTS: The microbial community structure of the hMPV-infected group was clearly separated from that of the healthy control group. Opportunistic pathogens such as Finegoldia, Anaerococcus, and Peptoniphilus were enriched, while beneficial commensals including Bifidobacterium, Blautia, and Faecalibacterium were reduced. Serum metabolic profiles showed global divergence between the two groups, with 558 upregulated and 213 downregulated metabolites identified. Using a VIP threshold >1.5, 24 core differential metabolites were ultimately selected. KEGG enrichment and MetPA topological analyses revealed that these differential metabolites were mainly enriched in pathways including glycerophospholipid metabolism, nucleotide metabolism, alpha-linolenic acid metabolism, and arachidonic acid metabolism. Correlation analysis showed that beneficial commensals with reduced abundance in the infected group, such as Bifidobacterium and Blautia, were positively correlated with anti-inflammatory and barrier-protective metabolites (e.g., alpha-linolenic acid, 11,12-DiHETrE, GPCho(20:4/14:0)), and negatively correlated with pro-inflammatory lipid mediators (e.g., 12,13-DiHOME, 9-OxoODE, vernolic acid).
CONCLUSION: This study indicated that hMPV infection might be associated with intestinal microecological imbalance and serum metabolic disturbances in children. The screened core differential metabolites hold the potential for further evaluation of their diagnostic value. Significant correlations exist between gut microbiota alterations and serum metabolic disorders, providing preliminary clues for the future development of preventive and therapeutic strategies targeting gut microbiota or metabolic pathways.},
}
MeSH Terms:
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Humans
*Paramyxoviridae Infections/blood/microbiology/virology/metabolism
*Metapneumovirus
Male
Female
*Metabolome
*Gastrointestinal Microbiome
Child, Preschool
Multiomics
Metabolomics/methods
Child
Feces/microbiology
RNA, Ribosomal, 16S/genetics
Dysbiosis/blood
Infant
Biomarkers/blood
RevDate: 2026-08-12
Psychobiotic Strategies for Managing Anxiety, Depression, and Schizophrenia: A Narrative Review.
Journal of restorative medicine, 2026:.
The gut microbiome exerts significant influence over mental health through the bidirectional communication network of the gut-brain axis. Growing evidence implicates disruptions in gut microbial composition in the pathophysiology of a range of neuropsychiatric conditions, including anxiety, major depressive disorder (MDD), and schizophrenia. Psychobiotics have emerged as a promising adjunctive strategy for modulating mental health outcomes through several interconnected mechanisms, including neurotransmitter modulation, immune regulation, short-chain fatty acid production, and hypothalamic-pituitary-adrenal axis stabilization, among others. This narrative review, intended for clinicians and researchers in integrative and functional medicine, synthesizes current clinical and translational evidence for probiotic interventions across anxiety, MDD, bipolar disorder, and schizophrenia, highlighting key strains, mechanisms, and outcomes. Findings demonstrate that specific Lactobacillus and Bifidobacterium strains show measurable benefit in reducing anxiety and depressive symptom severity, while emerging evidence suggests potential utility in psychotic disorders. Limitations include significant heterogeneity in strain selection, dosing protocols, study populations, and outcome measures, which constrain clinical translation. Future research should prioritize standardized protocols, longitudinal designs, and functional microbiome profiling to support personalized, microbiome-informed approaches to mental health care.
Additional Links: PMID-42583597
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Citation:
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@article {pmid42583597,
year = {2026},
author = {Thextona, A and Liberty, M and Alexandra, V and Rebecca, H and Jamie, M and Kate, P and Heather, Z},
title = {Psychobiotic Strategies for Managing Anxiety, Depression, and Schizophrenia: A Narrative Review.},
journal = {Journal of restorative medicine},
volume = {2026},
number = {},
pages = {},
pmid = {42583597},
issn = {2330-2941},
abstract = {The gut microbiome exerts significant influence over mental health through the bidirectional communication network of the gut-brain axis. Growing evidence implicates disruptions in gut microbial composition in the pathophysiology of a range of neuropsychiatric conditions, including anxiety, major depressive disorder (MDD), and schizophrenia. Psychobiotics have emerged as a promising adjunctive strategy for modulating mental health outcomes through several interconnected mechanisms, including neurotransmitter modulation, immune regulation, short-chain fatty acid production, and hypothalamic-pituitary-adrenal axis stabilization, among others. This narrative review, intended for clinicians and researchers in integrative and functional medicine, synthesizes current clinical and translational evidence for probiotic interventions across anxiety, MDD, bipolar disorder, and schizophrenia, highlighting key strains, mechanisms, and outcomes. Findings demonstrate that specific Lactobacillus and Bifidobacterium strains show measurable benefit in reducing anxiety and depressive symptom severity, while emerging evidence suggests potential utility in psychotic disorders. Limitations include significant heterogeneity in strain selection, dosing protocols, study populations, and outcome measures, which constrain clinical translation. Future research should prioritize standardized protocols, longitudinal designs, and functional microbiome profiling to support personalized, microbiome-informed approaches to mental health care.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
A Two-Sample Mendelian Randomisation Analysis of the Oral Microbiome and Oral/Oropharyngeal/Tongue Cancers.
Oral health & preventive dentistry, 24:613-621 pii:7074287.
OBJECTIVE: To assess the potential causal relationships of the oral microbiome with the risks of oral cancer, oropharyngeal cancer, and tongue cancer using two-sample Mendelian randomisation (MR) analysis, while distinguishing these from reverse causal effects of the cancers on microbial abundance.
METHODS AND MATERIALS: Using single-nucleotide polymorphisms as instrumental variables, we applied the MR inverse-variance-weighted approach to evaluate the effects of the dorsal-tongue and salivary microbiomes on oral, oropharyngeal, and tongue cancers. Analyses were conducted with the R package TwoSampleMR, leveraging genome-wide association study (GWAS) summary statistics from CNGBdb, the FinnGen consortium, and other sources. Sensitivity, heterogeneity, and pleiotropy assessments were performed. Additionally, reverse MR sensitivity analyses were conducted to explore the possible causal influence of cancers on the oral microbiota.
RESULTS: Using a single nucleotide polymorphism (SNP) significance threshold of p 5 × 10-6, our large-scale MR study revealed genetically supported causal relationships between microbial taxa derived from saliva and the tongue and the risk of oral, oropharyngeal, and tongue cancers. Integrating these results, we found that both 's Veillonella_rogosae_mgs_2008' and 's unclassified_mgs_1048' conferred a reduced risk of oropharyngeal and tongue cancers. Sensitivity analyses based on heterogeneity tests and pleiotropy evaluations further corroborated the robustness of our findings, lending additional credibility to the conclusions.
CONCLUSION: This study leveraged large-scale publicly available genetic data and identified significant causal relationships between the oral microbiota and cancers of the oral cavity, oropharynx, and tongue. Reverse MR analyses indicated that oral and tongue cancers may in turn alter the abundance of specific oral microbes, suggesting a potential bidirectional causal loop. Future work should integrate metagenomic data to further validate these microbiota-cancer associations.
Additional Links: PMID-42583788
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PubMed:
Citation:
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@article {pmid42583788,
year = {2026},
author = {Han, L and Wu, X and Gong, B and Li, X and Li, X and Wang, Z},
title = {A Two-Sample Mendelian Randomisation Analysis of the Oral Microbiome and Oral/Oropharyngeal/Tongue Cancers.},
journal = {Oral health & preventive dentistry},
volume = {24},
number = {},
pages = {613-621},
doi = {10.3290/j.ohpd.c_2778},
pmid = {42583788},
issn = {1757-9996},
mesh = {Humans ; *Mendelian Randomization Analysis ; *Microbiota/genetics ; *Tongue Neoplasms/microbiology ; *Oropharyngeal Neoplasms/microbiology ; Polymorphism, Single Nucleotide ; Genome-Wide Association Study ; *Mouth Neoplasms/microbiology ; Saliva/microbiology ; *Mouth/microbiology ; Tongue/microbiology ; },
abstract = {OBJECTIVE: To assess the potential causal relationships of the oral microbiome with the risks of oral cancer, oropharyngeal cancer, and tongue cancer using two-sample Mendelian randomisation (MR) analysis, while distinguishing these from reverse causal effects of the cancers on microbial abundance.
METHODS AND MATERIALS: Using single-nucleotide polymorphisms as instrumental variables, we applied the MR inverse-variance-weighted approach to evaluate the effects of the dorsal-tongue and salivary microbiomes on oral, oropharyngeal, and tongue cancers. Analyses were conducted with the R package TwoSampleMR, leveraging genome-wide association study (GWAS) summary statistics from CNGBdb, the FinnGen consortium, and other sources. Sensitivity, heterogeneity, and pleiotropy assessments were performed. Additionally, reverse MR sensitivity analyses were conducted to explore the possible causal influence of cancers on the oral microbiota.
RESULTS: Using a single nucleotide polymorphism (SNP) significance threshold of p 5 × 10-6, our large-scale MR study revealed genetically supported causal relationships between microbial taxa derived from saliva and the tongue and the risk of oral, oropharyngeal, and tongue cancers. Integrating these results, we found that both 's Veillonella_rogosae_mgs_2008' and 's unclassified_mgs_1048' conferred a reduced risk of oropharyngeal and tongue cancers. Sensitivity analyses based on heterogeneity tests and pleiotropy evaluations further corroborated the robustness of our findings, lending additional credibility to the conclusions.
CONCLUSION: This study leveraged large-scale publicly available genetic data and identified significant causal relationships between the oral microbiota and cancers of the oral cavity, oropharynx, and tongue. Reverse MR analyses indicated that oral and tongue cancers may in turn alter the abundance of specific oral microbes, suggesting a potential bidirectional causal loop. Future work should integrate metagenomic data to further validate these microbiota-cancer associations.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Mendelian Randomization Analysis
*Microbiota/genetics
*Tongue Neoplasms/microbiology
*Oropharyngeal Neoplasms/microbiology
Polymorphism, Single Nucleotide
Genome-Wide Association Study
*Mouth Neoplasms/microbiology
Saliva/microbiology
*Mouth/microbiology
Tongue/microbiology
RevDate: 2026-08-12
Fecal microbiota transplantation accelerates clearance of carbapenemase-producing Enterobacterales intestinal carriage: influence of recipient gut microbiome ecology.
The Journal of infectious diseases pii:8759462 [Epub ahead of print].
BACKGROUND: Persistent intestinal carbapenemase-producing Enterobacterales (CPE) carriage challenges infection prevention and antimicrobial stewardship. We evaluated fecal microbiota transplantation (FMT) for decolonization and response-associated recipient microbiome features.
METHODS: This prospective cohort study assessed intestinal CPE clearance in 131 adult carriers (68 receiving FMT; 63 under observation). Responders achieved clearance, defined as three consecutive negative rectal surveillance cultures for CPE, obtained at 3-day intervals within 1 month after FMT. Following least absolute shrinkage and selection operator (LASSO)-based covariate selection, Cox proportional hazards models estimated associations between FMT and time to successful decolonization within prespecified 0-30-day and 0-90-day windows. A longitudinal metagenomic subcohort of 21 FMT recipients (102 fecal samples) underwent shotgun sequencing to characterize taxonomic composition, microbial network organization, functional pathways, antimicrobial resistance genes (ARGs), and donor engraftment.
RESULTS: After LASSO-based covariate selection, FMT was associated with faster CPE clearance than observation at 1 month (hazard ratio, 4.02; 95% confidence interval, 1.84-8.79), with effects sustained at 3 months. Responders showed relatively preserved baseline microbial network organization and enrichment of taxa annotated with arginine-related pathway features, suggesting metabolic relevance to microbial niche competition. After FMT, responders had greater engraftment of donor-associated taxa and donor-like ecological reassembly, with reduced Klebsiella pneumoniae dominance and ARG abundance.
CONCLUSIONS: FMT may accelerate intestinal decolonization in CPE carriers; response variability was associated with recipient gut-microbiome ecology, suggesting microbiome-guided patient selection could optimize microbiota-based strategies.
Additional Links: PMID-42583799
Publisher:
PubMed:
Citation:
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@article {pmid42583799,
year = {2026},
author = {Lee, I and Suk, KT and Park, JY and Yong, D and Kim, DJ and Kim, BS and Lee, SS},
title = {Fecal microbiota transplantation accelerates clearance of carbapenemase-producing Enterobacterales intestinal carriage: influence of recipient gut microbiome ecology.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiag414},
pmid = {42583799},
issn = {1537-6613},
abstract = {BACKGROUND: Persistent intestinal carbapenemase-producing Enterobacterales (CPE) carriage challenges infection prevention and antimicrobial stewardship. We evaluated fecal microbiota transplantation (FMT) for decolonization and response-associated recipient microbiome features.
METHODS: This prospective cohort study assessed intestinal CPE clearance in 131 adult carriers (68 receiving FMT; 63 under observation). Responders achieved clearance, defined as three consecutive negative rectal surveillance cultures for CPE, obtained at 3-day intervals within 1 month after FMT. Following least absolute shrinkage and selection operator (LASSO)-based covariate selection, Cox proportional hazards models estimated associations between FMT and time to successful decolonization within prespecified 0-30-day and 0-90-day windows. A longitudinal metagenomic subcohort of 21 FMT recipients (102 fecal samples) underwent shotgun sequencing to characterize taxonomic composition, microbial network organization, functional pathways, antimicrobial resistance genes (ARGs), and donor engraftment.
RESULTS: After LASSO-based covariate selection, FMT was associated with faster CPE clearance than observation at 1 month (hazard ratio, 4.02; 95% confidence interval, 1.84-8.79), with effects sustained at 3 months. Responders showed relatively preserved baseline microbial network organization and enrichment of taxa annotated with arginine-related pathway features, suggesting metabolic relevance to microbial niche competition. After FMT, responders had greater engraftment of donor-associated taxa and donor-like ecological reassembly, with reduced Klebsiella pneumoniae dominance and ARG abundance.
CONCLUSIONS: FMT may accelerate intestinal decolonization in CPE carriers; response variability was associated with recipient gut-microbiome ecology, suggesting microbiome-guided patient selection could optimize microbiota-based strategies.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Systemic pathways linking subcutaneous therapies to gastrointestinal adverse effects: A Narrative review of mechanisms and mitigation strategies.
Indian journal of pharmacology, 58(4):307-318.
To systematically evaluate the spectrum, mechanisms, and prevention strategies of gastrointestinal (GI) adverse effects associated with subcutaneously administered drug therapies across multiple therapeutic classes. A comprehensive literature search was conducted in PubMed, EMBASE, and the Cochrane Library for studies published from January 2000 to June 2025. Eligible publications included randomized trials, observational studies, systematic reviews, meta-analyses, and regulatory label data reporting GI adverse effects of subcutaneous therapies. Drug classes analyzed included metabolic and endocrine agents, hematopoietic and bone-active drugs, cytokine modulators, biologic immunotherapies, vaccines, and selected miscellaneous agents. Data were extracted on incidence, clinical manifestations, mechanistic pathways, and mitigation strategies. Subcutaneously administered drugs were consistently associated with a wide range of GI adverse effects, including nausea, vomiting, diarrhea, abdominal pain, dyspepsia, and mucosal inflammation. Prominent contributors included glucagon-like peptide-1 receptor agonists, insulin analogs, growth factors, cytokine modulators, and biologic therapies. Mechanistic pathways identified included delayed gastric emptying, vagal and enteric nervous system activation, cytokine-mediated epithelial dysfunction, immune activation, and alterations of the gut microbiome. Interindividual variability in metabolic, immunologic, and neurohumoral responses influenced susceptibility. Despite bypassing the GI tract, subcutaneous therapies can induce clinically relevant GI toxicity through systemic neurohormonal, immune, and microbial pathways. Recognition of these mechanisms supports the use of dose titration, administration timing, dietary modification, and prophylactic pharmacotherapy to improve tolerability and treatment adherence.
Additional Links: PMID-42583966
PubMed:
Citation:
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@article {pmid42583966,
year = {2026},
author = {Singh, A and Yadav, D and Singh, MP},
title = {Systemic pathways linking subcutaneous therapies to gastrointestinal adverse effects: A Narrative review of mechanisms and mitigation strategies.},
journal = {Indian journal of pharmacology},
volume = {58},
number = {4},
pages = {307-318},
pmid = {42583966},
issn = {1998-3751},
mesh = {Humans ; *Gastrointestinal Diseases/chemically induced/prevention & control ; Animals ; Injections, Subcutaneous/adverse effects ; *Gastrointestinal Tract/drug effects ; },
abstract = {To systematically evaluate the spectrum, mechanisms, and prevention strategies of gastrointestinal (GI) adverse effects associated with subcutaneously administered drug therapies across multiple therapeutic classes. A comprehensive literature search was conducted in PubMed, EMBASE, and the Cochrane Library for studies published from January 2000 to June 2025. Eligible publications included randomized trials, observational studies, systematic reviews, meta-analyses, and regulatory label data reporting GI adverse effects of subcutaneous therapies. Drug classes analyzed included metabolic and endocrine agents, hematopoietic and bone-active drugs, cytokine modulators, biologic immunotherapies, vaccines, and selected miscellaneous agents. Data were extracted on incidence, clinical manifestations, mechanistic pathways, and mitigation strategies. Subcutaneously administered drugs were consistently associated with a wide range of GI adverse effects, including nausea, vomiting, diarrhea, abdominal pain, dyspepsia, and mucosal inflammation. Prominent contributors included glucagon-like peptide-1 receptor agonists, insulin analogs, growth factors, cytokine modulators, and biologic therapies. Mechanistic pathways identified included delayed gastric emptying, vagal and enteric nervous system activation, cytokine-mediated epithelial dysfunction, immune activation, and alterations of the gut microbiome. Interindividual variability in metabolic, immunologic, and neurohumoral responses influenced susceptibility. Despite bypassing the GI tract, subcutaneous therapies can induce clinically relevant GI toxicity through systemic neurohormonal, immune, and microbial pathways. Recognition of these mechanisms supports the use of dose titration, administration timing, dietary modification, and prophylactic pharmacotherapy to improve tolerability and treatment adherence.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Diseases/chemically induced/prevention & control
Animals
Injections, Subcutaneous/adverse effects
*Gastrointestinal Tract/drug effects
RevDate: 2026-08-12
A systematic review evaluating efficacy of probiotics in prevention and treatment of bacterial infections.
Future microbiology [Epub ahead of print].
AIMS: To evaluate the efficacy of probiotics in preventing or treating bacterial infections across different infection types in recently published randomized controlled trials (RCTs).
PATIENTS AND METHODS: Systematic review of 12 RCTs (2021-2026) addressing probiotics (single or multistrain) for recurrent urinary tract infections (rUTI), Helicobacter pylori eradication, respiratory tract infections (RTI), acne vulgaris, and multidrug-resistant (MDR) bacterial colonization. RoB assessed using Cochrane RoB 2.0; qualitative GRADE certainty assessment performed for all primary outcomes. Narrative synthesis with vote-counting analysis conducted due to heterogeneous study designs and outcomes.
RESULTS: Across 12 RCTs (n = 1200 participants), probiotics demonstrated consistent directional benefit for rUTI (2 RCTs: 75% recurrence-free vs. 33% placebo), H. pylori eradication (3 RCTs: 70-86% eradication rates), and RTI symptom reduction (3 RCTs: 64-96% improvement). Acne lesion reduction was observed in two RCTs. MDR colonization results were inconsistent (two RCTs). GRADE certainty of evidence ranged from low to moderate across all outcomes, primarily due to imprecision from small sample size and heterogenicity.
CONCLUSIONS: Probiotics show promise as adjuvant therapy for select bacterial infections, but evidence certainty is low. Larger structured RCTs with standardized outcome measures are required before routine clinical recommendations can be established.
PROTOCOL REGISTRATION: PROSPERO; https://www.crd.york.ac.uk/PROSPERO identifier is CRD420261339142.
Additional Links: PMID-42584057
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PubMed:
Citation:
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@article {pmid42584057,
year = {2026},
author = {Bhagat, T and Goyal, A and Chatterji, T},
title = {A systematic review evaluating efficacy of probiotics in prevention and treatment of bacterial infections.},
journal = {Future microbiology},
volume = {},
number = {},
pages = {1-13},
doi = {10.1080/17460913.2026.2715938},
pmid = {42584057},
issn = {1746-0921},
abstract = {AIMS: To evaluate the efficacy of probiotics in preventing or treating bacterial infections across different infection types in recently published randomized controlled trials (RCTs).
PATIENTS AND METHODS: Systematic review of 12 RCTs (2021-2026) addressing probiotics (single or multistrain) for recurrent urinary tract infections (rUTI), Helicobacter pylori eradication, respiratory tract infections (RTI), acne vulgaris, and multidrug-resistant (MDR) bacterial colonization. RoB assessed using Cochrane RoB 2.0; qualitative GRADE certainty assessment performed for all primary outcomes. Narrative synthesis with vote-counting analysis conducted due to heterogeneous study designs and outcomes.
RESULTS: Across 12 RCTs (n = 1200 participants), probiotics demonstrated consistent directional benefit for rUTI (2 RCTs: 75% recurrence-free vs. 33% placebo), H. pylori eradication (3 RCTs: 70-86% eradication rates), and RTI symptom reduction (3 RCTs: 64-96% improvement). Acne lesion reduction was observed in two RCTs. MDR colonization results were inconsistent (two RCTs). GRADE certainty of evidence ranged from low to moderate across all outcomes, primarily due to imprecision from small sample size and heterogenicity.
CONCLUSIONS: Probiotics show promise as adjuvant therapy for select bacterial infections, but evidence certainty is low. Larger structured RCTs with standardized outcome measures are required before routine clinical recommendations can be established.
PROTOCOL REGISTRATION: PROSPERO; https://www.crd.york.ac.uk/PROSPERO identifier is CRD420261339142.},
}
RevDate: 2026-08-12
Dental wastewater reveals a hidden reservoir of oral bacteriophage diversity.
Microbiology spectrum [Epub ahead of print].
Bacteriophages (phages) are being explored as alternatives or complements to antibiotics because of their ability to selectively kill bacterial pathogens. However, phages that infect many oral bacteria remain undiscovered. Here, we discovered that dental wastewater harbors previously underexplored phage diversity. Viral particles concentrated from dental wastewater displayed diverse morphologies, including abundant filamentous phage-like particles. Deep long-read metagenomic sequencing of concentrated viral particles generated 7.4 billion bases of sequence data and yielded 255 medium- to high-quality viral operational taxonomic units (vOTUs), including 46 predicted complete genomes. Comparison with large phage databases revealed that 63 of these 255 vOTUs had no detectable match, indicating that extensive sequencing of dental wastewater substantially expands the number of potential bacteriophages associated with the human oral microbiome. Host prediction linked many vOTUs to oral-associated bacterial taxa, including species with few or no previously reported phages, such as Porphyromonas gingivalis, Tannerella forsythia, and Candidatus Saccharibacteria. Functional annotation identified diverse genes associated with antiphage defense systems within a subset of vOTUs, suggesting that oral phages may contribute to the movement of genes encoding bacterial immune functions within the oral microbiome. Together, these findings expand the known oral phageome and show that dental wastewater contains a largely untapped diversity of phages.IMPORTANCEThe human oral cavity contains a diverse microbial community, but the bacteriophages (phages) that infect many oral bacteria remain poorly characterized. This gap limits our understanding of how phages shape oral microbial communities. Here, we show that dental wastewater is an underexplored source of oral phage diversity. Deep long-read metagenomic sequencing revealed 255 medium- to high-quality phage operational taxonomic units, many of which are not present in existing oral phage databases. These genomes include predicted phages of periodontal disease-associated bacteria and other oral taxa with few or no known phages. Dental wastewater therefore expands the known human oral phageome and reveals candidate phages linked to bacteria associated with oral health and disease.
Additional Links: PMID-42584065
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PubMed:
Citation:
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@article {pmid42584065,
year = {2026},
author = {Roush, C and Whiteley, M},
title = {Dental wastewater reveals a hidden reservoir of oral bacteriophage diversity.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0182026},
doi = {10.1128/spectrum.01820-26},
pmid = {42584065},
issn = {2165-0497},
abstract = {Bacteriophages (phages) are being explored as alternatives or complements to antibiotics because of their ability to selectively kill bacterial pathogens. However, phages that infect many oral bacteria remain undiscovered. Here, we discovered that dental wastewater harbors previously underexplored phage diversity. Viral particles concentrated from dental wastewater displayed diverse morphologies, including abundant filamentous phage-like particles. Deep long-read metagenomic sequencing of concentrated viral particles generated 7.4 billion bases of sequence data and yielded 255 medium- to high-quality viral operational taxonomic units (vOTUs), including 46 predicted complete genomes. Comparison with large phage databases revealed that 63 of these 255 vOTUs had no detectable match, indicating that extensive sequencing of dental wastewater substantially expands the number of potential bacteriophages associated with the human oral microbiome. Host prediction linked many vOTUs to oral-associated bacterial taxa, including species with few or no previously reported phages, such as Porphyromonas gingivalis, Tannerella forsythia, and Candidatus Saccharibacteria. Functional annotation identified diverse genes associated with antiphage defense systems within a subset of vOTUs, suggesting that oral phages may contribute to the movement of genes encoding bacterial immune functions within the oral microbiome. Together, these findings expand the known oral phageome and show that dental wastewater contains a largely untapped diversity of phages.IMPORTANCEThe human oral cavity contains a diverse microbial community, but the bacteriophages (phages) that infect many oral bacteria remain poorly characterized. This gap limits our understanding of how phages shape oral microbial communities. Here, we show that dental wastewater is an underexplored source of oral phage diversity. Deep long-read metagenomic sequencing revealed 255 medium- to high-quality phage operational taxonomic units, many of which are not present in existing oral phage databases. These genomes include predicted phages of periodontal disease-associated bacteria and other oral taxa with few or no known phages. Dental wastewater therefore expands the known human oral phageome and reveals candidate phages linked to bacteria associated with oral health and disease.},
}
RevDate: 2026-08-12
Temporal succession of microbiomes and resistomes during buried rat carcass decomposition.
mSphere [Epub ahead of print].
Burial is a prevalent approach for disposing of human and animal carcass. Carcass decomposition is a key natural disturbance that reshapes microbial communities and modulates biogeochemical cycles. Animal intestines serve as critical natural reservoirs of antibiotic resistance genes (ARGs), and carcass decomposition concurrently remodels intestinal bacterial assemblages and resistome profiles. Most previous studies have characterized microbial succession in surface-exposed carcasses, yet the coordinated temporal shifts of intestinal microbiota, resistomes, and horizontal gene transfer (HGT) signatures within buried carcasses remain underexplored. We established a buried rat carcass model and performed metagenomic sequencing to characterize temporal dynamics of intestinal bacteria, ARGs, mobile genetic elements (MGEs), and HGT events. Bacterial communities underwent directional succession accompanied by reduced α-diversity and stage-specific β-diversity. Proteobacteria gradually outcompeted Firmicutes and Bacteroidetes to become dominant taxa. The resistome followed regular temporal changes: tetracycline and macrolide-lincosamide-streptogramin (MLS) ARGs prevailed in early decomposition, while multidrug, β-lactam, polymyxin, and quinolone ARGs accumulated in mid-late stages, with ARG richness peaking on day 28. Approximately 83% of temporally dynamic ARG subtypes were positively correlated with decomposition duration. Procrustes analysis (R[2] = 0.859) revealed strong correlations between bacterial succession and resistome dynamics, with Proteobacteria as potential multidrug-resistant hosts and major HGT donors. This study identifies a correlative cascade of microbial succession that drives MGE functional shift, which in turn increased HGT potential and ultimately leads to resistome accumulation in buried carcass intestinal habitats. These findings expand the theoretical framework of disturbance-driven microbial-resistome co-succession and offer insights into drivers of antibiotic resistance propagation in terrestrial cadaver systems.IMPORTANCEAnimal carcass burial is a ubiquitous natural terrestrial disturbance, and carcass intestinal contents represent a major endogenous reservoir of environmental antibiotic resistance genes (ARGs). Although extensive research has characterized microbial succession of exposed carcasses, the co-occurrence patterns of gut microbiome and resistome together with associated horizontal gene transfer (HGT) under buried conditions remain underexplored. Using metagenomic profiling of decomposing rat intestinal feces, this study explores a potential correlative cascade spanning bacterial succession, mobile genetic element (MGE) functional shifts, increased HGT potential, and gradual ARG enrichment. Our findings expand the ecological data set focused on subsurface buried carcass habitats and advance mechanistic knowledge of coupled microbiome-resistome succession driven by postmortem decomposition.
Additional Links: PMID-42584101
Publisher:
PubMed:
Citation:
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@article {pmid42584101,
year = {2026},
author = {Yu, D and Zhang, L and Agu, D and Gao, N and Xiao, Y and Zhang, M and Zhang, J and Yan, J},
title = {Temporal succession of microbiomes and resistomes during buried rat carcass decomposition.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0043726},
doi = {10.1128/msphere.00437-26},
pmid = {42584101},
issn = {2379-5042},
abstract = {Burial is a prevalent approach for disposing of human and animal carcass. Carcass decomposition is a key natural disturbance that reshapes microbial communities and modulates biogeochemical cycles. Animal intestines serve as critical natural reservoirs of antibiotic resistance genes (ARGs), and carcass decomposition concurrently remodels intestinal bacterial assemblages and resistome profiles. Most previous studies have characterized microbial succession in surface-exposed carcasses, yet the coordinated temporal shifts of intestinal microbiota, resistomes, and horizontal gene transfer (HGT) signatures within buried carcasses remain underexplored. We established a buried rat carcass model and performed metagenomic sequencing to characterize temporal dynamics of intestinal bacteria, ARGs, mobile genetic elements (MGEs), and HGT events. Bacterial communities underwent directional succession accompanied by reduced α-diversity and stage-specific β-diversity. Proteobacteria gradually outcompeted Firmicutes and Bacteroidetes to become dominant taxa. The resistome followed regular temporal changes: tetracycline and macrolide-lincosamide-streptogramin (MLS) ARGs prevailed in early decomposition, while multidrug, β-lactam, polymyxin, and quinolone ARGs accumulated in mid-late stages, with ARG richness peaking on day 28. Approximately 83% of temporally dynamic ARG subtypes were positively correlated with decomposition duration. Procrustes analysis (R[2] = 0.859) revealed strong correlations between bacterial succession and resistome dynamics, with Proteobacteria as potential multidrug-resistant hosts and major HGT donors. This study identifies a correlative cascade of microbial succession that drives MGE functional shift, which in turn increased HGT potential and ultimately leads to resistome accumulation in buried carcass intestinal habitats. These findings expand the theoretical framework of disturbance-driven microbial-resistome co-succession and offer insights into drivers of antibiotic resistance propagation in terrestrial cadaver systems.IMPORTANCEAnimal carcass burial is a ubiquitous natural terrestrial disturbance, and carcass intestinal contents represent a major endogenous reservoir of environmental antibiotic resistance genes (ARGs). Although extensive research has characterized microbial succession of exposed carcasses, the co-occurrence patterns of gut microbiome and resistome together with associated horizontal gene transfer (HGT) under buried conditions remain underexplored. Using metagenomic profiling of decomposing rat intestinal feces, this study explores a potential correlative cascade spanning bacterial succession, mobile genetic element (MGE) functional shifts, increased HGT potential, and gradual ARG enrichment. Our findings expand the ecological data set focused on subsurface buried carcass habitats and advance mechanistic knowledge of coupled microbiome-resistome succession driven by postmortem decomposition.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Multiomics Dissection of the Mechanisms Underlying Eicosapentaenoic Acid Astaxanthin Ester-Mediated Protection Against High-Fat Diet-Induced Gut Barrier Injury.
Journal of agricultural and food chemistry, 74(31):24263-24276.
The intestinal barrier proves exquisitely sensitive to dietary cues and is intimately linked to the progression of intestinal, metabolic, and systemic disorders. This study explored the effects of eicosapentaenoic acid astaxanthin ester (EA) on high-fat-diet (HFD)-induced intestinal barrier damage based on the modification of gut microecology. The results showed that EA inhibited obesity development, dyslipidemia, and colon inflammation, suppressed colon pathological damage, and restored the intestinal barrier by upregulating ZO-1 and Occludin, but these improvement effects were lost in pseudogerm-free mice. 16S rRNA sequencing revealed that EA reconfigured the dysbiotic microbiome and selectively expanded barrier-protective genera such as Akkermansia, Muribaculum, Parabacteroides, and Lactobacillus. Transcriptomic analysis indicated that EA regulated cholesterol metabolism and bile secretion. Moreover, EA increased the levels of total bile acids (BAs), secondary BAs, and unconjugated BAs, and the upregulated BAs activated the intestinal farnesoid X receptor. Collectively, these findings provided novel evidence that EA alleviated HFD-induced gut barrier injury.
Additional Links: PMID-42584113
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PubMed:
Citation:
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@article {pmid42584113,
year = {2026},
author = {Li, X and Jing, B and Xia, C and Duan, J and Zhang, T and Li, H and Che, H},
title = {Multiomics Dissection of the Mechanisms Underlying Eicosapentaenoic Acid Astaxanthin Ester-Mediated Protection Against High-Fat Diet-Induced Gut Barrier Injury.},
journal = {Journal of agricultural and food chemistry},
volume = {74},
number = {31},
pages = {24263-24276},
doi = {10.1021/acs.jafc.5c16899},
pmid = {42584113},
issn = {1520-5118},
support = {32302103//National Natural Science Foundation of China/ ; },
mesh = {Animals ; Diet, High-Fat/adverse effects ; Intestinal Barrier Function/drug effects ; Mice ; *Eicosapentaenoic Acid/administration & dosage/chemistry ; Male ; Xanthophylls/administration & dosage ; Humans ; Gastrointestinal Microbiome/drug effects ; Mice, Inbred C57BL ; Bacteria/classification/isolation & purification/genetics/metabolism ; Bile Acids and Salts/metabolism ; *Intestinal Mucosa/metabolism/drug effects/microbiology ; *Protective Agents/administration & dosage ; Esters/administration & dosage ; },
abstract = {The intestinal barrier proves exquisitely sensitive to dietary cues and is intimately linked to the progression of intestinal, metabolic, and systemic disorders. This study explored the effects of eicosapentaenoic acid astaxanthin ester (EA) on high-fat-diet (HFD)-induced intestinal barrier damage based on the modification of gut microecology. The results showed that EA inhibited obesity development, dyslipidemia, and colon inflammation, suppressed colon pathological damage, and restored the intestinal barrier by upregulating ZO-1 and Occludin, but these improvement effects were lost in pseudogerm-free mice. 16S rRNA sequencing revealed that EA reconfigured the dysbiotic microbiome and selectively expanded barrier-protective genera such as Akkermansia, Muribaculum, Parabacteroides, and Lactobacillus. Transcriptomic analysis indicated that EA regulated cholesterol metabolism and bile secretion. Moreover, EA increased the levels of total bile acids (BAs), secondary BAs, and unconjugated BAs, and the upregulated BAs activated the intestinal farnesoid X receptor. Collectively, these findings provided novel evidence that EA alleviated HFD-induced gut barrier injury.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Diet, High-Fat/adverse effects
Intestinal Barrier Function/drug effects
Mice
*Eicosapentaenoic Acid/administration & dosage/chemistry
Male
Xanthophylls/administration & dosage
Humans
Gastrointestinal Microbiome/drug effects
Mice, Inbred C57BL
Bacteria/classification/isolation & purification/genetics/metabolism
Bile Acids and Salts/metabolism
*Intestinal Mucosa/metabolism/drug effects/microbiology
*Protective Agents/administration & dosage
Esters/administration & dosage
RevDate: 2026-08-12
Virome DNA stable isotope probing reveals diverse active soil virus communities across ecosystem contexts.
mSystems [Epub ahead of print].
Viruses are increasingly recognized as important players in soil ecosystems, but the active lytic virus populations that influence microbe-mediated terrestrial ecosystem processes remain mostly uncharacterized. Here, we trace [13]C-labeled glucose from host microorganisms into virus genomic DNA to identify virus populations actively involved in soil carbon (C) cycling, i.e., viruses that lysed [13]C-incorporating microbes. We present experimental evidence of isotope labeling (i.e., lytic activity) of more than 5,000 virus populations. The active viruses lysed hosts from 197 microbial families across 28 prokaryotic phyla. Viral lysis was greater in C-limited agricultural soils compared with C-rich forest soils, highlighting C availability/inputs as key factors that mediate virus life cycles. Active viruses disproportionately lysed microorganisms in the Bacillota, Bacteroidota, and Pseudomonadota phyla, likely reflecting glucose-induced growth responses of microbial copiotrophs within those groups. Supporting this, we observed that the degree of virus genome isotope labeling was positively correlated with the growth potential of the microbial hosts. Furthermore, the active viruses exhibited unique genomic characteristics compared to the inactive viruses, including a greater prevalence of lysogeny-associated genes and distinct profiles of putative auxiliary metabolism genes in the active virus genomes. Overall, our results demonstrate a link between microbial growth traits and virus activity and suggest that substrate-induced viral lysis significantly influences microbial population turnover in soil. Our results also show that virus activity in response to C inputs is highly variable among soil contexts, with implications for the varying ecosystem-scale influences of viruses among terrestrial environments.IMPORTANCEIn this study, we used a new method of detecting active viruses that lyse (kill) their microorganism hosts in soil. We accomplished this by tracing "heavy" versions of carbon from soil microorganisms into the DNA of their virus parasites. This showed that there are thousands of different potentially active virus populations in soil and that the microorganisms that get lysed the most are those that grow the fastest. However, the activity of viruses was very high in some ecosystems (agricultural soils) and much lower in others (forest soils). Our results show that viruses can play an important role in influencing soil microbial communities, but that the size of their effects is very different in different types of ecosystems. Our study also describes a new method that can be extended to further explore the roles and importance of viruses across different environmental conditions and different ecosystem types.
Additional Links: PMID-42584163
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@article {pmid42584163,
year = {2026},
author = {Osburn, ED and Kim, M},
title = {Virome DNA stable isotope probing reveals diverse active soil virus communities across ecosystem contexts.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0073326},
doi = {10.1128/msystems.00733-26},
pmid = {42584163},
issn = {2379-5077},
abstract = {Viruses are increasingly recognized as important players in soil ecosystems, but the active lytic virus populations that influence microbe-mediated terrestrial ecosystem processes remain mostly uncharacterized. Here, we trace [13]C-labeled glucose from host microorganisms into virus genomic DNA to identify virus populations actively involved in soil carbon (C) cycling, i.e., viruses that lysed [13]C-incorporating microbes. We present experimental evidence of isotope labeling (i.e., lytic activity) of more than 5,000 virus populations. The active viruses lysed hosts from 197 microbial families across 28 prokaryotic phyla. Viral lysis was greater in C-limited agricultural soils compared with C-rich forest soils, highlighting C availability/inputs as key factors that mediate virus life cycles. Active viruses disproportionately lysed microorganisms in the Bacillota, Bacteroidota, and Pseudomonadota phyla, likely reflecting glucose-induced growth responses of microbial copiotrophs within those groups. Supporting this, we observed that the degree of virus genome isotope labeling was positively correlated with the growth potential of the microbial hosts. Furthermore, the active viruses exhibited unique genomic characteristics compared to the inactive viruses, including a greater prevalence of lysogeny-associated genes and distinct profiles of putative auxiliary metabolism genes in the active virus genomes. Overall, our results demonstrate a link between microbial growth traits and virus activity and suggest that substrate-induced viral lysis significantly influences microbial population turnover in soil. Our results also show that virus activity in response to C inputs is highly variable among soil contexts, with implications for the varying ecosystem-scale influences of viruses among terrestrial environments.IMPORTANCEIn this study, we used a new method of detecting active viruses that lyse (kill) their microorganism hosts in soil. We accomplished this by tracing "heavy" versions of carbon from soil microorganisms into the DNA of their virus parasites. This showed that there are thousands of different potentially active virus populations in soil and that the microorganisms that get lysed the most are those that grow the fastest. However, the activity of viruses was very high in some ecosystems (agricultural soils) and much lower in others (forest soils). Our results show that viruses can play an important role in influencing soil microbial communities, but that the size of their effects is very different in different types of ecosystems. Our study also describes a new method that can be extended to further explore the roles and importance of viruses across different environmental conditions and different ecosystem types.},
}
RevDate: 2026-08-12
Prevotella in the airway: implications for lung health and pathogen defense mediated by Prevotella-host interactions.
Journal of bacteriology [Epub ahead of print].
Prevotella species are an extremely common and abundant bacteria detected within the low microbial biomass of the lungs and are a core component of the oral microbiome. Clinical studies have drawn associations between Prevotella abundance and lung homeostasis, indicating potential relationships between Prevotella and lung inflammation, infection defense, and lung function. Across several studies in critically ill patients, the depletion of Prevotella and other obligate anaerobes is linked to significantly reduced survival, leading to calls for anaerobe preservation in empiric antibiotic therapy regimens. In recent years, mechanistic studies have provided new information regarding Prevotella-host relationships, highlighting several processes by which Prevotella exposure activates epithelial, innate, and adaptive immune responses. Prevotella species also have direct and indirect effects on important lung bacterial pathogens, including Streptococcus pneumoniae, Staphylococcus aureus, and Pseudomonas aeruginosa, with Prevotella species-dependent consequences for pathogen infection and regulation of pathogen-induced inflammation. This review summarizes our current understanding regarding how Prevotella regulate lung immune homeostasis, with a discussion of key knowledge gaps necessary for the translation of these insights into new therapeutic approaches to reduce the burden of lung infection and disease.
Additional Links: PMID-42584416
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@article {pmid42584416,
year = {2026},
author = {Stoner, SN and Fairbanks-Mahnke, A and Clark, SE},
title = {Prevotella in the airway: implications for lung health and pathogen defense mediated by Prevotella-host interactions.},
journal = {Journal of bacteriology},
volume = {},
number = {},
pages = {e0022826},
doi = {10.1128/jb.00228-26},
pmid = {42584416},
issn = {1098-5530},
abstract = {Prevotella species are an extremely common and abundant bacteria detected within the low microbial biomass of the lungs and are a core component of the oral microbiome. Clinical studies have drawn associations between Prevotella abundance and lung homeostasis, indicating potential relationships between Prevotella and lung inflammation, infection defense, and lung function. Across several studies in critically ill patients, the depletion of Prevotella and other obligate anaerobes is linked to significantly reduced survival, leading to calls for anaerobe preservation in empiric antibiotic therapy regimens. In recent years, mechanistic studies have provided new information regarding Prevotella-host relationships, highlighting several processes by which Prevotella exposure activates epithelial, innate, and adaptive immune responses. Prevotella species also have direct and indirect effects on important lung bacterial pathogens, including Streptococcus pneumoniae, Staphylococcus aureus, and Pseudomonas aeruginosa, with Prevotella species-dependent consequences for pathogen infection and regulation of pathogen-induced inflammation. This review summarizes our current understanding regarding how Prevotella regulate lung immune homeostasis, with a discussion of key knowledge gaps necessary for the translation of these insights into new therapeutic approaches to reduce the burden of lung infection and disease.},
}
RevDate: 2026-08-12
Livestock Multi-Omics Integration: A Systematic Framework From Statistical Association to Causal Interpretation.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Livestock multi-omics integration is key to unraveling complex trait regulation, yet systematic, livestock-specific strategies remain scarce. This review traces the progression from single-omics accumulation to multi-dimensional integration, highlighting how large-scale genomic, epigenomic, and transcriptomic projects lay the foundation for functional dissection. We identify core impediments: extreme species diversity, marked data heterogeneity, limited sample sizes, and a pervasive reduction of multi-omics data to simplistic differential screens, resulting in low translational efficiency. We critically appraise four common pitfalls-overinterpreting correlation as causation, relegating proteomics to corroborating transcriptomics, incomplete microbiome-host integration lacking environmental context, and systematic neglect of metabolic fluxomics-and show how exposomics and fluxomics add necessary causal and dynamic dimensions. To address these, we propose a livestock-adapted three-tier analytical framework: (1) statistical association of cross-omics covariation patterns; (2) machine learning-driven feature mining and integrative modeling; and (3) causal interpretation encompassing Mendelian randomization, prior-knowledge-guided network inference, and physical causal evidence via fluxomics and metabolic control analysis. We further discuss how multimodal sequencing (single-cell, spatial, temporal) and generative AI can fundamentally mitigate heterogeneity and strengthen causal evidence. Finally, we outline future priorities in database standardization, livestock-specific benchmarking, and translational pipelines, charting a path from correlation-centric reporting to mechanistic causality and precision breeding.
Additional Links: PMID-42584423
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@article {pmid42584423,
year = {2026},
author = {Wen, J and Wang, Z and Huang, J and Li, F and Chen, N and Ma, Y},
title = {Livestock Multi-Omics Integration: A Systematic Framework From Statistical Association to Causal Interpretation.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e77094},
pmid = {42584423},
issn = {2198-3844},
support = {U22A20506//National Natural Science Foundation of China/ ; 32472871//National Natural Science Foundation of China/ ; 32341054//National Natural Science Foundation of China/ ; 2024BBF01007//Key Research and Development Program of Ningxia Projects/ ; 2023BCF01006//Key Research and Development Program of Ningxia Projects/ ; CARS-37//China Agriculture Research System of MOF and MARA/ ; },
abstract = {Livestock multi-omics integration is key to unraveling complex trait regulation, yet systematic, livestock-specific strategies remain scarce. This review traces the progression from single-omics accumulation to multi-dimensional integration, highlighting how large-scale genomic, epigenomic, and transcriptomic projects lay the foundation for functional dissection. We identify core impediments: extreme species diversity, marked data heterogeneity, limited sample sizes, and a pervasive reduction of multi-omics data to simplistic differential screens, resulting in low translational efficiency. We critically appraise four common pitfalls-overinterpreting correlation as causation, relegating proteomics to corroborating transcriptomics, incomplete microbiome-host integration lacking environmental context, and systematic neglect of metabolic fluxomics-and show how exposomics and fluxomics add necessary causal and dynamic dimensions. To address these, we propose a livestock-adapted three-tier analytical framework: (1) statistical association of cross-omics covariation patterns; (2) machine learning-driven feature mining and integrative modeling; and (3) causal interpretation encompassing Mendelian randomization, prior-knowledge-guided network inference, and physical causal evidence via fluxomics and metabolic control analysis. We further discuss how multimodal sequencing (single-cell, spatial, temporal) and generative AI can fundamentally mitigate heterogeneity and strengthen causal evidence. Finally, we outline future priorities in database standardization, livestock-specific benchmarking, and translational pipelines, charting a path from correlation-centric reporting to mechanistic causality and precision breeding.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Use, understanding, and perceptions of gut microbiome research and practices in oncology.
Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer, 34(9):.
PURPOSE: The gut microbiome has gained increasing recognition as an important factor influencing cancer treatment efficacy and toxicity. However, translation of this knowledge to deliver clinical benefit has been hampered by inconsistent approaches to both biospecimen sampling and investigation of microbial-based interventions, potentially reflecting inherent biases and/or barriers across research environments. Accordingly, we aimed to characterize the current practices and perceptions surrounding the gut microbiome among members of the Multinational Association of Supportive Care in Cancer (MASCC).
METHODS: A mixed-methods survey, probing current research and/or clinical use, plans, and perceptions of the gut microbiome in oncology, was developed in 2022 and distributed MASCC-wide via REDCap. Quantitative data were summarized using descriptive analyses, and qualitative responses were independently dual-coded using inductive thematic analysis.
RESULTS: Out of 117 respondents, the majority (83%) held the belief that the gut microbiome plays an important role in disease states such as cancer. 44.4% of survey respondents reported ongoing research or clinical practice regarding the gut microbiome at their center, with 70.5% also expressing an interest in developing such a program. Qualitative analysis revealed 6 main themes: (1) state of the evidence, (2) significance of the microbiome, (3) uncertainty, (4) aspirations, (5) preferences, and (6) critique.
CONCLUSIONS: This survey identifies general concordance on the importance of the gut microbiome in cancer. Despite interest in this field, there is a clear need for resource support (i.e., funding and infrastructure) and increased expertise to support high-quality trials generating the evidence required for implementation of microbial-based sampling or therapeutics in clinical practice.
Additional Links: PMID-42584704
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Citation:
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@article {pmid42584704,
year = {2026},
author = {Cross, CB and Davies, MR and Irestorm, E and Thornton, CP and Elgarten, CW and Wardill, HR and Stein, MT and Cheung, YT and Beeler, DM and Freedman, JL},
title = {Use, understanding, and perceptions of gut microbiome research and practices in oncology.},
journal = {Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer},
volume = {34},
number = {9},
pages = {},
pmid = {42584704},
issn = {1433-7339},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Neoplasms/microbiology/therapy ; *Medical Oncology/methods ; Surveys and Questionnaires ; Attitude of Health Personnel ; },
abstract = {PURPOSE: The gut microbiome has gained increasing recognition as an important factor influencing cancer treatment efficacy and toxicity. However, translation of this knowledge to deliver clinical benefit has been hampered by inconsistent approaches to both biospecimen sampling and investigation of microbial-based interventions, potentially reflecting inherent biases and/or barriers across research environments. Accordingly, we aimed to characterize the current practices and perceptions surrounding the gut microbiome among members of the Multinational Association of Supportive Care in Cancer (MASCC).
METHODS: A mixed-methods survey, probing current research and/or clinical use, plans, and perceptions of the gut microbiome in oncology, was developed in 2022 and distributed MASCC-wide via REDCap. Quantitative data were summarized using descriptive analyses, and qualitative responses were independently dual-coded using inductive thematic analysis.
RESULTS: Out of 117 respondents, the majority (83%) held the belief that the gut microbiome plays an important role in disease states such as cancer. 44.4% of survey respondents reported ongoing research or clinical practice regarding the gut microbiome at their center, with 70.5% also expressing an interest in developing such a program. Qualitative analysis revealed 6 main themes: (1) state of the evidence, (2) significance of the microbiome, (3) uncertainty, (4) aspirations, (5) preferences, and (6) critique.
CONCLUSIONS: This survey identifies general concordance on the importance of the gut microbiome in cancer. Despite interest in this field, there is a clear need for resource support (i.e., funding and infrastructure) and increased expertise to support high-quality trials generating the evidence required for implementation of microbial-based sampling or therapeutics in clinical practice.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome
*Neoplasms/microbiology/therapy
*Medical Oncology/methods
Surveys and Questionnaires
Attitude of Health Personnel
RevDate: 2026-08-12
CmpDate: 2026-08-12
Microplastics and nanoplastics in human toxicity: ROS-mediated mechanisms, cellular damage and systemic effects.
Molecular biology reports, 53(1):.
Microplastics (MPs, less than 5 mm) and nanoplastics (NPs, less than 1 μm) have become widespread environmental contaminants with significant implications for human health. Owing to their small size, large surface area, and physicochemical reactivity, MPs and NPs readily interact with biological membranes, promote cellular uptake, and accumulate within organelles such as mitochondria, lysosomes, and the endoplasmic reticulum. ROS overproduction disrupts mitochondrial dynamics, induces DNA damage, alters lipid metabolism, and affects redox-sensitive signalling pathways, including MAPK, PI3K/Akt, NF-κB, p53, and TGF-β. These molecular events collectively initiate apoptosis, autophagy, inflammation, and genotoxicity. At the systemic level, experimental MP and NP exposure has been associated with hepatotoxicity, nephrotoxicity, cardiopulmonary injury, reproductive impairment, neurotoxicity, gut microbiome dysbiosis, endocrine disruption, and elevated cancer risk. Furthermore, MPs and NPs can act as vectors of co-contaminants, increasing the bioavailability and toxicity of associated pollutants such as plasticizers and heavy metals. This review consolidates current understanding of the sources, cellular uptake, ROS-mediated mechanisms, and multi-organ toxicological effects of MPs and NPs.
Additional Links: PMID-42584724
PubMed:
Citation:
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@article {pmid42584724,
year = {2026},
author = {Chakraborty, S and Chakraborty, A and Ghosh, A and Bishwanath Singh, N and Ghosh, D and Kundu, T and Das, A},
title = {Microplastics and nanoplastics in human toxicity: ROS-mediated mechanisms, cellular damage and systemic effects.},
journal = {Molecular biology reports},
volume = {53},
number = {1},
pages = {},
pmid = {42584724},
issn = {1573-4978},
mesh = {Humans ; *Reactive Oxygen Species/metabolism ; *Microplastics/toxicity ; DNA Damage/drug effects ; Animals ; Oxidative Stress/drug effects ; *Environmental Pollutants/toxicity ; Signal Transduction/drug effects ; *Nanoparticles/toxicity ; Mitochondria/metabolism/drug effects ; },
abstract = {Microplastics (MPs, less than 5 mm) and nanoplastics (NPs, less than 1 μm) have become widespread environmental contaminants with significant implications for human health. Owing to their small size, large surface area, and physicochemical reactivity, MPs and NPs readily interact with biological membranes, promote cellular uptake, and accumulate within organelles such as mitochondria, lysosomes, and the endoplasmic reticulum. ROS overproduction disrupts mitochondrial dynamics, induces DNA damage, alters lipid metabolism, and affects redox-sensitive signalling pathways, including MAPK, PI3K/Akt, NF-κB, p53, and TGF-β. These molecular events collectively initiate apoptosis, autophagy, inflammation, and genotoxicity. At the systemic level, experimental MP and NP exposure has been associated with hepatotoxicity, nephrotoxicity, cardiopulmonary injury, reproductive impairment, neurotoxicity, gut microbiome dysbiosis, endocrine disruption, and elevated cancer risk. Furthermore, MPs and NPs can act as vectors of co-contaminants, increasing the bioavailability and toxicity of associated pollutants such as plasticizers and heavy metals. This review consolidates current understanding of the sources, cellular uptake, ROS-mediated mechanisms, and multi-organ toxicological effects of MPs and NPs.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Reactive Oxygen Species/metabolism
*Microplastics/toxicity
DNA Damage/drug effects
Animals
Oxidative Stress/drug effects
*Environmental Pollutants/toxicity
Signal Transduction/drug effects
*Nanoparticles/toxicity
Mitochondria/metabolism/drug effects
RevDate: 2026-08-12
Anxiety and Depression in Pancreatitis: Mechanisms, Assessment, and Treatment.
Digestive diseases (Basel, Switzerland) pii:000553789 [Epub ahead of print].
BACKGROUND: Numerous studies have detailed that patients with pancreatitis frequently experience comorbid anxiety and depression, which may arise from physiological factors or psychosocial influences, and these conditions adversely affect daily functioning and quality of life. However, there is still a lack of reviews on epidemiological and mechanistic studies of anxiety and depression in patients with pancreatitis.
SUMMARY: Patients with pancreatitis commonly present with comorbid anxiety and depression, with chronic pancreatitis patients being more susceptible than those with acute pancreatitis. The mechanisms underlying this comorbidity are complex and likely multifactorial. Biological factors encompass inflammation-driven cytokine signalling to the brain, Hypothalamic-Pituitary-Adrenal (HPA) axis hyperactivity, gut microbiome dysbiosis, and altered central nervous system plasticity. Psychosocial factors include the emotional burden of pancreatitis, persistent sleep disturbances, substance abuse, and diminished family and social support. Assessment primarily relies on various types of scales, while treatment encompasses a comprehensive approach involving medication, psychological interventions, and family and social support.
KEY MESSAGES: This paper reviews the epidemiological characteristics of anxiety and depression in patients with pancreatitis, explores their biological and psychosocial mechanisms, and summarizes key points for the assessment and treatment of this comorbidity.
Additional Links: PMID-42585120
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PubMed:
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@article {pmid42585120,
year = {2026},
author = {Xiong, C and Zheng, Z and Qiao, WG and Ren, Y},
title = {Anxiety and Depression in Pancreatitis: Mechanisms, Assessment, and Treatment.},
journal = {Digestive diseases (Basel, Switzerland)},
volume = {},
number = {},
pages = {1},
doi = {10.1159/ddi/acnag001},
pmid = {42585120},
issn = {1421-9875},
abstract = {BACKGROUND: Numerous studies have detailed that patients with pancreatitis frequently experience comorbid anxiety and depression, which may arise from physiological factors or psychosocial influences, and these conditions adversely affect daily functioning and quality of life. However, there is still a lack of reviews on epidemiological and mechanistic studies of anxiety and depression in patients with pancreatitis.
SUMMARY: Patients with pancreatitis commonly present with comorbid anxiety and depression, with chronic pancreatitis patients being more susceptible than those with acute pancreatitis. The mechanisms underlying this comorbidity are complex and likely multifactorial. Biological factors encompass inflammation-driven cytokine signalling to the brain, Hypothalamic-Pituitary-Adrenal (HPA) axis hyperactivity, gut microbiome dysbiosis, and altered central nervous system plasticity. Psychosocial factors include the emotional burden of pancreatitis, persistent sleep disturbances, substance abuse, and diminished family and social support. Assessment primarily relies on various types of scales, while treatment encompasses a comprehensive approach involving medication, psychological interventions, and family and social support.
KEY MESSAGES: This paper reviews the epidemiological characteristics of anxiety and depression in patients with pancreatitis, explores their biological and psychosocial mechanisms, and summarizes key points for the assessment and treatment of this comorbidity.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
DELTA: Strengthening human biological resilience with an N=1 digital health and dynamic biomarker protocol.
PloS one, 21(8):e0354234 pii:PONE-D-25-65417.
Societies are aging rapidly in parallel with the increasingly earlier onset of serious diseases in younger populations. These and other factors are creating a substantial disparity between healthspan, the period of life where an individual is free from serious chronic disease or disability, and lifespan - expanding the morbidity span. Extending healthspan has thus become a major priority. To pursue an integrated strategy toward healthspan support, we launched DELTA, a prospective, open-label, interventional, and participatory N = 1 study (NCT06630637) conducted on a healthy individual (DELTA001, author D.H.). The study was conducted with methodological rigor to support repeatability, transparency, and balanced reporting. The core focus of the DELTA protocol was to assess and enhance human biological resilience. This was demonstrated through the subject's adaptive capacity, revealed through changes and trajectories in cardiometabolic and pleiotropic biomarker levels based upon systematically administered challenges (e.g., fasting). Specifically, the interventional DELTA protocol integrates time-restricted eating (TRE, fasting), strength and cardiovascular fitness regimens, a Mediterranean-inspired dietary protocol, and supplementation alongside an analytics and reporting framework comprised of artificial intelligence (AI), digital health, and wearables-based sleep performance monitoring, microbiome assessment, and longitudinal tracking of biomarker dynamics and performance outcomes. This study introduces new methods and metrics for assessing these biomarker dynamics, including the development of digital biomarkers that reflect dynamic human functional resilience. Findings from DELTA may actionably guide the design of larger participatory human trials to monitor biomarker resilience, design appropriate interventions for dynamic administration, and subsequently strengthen healthspan at a population level.
Additional Links: PMID-42585167
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PubMed:
Citation:
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@article {pmid42585167,
year = {2026},
author = {Wang, P and Foo, N and Su, C and Leung, NYT and Song, SW and Seres, G and Sapanel, Y and Hooi, L and Wong, A and Ong, YH and Rai, P and Park, H and Chew, HSJ and Wang, LYT and Lee, JWJ and Tadeo, X and Ho, D},
title = {DELTA: Strengthening human biological resilience with an N=1 digital health and dynamic biomarker protocol.},
journal = {PloS one},
volume = {21},
number = {8},
pages = {e0354234},
doi = {10.1371/journal.pone.0354234},
pmid = {42585167},
issn = {1932-6203},
mesh = {Humans ; Digital Health ; *Biomarkers ; Female ; Male ; Prospective Studies ; Adult ; Fasting ; },
abstract = {Societies are aging rapidly in parallel with the increasingly earlier onset of serious diseases in younger populations. These and other factors are creating a substantial disparity between healthspan, the period of life where an individual is free from serious chronic disease or disability, and lifespan - expanding the morbidity span. Extending healthspan has thus become a major priority. To pursue an integrated strategy toward healthspan support, we launched DELTA, a prospective, open-label, interventional, and participatory N = 1 study (NCT06630637) conducted on a healthy individual (DELTA001, author D.H.). The study was conducted with methodological rigor to support repeatability, transparency, and balanced reporting. The core focus of the DELTA protocol was to assess and enhance human biological resilience. This was demonstrated through the subject's adaptive capacity, revealed through changes and trajectories in cardiometabolic and pleiotropic biomarker levels based upon systematically administered challenges (e.g., fasting). Specifically, the interventional DELTA protocol integrates time-restricted eating (TRE, fasting), strength and cardiovascular fitness regimens, a Mediterranean-inspired dietary protocol, and supplementation alongside an analytics and reporting framework comprised of artificial intelligence (AI), digital health, and wearables-based sleep performance monitoring, microbiome assessment, and longitudinal tracking of biomarker dynamics and performance outcomes. This study introduces new methods and metrics for assessing these biomarker dynamics, including the development of digital biomarkers that reflect dynamic human functional resilience. Findings from DELTA may actionably guide the design of larger participatory human trials to monitor biomarker resilience, design appropriate interventions for dynamic administration, and subsequently strengthen healthspan at a population level.},
}
MeSH Terms:
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Humans
Digital Health
*Biomarkers
Female
Male
Prospective Studies
Adult
Fasting
RevDate: 2026-08-12
CmpDate: 2026-08-12
Effect of reused litter on early cecal microbiota succession and the immune cells distribution in layer chickens.
PloS one, 21(8):e0355745 pii:PONE-D-26-13127.
This study was designed to evaluate early immune development and gut microbiome establishment in layer chicks reared on reused or fresh litter. A total of 160 newly hatched female Hy-Line W80 layer were housed on fresh or used litter (n = 80/group). Body weight was recorded weekly, ceca, ileum and spleen samples were collected at days 7 and 35 for gut microbiome analysis and intraepithelial lymphocytes (IELs) study. Results showed that layer chicks reared on fresh litter exhibited significantly higher body weight compared with layer chicks reared on used litter from day 14 to day 35 (P < 0.05), while mortality remained low and was not significantly different between groups. Cecal microbiota analysis revealed significant litter-associated differences in alpha and beta diversity at day 7 (P < 0.05). However, by day 35, microbial richness and overall community composition were no longer significantly different between treatments. At the phylum level, Bacillota was the dominant phylum in both litter groups at days 7 and 35. Pseudomonadota was the second most abundant phylum at day 7, whereas Bacteroidota became the second most abundant phylum by day 35. This shift indicates age related maturation of the cecal microbial community. In terms of immune responses, no significant difference was found in IEL subsets at day 7 between litter groups. However, by 35 days, the used litter exposure resulted in a significant expansion of TCR [-] , TCRγδ + , TCRαβ, TCRαβ [+] CD8αβ[+] and TCRαβ + CD8αα + IEL subsets (P < 0.05). Similarly, splenic TCRγδ+ and TCRαβ + CD8αβ+ populations were significantly elevated in used litter layer chicks at day 35. These findings highlight that exposure to different litter environment was associated with distinct cecal microbial profiles and immune-cell distributions in layer chicks. Given the limited information available in laying hens, these results provide novel baseline data and support further studies investigating the role of litter-associated microbial exposure in shaping early immune development.
Additional Links: PMID-42585188
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PubMed:
Citation:
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@article {pmid42585188,
year = {2026},
author = {Khalid, N and Majeed, S and Shah, BR and Nazmi, A},
title = {Effect of reused litter on early cecal microbiota succession and the immune cells distribution in layer chickens.},
journal = {PloS one},
volume = {21},
number = {8},
pages = {e0355745},
doi = {10.1371/journal.pone.0355745},
pmid = {42585188},
issn = {1932-6203},
mesh = {Animals ; *Chickens/microbiology/immunology ; *Cecum/microbiology/immunology ; Female ; *Microbiota ; Spleen/immunology ; Housing, Animal ; Intraepithelial Lymphocytes/immunology ; Body Weight ; },
abstract = {This study was designed to evaluate early immune development and gut microbiome establishment in layer chicks reared on reused or fresh litter. A total of 160 newly hatched female Hy-Line W80 layer were housed on fresh or used litter (n = 80/group). Body weight was recorded weekly, ceca, ileum and spleen samples were collected at days 7 and 35 for gut microbiome analysis and intraepithelial lymphocytes (IELs) study. Results showed that layer chicks reared on fresh litter exhibited significantly higher body weight compared with layer chicks reared on used litter from day 14 to day 35 (P < 0.05), while mortality remained low and was not significantly different between groups. Cecal microbiota analysis revealed significant litter-associated differences in alpha and beta diversity at day 7 (P < 0.05). However, by day 35, microbial richness and overall community composition were no longer significantly different between treatments. At the phylum level, Bacillota was the dominant phylum in both litter groups at days 7 and 35. Pseudomonadota was the second most abundant phylum at day 7, whereas Bacteroidota became the second most abundant phylum by day 35. This shift indicates age related maturation of the cecal microbial community. In terms of immune responses, no significant difference was found in IEL subsets at day 7 between litter groups. However, by 35 days, the used litter exposure resulted in a significant expansion of TCR [-] , TCRγδ + , TCRαβ, TCRαβ [+] CD8αβ[+] and TCRαβ + CD8αα + IEL subsets (P < 0.05). Similarly, splenic TCRγδ+ and TCRαβ + CD8αβ+ populations were significantly elevated in used litter layer chicks at day 35. These findings highlight that exposure to different litter environment was associated with distinct cecal microbial profiles and immune-cell distributions in layer chicks. Given the limited information available in laying hens, these results provide novel baseline data and support further studies investigating the role of litter-associated microbial exposure in shaping early immune development.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Chickens/microbiology/immunology
*Cecum/microbiology/immunology
Female
*Microbiota
Spleen/immunology
Housing, Animal
Intraepithelial Lymphocytes/immunology
Body Weight
RevDate: 2026-08-12
CmpDate: 2026-08-12
The gut takes it all: Enteroendocrine control of developmental growth.
PLoS biology, 24(8):e3003921 pii:PBIOLOGY-D-26-02041.
How developing animals sense nutritional shortages to adjust growth? A new study in PLOS Biology shows that the developing intestine is a central regulator of animal growth in response to microbiome composition and nutritional deficiency.
Additional Links: PMID-42585212
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PubMed:
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@article {pmid42585212,
year = {2026},
author = {Cordero, JB},
title = {The gut takes it all: Enteroendocrine control of developmental growth.},
journal = {PLoS biology},
volume = {24},
number = {8},
pages = {e3003921},
doi = {10.1371/journal.pbio.3003921},
pmid = {42585212},
issn = {1545-7885},
mesh = {Animals ; *Enteroendocrine Cells/physiology/metabolism ; *Intestines/microbiology/growth & development ; },
abstract = {How developing animals sense nutritional shortages to adjust growth? A new study in PLOS Biology shows that the developing intestine is a central regulator of animal growth in response to microbiome composition and nutritional deficiency.},
}
MeSH Terms:
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Animals
*Enteroendocrine Cells/physiology/metabolism
*Intestines/microbiology/growth & development
RevDate: 2026-08-12
CmpDate: 2026-08-12
TMAO is associated with higher age, cardiometabolic risk factors and degenerative alterations of the brain in healthy elderly adults.
Aging, 18(1):991-1003.
Trimethylamine N-oxide (TMAO) is a microbiome-based metabolite known to increase with age, cardiovascular and other diseases, with average concentrations mostly higher in males. It was recently found to be associated with neurodegenerative diseases. In this context we aimed to investigate associations between TMAO, cardiometabolic risk factors, cognitive function and brain atrophy in older individuals (67.81 ± 8.86 years of age) with normal neurological status. TMAO was measured by liquid-chromatography tandem mass spectrometry in serum samples from 487 individuals. All participants underwent cognitive testing capturing executive function, motor and memory abilities. In 180 of these individuals, brain MRI was performed to investigate vascular and neurodegenerative changes. In the total cohort higher TMAO concentrations were positively associated with advanced age (p=0.01), BMI (p<0.01), fasting blood sugar (p<0.01), HbA1c (p<0.01) and diabetes (p=0.02). In contrast, we observed negative associations with total cholesterol (p=0.01), LDL (p=0.04) and HDL cholesterol (p=0.04). No significant differences in TMAO concentrations were found between females and males. MRI revealed higher TMAO levels to be associated with lower total grey matter, frontal lobar and hippocampal volume (p=0.01). Summarized, TMAO is associated with higher age, cardiometabolic risk factors and brain atrophy, while there was no difference between the two sexes of this community-dwelling elderly cohort. These findings support that TMAO is mainly a marker of aging processes but also associated with neurodegeneration, even though associations with cognitive functioning were not observed.
Additional Links: PMID-42585667
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@article {pmid42585667,
year = {2026},
author = {Almer, G and Hofer, E and Schmidt, R and Meinitzer, A and Herrmann, M and Enko, D},
title = {TMAO is associated with higher age, cardiometabolic risk factors and degenerative alterations of the brain in healthy elderly adults.},
journal = {Aging},
volume = {18},
number = {1},
pages = {991-1003},
doi = {10.18632/aging.206401},
pmid = {42585667},
issn = {1945-4589},
mesh = {Humans ; Male ; Aged ; *Methylamines/blood ; Female ; *Brain/pathology/diagnostic imaging ; *Aging/blood ; *Cardiometabolic Risk Factors ; Cognition/physiology ; Magnetic Resonance Imaging ; Middle Aged ; Atrophy ; Risk Factors ; },
abstract = {Trimethylamine N-oxide (TMAO) is a microbiome-based metabolite known to increase with age, cardiovascular and other diseases, with average concentrations mostly higher in males. It was recently found to be associated with neurodegenerative diseases. In this context we aimed to investigate associations between TMAO, cardiometabolic risk factors, cognitive function and brain atrophy in older individuals (67.81 ± 8.86 years of age) with normal neurological status. TMAO was measured by liquid-chromatography tandem mass spectrometry in serum samples from 487 individuals. All participants underwent cognitive testing capturing executive function, motor and memory abilities. In 180 of these individuals, brain MRI was performed to investigate vascular and neurodegenerative changes. In the total cohort higher TMAO concentrations were positively associated with advanced age (p=0.01), BMI (p<0.01), fasting blood sugar (p<0.01), HbA1c (p<0.01) and diabetes (p=0.02). In contrast, we observed negative associations with total cholesterol (p=0.01), LDL (p=0.04) and HDL cholesterol (p=0.04). No significant differences in TMAO concentrations were found between females and males. MRI revealed higher TMAO levels to be associated with lower total grey matter, frontal lobar and hippocampal volume (p=0.01). Summarized, TMAO is associated with higher age, cardiometabolic risk factors and brain atrophy, while there was no difference between the two sexes of this community-dwelling elderly cohort. These findings support that TMAO is mainly a marker of aging processes but also associated with neurodegeneration, even though associations with cognitive functioning were not observed.},
}
MeSH Terms:
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Humans
Male
Aged
*Methylamines/blood
Female
*Brain/pathology/diagnostic imaging
*Aging/blood
*Cardiometabolic Risk Factors
Cognition/physiology
Magnetic Resonance Imaging
Middle Aged
Atrophy
Risk Factors
RevDate: 2026-08-12
Phosphorus source shapes rhizosphere microbiome assembly and plant oxidative stress regulation in a volcanic Andisol: a path-analysis approach.
Plant physiology and biochemistry : PPB, 238:111618 pii:S0981-9428(26)00604-2 [Epub ahead of print].
Volcanic Andisols in southern Chile severely limit pasture productivity due to their high phosphorus (P) sorption capacity. This study evaluated how contrasting P sources shape the rhizosphere microbiome of perennial ryegrass (Lolium perenne) and the pathways linking microbial community composition, plant biochemical responses, and biomass production under P-limiting conditions. A greenhouse experiment using an Andisol (Freire series) tested four P sources; Triple Superphosphate (TSP), Phosphate Rock (PR), Cattle Dung (CD), and Poultry Manure (PM); at two nitrogen (N) rates (100 and 200 mg kg[-1]) alongside no-P control that received the same two N rates and basal nutrients but no added P. Rhizosphere communities were characterized by 16S rRNA amplicon sequencing coupled with functional gene prediction (PICRUSt2), antioxidant enzyme activity and lipid peroxidation markers (superoxide dismutase, catalase, malondialdehyde), P-starvation transporter and phosphatase gene expression (LpPHT1;1, LpPHT1;4, LpPAP1), and soil chemistry. P source was the dominant driver of both plant performance and community composition, with N rate exerting a secondary, modulatory role; attenuating P-starvation gene expression at higher doses and subtly influencing community beta-diversity. Soil P availability, pH, and exchangeable aluminum were the significant drivers of community structure. Path analysis revealed that the rhizosphere microbiome had no significant direct effect on shoot P uptake but was strongly associated with reduced foliar oxidative stress (β = -0.759, p < 0.001), with its indirect effect on shoot biomass statistically consistent with mediation through this antioxidant buffering response. Organic amendments enriched predicted genes related to P mineralization and biological N-P cycling while suppressing denitrification-associated genes. These findings suggest that in high P-fixing volcanic soils, rhizosphere community shifts benefit plant growth primarily by alleviating P deficiency-induced oxidative stress rather than by directly enhancing P uptake, highlighting the agronomic value of organic amendments beyond nutrient supply alone.
Additional Links: PMID-42585736
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PubMed:
Citation:
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@article {pmid42585736,
year = {2026},
author = {Barra, PJ and Parra-Almuna, L and Pontigo, S and Paredes, C and Larama, G and Valdebenito, D and Jerez-Quezada, C and Menezes-Blackburn, D and Mora, ML},
title = {Phosphorus source shapes rhizosphere microbiome assembly and plant oxidative stress regulation in a volcanic Andisol: a path-analysis approach.},
journal = {Plant physiology and biochemistry : PPB},
volume = {238},
number = {},
pages = {111618},
doi = {10.1016/j.plaphy.2026.111618},
pmid = {42585736},
issn = {1873-2690},
abstract = {Volcanic Andisols in southern Chile severely limit pasture productivity due to their high phosphorus (P) sorption capacity. This study evaluated how contrasting P sources shape the rhizosphere microbiome of perennial ryegrass (Lolium perenne) and the pathways linking microbial community composition, plant biochemical responses, and biomass production under P-limiting conditions. A greenhouse experiment using an Andisol (Freire series) tested four P sources; Triple Superphosphate (TSP), Phosphate Rock (PR), Cattle Dung (CD), and Poultry Manure (PM); at two nitrogen (N) rates (100 and 200 mg kg[-1]) alongside no-P control that received the same two N rates and basal nutrients but no added P. Rhizosphere communities were characterized by 16S rRNA amplicon sequencing coupled with functional gene prediction (PICRUSt2), antioxidant enzyme activity and lipid peroxidation markers (superoxide dismutase, catalase, malondialdehyde), P-starvation transporter and phosphatase gene expression (LpPHT1;1, LpPHT1;4, LpPAP1), and soil chemistry. P source was the dominant driver of both plant performance and community composition, with N rate exerting a secondary, modulatory role; attenuating P-starvation gene expression at higher doses and subtly influencing community beta-diversity. Soil P availability, pH, and exchangeable aluminum were the significant drivers of community structure. Path analysis revealed that the rhizosphere microbiome had no significant direct effect on shoot P uptake but was strongly associated with reduced foliar oxidative stress (β = -0.759, p < 0.001), with its indirect effect on shoot biomass statistically consistent with mediation through this antioxidant buffering response. Organic amendments enriched predicted genes related to P mineralization and biological N-P cycling while suppressing denitrification-associated genes. These findings suggest that in high P-fixing volcanic soils, rhizosphere community shifts benefit plant growth primarily by alleviating P deficiency-induced oxidative stress rather than by directly enhancing P uptake, highlighting the agronomic value of organic amendments beyond nutrient supply alone.},
}
RevDate: 2026-08-12
Synbiotic and postbiotic reuterin attenuate heat stress in rabbits by improving intestinal barrier function and modulating TLR4-NF-κB signalling.
Research in veterinary science, 210:106353 pii:S0034-5288(26)00307-3 [Epub ahead of print].
Heat stress disrupts intestinal barrier integrity, immune homeostasis, and growth in rabbits, a species highly sensitive to thermal challenges. Microbiota-targeted interventions represent a potential strategy to mitigate these effects. This study evaluated the protective effects of a probiotic (Limosilactobacillus reuteri), a prebiotic (inulin), a postbiotic (reuterin), and a synbiotic (reuterin + β-galacto-oligosaccharides) under natural summer conditions. Rabbits (n = 6 per group) were assessed for thermoregulation, growth, intestinal barrier markers (jejunal zonula occludens-1 [ZO-1], plasma D-lactate), oxidative stress (malondialdehyde [MDA], superoxide dismutase [SOD], catalase [CAT], glutathione [GSH]), inflammatory signalling (TLR4-MyD88-NF-κB, TNF-α, IL-6, IL-10), and gut microbiota composition. All treatments improved thermoregulation, growth, barrier integrity, and redox balance, while suppressing pro-inflammatory signalling, with the synbiotic showing the most consistent benefits, including enrichment of beneficial microbes. In silico analyses indicated that inulin and reuterin interact with key immunoregulatory and metabolic proteins, supporting their functional bioactivity. Mechanistically, these interventions restore intestinal homeostasis by reshaping the microbiota, attenuating endotoxin-driven activation of the TLR4-MyD88-NF-κB axis, strengthening tight junctions, and enhancing antioxidant defenses, thereby reducing epithelial permeability and systemic inflammation. Synbiotic and reuterin-based treatments show the strongest effects, likely via synergistic modulation of host-microbe interactions and intracellular signalling pathways that stabilize barrier integrity, immune balance, and metabolic performance under heat stress.
Additional Links: PMID-42585802
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PubMed:
Citation:
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@article {pmid42585802,
year = {2026},
author = {El Ghany, KA and Yassin, HM and Mosaad, RM and El-Garhy, HAS and Saif El Nasr, WS and Khattab, RH and Aika, EAM and Al Saihati, HA and Warda, M and Shadidizaji, A and Ahmed-Farid, OA},
title = {Synbiotic and postbiotic reuterin attenuate heat stress in rabbits by improving intestinal barrier function and modulating TLR4-NF-κB signalling.},
journal = {Research in veterinary science},
volume = {210},
number = {},
pages = {106353},
doi = {10.1016/j.rvsc.2026.106353},
pmid = {42585802},
issn = {1532-2661},
abstract = {Heat stress disrupts intestinal barrier integrity, immune homeostasis, and growth in rabbits, a species highly sensitive to thermal challenges. Microbiota-targeted interventions represent a potential strategy to mitigate these effects. This study evaluated the protective effects of a probiotic (Limosilactobacillus reuteri), a prebiotic (inulin), a postbiotic (reuterin), and a synbiotic (reuterin + β-galacto-oligosaccharides) under natural summer conditions. Rabbits (n = 6 per group) were assessed for thermoregulation, growth, intestinal barrier markers (jejunal zonula occludens-1 [ZO-1], plasma D-lactate), oxidative stress (malondialdehyde [MDA], superoxide dismutase [SOD], catalase [CAT], glutathione [GSH]), inflammatory signalling (TLR4-MyD88-NF-κB, TNF-α, IL-6, IL-10), and gut microbiota composition. All treatments improved thermoregulation, growth, barrier integrity, and redox balance, while suppressing pro-inflammatory signalling, with the synbiotic showing the most consistent benefits, including enrichment of beneficial microbes. In silico analyses indicated that inulin and reuterin interact with key immunoregulatory and metabolic proteins, supporting their functional bioactivity. Mechanistically, these interventions restore intestinal homeostasis by reshaping the microbiota, attenuating endotoxin-driven activation of the TLR4-MyD88-NF-κB axis, strengthening tight junctions, and enhancing antioxidant defenses, thereby reducing epithelial permeability and systemic inflammation. Synbiotic and reuterin-based treatments show the strongest effects, likely via synergistic modulation of host-microbe interactions and intracellular signalling pathways that stabilize barrier integrity, immune balance, and metabolic performance under heat stress.},
}
RevDate: 2026-08-12
Cancer immunotherapy under immune pressure: Mechanisms of resistance and the shift toward precision immune engineering.
International immunopharmacology, 187:117271 pii:S1567-5769(26)01117-3 [Epub ahead of print].
Cancer immunotherapy has transformed the treatment landscape across multiple malignancies; however, durable responses remain limited to a subset of patients due to the emergence of intrinsic and acquired resistance. Increasing evidence suggests that therapeutic immune pressure itself acts as a selective force that shapes tumour evolution, driving the outgrowth of resistant clones. In this review, we synthesise current understanding of the molecular and cellular mechanisms underlying resistance to major immunotherapeutic modalities, including immune checkpoint inhibitors, adoptive cell therapies, and cancer vaccines. We discuss tumour-intrinsic alterations such as defects in antigen presentation and immune signalling pathways, alongside tumour-extrinsic factors including immunosuppressive cell populations, metabolic constraints, and microbiome-mediated modulation. We further examine how these mechanisms converge within the tumour microenvironment to limit therapeutic efficacy. Emerging strategies to overcome resistance are highlighted, including rational combination therapies, next-generation engineered cellular platforms, and precision-guided approaches enabled by multi-omics profiling and artificial intelligence. Collectively, we propose that resistance should be understood as an adaptive consequence of therapeutic immune pressure. Building upon the principles of cancer immunoediting, we discuss how precision immune engineering, the rational design of personalised immunotherapeutic strategies informed by tumour biology, immune context, and predictive biomarkers, may be used to anticipate and overcome evolutionary escape mechanisms.
Additional Links: PMID-42585834
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PubMed:
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@article {pmid42585834,
year = {2026},
author = {Anwer, M},
title = {Cancer immunotherapy under immune pressure: Mechanisms of resistance and the shift toward precision immune engineering.},
journal = {International immunopharmacology},
volume = {187},
number = {},
pages = {117271},
doi = {10.1016/j.intimp.2026.117271},
pmid = {42585834},
issn = {1878-1705},
abstract = {Cancer immunotherapy has transformed the treatment landscape across multiple malignancies; however, durable responses remain limited to a subset of patients due to the emergence of intrinsic and acquired resistance. Increasing evidence suggests that therapeutic immune pressure itself acts as a selective force that shapes tumour evolution, driving the outgrowth of resistant clones. In this review, we synthesise current understanding of the molecular and cellular mechanisms underlying resistance to major immunotherapeutic modalities, including immune checkpoint inhibitors, adoptive cell therapies, and cancer vaccines. We discuss tumour-intrinsic alterations such as defects in antigen presentation and immune signalling pathways, alongside tumour-extrinsic factors including immunosuppressive cell populations, metabolic constraints, and microbiome-mediated modulation. We further examine how these mechanisms converge within the tumour microenvironment to limit therapeutic efficacy. Emerging strategies to overcome resistance are highlighted, including rational combination therapies, next-generation engineered cellular platforms, and precision-guided approaches enabled by multi-omics profiling and artificial intelligence. Collectively, we propose that resistance should be understood as an adaptive consequence of therapeutic immune pressure. Building upon the principles of cancer immunoediting, we discuss how precision immune engineering, the rational design of personalised immunotherapeutic strategies informed by tumour biology, immune context, and predictive biomarkers, may be used to anticipate and overcome evolutionary escape mechanisms.},
}
RevDate: 2026-08-12
Mechanized Qu-making may contribute to lactic acid bacteria overproliferation in Hongqu rice wine brewing: Insights into microbial dysbiosis and flavor quality deterioration.
International journal of food microbiology, 461:112013 pii:S0168-1605(26)00394-6 [Epub ahead of print].
Hongqu (HQ) serves as the core saccharification and fermentation starter (commonly referred to as "Qu") for Hongqu rice wine (HQW), a traditional Chinese fermented alcoholic beverage celebrated for its unique sensory characteristics and potential health-promoting properties. Driven by industrialization, mechanized Qu production has been progressively implemented to enhance process reproducibility, scalability, and operational efficiency. However, the implications of this technological transition on microbial community assembly, metabolic function and flavor formation during HQW brewing remain insufficiently characterized. To address this gap, this study employed an integrated metagenomic and metabolomic approach to comparatively analyze the taxonomic composition and functional metabolic profiles of mechanized Hongqu (MHQ) and traditional Hongqu (THQ), and further monitored their dynamic succession throughout HQW brewing process. Results demonstrated that MHQ exhibited significantly higher saccharification capacity and markedly enriched abundance of Saccharomyces cerevisiae, yet displayed a substantial reduction in Aspergillus niger compared with THQ (1.06% versus 43.41%). Paradoxically, despite these favorable starter attributes, HQW fermentation inoculated with MHQ induced an uncontrollable proliferation of lactic acid bacteria (LAB), predominantly represented by Pediococcus acidilactici, Lactiplantibacillus plantarum and Weissella paramesenteroides. This LAB-dominant consortium proliferated markedly during HQW fermentation, resulting in a community compositional shift toward bacterial dominance, evidenced by a fungi-to-bacteria ratio of 1.00:5.88 in MHQW, whereas THQW retained fungal dominance, with a corresponding ratio of 1.00:0.26. This structural shift coincided with significant declines in the relative abundances of functional fungi, including Saccharomyces cerevisiae and Monascus purpureus, possibly involving changes in niche occupation and acidification. These microbial community changes were associated with a metabolic shift characterized by excessive accumulation of organic acids, dysregulated biogenic amine profiles, depletion of free amino acids, and diminished synthesis of key volatile flavor compounds. Quantitatively, MHQW exhibited significantly higher final titratable acidity (12.67 g/L vs. 5.76 g/L), lower ethanol yield (17.29% v/v vs. 20.39% v/v), elevated total organic acid content (16.62 g/L vs. 6.28 g/L), and reduced total free amino acid concentration (3366.23 mg/L vs. 4303.93 mg/L) relative to THQW. Collectively, these findings indicate that mechanized Qu-making may disrupt the delicate "fungi-bacteria" ecological equilibrium essential for robust and balanced HQW fermentation, potentially favoring LAB proliferation. This study highlights the potential value of rational microbiome design to control LAB proliferation while maintaining functional fungi, which is important for optimizing mechanized Qu-making processes and improving flavor quality and fermentation robustness in HQW production. Collectively, our work provides a mechanism-informed framework for advancing Huangjiu modernization through rational microbiome engineering.
Additional Links: PMID-42585873
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@article {pmid42585873,
year = {2026},
author = {Wang, H and Liang, Z and Guo, W and Ni, L and Lv, X},
title = {Mechanized Qu-making may contribute to lactic acid bacteria overproliferation in Hongqu rice wine brewing: Insights into microbial dysbiosis and flavor quality deterioration.},
journal = {International journal of food microbiology},
volume = {461},
number = {},
pages = {112013},
doi = {10.1016/j.ijfoodmicro.2026.112013},
pmid = {42585873},
issn = {1879-3460},
abstract = {Hongqu (HQ) serves as the core saccharification and fermentation starter (commonly referred to as "Qu") for Hongqu rice wine (HQW), a traditional Chinese fermented alcoholic beverage celebrated for its unique sensory characteristics and potential health-promoting properties. Driven by industrialization, mechanized Qu production has been progressively implemented to enhance process reproducibility, scalability, and operational efficiency. However, the implications of this technological transition on microbial community assembly, metabolic function and flavor formation during HQW brewing remain insufficiently characterized. To address this gap, this study employed an integrated metagenomic and metabolomic approach to comparatively analyze the taxonomic composition and functional metabolic profiles of mechanized Hongqu (MHQ) and traditional Hongqu (THQ), and further monitored their dynamic succession throughout HQW brewing process. Results demonstrated that MHQ exhibited significantly higher saccharification capacity and markedly enriched abundance of Saccharomyces cerevisiae, yet displayed a substantial reduction in Aspergillus niger compared with THQ (1.06% versus 43.41%). Paradoxically, despite these favorable starter attributes, HQW fermentation inoculated with MHQ induced an uncontrollable proliferation of lactic acid bacteria (LAB), predominantly represented by Pediococcus acidilactici, Lactiplantibacillus plantarum and Weissella paramesenteroides. This LAB-dominant consortium proliferated markedly during HQW fermentation, resulting in a community compositional shift toward bacterial dominance, evidenced by a fungi-to-bacteria ratio of 1.00:5.88 in MHQW, whereas THQW retained fungal dominance, with a corresponding ratio of 1.00:0.26. This structural shift coincided with significant declines in the relative abundances of functional fungi, including Saccharomyces cerevisiae and Monascus purpureus, possibly involving changes in niche occupation and acidification. These microbial community changes were associated with a metabolic shift characterized by excessive accumulation of organic acids, dysregulated biogenic amine profiles, depletion of free amino acids, and diminished synthesis of key volatile flavor compounds. Quantitatively, MHQW exhibited significantly higher final titratable acidity (12.67 g/L vs. 5.76 g/L), lower ethanol yield (17.29% v/v vs. 20.39% v/v), elevated total organic acid content (16.62 g/L vs. 6.28 g/L), and reduced total free amino acid concentration (3366.23 mg/L vs. 4303.93 mg/L) relative to THQW. Collectively, these findings indicate that mechanized Qu-making may disrupt the delicate "fungi-bacteria" ecological equilibrium essential for robust and balanced HQW fermentation, potentially favoring LAB proliferation. This study highlights the potential value of rational microbiome design to control LAB proliferation while maintaining functional fungi, which is important for optimizing mechanized Qu-making processes and improving flavor quality and fermentation robustness in HQW production. Collectively, our work provides a mechanism-informed framework for advancing Huangjiu modernization through rational microbiome engineering.},
}
RevDate: 2026-08-12
Integrative multi-omics reveals comprehensive gut-liver-adipose metabolic changes in peak laying hens with high or low egg production.
Poultry science, 105(11):107493 pii:S0032-5791(26)01126-0 [Epub ahead of print].
Eggs serve as an indispensable global nutritional resource, sustaining the economic foundation of the commercial poultry industry. To meet this continuous demand, egg formation involves an exceptionally energy-intensive biological process requiring continuous yolk precursor synthesis, which imposes a massive metabolic burden on laying hens. However, the comprehensive metabolic differences across the gut-liver-adipose axis between peak laying hens with high or low egg production remain incompletely characterized. A total of 180 healthy Hy-Line Brown laying hens (45-week-old) were continuously fed and monitored for production performance over a 6-week period. Following the exclusion of individuals with extremely low egg production (≤10 eggs during the 6-week monitoring period; n = 5) and candidate hens that repeatedly produced unqualified eggs over multiple weeks (n = 20), the remaining hens were ranked by 6-week average laying rate and allocated into FH (high-production hens at 50 weeks of age, n = 15) and FL (low-production hens at 50 weeks of age, n = 14) groups. Initial body weight did not differ significantly between groups (FH: 1936 ± 29.0 g; FL: 1894 ± 48.2 g; P-value = 0.446). We integrated transcriptomic, untargeted metabolomic, targeted bile acid metabolomics, and microbiome (16S rRNA and metagenomic) profiles to characterize comprehensive metabolic changes across the gut-liver-adipose axis associated with divergent egg-production phenotypes. The results showed that: (1) FH hens exhibited higher serum APOB and lower conjugated bile acids (TCDCA, TCA, and THDCA), with hepatic upregulation of FASN, PPARA, CPT1A, and VTG1 along with downregulation of CYP7A1, CYP7B1, CYP8B1, and CYP27A1; (2) intersecting module hub genes (MHGs) with differentially expressed genes (DEGs) identified 354 upregulated and 299 downregulated core genes, with EEF2 identified as the primary hepatic downregulated hub gene; (3) in abdominal fat, GSEA revealed significant enrichment in fatty acid transport (NES = 1.54), long-chain fatty acid metabolic process (NES = 1.39), and steroid hormone biosynthesis (NES = 1.85), accompanied by significant downregulation of ANGPTL4 and upregulation of HSD3B1, VTG1, VTG2, and VTG3; (4) ileal mucosal transcriptomics identified 619 DEGs (502 upregulated), with GSEA highlighting enrichment in cell junction organization (NES = 1.52) and tube morphogenesis (NES = 1.39), which were further categorized into functional modules including enteric synaptic signaling, epithelial adhesion, mucosal vascularization, and tissue renewal; (5) the functional profile of the ileal microbiota in FH hens showed enrichment of functions related to complex carbohydrate degradation and carbohydrate-binding modules, with keystone taxa including Blautia and Bifidobacterium associated with production and lipid markers. Collectively, these findings suggest that high egg production during the peak laying period is associated with coordinated metabolic differences across the liver, abdominal fat tissue, and intestine. The observed profiles included reduced hepatic translation-related and primary bile acid synthesis-related signatures, adipose endocrine-related changes and microbial functional potential related to carbohydrate utilization and antioxidant-related functional potential. These findings provide candidate multi-omics features for precision nutritional strategies and genetic improvement in commercial poultry.
Additional Links: PMID-42585927
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PubMed:
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@article {pmid42585927,
year = {2026},
author = {Ma, J and Qin, K and Qiao, Z and Ren, Z and Yang, X and Liu, Y},
title = {Integrative multi-omics reveals comprehensive gut-liver-adipose metabolic changes in peak laying hens with high or low egg production.},
journal = {Poultry science},
volume = {105},
number = {11},
pages = {107493},
doi = {10.1016/j.psj.2026.107493},
pmid = {42585927},
issn = {1525-3171},
abstract = {Eggs serve as an indispensable global nutritional resource, sustaining the economic foundation of the commercial poultry industry. To meet this continuous demand, egg formation involves an exceptionally energy-intensive biological process requiring continuous yolk precursor synthesis, which imposes a massive metabolic burden on laying hens. However, the comprehensive metabolic differences across the gut-liver-adipose axis between peak laying hens with high or low egg production remain incompletely characterized. A total of 180 healthy Hy-Line Brown laying hens (45-week-old) were continuously fed and monitored for production performance over a 6-week period. Following the exclusion of individuals with extremely low egg production (≤10 eggs during the 6-week monitoring period; n = 5) and candidate hens that repeatedly produced unqualified eggs over multiple weeks (n = 20), the remaining hens were ranked by 6-week average laying rate and allocated into FH (high-production hens at 50 weeks of age, n = 15) and FL (low-production hens at 50 weeks of age, n = 14) groups. Initial body weight did not differ significantly between groups (FH: 1936 ± 29.0 g; FL: 1894 ± 48.2 g; P-value = 0.446). We integrated transcriptomic, untargeted metabolomic, targeted bile acid metabolomics, and microbiome (16S rRNA and metagenomic) profiles to characterize comprehensive metabolic changes across the gut-liver-adipose axis associated with divergent egg-production phenotypes. The results showed that: (1) FH hens exhibited higher serum APOB and lower conjugated bile acids (TCDCA, TCA, and THDCA), with hepatic upregulation of FASN, PPARA, CPT1A, and VTG1 along with downregulation of CYP7A1, CYP7B1, CYP8B1, and CYP27A1; (2) intersecting module hub genes (MHGs) with differentially expressed genes (DEGs) identified 354 upregulated and 299 downregulated core genes, with EEF2 identified as the primary hepatic downregulated hub gene; (3) in abdominal fat, GSEA revealed significant enrichment in fatty acid transport (NES = 1.54), long-chain fatty acid metabolic process (NES = 1.39), and steroid hormone biosynthesis (NES = 1.85), accompanied by significant downregulation of ANGPTL4 and upregulation of HSD3B1, VTG1, VTG2, and VTG3; (4) ileal mucosal transcriptomics identified 619 DEGs (502 upregulated), with GSEA highlighting enrichment in cell junction organization (NES = 1.52) and tube morphogenesis (NES = 1.39), which were further categorized into functional modules including enteric synaptic signaling, epithelial adhesion, mucosal vascularization, and tissue renewal; (5) the functional profile of the ileal microbiota in FH hens showed enrichment of functions related to complex carbohydrate degradation and carbohydrate-binding modules, with keystone taxa including Blautia and Bifidobacterium associated with production and lipid markers. Collectively, these findings suggest that high egg production during the peak laying period is associated with coordinated metabolic differences across the liver, abdominal fat tissue, and intestine. The observed profiles included reduced hepatic translation-related and primary bile acid synthesis-related signatures, adipose endocrine-related changes and microbial functional potential related to carbohydrate utilization and antioxidant-related functional potential. These findings provide candidate multi-omics features for precision nutritional strategies and genetic improvement in commercial poultry.},
}
RevDate: 2026-08-12
Microplastics disrupt bacterial defense within the plant-AMF-bacteria continuum to amplify Cd bioavailability.
Journal of hazardous materials, 515:143257 pii:S0304-3894(26)02237-5 [Epub ahead of print].
The plant-arbuscular mycorrhizal fungi (AMF)-bacteria continuum provides a critical barrier against heavy-metal toxicity, but how microplastics (MPs) disrupt rhizosphere functions and exacerbate phytotoxicity remains unresolved. Using a maize-AMF-bacteria system in cadmium (Cd)-contaminated soil, we investigated two MP fractions differing in size and morphology added at increasing Cd contents. Although AMF colonization remained resilient, MPs induced fraction-dependent bacterial functional decoupling. Small MPs shifted the microbiome from extracellular Cd-immobilizing taxa (Sphingomonadaceae and Rhizobiaceae) toward intracellular stress-tolerant lineages. Large MPs restricted bacterial contacts, suppressing density-dependent cooperation. Metagenomic profiling and analysis of metagenome-assembled genomes (MAGs) revealed reduced potential for quorum sensing, ABC transporters, and alpha-linolenic acid metabolism under large MP exposure, compromising biofilm formation and extracellular Cd sequestration. Partial least squares path modeling indicated that bulk-soil chemistry did not define Cd uptake by plants. Instead, depletion of available Cd in soil reflected a biological sink associated with enhanced plant uptake. Enhanced Cd accumulation was associated with loss of rhizosphere defense mechanisms: potential root-barrier disruption by large MPs and weakened microbial buffering. Consequently, large MPs increased the Cd bioconcentration factor by 57.5%, compared with 32.1% for small MPs. These findings show that MPs amplify legacy Cd risks without increasing bulk-soil Cd availability, through disruption of root-interface integrity and microbial protection.
Additional Links: PMID-42585955
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PubMed:
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@article {pmid42585955,
year = {2026},
author = {Han, X and Gao, Y and Chen, J and Yang, P and Liang, X and Wang, L and Ge, Y and Gui, H and He, Y and Zhan, F and Zhang, X and Kuzyakov, Y},
title = {Microplastics disrupt bacterial defense within the plant-AMF-bacteria continuum to amplify Cd bioavailability.},
journal = {Journal of hazardous materials},
volume = {515},
number = {},
pages = {143257},
doi = {10.1016/j.jhazmat.2026.143257},
pmid = {42585955},
issn = {1873-3336},
abstract = {The plant-arbuscular mycorrhizal fungi (AMF)-bacteria continuum provides a critical barrier against heavy-metal toxicity, but how microplastics (MPs) disrupt rhizosphere functions and exacerbate phytotoxicity remains unresolved. Using a maize-AMF-bacteria system in cadmium (Cd)-contaminated soil, we investigated two MP fractions differing in size and morphology added at increasing Cd contents. Although AMF colonization remained resilient, MPs induced fraction-dependent bacterial functional decoupling. Small MPs shifted the microbiome from extracellular Cd-immobilizing taxa (Sphingomonadaceae and Rhizobiaceae) toward intracellular stress-tolerant lineages. Large MPs restricted bacterial contacts, suppressing density-dependent cooperation. Metagenomic profiling and analysis of metagenome-assembled genomes (MAGs) revealed reduced potential for quorum sensing, ABC transporters, and alpha-linolenic acid metabolism under large MP exposure, compromising biofilm formation and extracellular Cd sequestration. Partial least squares path modeling indicated that bulk-soil chemistry did not define Cd uptake by plants. Instead, depletion of available Cd in soil reflected a biological sink associated with enhanced plant uptake. Enhanced Cd accumulation was associated with loss of rhizosphere defense mechanisms: potential root-barrier disruption by large MPs and weakened microbial buffering. Consequently, large MPs increased the Cd bioconcentration factor by 57.5%, compared with 32.1% for small MPs. These findings show that MPs amplify legacy Cd risks without increasing bulk-soil Cd availability, through disruption of root-interface integrity and microbial protection.},
}
RevDate: 2026-08-12
CmpDate: 2026-08-12
Soil microbiomes and regenerative agriculture.
Cell host & microbe, 34(8):1489-1493.
Regenerative agriculture is gaining attention as a way to make agriculture more sustainable and to better integrate natural processes. Here, we highlight how the soil microbiome critically contributes to regenerative agriculture by providing multiple functions that support soil health and plant growth under future climate change.
Additional Links: PMID-42586035
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PubMed:
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@article {pmid42586035,
year = {2026},
author = {Bardgett, RD and van der Heijden, MGA},
title = {Soil microbiomes and regenerative agriculture.},
journal = {Cell host & microbe},
volume = {34},
number = {8},
pages = {1489-1493},
doi = {10.1016/j.chom.2026.07.002},
pmid = {42586035},
issn = {1934-6069},
mesh = {*Soil Microbiology ; *Microbiota ; *Agriculture/methods ; Climate Change ; Plant Development ; },
abstract = {Regenerative agriculture is gaining attention as a way to make agriculture more sustainable and to better integrate natural processes. Here, we highlight how the soil microbiome critically contributes to regenerative agriculture by providing multiple functions that support soil health and plant growth under future climate change.},
}
MeSH Terms:
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*Soil Microbiology
*Microbiota
*Agriculture/methods
Climate Change
Plant Development
RevDate: 2026-08-12
CmpDate: 2026-08-12
Next-generation coral microbiome stewardship: From holobiont restoration to ecosystem resilience.
Cell host & microbe, 34(8):1494-1498.
Marine bacterial microbiomes comprise an invisible biological infrastructure supporting ecosystem resilience. As climate stressors drive coral reef dysbiosis, microbial-based interventions, including probiotics, bioengineering, and holobiont priming, offer emerging strategies to restore holobiont function and enhance resilience. We explore state-of-the-art tools and outline challenges and policy-aligned pathways for translation.
Additional Links: PMID-42586036
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PubMed:
Citation:
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@article {pmid42586036,
year = {2026},
author = {Peixoto, RS and Monti, M and Beenham, L and Luo, H and Voolstra, CR},
title = {Next-generation coral microbiome stewardship: From holobiont restoration to ecosystem resilience.},
journal = {Cell host & microbe},
volume = {34},
number = {8},
pages = {1494-1498},
doi = {10.1016/j.chom.2026.07.010},
pmid = {42586036},
issn = {1934-6069},
mesh = {Animals ; *Microbiota/physiology ; *Ecosystem ; *Anthozoa/microbiology ; Coral Reefs ; Symbiosis ; Probiotics ; Dysbiosis ; Bioengineering ; },
abstract = {Marine bacterial microbiomes comprise an invisible biological infrastructure supporting ecosystem resilience. As climate stressors drive coral reef dysbiosis, microbial-based interventions, including probiotics, bioengineering, and holobiont priming, offer emerging strategies to restore holobiont function and enhance resilience. We explore state-of-the-art tools and outline challenges and policy-aligned pathways for translation.},
}
MeSH Terms:
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Animals
*Microbiota/physiology
*Ecosystem
*Anthozoa/microbiology
Coral Reefs
Symbiosis
Probiotics
Dysbiosis
Bioengineering
RevDate: 2026-08-12
Targeting the Hallmarks of Ageing: Pharmacological Challenges and Breakthroughs in CRISPR Delivery Systems and Future Prospects.
Ageing research reviews pii:S1568-1637(26)00293-X [Epub ahead of print].
CRISPR has emerged as a next-generation gene-editing tool with the potential to target the molecular pathways associated with ageing and related disorders. It functions through RNA-guided Cas nucleases, directing DNA cleavage and utilizing the native DNA repair machinery for genetic manipulations. Advances in CRISPR technology have significantly enhanced the precision and flexibility of techniques for genome editing. The enzyme Cas9's ability to cut DNA at exact site has revolutionized genome editing by enabling accurate modifications within living eukaryotic cells. This review critically examines recent developments in CRISPR-based technologies, including Cas9, Cas12, base editing, prime editing, and CRISPR-mediated gene regulation. It highlights their rising applications in ageing research, with more emphasis on neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. The review also discusses the major pharmacological and translational challenges that currently limit clinical applications, including inefficient tissue-specific delivery, off-target genome editing, immunogenicity, manufacturing complexity, and long-term safety concerns. Also, recent progress in both, viral and non-viral delivery methods are critically evaluated, including adeno-associated viruses, lentivirus vectors, lipid nanoparticles, gold nanoparticles, exosomes, electroporation, and microinjection, is thoroughly discussed to highlight their therapeutic potential and translational limitations. Current studies indicate that CRISPR-based approaches have preclinical potential for targeting important hallmarks of ageing, particularly genomic instability, telomere attrition, and mitochondrial dysfunction. Other hallmarks of ageing, such as stem cell exhaustion, epigenetic modifications, and microbiome changes, are at earlier stages of development. Overall, this review describes future strategies for developing safe, precise, and clinically translatable CRISPR-based treatments to promote healthy ageing.
Additional Links: PMID-42586245
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PubMed:
Citation:
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@article {pmid42586245,
year = {2026},
author = {Rathore, S and Gupta, A and Shah, K and Chauhan, NS and Gupta, SK},
title = {Targeting the Hallmarks of Ageing: Pharmacological Challenges and Breakthroughs in CRISPR Delivery Systems and Future Prospects.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {103301},
doi = {10.1016/j.arr.2026.103301},
pmid = {42586245},
issn = {1872-9649},
abstract = {CRISPR has emerged as a next-generation gene-editing tool with the potential to target the molecular pathways associated with ageing and related disorders. It functions through RNA-guided Cas nucleases, directing DNA cleavage and utilizing the native DNA repair machinery for genetic manipulations. Advances in CRISPR technology have significantly enhanced the precision and flexibility of techniques for genome editing. The enzyme Cas9's ability to cut DNA at exact site has revolutionized genome editing by enabling accurate modifications within living eukaryotic cells. This review critically examines recent developments in CRISPR-based technologies, including Cas9, Cas12, base editing, prime editing, and CRISPR-mediated gene regulation. It highlights their rising applications in ageing research, with more emphasis on neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. The review also discusses the major pharmacological and translational challenges that currently limit clinical applications, including inefficient tissue-specific delivery, off-target genome editing, immunogenicity, manufacturing complexity, and long-term safety concerns. Also, recent progress in both, viral and non-viral delivery methods are critically evaluated, including adeno-associated viruses, lentivirus vectors, lipid nanoparticles, gold nanoparticles, exosomes, electroporation, and microinjection, is thoroughly discussed to highlight their therapeutic potential and translational limitations. Current studies indicate that CRISPR-based approaches have preclinical potential for targeting important hallmarks of ageing, particularly genomic instability, telomere attrition, and mitochondrial dysfunction. Other hallmarks of ageing, such as stem cell exhaustion, epigenetic modifications, and microbiome changes, are at earlier stages of development. Overall, this review describes future strategies for developing safe, precise, and clinically translatable CRISPR-based treatments to promote healthy ageing.},
}
RevDate: 2026-08-12
From Food to Function: Nutraceutical-Based Modulation of Mitochondrial, Inflammatory, and Epigenetic Networks in Retinal Neurodegeneration.
Ageing research reviews pii:S1568-1637(26)00280-1 [Epub ahead of print].
Retinal neurodegenerative diseases, such as age-related macular degeneration, diabetic retinopathy, glaucoma, and inherited retinal dystrophies, are major causes of irreversible vision loss worldwide. Although they originate from different causes, these disorders increasingly appear to share a network of cellular stress pathways, including impaired mitochondrial function, oxidative stress, endoplasmic reticulum proteostasis collapse, chronic neuroinflammation, epigenetic dysregulation, and activation of regulated cell death pathways. The interactions among these processes create an integrated stress network that gradually disrupts retinal homeostasis and promotes neuronal degeneration, which explains the failure of therapies targeting single molecular pathways. Nutraceutical compounds found in food are gaining interest as potential agents to support retinal health because many exhibit pleiotropic biological activities that influence mitochondrial function, inflammatory signaling, antioxidant defenses, and transcriptional regulation. Herein, we consolidate knowledge of the molecular mechanisms underlying retinal neurodegeneration and how major classes of nutraceuticals (polyphenols, carotenoids, omega-3 fatty acids, and metabolic modulators) may interact with these pathways. We also discuss key translational challenges in developing therapies, including poor bioavailability and differences between human phenotypes and model systems. Additionally, we highlight emerging concepts such as microbiome-dependent metabolism of nutraceuticals, personalized nutrition strategies, and advanced ocular drug-delivery technologies. Collectively, these findings support a systems-level framework in which selected nutraceuticals may influence multiple nodes of retinal stress biology, although clinical validation remains limited.
Additional Links: PMID-42586246
Publisher:
PubMed:
Citation:
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@article {pmid42586246,
year = {2026},
author = {Manjunatha, HJ and Mahalingappa, G and Varadaraju, SR and Manjunath, SH and Prashantha, K and Damle, A and Lee, C and Kumar, A},
title = {From Food to Function: Nutraceutical-Based Modulation of Mitochondrial, Inflammatory, and Epigenetic Networks in Retinal Neurodegeneration.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {103288},
doi = {10.1016/j.arr.2026.103288},
pmid = {42586246},
issn = {1872-9649},
abstract = {Retinal neurodegenerative diseases, such as age-related macular degeneration, diabetic retinopathy, glaucoma, and inherited retinal dystrophies, are major causes of irreversible vision loss worldwide. Although they originate from different causes, these disorders increasingly appear to share a network of cellular stress pathways, including impaired mitochondrial function, oxidative stress, endoplasmic reticulum proteostasis collapse, chronic neuroinflammation, epigenetic dysregulation, and activation of regulated cell death pathways. The interactions among these processes create an integrated stress network that gradually disrupts retinal homeostasis and promotes neuronal degeneration, which explains the failure of therapies targeting single molecular pathways. Nutraceutical compounds found in food are gaining interest as potential agents to support retinal health because many exhibit pleiotropic biological activities that influence mitochondrial function, inflammatory signaling, antioxidant defenses, and transcriptional regulation. Herein, we consolidate knowledge of the molecular mechanisms underlying retinal neurodegeneration and how major classes of nutraceuticals (polyphenols, carotenoids, omega-3 fatty acids, and metabolic modulators) may interact with these pathways. We also discuss key translational challenges in developing therapies, including poor bioavailability and differences between human phenotypes and model systems. Additionally, we highlight emerging concepts such as microbiome-dependent metabolism of nutraceuticals, personalized nutrition strategies, and advanced ocular drug-delivery technologies. Collectively, these findings support a systems-level framework in which selected nutraceuticals may influence multiple nodes of retinal stress biology, although clinical validation remains limited.},
}
RevDate: 2026-08-12
The gut microbiome-immunity-virus axis in lepidopteran antiviral defensee.
Current opinion in insect science pii:S2214-5745(26)00118-5 [Epub ahead of print].
The gut microbiota forms a competitive biological barrier against enteric pathogens and may also modulate antiviral immunity and disease prevention. This review presents recent advances demonstrating the tripartite model of the gut microbiome-immunity-virus axis in lepidopteran insects. Emerging evidence indicates that their gut microbiota regulates antiviral immunity through context-dependent mechanisms shaped by host species identity, microbial community composition, and strain-specific differences in viral resistance. Rather than acting as a uniformly protective factor, gut microbes fine-tune the local immune environment chiefly through antimicrobial peptide induction, modulation of PPO/melanization, Duox/ROS regulation, and maintenance of epithelial homeostasis. Although RNAi, STING-related, and JAK/STAT signalling are established antiviral pathways in Lepidoptera, their direct regulation by gut microorganisms during viral infection remains elusive. These microbiota-conditioned immune states can either restrict viral replication and maintain gut barrier integrity or, conversely, favor virus pathogenesis when infection disrupts gut homeostasis, drives dysbiosis, or suppresses key antiviral effectors. Furthermore, strain-specific microbiome signatures correlate with differential viral resistance in susceptible and resistant hosts. By positioning the gut microbiome as a crucial immunological interface, this review integrates symbiosis biology into insect antiviral immunity and highlights microbiome-informed opportunities for sustainable pest management and the protection of beneficial insects.
Additional Links: PMID-42586315
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PubMed:
Citation:
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@article {pmid42586315,
year = {2026},
author = {Muhammad, A and Sun, C and Shao, Y},
title = {The gut microbiome-immunity-virus axis in lepidopteran antiviral defensee.},
journal = {Current opinion in insect science},
volume = {},
number = {},
pages = {101602},
doi = {10.1016/j.cois.2026.101602},
pmid = {42586315},
issn = {2214-5753},
abstract = {The gut microbiota forms a competitive biological barrier against enteric pathogens and may also modulate antiviral immunity and disease prevention. This review presents recent advances demonstrating the tripartite model of the gut microbiome-immunity-virus axis in lepidopteran insects. Emerging evidence indicates that their gut microbiota regulates antiviral immunity through context-dependent mechanisms shaped by host species identity, microbial community composition, and strain-specific differences in viral resistance. Rather than acting as a uniformly protective factor, gut microbes fine-tune the local immune environment chiefly through antimicrobial peptide induction, modulation of PPO/melanization, Duox/ROS regulation, and maintenance of epithelial homeostasis. Although RNAi, STING-related, and JAK/STAT signalling are established antiviral pathways in Lepidoptera, their direct regulation by gut microorganisms during viral infection remains elusive. These microbiota-conditioned immune states can either restrict viral replication and maintain gut barrier integrity or, conversely, favor virus pathogenesis when infection disrupts gut homeostasis, drives dysbiosis, or suppresses key antiviral effectors. Furthermore, strain-specific microbiome signatures correlate with differential viral resistance in susceptible and resistant hosts. By positioning the gut microbiome as a crucial immunological interface, this review integrates symbiosis biology into insect antiviral immunity and highlights microbiome-informed opportunities for sustainable pest management and the protection of beneficial insects.},
}
RevDate: 2026-08-12
Ecotoxicological Effects of Pharmaceuticals and Personal Care Products on the Microbiome and Oxidative Stress of Freshwater Crayfish Faxonius obscurus.
Environmental pollution (Barking, Essex : 1987) pii:S0269-7491(26)01320-5 [Epub ahead of print].
The ecotoxicity of individual pharmaceuticals and personal care products (PPCPs) in freshwaters is well documented. However, their combined effects as mixtures on aquatic animals and their associated microbiomes remain poorly understood. This study examined the response of freshwater crayfish, Faxonius obscurus, to a mixture of three frequently co-occurring PPCPs, i.e., carbamazepine, estradiol, and triclosan, at environmentally relevant concentrations (10 or 100 μg/L). Our results revealed dose-dependent disruptions of crayfish microbiomes across multiple body locations upon a 96-hr PPCP exposure. These were characterized by an increase in the Firmicutes/Bacteroidetes ratio, an enrichment of opportunistic pathogens (e.g., Staphylococcus), and an elimination of commensal taxa (e.g., Dechloromonas). The taxonomic changes were accompanied by the enrichment of microbial detoxification and oxidative stress response pathways. Meanwhile, systemic oxidative stress was induced in the host crayfish across the carapace, gill, and abdominal muscle. Our findings underscore the urgent need for mixture-based monitoring efforts and risk assessments in environmental management to better protect freshwater ecosystems from the cumulative ecotoxicity of PPCPs.
Additional Links: PMID-42586354
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PubMed:
Citation:
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@article {pmid42586354,
year = {2026},
author = {Dutta, S and Leff, LG and Mou, X},
title = {Ecotoxicological Effects of Pharmaceuticals and Personal Care Products on the Microbiome and Oxidative Stress of Freshwater Crayfish Faxonius obscurus.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {128950},
doi = {10.1016/j.envpol.2026.128950},
pmid = {42586354},
issn = {1873-6424},
abstract = {The ecotoxicity of individual pharmaceuticals and personal care products (PPCPs) in freshwaters is well documented. However, their combined effects as mixtures on aquatic animals and their associated microbiomes remain poorly understood. This study examined the response of freshwater crayfish, Faxonius obscurus, to a mixture of three frequently co-occurring PPCPs, i.e., carbamazepine, estradiol, and triclosan, at environmentally relevant concentrations (10 or 100 μg/L). Our results revealed dose-dependent disruptions of crayfish microbiomes across multiple body locations upon a 96-hr PPCP exposure. These were characterized by an increase in the Firmicutes/Bacteroidetes ratio, an enrichment of opportunistic pathogens (e.g., Staphylococcus), and an elimination of commensal taxa (e.g., Dechloromonas). The taxonomic changes were accompanied by the enrichment of microbial detoxification and oxidative stress response pathways. Meanwhile, systemic oxidative stress was induced in the host crayfish across the carapace, gill, and abdominal muscle. Our findings underscore the urgent need for mixture-based monitoring efforts and risk assessments in environmental management to better protect freshwater ecosystems from the cumulative ecotoxicity of PPCPs.},
}
RevDate: 2026-08-10
Global gut microbiome atlas identifies epidemiologic-stage-specific signatures in inflammatory bowel disease.
Cell reports. Medicine pii:S2666-3791(26)00391-5 [Epub ahead of print].
The global rise of inflammatory bowel disease (IBD) reflects environmental shifts, yet how these changes are embedded in the gut microbial ecology remains unclear. We construct a microbiome atlas comprising 245,627 profiles. By classifying countries into three epidemiologic stages, we establish a framework. As the IBD burden increases, the gut microbial alpha diversity declines, and community structures form distinct clusters. This transition is characterized by a gradient of core genera. Integrating six shotgun metagenomic cohorts, we identify the depletion of anabolic pathways in IBD patients. Strain-level analysis reveals that epidemiologic staging shapes genetic architecture within species, identifying an IBD-enriched subclade of Eisenbergiella associated with elevated fecal cholic acid. We develop a microbial inflammatory risk score (MIRS), based on 19 genera, that discriminates IBD from controls (area under the curve [AUC] = 0.92). MIRS correlates with IBD prevalence. Our study provides an atlas linking epidemiology to microbiome ecology and strain evolution, offering a foundation for population-level surveillance and interventions in IBD.
Additional Links: PMID-42575094
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PubMed:
Citation:
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@article {pmid42575094,
year = {2026},
author = {Zhai, J and Li, Y and Liu, J and Su, X and Cui, R and Zheng, D and Sun, Y and Yu, J and Dai, C},
title = {Global gut microbiome atlas identifies epidemiologic-stage-specific signatures in inflammatory bowel disease.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102974},
doi = {10.1016/j.xcrm.2026.102974},
pmid = {42575094},
issn = {2666-3791},
abstract = {The global rise of inflammatory bowel disease (IBD) reflects environmental shifts, yet how these changes are embedded in the gut microbial ecology remains unclear. We construct a microbiome atlas comprising 245,627 profiles. By classifying countries into three epidemiologic stages, we establish a framework. As the IBD burden increases, the gut microbial alpha diversity declines, and community structures form distinct clusters. This transition is characterized by a gradient of core genera. Integrating six shotgun metagenomic cohorts, we identify the depletion of anabolic pathways in IBD patients. Strain-level analysis reveals that epidemiologic staging shapes genetic architecture within species, identifying an IBD-enriched subclade of Eisenbergiella associated with elevated fecal cholic acid. We develop a microbial inflammatory risk score (MIRS), based on 19 genera, that discriminates IBD from controls (area under the curve [AUC] = 0.92). MIRS correlates with IBD prevalence. Our study provides an atlas linking epidemiology to microbiome ecology and strain evolution, offering a foundation for population-level surveillance and interventions in IBD.},
}
RevDate: 2026-08-10
Bifid triple viable tablets are associated with renal biochemical improvement and qualitative gastrointestinal changes in 5/6-nephrectomized rats: An exploratory microbiome-metabolome study.
Biochimica et biophysica acta. General subjects pii:S0304-4165(26)00087-5 [Epub ahead of print].
BACKGROUND: Chronic kidney disease (CKD) is accompanied by renal injury, gut-barrier disruption, dysbiosis, inflammation, and disordered iron regulation. We examined whether a clinical multi-strain probiotic produces coordinated renal, intestinal, and metabolic effects in experimental CKD.
METHODS: Male Sprague-Dawley rats underwent 5/6 nephrectomy (5/6 Nx). Dose-response phenotyping compared sham, untreated 5/6 Nx, three Bifid Triple Viable Tablets (BTV) doses, and valsartan (n = 3/group). Independent cohorts provided targeted validation (untreated versus high-dose BTV; n = 6/group) and paired fecal 16S rRNA/serum metabolomics (n = 4/group). Technical replicates were averaged within animals.
RESULTS: High-dose BTV was associated with lower blood urea nitrogen (BUN), serum creatinine (Scr), inflammatory cytokines, and hepcidin, plus qualitatively less renal and gastrointestinal injury. Occludin and zonula occludens-1 (ZO-1) integrated fluorescence did not differ from untreated 5/6 Nx rats (all adjusted P > 0.05; n = 3/group). Validation confirmed lower BUN (27.87 ± 2.09 vs 16.64 ± 3.82 mmol/L; P = 0.000264), Scr (235.75 ± 27.41 vs 132.05 ± 19.50 μmol/L; P = 0.0000343), and interleukin-6 (IL-6; 188.11 ± 8.67 vs 92.21 ± 14.51 pg/mL; P = 5.72 × 10-7) with high-dose BTV. Omics detected 1966 metabolites, 393 differential metabolites, and 160 nominal genus-metabolite associations.
CONCLUSIONS: BTV was associated with reproducible renal biochemical and inflammatory improvement, qualitative gastrointestinal differences, and exploratory microbial-metabolic changes. Barrier-protein findings were nonsignificant, and small, separate cohorts preclude causal inference.
Additional Links: PMID-42575254
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PubMed:
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@article {pmid42575254,
year = {2026},
author = {Di, J and Hu, J and Zhao, F and Qi, J and Wu, Y},
title = {Bifid triple viable tablets are associated with renal biochemical improvement and qualitative gastrointestinal changes in 5/6-nephrectomized rats: An exploratory microbiome-metabolome study.},
journal = {Biochimica et biophysica acta. General subjects},
volume = {},
number = {},
pages = {130987},
doi = {10.1016/j.bbagen.2026.130987},
pmid = {42575254},
issn = {1872-8006},
abstract = {BACKGROUND: Chronic kidney disease (CKD) is accompanied by renal injury, gut-barrier disruption, dysbiosis, inflammation, and disordered iron regulation. We examined whether a clinical multi-strain probiotic produces coordinated renal, intestinal, and metabolic effects in experimental CKD.
METHODS: Male Sprague-Dawley rats underwent 5/6 nephrectomy (5/6 Nx). Dose-response phenotyping compared sham, untreated 5/6 Nx, three Bifid Triple Viable Tablets (BTV) doses, and valsartan (n = 3/group). Independent cohorts provided targeted validation (untreated versus high-dose BTV; n = 6/group) and paired fecal 16S rRNA/serum metabolomics (n = 4/group). Technical replicates were averaged within animals.
RESULTS: High-dose BTV was associated with lower blood urea nitrogen (BUN), serum creatinine (Scr), inflammatory cytokines, and hepcidin, plus qualitatively less renal and gastrointestinal injury. Occludin and zonula occludens-1 (ZO-1) integrated fluorescence did not differ from untreated 5/6 Nx rats (all adjusted P > 0.05; n = 3/group). Validation confirmed lower BUN (27.87 ± 2.09 vs 16.64 ± 3.82 mmol/L; P = 0.000264), Scr (235.75 ± 27.41 vs 132.05 ± 19.50 μmol/L; P = 0.0000343), and interleukin-6 (IL-6; 188.11 ± 8.67 vs 92.21 ± 14.51 pg/mL; P = 5.72 × 10-7) with high-dose BTV. Omics detected 1966 metabolites, 393 differential metabolites, and 160 nominal genus-metabolite associations.
CONCLUSIONS: BTV was associated with reproducible renal biochemical and inflammatory improvement, qualitative gastrointestinal differences, and exploratory microbial-metabolic changes. Barrier-protein findings were nonsignificant, and small, separate cohorts preclude causal inference.},
}
RevDate: 2026-08-10
The Exposome-Autoimmunity Axis: Environmental Xenobiotics, Gut Dysbiosis, and Potential Pathways to Immunosenescence.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association pii:S0278-6915(26)00406-0 [Epub ahead of print].
The escalating incidence of autoimmune diseases cannot be fully explained by genetics alone. It is increasingly linked to the exposome-the cumulative burden of lifelong environmental exposures. This review examines how pollutants (particulate matter, microplastics, agrochemicals, heavy metals) reshape the gut microbiota-immune axis and disrupt intestinal homeostasis. This triggers profound dysbiosis, characterized by reduced commensal diversity and expanded pathobionts. We highlight three mechanisms driving pollution-induced immune reprogramming: (i) barrier compromise facilitating metabolic endotoxemia; (ii) toxic Aryl Hydrocarbon Receptor (AhR) overactivation skewing the Th17/Treg balance; and (iii) epigenetic modifications like aberrant DNA methylation. Chronic environmental exposure accelerates telomere attrition, inducing premature immunosenescence and inflammaging. This promotes the pathological accumulation of senescent T cells and Age-associated B Cells (ABCs), linking environmental stress to tissue damage and autoantibody generation. However, a major limitation of the current literature is that many in vivo and in vitro models employ supraphysiological concentrations of pollutants that do not reflect actual human exposure scenarios. Without evaluating these specific exposure scenarios against realistic human gut concentrations, it is difficult to determine under which exact conditions the postulated dysbiotic effects occur. Ultimately, mitigating environmental risks and employing microbiota-targeted therapeutics are vital to restore barrier integrity.
Additional Links: PMID-42575421
Publisher:
PubMed:
Citation:
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@article {pmid42575421,
year = {2026},
author = {Daşdemir, FO and Sari, MF and Aktaş, B and Kocazeybek, B},
title = {The Exposome-Autoimmunity Axis: Environmental Xenobiotics, Gut Dysbiosis, and Potential Pathways to Immunosenescence.},
journal = {Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association},
volume = {},
number = {},
pages = {116331},
doi = {10.1016/j.fct.2026.116331},
pmid = {42575421},
issn = {1873-6351},
abstract = {The escalating incidence of autoimmune diseases cannot be fully explained by genetics alone. It is increasingly linked to the exposome-the cumulative burden of lifelong environmental exposures. This review examines how pollutants (particulate matter, microplastics, agrochemicals, heavy metals) reshape the gut microbiota-immune axis and disrupt intestinal homeostasis. This triggers profound dysbiosis, characterized by reduced commensal diversity and expanded pathobionts. We highlight three mechanisms driving pollution-induced immune reprogramming: (i) barrier compromise facilitating metabolic endotoxemia; (ii) toxic Aryl Hydrocarbon Receptor (AhR) overactivation skewing the Th17/Treg balance; and (iii) epigenetic modifications like aberrant DNA methylation. Chronic environmental exposure accelerates telomere attrition, inducing premature immunosenescence and inflammaging. This promotes the pathological accumulation of senescent T cells and Age-associated B Cells (ABCs), linking environmental stress to tissue damage and autoantibody generation. However, a major limitation of the current literature is that many in vivo and in vitro models employ supraphysiological concentrations of pollutants that do not reflect actual human exposure scenarios. Without evaluating these specific exposure scenarios against realistic human gut concentrations, it is difficult to determine under which exact conditions the postulated dysbiotic effects occur. Ultimately, mitigating environmental risks and employing microbiota-targeted therapeutics are vital to restore barrier integrity.},
}
RevDate: 2026-08-10
Gut microbiome: a key driver and therapeutic target of intestinal fibrosis in Crohn's disease.
Intestinal research pii:ir.2026.00013 [Epub ahead of print].
Intestinal fibrosis is a debilitating complication of Crohn's disease that often leads to stricture formation, requiring surgical intervention. Despite its clinical significance, effective anti-fibrotic therapies remain an unmet need. Emerging evidence highlights the gut microbiome as a central orchestrator of fibrogenesis, beyond its role in inflammation. This review provides a comprehensive overview of how microbial dysbiosis, which is marked by the expansion of pathobionts such as adherent-invasive Escherichia coli and Clostridium innocuum, drives intestinal fibrosis through multifaceted pathways. We delineate the direct activation of fibroblasts via pattern recognition receptors and indirect mechanisms involving macrophage polarization, T helper 17 cell responses, and the emerging role of the "creeping fat" axis. Furthermore, we discuss how microbial translocation into the mesenteric adipose tissue triggers a profibrotic environment. By synthesizing these mechanistic insights, we suggest that targeting the microbiome-fibrosis axis, through precision modulation of the microbiome or metabolite-based interventions, represents a promising frontier for preventing and reversing fibrostenotic Crohn's disease.
Additional Links: PMID-42575494
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PubMed:
Citation:
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@article {pmid42575494,
year = {2026},
author = {Kim, JH and Choi, YJ and Yoo, JH},
title = {Gut microbiome: a key driver and therapeutic target of intestinal fibrosis in Crohn's disease.},
journal = {Intestinal research},
volume = {},
number = {},
pages = {},
doi = {10.5217/ir.2026.00013},
pmid = {42575494},
issn = {1598-9100},
abstract = {Intestinal fibrosis is a debilitating complication of Crohn's disease that often leads to stricture formation, requiring surgical intervention. Despite its clinical significance, effective anti-fibrotic therapies remain an unmet need. Emerging evidence highlights the gut microbiome as a central orchestrator of fibrogenesis, beyond its role in inflammation. This review provides a comprehensive overview of how microbial dysbiosis, which is marked by the expansion of pathobionts such as adherent-invasive Escherichia coli and Clostridium innocuum, drives intestinal fibrosis through multifaceted pathways. We delineate the direct activation of fibroblasts via pattern recognition receptors and indirect mechanisms involving macrophage polarization, T helper 17 cell responses, and the emerging role of the "creeping fat" axis. Furthermore, we discuss how microbial translocation into the mesenteric adipose tissue triggers a profibrotic environment. By synthesizing these mechanistic insights, we suggest that targeting the microbiome-fibrosis axis, through precision modulation of the microbiome or metabolite-based interventions, represents a promising frontier for preventing and reversing fibrostenotic Crohn's disease.},
}
RevDate: 2026-08-10
CmpDate: 2026-08-10
Nanopore Long-Read Metagenomics Reveals Pollution-Driven Antibiotic Resistance and Xenobiotic Degradation in Urban Beach Microbiomes.
Environmental microbiology reports, 18(4):e70396.
Coastal ecosystems are vital for biodiversity but are increasingly threatened by urbanisation and pollution, which significantly alter local microbial communities. This study assessed bacterial diversity and functional profiles in urban and island beaches in Belém, Brazil. Urban beaches showed significantly higher microbial diversity and evenness, alongside functional plasticity due to pollutant input, while island beaches hosted more specialised and stable communities. Taxonomic analysis revealed the significant enrichment of opportunistic genera such as Comamonas, Clostridium and Paenibacillus in urban areas, and the massive dominance of Prochlorococcus and Candidatus Pelagibacter in island sites. Furthermore, shotgun metagenomics identified a robust genomic potential for xenobiotic degradation and antibiotic resistance in urban microbiomes, whereas island microbiomes were significantly enriched in genes for energy production and biosynthesis. These results underscore the ecological divergence between anthropogenically impacted and natural coastal environments, highlighting the importance of microbiome monitoring for sustainable coastal management.
Additional Links: PMID-42575708
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PubMed:
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@article {pmid42575708,
year = {2026},
author = {de Oliveira, AFB and Carneiro, BS and de Carvalho, JB and de Oliveira, AR and da Costa da Silva, AL and de Oliveira Veras, AA and Baraúna, RA and das Graças, DA},
title = {Nanopore Long-Read Metagenomics Reveals Pollution-Driven Antibiotic Resistance and Xenobiotic Degradation in Urban Beach Microbiomes.},
journal = {Environmental microbiology reports},
volume = {18},
number = {4},
pages = {e70396},
doi = {10.1111/1758-2229.70396},
pmid = {42575708},
issn = {1758-2229},
support = {445350/2024-5//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; },
mesh = {*Metagenomics ; *Microbiota/genetics ; *Bacteria/genetics/classification/isolation & purification/metabolism/drug effects ; *Xenobiotics/metabolism ; Brazil ; *Bathing Beaches ; *Drug Resistance, Bacterial ; Biodiversity ; *Drug Resistance, Microbial ; Phylogeny ; Biodegradation, Environmental ; Cities ; },
abstract = {Coastal ecosystems are vital for biodiversity but are increasingly threatened by urbanisation and pollution, which significantly alter local microbial communities. This study assessed bacterial diversity and functional profiles in urban and island beaches in Belém, Brazil. Urban beaches showed significantly higher microbial diversity and evenness, alongside functional plasticity due to pollutant input, while island beaches hosted more specialised and stable communities. Taxonomic analysis revealed the significant enrichment of opportunistic genera such as Comamonas, Clostridium and Paenibacillus in urban areas, and the massive dominance of Prochlorococcus and Candidatus Pelagibacter in island sites. Furthermore, shotgun metagenomics identified a robust genomic potential for xenobiotic degradation and antibiotic resistance in urban microbiomes, whereas island microbiomes were significantly enriched in genes for energy production and biosynthesis. These results underscore the ecological divergence between anthropogenically impacted and natural coastal environments, highlighting the importance of microbiome monitoring for sustainable coastal management.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Metagenomics
*Microbiota/genetics
*Bacteria/genetics/classification/isolation & purification/metabolism/drug effects
*Xenobiotics/metabolism
Brazil
*Bathing Beaches
*Drug Resistance, Bacterial
Biodiversity
*Drug Resistance, Microbial
Phylogeny
Biodegradation, Environmental
Cities
RevDate: 2026-08-10
Review: Trends in feed technology and feed additives for a sustainable and resilient livestock production.
Animal : an international journal of animal bioscience pii:S1751-7311(26)00156-4 [Epub ahead of print].
Achieving sustainable and resilient livestock production depends on continued innovation in feed technology and feed additives. Automation, robotics, predictive modelling of effects, machine learning, encapsulation of nutrients and feed additives, precision nutrition, synbiotics, postbiotics and precision biotics are trending in the feed industry, although many are still in early stages of development. A deeper understanding is needed on how the nutritional composition of the feed influences the complex metabolic interactions, digestibility and performance of the host. These insights will allow a more precise feed formulation, improving feed efficiency, animal health and welfare, while reducing emissions and environmental impact of livestock production. This manuscript compiles trends and future perspectives in feed technology and feed additives that will contribute to more sustainable and resilient livestock production systems. Furthermore, the aim of this review article was to identify gaps in research in both areas in order to accelerate the introduction of promising innovations.
Additional Links: PMID-42575748
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@article {pmid42575748,
year = {2026},
author = {Lourenço, M},
title = {Review: Trends in feed technology and feed additives for a sustainable and resilient livestock production.},
journal = {Animal : an international journal of animal bioscience},
volume = {},
number = {},
pages = {101909},
doi = {10.1016/j.animal.2026.101909},
pmid = {42575748},
issn = {1751-732X},
abstract = {Achieving sustainable and resilient livestock production depends on continued innovation in feed technology and feed additives. Automation, robotics, predictive modelling of effects, machine learning, encapsulation of nutrients and feed additives, precision nutrition, synbiotics, postbiotics and precision biotics are trending in the feed industry, although many are still in early stages of development. A deeper understanding is needed on how the nutritional composition of the feed influences the complex metabolic interactions, digestibility and performance of the host. These insights will allow a more precise feed formulation, improving feed efficiency, animal health and welfare, while reducing emissions and environmental impact of livestock production. This manuscript compiles trends and future perspectives in feed technology and feed additives that will contribute to more sustainable and resilient livestock production systems. Furthermore, the aim of this review article was to identify gaps in research in both areas in order to accelerate the introduction of promising innovations.},
}
RevDate: 2026-08-10
CmpDate: 2026-08-11
Transcriptome, glycome, and mucinome analysis reveal zinc is essential for the composition of mucus in the human goblet cell model HT-29-MTX.
Scientific reports, 16(1):.
Zinc (Zn) deficiency affects approximately 1 billion people worldwide with severe consequences for their health, including increased intestinal infections, inflammation, and diarrhea. Accordingly, the intestinal defense barrier is compromised, leading to epithelial destruction and alteration of mucus. However, the processes and the extent to which Zn deficiency affects mucin synthesis in intestinal goblet cells (GCs) remain poorly understood. To this end, we investigated the impact of Zn deficiency on mucin expression and glycosylation in the human GC model HT-29-MTX. Zn deprivation altered the GC transcriptome, affecting genes involved in Zn transport, mucin synthesis and glycosylation. Accordingly, mucus composition was changed in Zn-deficient GCs, significantly increasing MUC2 and MUC17 on the mRNA and protein level. Several Zn transporters, mostly those associated with the early secretory pathway (ESP), were dysregulated, indicating an adaptive response of cellular Zn homeostasis. Additionally, free Zn was markedly reduced in the ESP, a critical location for glycosylation. Zn deficit substantially changed mucin glycosylation, characterized by an increase in sialylation and a strong decrease in complex N-glycans. All these changes involved widespread dysregulation of glycosyltransferase expression, including an increase in COSMC, a Zn-binding chaperone essential for the core 1 O-glycan formation. Collectively, our in vitro findings demonstrate that Zn is a critical regulator of mucin production and glycosylation in GCs. Zn deficiency might weaken the protective and functional qualities of intestinal mucus, increasing the risk of infections and potentially disrupting host-microbiome interactions.
Additional Links: PMID-42575931
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Citation:
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@article {pmid42575931,
year = {2026},
author = {Schüßler, C and Chung, N and Léonard, R and Sprenger, H and Rödel, T and Mahoney, KE and Thomsen, S and Ocket, E and Matthaeus, C and Denis, J and Ebert, F and Wolf, M and Morelle, W and Foulquier, F and Braeuning, A and Masselot, CR and Malaker, SA and Maares, M},
title = {Transcriptome, glycome, and mucinome analysis reveal zinc is essential for the composition of mucus in the human goblet cell model HT-29-MTX.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42575931},
issn = {2045-2322},
mesh = {Humans ; *Zinc/metabolism/deficiency ; *Goblet Cells/metabolism ; *Mucins/metabolism/genetics ; Glycosylation ; *Mucus/metabolism ; *Transcriptome ; HT29 Cells ; Intestinal Mucosa/metabolism ; Glycomics ; },
abstract = {Zinc (Zn) deficiency affects approximately 1 billion people worldwide with severe consequences for their health, including increased intestinal infections, inflammation, and diarrhea. Accordingly, the intestinal defense barrier is compromised, leading to epithelial destruction and alteration of mucus. However, the processes and the extent to which Zn deficiency affects mucin synthesis in intestinal goblet cells (GCs) remain poorly understood. To this end, we investigated the impact of Zn deficiency on mucin expression and glycosylation in the human GC model HT-29-MTX. Zn deprivation altered the GC transcriptome, affecting genes involved in Zn transport, mucin synthesis and glycosylation. Accordingly, mucus composition was changed in Zn-deficient GCs, significantly increasing MUC2 and MUC17 on the mRNA and protein level. Several Zn transporters, mostly those associated with the early secretory pathway (ESP), were dysregulated, indicating an adaptive response of cellular Zn homeostasis. Additionally, free Zn was markedly reduced in the ESP, a critical location for glycosylation. Zn deficit substantially changed mucin glycosylation, characterized by an increase in sialylation and a strong decrease in complex N-glycans. All these changes involved widespread dysregulation of glycosyltransferase expression, including an increase in COSMC, a Zn-binding chaperone essential for the core 1 O-glycan formation. Collectively, our in vitro findings demonstrate that Zn is a critical regulator of mucin production and glycosylation in GCs. Zn deficiency might weaken the protective and functional qualities of intestinal mucus, increasing the risk of infections and potentially disrupting host-microbiome interactions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Zinc/metabolism/deficiency
*Goblet Cells/metabolism
*Mucins/metabolism/genetics
Glycosylation
*Mucus/metabolism
*Transcriptome
HT29 Cells
Intestinal Mucosa/metabolism
Glycomics
RevDate: 2026-08-10
Antisense transcription reveals disease-associated adaptations in the human gut microbiome.
Nature microbiology [Epub ahead of print].
The gut microbiome is a dynamic ecosystem in which microorganisms constantly adjust their transcriptional programmes. Here we developed metastrand, a framework that integrates strand-aware metatranscriptomics and metagenomics to quantify mRNAs and antisense RNAs (asRNAs) in complex microbial communities at gene-level resolution. In inflammatory bowel disease (IBD), microbial asRNA programmes converged across patients during active disease, correlated with faecal metabolites and calprotectin levels and remained stable during persistent inflammation, highlighting their potential as biomarkers of inflammatory activity in the gut. These programmes involved antisense-to-sense transcriptional shifts at insertion sequence elements with functionally diverse passenger genes and preceded their detection at new genomic locations, linking asRNA dynamics to structural genome rearrangements and redistribution of adaptive functions under selective pressure. Similar dynamics were observed in a mouse model of colitis, oxidative stress in vitro and in patients with pathogen-confirmed gastroenteritis, establishing asRNAs as an important dimension of microbial adaptation in health and disease.
Additional Links: PMID-42575975
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Citation:
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@article {pmid42575975,
year = {2026},
author = {Pust, MM and Mohamed, AMT and Stražar, M and Arias-Rojas, A and Cunningham-Oakes, E and Brown, EM and Bumber, A and Pishchany, G and Li, C and Ananthakrishnan, AN and Darby, AC and Vlamakis, H and Plichta, DR and Xavier, RJ},
title = {Antisense transcription reveals disease-associated adaptations in the human gut microbiome.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {42575975},
issn = {2058-5276},
support = {P30 DK043351//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; R01 DK127171//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; R01 AI172147//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; 530694780//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; },
abstract = {The gut microbiome is a dynamic ecosystem in which microorganisms constantly adjust their transcriptional programmes. Here we developed metastrand, a framework that integrates strand-aware metatranscriptomics and metagenomics to quantify mRNAs and antisense RNAs (asRNAs) in complex microbial communities at gene-level resolution. In inflammatory bowel disease (IBD), microbial asRNA programmes converged across patients during active disease, correlated with faecal metabolites and calprotectin levels and remained stable during persistent inflammation, highlighting their potential as biomarkers of inflammatory activity in the gut. These programmes involved antisense-to-sense transcriptional shifts at insertion sequence elements with functionally diverse passenger genes and preceded their detection at new genomic locations, linking asRNA dynamics to structural genome rearrangements and redistribution of adaptive functions under selective pressure. Similar dynamics were observed in a mouse model of colitis, oxidative stress in vitro and in patients with pathogen-confirmed gastroenteritis, establishing asRNAs as an important dimension of microbial adaptation in health and disease.},
}
RevDate: 2026-08-10
Prevalence and chronology of colibactin-associated mutational processes and their microbiome spectra in Japanese colorectal cancer.
Nature genetics [Epub ahead of print].
The incidence of colorectal cancer (CRC) has risen in recent decades, with a disproportionate increase observed among younger individuals in Japan and other countries. The etiological contribution of the gut microbiota to CRC pathogenesis is recognized, yet the mechanisms involved remain to be fully clarified. Here we integrated whole-genome sequencing (WGS) and transcriptome profiling of CRC with whole-genome metagenomic sequencing of fecal samples to interrogate host-microbiome interactions at high resolution. Application of interpretable artificial intelligence enabled the stratification of CRC into four distinct microbiome-informed subtypes. WGS analysis identified mutational signatures SBS88 and ID18, linked to colibactin exposure, as early clonal events detected in 44.8% of non-hypermutated patients. Notably, these signatures were significantly more frequent among patients born after the 1960s. Microbiome-based subclassification revealed subtype-specific clinical and molecular features. Collectively, our findings indicate that colibactin exposure constitutes a prevalent and potentially modifiable risk factor for CRC in the Japanese population.
Additional Links: PMID-42576026
PubMed:
Citation:
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@article {pmid42576026,
year = {2026},
author = {Shiba, S and Yachida, S and Mizutani, S and Totoki, Y and Nakamura, H and Hama, N and Miyoshi, N and Arai, Y and Saito-Adachi, M and Kimura, H and Hayashi, Y and Takamaru, H and Tanaka, K and Hayashi, R and Rokutan, H and Ikuta, S and Kanemitsu, Y and Doki, Y and Eguchi, H and Hattori, S and Saito, Y and Yamada, T and Shibata, T},
title = {Prevalence and chronology of colibactin-associated mutational processes and their microbiome spectra in Japanese colorectal cancer.},
journal = {Nature genetics},
volume = {},
number = {},
pages = {},
pmid = {42576026},
issn = {1546-1718},
support = {JP25ck0106800//Japan Agency for Medical Research and Development (AMED)/ ; JP26ck0106162//Japan Agency for Medical Research and Development (AMED)/ ; JP23jk0210009//Japan Agency for Medical Research and Development (AMED)/ ; JP21cm0106477//Japan Agency for Medical Research and Development (AMED)/ ; JP25gm2010009//Japan Agency for Medical Research and Development (AMED)/ ; JP25ck0106800//Japan Agency for Medical Research and Development (AMED)/ ; JP25ck0106800//Japan Agency for Medical Research and Development (AMED)/ ; JP22ck0106546//Japan Agency for Medical Research and Development (AMED)/ ; JP25ck0106799//Japan Agency for Medical Research and Development (AMED)/ ; JP25ck0106874//Japan Agency for Medical Research and Development (AMED)/ ; JP26ck0106162//Japan Agency for Medical Research and Development (AMED)/ ; JP21cm0106477//Japan Agency for Medical Research and Development (AMED)/ ; JP25ama221430//Japan Agency for Medical Research and Development (AMED)/ ; JP26gm2010009//Japan Agency for Medical Research and Development (AMED)/ ; JP26jf0126022//Japan Agency for Medical Research and Development (AMED)/ ; JP23jk0210009//Japan Agency for Medical Research and Development (AMED)/ ; JP26jf0126022//Japan Agency for Medical Research and Development (AMED)/ ; JP26gm2010009//Japan Agency for Medical Research and Development (AMED)/ ; JP22ck0106546//Japan Agency for Medical Research and Development (AMED)/ ; JP25ck0106799//Japan Agency for Medical Research and Development (AMED)/ ; JP25ck0106874//Japan Agency for Medical Research and Development (AMED)/ ; JP25ama221430//Japan Agency for Medical Research and Development (AMED)/ ; JP26gm2010009//Japan Agency for Medical Research and Development (AMED)/ ; JP22ck0106546//Japan Agency for Medical Research and Development (AMED)/ ; JP21cm0106477//Japan Agency for Medical Research and Development (AMED)/ ; JP25ama221430//Japan Agency for Medical Research and Development (AMED)/ ; JP26gm2010009//Japan Agency for Medical Research and Development (AMED)/ ; JP16H06279, 22K16336//MEXT | Japan Society for the Promotion of Science (JSPS)/ ; 20H03662, 23H02892, 25K21771//MEXT | Japan Science and Technology Agency (JST)/ ; },
abstract = {The incidence of colorectal cancer (CRC) has risen in recent decades, with a disproportionate increase observed among younger individuals in Japan and other countries. The etiological contribution of the gut microbiota to CRC pathogenesis is recognized, yet the mechanisms involved remain to be fully clarified. Here we integrated whole-genome sequencing (WGS) and transcriptome profiling of CRC with whole-genome metagenomic sequencing of fecal samples to interrogate host-microbiome interactions at high resolution. Application of interpretable artificial intelligence enabled the stratification of CRC into four distinct microbiome-informed subtypes. WGS analysis identified mutational signatures SBS88 and ID18, linked to colibactin exposure, as early clonal events detected in 44.8% of non-hypermutated patients. Notably, these signatures were significantly more frequent among patients born after the 1960s. Microbiome-based subclassification revealed subtype-specific clinical and molecular features. Collectively, our findings indicate that colibactin exposure constitutes a prevalent and potentially modifiable risk factor for CRC in the Japanese population.},
}
RevDate: 2026-08-11
Correction: Pathology-derived clinical micro-architectural diagnostics of tumour-microbiome interactions in colorectal cancer.
Journal of translational medicine, 24(1): pii:10.1186/s12967-026-08715-9.
Additional Links: PMID-42576221
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PubMed:
Citation:
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@article {pmid42576221,
year = {2026},
author = {Steele, S and Mazengenya, P and Chambuso, R},
title = {Correction: Pathology-derived clinical micro-architectural diagnostics of tumour-microbiome interactions in colorectal cancer.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
doi = {10.1186/s12967-026-08715-9},
pmid = {42576221},
issn = {1479-5876},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
Antibiotic exposure during weaning disrupts oral microbiota assembly in piglets.
Journal of animal science and biotechnology, 17(1):.
BACKGROUND: The use of antibiotics in swine production during the stressful weaning period is widespread. While their impact on the gut microbiome is documented, their effect on the developing oral microbiota, a critical gateway to systemic health, remains poorly understood. This study investigated how chronic exposure to tylosin (TYL) or a chlortetracycline-sulfadiazine-penicillin combination (CSP) shapes oral microbiota assembly in piglets from 21 to 60 days of age.
RESULTS: Healthy piglets exhibited a defined ecological succession, transitioning from an early, Pseudomonadota-dominated types of oral microbiota, or referred to as orotypes (driven by Moraxellaceae) at weaning to a stable, mature Bacillota-dominated state (driven by Lachnospiraceae) by 40 days of age. Antibiotic exposure disrupted this developmental program. CSP treatment locked the microbiota in an immature, Pseudomonadota-dominated state, while TYL promoted a dispersed and unstable Bacillota community. Dysbiosis was marked by enrichment of pathobionts (e.g., Moraxella, Bergeyella) and depletion of beneficial commensals like Veillonella and Phocaeicola, with the latter reduced in both the oral and gut microbiota. These structural shifts were linked to dysregulated microbial energy and lipid metabolism. Crucially, antibiotics compromised mucosal immunity, reducing salivary secretory IgA (SIgA), and provoked inflammation, evidenced by elevated salivary extracellular ATP (eATP), histological damage and transcriptome alteration in oral tissue, and changed serum metabolites.
CONCLUSIONS: Our findings demonstrate that early-life antibiotic exposure disrupts the developmental programming of the oral ecosystem. The oral microbiota serves as a sensitive indicator of antibiotic impact and a key mediator of systemic health, highlighting the need for strategies that safeguard microbial succession to promote sustainable swine health.
Additional Links: PMID-42576226
PubMed:
Citation:
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@article {pmid42576226,
year = {2026},
author = {Zhu, C and Hu, P and Yuan, P and Yu, J and Zhu, M and Ogamune, KJ and Huang, H and Kim, IH and Manyelo, TG and Ahmed, AA and Cai, D and Liu, H},
title = {Antibiotic exposure during weaning disrupts oral microbiota assembly in piglets.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {42576226},
issn = {1674-9782},
support = {SJCX25_2359.//the Postgraduate Research & Practice Innovation Program of Jiangsu Province/ ; 32202717//Natural Science Foundation of China/ ; 2023YFD1301200//National Key R&D Program of China/ ; 2023YFD1801100//National Key R&D Program of China/ ; },
abstract = {BACKGROUND: The use of antibiotics in swine production during the stressful weaning period is widespread. While their impact on the gut microbiome is documented, their effect on the developing oral microbiota, a critical gateway to systemic health, remains poorly understood. This study investigated how chronic exposure to tylosin (TYL) or a chlortetracycline-sulfadiazine-penicillin combination (CSP) shapes oral microbiota assembly in piglets from 21 to 60 days of age.
RESULTS: Healthy piglets exhibited a defined ecological succession, transitioning from an early, Pseudomonadota-dominated types of oral microbiota, or referred to as orotypes (driven by Moraxellaceae) at weaning to a stable, mature Bacillota-dominated state (driven by Lachnospiraceae) by 40 days of age. Antibiotic exposure disrupted this developmental program. CSP treatment locked the microbiota in an immature, Pseudomonadota-dominated state, while TYL promoted a dispersed and unstable Bacillota community. Dysbiosis was marked by enrichment of pathobionts (e.g., Moraxella, Bergeyella) and depletion of beneficial commensals like Veillonella and Phocaeicola, with the latter reduced in both the oral and gut microbiota. These structural shifts were linked to dysregulated microbial energy and lipid metabolism. Crucially, antibiotics compromised mucosal immunity, reducing salivary secretory IgA (SIgA), and provoked inflammation, evidenced by elevated salivary extracellular ATP (eATP), histological damage and transcriptome alteration in oral tissue, and changed serum metabolites.
CONCLUSIONS: Our findings demonstrate that early-life antibiotic exposure disrupts the developmental programming of the oral ecosystem. The oral microbiota serves as a sensitive indicator of antibiotic impact and a key mediator of systemic health, highlighting the need for strategies that safeguard microbial succession to promote sustainable swine health.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
Antimicrobial Peptides of the Skin: Roles in Skin Cancer and Clinical Applications.
Experimental dermatology, 35(8):e70341.
Cutaneous antimicrobial peptides (AMPs) are increasingly recognized for their multifaceted roles in skin disease and cancer, and thus application for therapeutic potential. Beyond their contributions to innate defence and the skin's microbiome, AMPs have been implicated in inflammatory skin conditions and cutaneous malignancies. Comprehensive summaries of AMPs' roles in skin cancer and related current clinical developments remain scarce, despite abundant emerging evidence of pro- and anti-tumour properties in other fields. This review provides a comprehensive discussion of AMPs, including dermcidin, psoriasin (S100A7), human cathelicidin (LL-37), RNase-7 and the human β-defensins, in the context of skin cancer research and clinical developments. These AMPs influence skin tumorigenesis through microbiome regulation, innate immune pathways and chronic inflammation, and although the mechanistic details are subject to scrutiny, several AMP-derived therapies, including LL-37 and LTX-315, have been developed for their potential in cutaneous oncology.
Additional Links: PMID-42576411
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PubMed:
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@article {pmid42576411,
year = {2026},
author = {Botto, E and Lipman, ZM and Temiz, LA and Corea-Selm, L and Grichnik, JM},
title = {Antimicrobial Peptides of the Skin: Roles in Skin Cancer and Clinical Applications.},
journal = {Experimental dermatology},
volume = {35},
number = {8},
pages = {e70341},
doi = {10.1111/exd.70341},
pmid = {42576411},
issn = {1600-0625},
mesh = {Humans ; *Skin Neoplasms/metabolism/drug therapy ; Cathelicidins ; *Antimicrobial Peptides/therapeutic use/metabolism ; *Skin/metabolism ; *Antimicrobial Cationic Peptides/therapeutic use/metabolism ; S100 Calcium Binding Protein A7 ; Ribonucleases/metabolism ; Animals ; Skin Microbiome ; beta-Defensins/metabolism ; Peptides/metabolism ; Immunity, Innate ; S100 Proteins/metabolism ; },
abstract = {Cutaneous antimicrobial peptides (AMPs) are increasingly recognized for their multifaceted roles in skin disease and cancer, and thus application for therapeutic potential. Beyond their contributions to innate defence and the skin's microbiome, AMPs have been implicated in inflammatory skin conditions and cutaneous malignancies. Comprehensive summaries of AMPs' roles in skin cancer and related current clinical developments remain scarce, despite abundant emerging evidence of pro- and anti-tumour properties in other fields. This review provides a comprehensive discussion of AMPs, including dermcidin, psoriasin (S100A7), human cathelicidin (LL-37), RNase-7 and the human β-defensins, in the context of skin cancer research and clinical developments. These AMPs influence skin tumorigenesis through microbiome regulation, innate immune pathways and chronic inflammation, and although the mechanistic details are subject to scrutiny, several AMP-derived therapies, including LL-37 and LTX-315, have been developed for their potential in cutaneous oncology.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Skin Neoplasms/metabolism/drug therapy
Cathelicidins
*Antimicrobial Peptides/therapeutic use/metabolism
*Skin/metabolism
*Antimicrobial Cationic Peptides/therapeutic use/metabolism
S100 Calcium Binding Protein A7
Ribonucleases/metabolism
Animals
Skin Microbiome
beta-Defensins/metabolism
Peptides/metabolism
Immunity, Innate
S100 Proteins/metabolism
RevDate: 2026-08-11
Correction to: Rapid resolution of colon inflammation and microbiome remodeling with vancomycin therapy in a patient with primary sclerosing cholangitis.
Journal of Crohn's & colitis, 20(8):.
Additional Links: PMID-42576426
Publisher:
PubMed:
Citation:
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@article {pmid42576426,
year = {2026},
author = {},
title = {Correction to: Rapid resolution of colon inflammation and microbiome remodeling with vancomycin therapy in a patient with primary sclerosing cholangitis.},
journal = {Journal of Crohn's & colitis},
volume = {20},
number = {8},
pages = {},
doi = {10.1093/ecco-jcc/jjag123},
pmid = {42576426},
issn = {1876-4479},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
Water Deficit During the Vegetative Stage Alters the Structure of Root-Associated Microbial Communities in Local North Sulawesi Rice.
Pakistan journal of biological sciences : PJBS, 29(5):243-250.
Background and Objective: Changes in rhizosphere microbial populations have been reported in response to drought, temperature fluctuations, CO2 levels and other environmental factors. However, the structure of the root-associated microbes in local North Sulawesi rice using a metagenomic approach has not yet been investigated. This study examined the microbial community structure in local North Sulawesi rice (cv. Superwin) under drought (water deficit) conditions compared to well-watered conditions at the vegetative phase. Materials and Methods: Rice plants were grown in polybags filled with a 5:1:1 mixture of garden soil, compost and rice husks and were allowed to grow until the four-fully-expanded leaf stage. They were then subjected to two treatments for 14 days: well-watered conditions (irrigated to 100% field capacity) and water deficit conditions (0% field capacity). Root samples were collected for next-generation sequencing analysis to assess molecular response of Superwin rice to water deficit. Results: During drought, several root-associated microbes were more prevalent, including Nitrospirota at the phylum level, Rubrobacteria at the class level, Micrococcales at the order level, Gaiellaceae at the family level, Gaiella at the genus level and Gaiella occulta at the species level. Conclusion: Root-associated microbes, including taxa Nitrospirota, Rubrobacteria, Micrococcales, Gaiellaceae, Gaiella and Gaiella occulta, have a higher relative abundance in rice plants under water deficit. Gaiella occulta serves as sensitive indicator of water deficit in North Sulawesi local rice, i.e. Superwin.
Additional Links: PMID-42576510
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@article {pmid42576510,
year = {2026},
author = {Nio, SA and Mantilen Ludong, DP},
title = {Water Deficit During the Vegetative Stage Alters the Structure of Root-Associated Microbial Communities in Local North Sulawesi Rice.},
journal = {Pakistan journal of biological sciences : PJBS},
volume = {29},
number = {5},
pages = {243-250},
doi = {10.3923/pjbs.2026.243.250},
pmid = {42576510},
issn = {1812-5735},
mesh = {*Oryza/microbiology/growth & development/metabolism ; *Plant Roots/microbiology ; Droughts ; Water/metabolism ; *Microbiota/physiology ; Indonesia ; Rhizosphere ; },
abstract = {Background and Objective: Changes in rhizosphere microbial populations have been reported in response to drought, temperature fluctuations, CO2 levels and other environmental factors. However, the structure of the root-associated microbes in local North Sulawesi rice using a metagenomic approach has not yet been investigated. This study examined the microbial community structure in local North Sulawesi rice (cv. Superwin) under drought (water deficit) conditions compared to well-watered conditions at the vegetative phase. Materials and Methods: Rice plants were grown in polybags filled with a 5:1:1 mixture of garden soil, compost and rice husks and were allowed to grow until the four-fully-expanded leaf stage. They were then subjected to two treatments for 14 days: well-watered conditions (irrigated to 100% field capacity) and water deficit conditions (0% field capacity). Root samples were collected for next-generation sequencing analysis to assess molecular response of Superwin rice to water deficit. Results: During drought, several root-associated microbes were more prevalent, including Nitrospirota at the phylum level, Rubrobacteria at the class level, Micrococcales at the order level, Gaiellaceae at the family level, Gaiella at the genus level and Gaiella occulta at the species level. Conclusion: Root-associated microbes, including taxa Nitrospirota, Rubrobacteria, Micrococcales, Gaiellaceae, Gaiella and Gaiella occulta, have a higher relative abundance in rice plants under water deficit. Gaiella occulta serves as sensitive indicator of water deficit in North Sulawesi local rice, i.e. Superwin.},
}
MeSH Terms:
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*Oryza/microbiology/growth & development/metabolism
*Plant Roots/microbiology
Droughts
Water/metabolism
*Microbiota/physiology
Indonesia
Rhizosphere
RevDate: 2026-08-11
Diabetes and the Nervous System: Linking Peripheral Neuropathy to Central Neurodegeneration.
Current diabetes reviews pii:CDR-EPUB-157446 [Epub ahead of print].
Diabetes mellitus affects both the peripheral and central nervous systems, giving rise to a spectrum of neurological complications that extend far beyond the traditional focus on diabetic peripheral neuropathy (DPN). Chronic hyperglycemia disrupts cellular homeostasis through increased formation of advanced glycation end-products, activation of inflammatory pathways, mitochondrial dysfunction, oxidative stress, and impaired neurovascular regulation. These disturbances converge to drive axonal degeneration, demyelination, synaptic injury, and progressive cognitive decline. Emerging evidence also highlights a critical role for gut dysbiosis and intestinal barrier dysfunction, which facilitate microbial translocation and systemic inflammation, ultimately disrupting the blood-brain barrier and amplifying neuroimmune injury. This narrative review synthesizes current mechanistic, clinical, and translational insights into how metabolic, inflammatory, vascular, and microbial pathways interact to produce diabetes-associated neurodegeneration. We summarize key molecular drivers-including mitochondrial ROS overproduction, microglial and astrocytic activation, endothelial dysfunction, and insulin resistance-while also describing their contributions to DPN, autonomic neuropathy, and diabetes-related cognitive impairment. We further integrate evidence from emerging therapeutic domains, including mitochondrial stabilizers, anti-inflammatory strategies, gut-microbiome modulation, and neurovascular-targeted interventions. Despite advances in understanding, disease-modifying therapies remain limited, and diagnostic tools for early detection are underutilized. Bridging these gaps will require longitudinal human studies, improved biomarkers, and integrative therapeutic approaches that target multiple convergent pathways. A deeper understanding of cross-talk among metabolic, immune, vascular, and microbial systems may enable earlier intervention and more effective strategies to mitigate the neurological burden of diabetes.
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@article {pmid42576522,
year = {2026},
author = {Hoque, MM and Akter, S and Mahir, JUK and Afrin, N and Shimu, SJ and Auny, FM and Sharker, SM and Mohib, MM and Uddin, MB and Mohiuddin, MS and Choubey, M},
title = {Diabetes and the Nervous System: Linking Peripheral Neuropathy to Central Neurodegeneration.},
journal = {Current diabetes reviews},
volume = {},
number = {},
pages = {},
doi = {10.2174/0115733998440886260306085847},
pmid = {42576522},
issn = {1875-6417},
abstract = {Diabetes mellitus affects both the peripheral and central nervous systems, giving rise to a spectrum of neurological complications that extend far beyond the traditional focus on diabetic peripheral neuropathy (DPN). Chronic hyperglycemia disrupts cellular homeostasis through increased formation of advanced glycation end-products, activation of inflammatory pathways, mitochondrial dysfunction, oxidative stress, and impaired neurovascular regulation. These disturbances converge to drive axonal degeneration, demyelination, synaptic injury, and progressive cognitive decline. Emerging evidence also highlights a critical role for gut dysbiosis and intestinal barrier dysfunction, which facilitate microbial translocation and systemic inflammation, ultimately disrupting the blood-brain barrier and amplifying neuroimmune injury. This narrative review synthesizes current mechanistic, clinical, and translational insights into how metabolic, inflammatory, vascular, and microbial pathways interact to produce diabetes-associated neurodegeneration. We summarize key molecular drivers-including mitochondrial ROS overproduction, microglial and astrocytic activation, endothelial dysfunction, and insulin resistance-while also describing their contributions to DPN, autonomic neuropathy, and diabetes-related cognitive impairment. We further integrate evidence from emerging therapeutic domains, including mitochondrial stabilizers, anti-inflammatory strategies, gut-microbiome modulation, and neurovascular-targeted interventions. Despite advances in understanding, disease-modifying therapies remain limited, and diagnostic tools for early detection are underutilized. Bridging these gaps will require longitudinal human studies, improved biomarkers, and integrative therapeutic approaches that target multiple convergent pathways. A deeper understanding of cross-talk among metabolic, immune, vascular, and microbial systems may enable earlier intervention and more effective strategies to mitigate the neurological burden of diabetes.},
}
RevDate: 2026-08-11
A qPCR-based approach targeting the microbial gene marker nanA of mucin-degrading Akkermansia in Parkinson's disease.
Journal of Parkinson's disease [Epub ahead of print].
BackgroundParkinson's disease (PD) is a multifactorial neurodegenerative disorder increasingly linked to gut microbiota alterations. However, despite advances in fecal microbiota profiling as a non-invasive approach to disease risk assessment, its clinical utility remains limited by a lack of functionally relevant microbial biomarkers.ObjectiveThis cross-sectional study aimed to identify a microbial gene marker reflecting metabolic potential associated with both the presence and severity of PD.MethodsFecal samples from patients with PD (n = 59) and healthy controls (n = 65) were analyzed by 16S rRNA sequencing to characterize taxonomic profiles. Quantitative PCR (qPCR) targeted the consensus sequence of the mucin-degrading nanA gene (nanAkk), a highly conserved within Akkermansia nan gene clusters. Differences in taxonomic composition and nanAkk abundance were examined, and correlations with clinical severity scores evaluated in the PD group.ResultsPatients with PD showed reduced abundance of short-chain fatty acid-producing taxa (Faecalibacterium, Blautia, and Anaerostipes) and increased levels of Akkermansia. Akkermansia abundance correlated positively with motor severity, including Hoehn-Yahr stage. Moreover, nanAkk levels also correlated positively with Hoehn-Yahr stage and were significantly elevated in PD patients compared with controls. Levels in the stage 4-5 group exceeded those in the stage 1-3 group (P = 0.0202), indicating a stage-related increase in mucin-degrading nanAkk abundance.ConclusionsWe have identified nanAkk as a microbial gene marker associated with both the presence and severity of PD. Our qPCR-based quantification shows potential as a non-invasive biomarker for disease stratification.
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@article {pmid42576570,
year = {2026},
author = {Mizutani, Y and Fujii, T and Maeda, Y and Funasaka, K and Ohno, E and Hirooka, Y and Watanabe, H and Tochio, T},
title = {A qPCR-based approach targeting the microbial gene marker nanA of mucin-degrading Akkermansia in Parkinson's disease.},
journal = {Journal of Parkinson's disease},
volume = {},
number = {},
pages = {1877718X261462342},
doi = {10.1177/1877718X261462342},
pmid = {42576570},
issn = {1877-718X},
abstract = {BackgroundParkinson's disease (PD) is a multifactorial neurodegenerative disorder increasingly linked to gut microbiota alterations. However, despite advances in fecal microbiota profiling as a non-invasive approach to disease risk assessment, its clinical utility remains limited by a lack of functionally relevant microbial biomarkers.ObjectiveThis cross-sectional study aimed to identify a microbial gene marker reflecting metabolic potential associated with both the presence and severity of PD.MethodsFecal samples from patients with PD (n = 59) and healthy controls (n = 65) were analyzed by 16S rRNA sequencing to characterize taxonomic profiles. Quantitative PCR (qPCR) targeted the consensus sequence of the mucin-degrading nanA gene (nanAkk), a highly conserved within Akkermansia nan gene clusters. Differences in taxonomic composition and nanAkk abundance were examined, and correlations with clinical severity scores evaluated in the PD group.ResultsPatients with PD showed reduced abundance of short-chain fatty acid-producing taxa (Faecalibacterium, Blautia, and Anaerostipes) and increased levels of Akkermansia. Akkermansia abundance correlated positively with motor severity, including Hoehn-Yahr stage. Moreover, nanAkk levels also correlated positively with Hoehn-Yahr stage and were significantly elevated in PD patients compared with controls. Levels in the stage 4-5 group exceeded those in the stage 1-3 group (P = 0.0202), indicating a stage-related increase in mucin-degrading nanAkk abundance.ConclusionsWe have identified nanAkk as a microbial gene marker associated with both the presence and severity of PD. Our qPCR-based quantification shows potential as a non-invasive biomarker for disease stratification.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
[The role of the nasal microbiome in regulating upper airway immune homeostasis].
Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery, 40(8):777-782.
The nasal microbiome serves as a pivotal regulator of immune homeostasis in the upper airway. Under physiological conditions, it maintains immune equilibrium through mechanisms such as reinforcing the epithelial barrier and modulating innate and adaptive immune responses. Microbial dysbiosis, however, is recognized as a key trigger in the pathogenesis of chronic rhinosinusitis (CRS) and allergic rhinitis (AR). This review summarizes how the nasal microbiome regulates immune homeostasis by influencing epithelial barrier function and immune responses in both health and disease states, with a focus on CRS and AR. It focuses on the characteristics of microbial dysbiosis and immunopathological mechanisms in CRS and AR, and provides perspectives on microbiome-based diagnostic biomarkers and microecological interventional therapeutic strategies.
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@article {pmid42576645,
year = {2026},
author = {Lin, X and Chen, Z and Lu, B and Huang, G},
title = {[The role of the nasal microbiome in regulating upper airway immune homeostasis].},
journal = {Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery},
volume = {40},
number = {8},
pages = {777-782},
doi = {10.13201/j.issn.2096-7993.2026.08.014},
pmid = {42576645},
issn = {2096-7993},
mesh = {Humans ; *Homeostasis ; *Microbiota ; *Rhinosinusitis/microbiology/immunology ; Rhinitis, Allergic ; Dysbiosis ; *Nasal Mucosa/microbiology ; Chronic Disease ; Immunity, Innate ; },
abstract = {The nasal microbiome serves as a pivotal regulator of immune homeostasis in the upper airway. Under physiological conditions, it maintains immune equilibrium through mechanisms such as reinforcing the epithelial barrier and modulating innate and adaptive immune responses. Microbial dysbiosis, however, is recognized as a key trigger in the pathogenesis of chronic rhinosinusitis (CRS) and allergic rhinitis (AR). This review summarizes how the nasal microbiome regulates immune homeostasis by influencing epithelial barrier function and immune responses in both health and disease states, with a focus on CRS and AR. It focuses on the characteristics of microbial dysbiosis and immunopathological mechanisms in CRS and AR, and provides perspectives on microbiome-based diagnostic biomarkers and microecological interventional therapeutic strategies.},
}
MeSH Terms:
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Humans
*Homeostasis
*Microbiota
*Rhinosinusitis/microbiology/immunology
Rhinitis, Allergic
Dysbiosis
*Nasal Mucosa/microbiology
Chronic Disease
Immunity, Innate
RevDate: 2026-08-11
CmpDate: 2026-08-11
Microbiome-Driven Mechanisms in Breast Cancer: Emerging Evidence From Gut Microbial Signatures to Therapeutic Response.
BioMed research international, 2026(1):e8376859.
Breast cancer remains the most frequently diagnosed malignancy among women worldwide, and increasing evidence indicates that the gut microbiome plays a significant role in tumor initiation, progression, and therapeutic response. Microbial dysbiosis and altered metabolite production have been associated with systemic inflammation, estrogen metabolism, immune regulation, and metabolic reprogramming, all of which contribute to breast cancer biology. This review summarizes current preclinical and clinical evidence describing the gut-breast cancer axis and its mechanistic and translational relevance. The review focuses on four major pathways through which gut microbiota may influence breast cancer development and treatment outcomes: immune modulation, estrobolome-mediated estrogen recycling, chronic inflammatory signaling, and microbial metabolite-driven epigenetic and metabolic regulation. Evidence from experimental models and human studies demonstrates that alterations in microbial diversity and enrichment of proinflammatory taxa are associated with tumor progression, subtype-specific biology, and variability in therapeutic response. Emerging findings further indicate that microbiome composition can influence the efficacy and toxicity of chemotherapy, endocrine therapy, radiotherapy, and immunotherapy, highlighting the potential of microbiome-informed precision oncology strategies. In addition, this review discusses current advances in microbiome-targeted interventions including probiotics, dietary modulation, postbiotics, and fecal microbiota transplantation. Despite promising translational potential, significant challenges remain regarding mechanistic validation, standardization of microbiome profiling, reproducibility across cohorts, and clinical implementation. Future research integrating longitudinal multiomics approaches, functional validation studies, and personalized microbiome-based therapeutic strategies may facilitate the development of clinically actionable microbiome interventions for breast cancer management.
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@article {pmid42576658,
year = {2026},
author = {Wali, AF and Talath, S and Rangraze, IR and El-Tanani, M and Khan, S},
title = {Microbiome-Driven Mechanisms in Breast Cancer: Emerging Evidence From Gut Microbial Signatures to Therapeutic Response.},
journal = {BioMed research international},
volume = {2026},
number = {1},
pages = {e8376859},
pmid = {42576658},
issn = {2314-6141},
mesh = {Humans ; *Breast Neoplasms/microbiology/therapy ; Female ; *Gastrointestinal Microbiome/physiology ; Dysbiosis/microbiology ; Animals ; Probiotics/therapeutic use ; },
abstract = {Breast cancer remains the most frequently diagnosed malignancy among women worldwide, and increasing evidence indicates that the gut microbiome plays a significant role in tumor initiation, progression, and therapeutic response. Microbial dysbiosis and altered metabolite production have been associated with systemic inflammation, estrogen metabolism, immune regulation, and metabolic reprogramming, all of which contribute to breast cancer biology. This review summarizes current preclinical and clinical evidence describing the gut-breast cancer axis and its mechanistic and translational relevance. The review focuses on four major pathways through which gut microbiota may influence breast cancer development and treatment outcomes: immune modulation, estrobolome-mediated estrogen recycling, chronic inflammatory signaling, and microbial metabolite-driven epigenetic and metabolic regulation. Evidence from experimental models and human studies demonstrates that alterations in microbial diversity and enrichment of proinflammatory taxa are associated with tumor progression, subtype-specific biology, and variability in therapeutic response. Emerging findings further indicate that microbiome composition can influence the efficacy and toxicity of chemotherapy, endocrine therapy, radiotherapy, and immunotherapy, highlighting the potential of microbiome-informed precision oncology strategies. In addition, this review discusses current advances in microbiome-targeted interventions including probiotics, dietary modulation, postbiotics, and fecal microbiota transplantation. Despite promising translational potential, significant challenges remain regarding mechanistic validation, standardization of microbiome profiling, reproducibility across cohorts, and clinical implementation. Future research integrating longitudinal multiomics approaches, functional validation studies, and personalized microbiome-based therapeutic strategies may facilitate the development of clinically actionable microbiome interventions for breast cancer management.},
}
MeSH Terms:
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Humans
*Breast Neoplasms/microbiology/therapy
Female
*Gastrointestinal Microbiome/physiology
Dysbiosis/microbiology
Animals
Probiotics/therapeutic use
RevDate: 2026-08-11
Postbiotic mechanisms of long-term fermented soybean foods in host immunometabolic regulation: a critical appraisal of evidence, contradictions, and precision nutrition perspectives.
Critical reviews in food science and nutrition [Epub ahead of print].
Traditionally made long-term fermented soybean (LTFS) foods, including doenjang, miso, ganjang, and douchi, are produced through months to years of fermentation under high-salinity conditions (12-20% NaCl), generating convergent postbiotic profiles comprising free amino acids, isoflavone aglycones, bioactive peptides, indole derivatives, and gamma-aminobutyric acid. These postbiotics engage host immune, metabolic, and redox signaling through AMPK-SIRT1 activation, NF-kB and RAAS suppression, Nrf2-Keap1 induction, and aryl hydrocarbon receptor signaling. Epidemiological evidence from Korean, Japanese, and Chinese cohorts consistently associates LTFS consumption with improved metabolic outcomes despite high concomitant sodium exposure, suggesting that fermentation-derived bioactive compounds suppress the adverse metabolic consequences of sodium. However, most mechanistic evidence derives from cell and animal models, and human intervention data directly measuring signaling endpoints remain sparse. Gut microbiota biotransformation of LTFS-derived bioactive compounds generates secondary metabolites with distinct biological activities, contributing to substantial inter-individual variability in physiological responses and underscoring the need for precision nutrition approaches that account for individual microbiota composition, metabolic phenotype, and genetic background. This review critically evaluates evidence within a postbiotic-to-signaling framework, distinguishes associative observational findings from preclinical mechanistic evidence, identifies contradictions and null findings, and highlights research priorities including standardized metabolite profiling and human intervention studies with mechanistic biomarker endpoints.
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@article {pmid42576686,
year = {2026},
author = {Jeong, DY and Daily, JW and Yang, HJ and Ryu, MS and Ha, GS and Seo, JW and Park, S},
title = {Postbiotic mechanisms of long-term fermented soybean foods in host immunometabolic regulation: a critical appraisal of evidence, contradictions, and precision nutrition perspectives.},
journal = {Critical reviews in food science and nutrition},
volume = {},
number = {},
pages = {1-17},
doi = {10.1080/10408398.2026.2715172},
pmid = {42576686},
issn = {1549-7852},
abstract = {Traditionally made long-term fermented soybean (LTFS) foods, including doenjang, miso, ganjang, and douchi, are produced through months to years of fermentation under high-salinity conditions (12-20% NaCl), generating convergent postbiotic profiles comprising free amino acids, isoflavone aglycones, bioactive peptides, indole derivatives, and gamma-aminobutyric acid. These postbiotics engage host immune, metabolic, and redox signaling through AMPK-SIRT1 activation, NF-kB and RAAS suppression, Nrf2-Keap1 induction, and aryl hydrocarbon receptor signaling. Epidemiological evidence from Korean, Japanese, and Chinese cohorts consistently associates LTFS consumption with improved metabolic outcomes despite high concomitant sodium exposure, suggesting that fermentation-derived bioactive compounds suppress the adverse metabolic consequences of sodium. However, most mechanistic evidence derives from cell and animal models, and human intervention data directly measuring signaling endpoints remain sparse. Gut microbiota biotransformation of LTFS-derived bioactive compounds generates secondary metabolites with distinct biological activities, contributing to substantial inter-individual variability in physiological responses and underscoring the need for precision nutrition approaches that account for individual microbiota composition, metabolic phenotype, and genetic background. This review critically evaluates evidence within a postbiotic-to-signaling framework, distinguishes associative observational findings from preclinical mechanistic evidence, identifies contradictions and null findings, and highlights research priorities including standardized metabolite profiling and human intervention studies with mechanistic biomarker endpoints.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
Temperature and microbe mediated impacts of the San Diego Bay ostreid herpesvirus (OsHV-1) microvariant on juvenile Pacific oysters.
Sustainable microbiology, 1(1):qvae014.
The ostreid herpesvirus (OsHV-1) was recently detected in San Diego Bay for the first time in farmed juvenile Pacific oysters (Crassostrea gigas). Due to the virus' ability to cause mass mortality (50%-100%), it is important to determine the factors that promote infection as well as the consequences of infection. Here, we assess the role of temperature in controlling OsHV-1 induced mortality. Pacific oysters were exposed to the San Diego Bay microvariant of OsHV-1 at four different temperatures (15°C, 18°C, 21°C, and 24°C). While OsHV-1 was able to replicate in oyster tissues at all temperatures, it did not induce mortality at 15°C, only at the higher temperatures. Additionally, we examined oyster tissue-associated bacterial response to OsHV-1 infection. As shown previously, bacterial richness increased following OsHV-1 exposure and then decreased as the oysters became sick and died. Four bacterial taxa linked to the San Diego Bay microvariant infection, including Arcobacter, Vibrio, Amphritea, and Pseudoalteromonas, were the same as those shown for other microvariant infections in other studies from globally distributed oysters, suggesting a similar spectrum of co-infection irrespective of geography and microvariant type. The significant shift in the bacterial community following exposure suggests a weakening of the host defenses as a result of OsHV-1 infection, which potentially leads to adverse opportunistic bacterial infection.
Additional Links: PMID-42576817
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@article {pmid42576817,
year = {2024},
author = {Kunselman, E and Manrique, D and Burge, CA and Allard, S and Daniel, Z and Mitta, G and Petton, B and Gilbert, JA},
title = {Temperature and microbe mediated impacts of the San Diego Bay ostreid herpesvirus (OsHV-1) microvariant on juvenile Pacific oysters.},
journal = {Sustainable microbiology},
volume = {1},
number = {1},
pages = {qvae014},
pmid = {42576817},
issn = {2755-1970},
abstract = {The ostreid herpesvirus (OsHV-1) was recently detected in San Diego Bay for the first time in farmed juvenile Pacific oysters (Crassostrea gigas). Due to the virus' ability to cause mass mortality (50%-100%), it is important to determine the factors that promote infection as well as the consequences of infection. Here, we assess the role of temperature in controlling OsHV-1 induced mortality. Pacific oysters were exposed to the San Diego Bay microvariant of OsHV-1 at four different temperatures (15°C, 18°C, 21°C, and 24°C). While OsHV-1 was able to replicate in oyster tissues at all temperatures, it did not induce mortality at 15°C, only at the higher temperatures. Additionally, we examined oyster tissue-associated bacterial response to OsHV-1 infection. As shown previously, bacterial richness increased following OsHV-1 exposure and then decreased as the oysters became sick and died. Four bacterial taxa linked to the San Diego Bay microvariant infection, including Arcobacter, Vibrio, Amphritea, and Pseudoalteromonas, were the same as those shown for other microvariant infections in other studies from globally distributed oysters, suggesting a similar spectrum of co-infection irrespective of geography and microvariant type. The significant shift in the bacterial community following exposure suggests a weakening of the host defenses as a result of OsHV-1 infection, which potentially leads to adverse opportunistic bacterial infection.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
House dust-a Pandora's box of antimicrobial resistance (AMR) activity?.
Sustainable microbiology, 2(4):qvaf022.
The presence and spread of Antibiotic Resistant Bacteria (ARB) and Antibiotic Resistant Genes (ARGs) in the environment is now recognised as one of the top ten global public health threats to humanity. In a previous study, we used citizen science and MiSeq to target 16S rRNA gene amplicons to investigate house dust microbiomes across diverse households and found a core microbiome. In this study, we used shotgun metagenomics to target antimicrobial resistance (AMR) genes in order to investigate the potential for functional differences and to test the hypothesis that there was a core resistome associated with this core microbiome, including any patterns in a core resistome in terms of likely origin and mechanisms of action. In this study we did not find a core resistome, but found that the predominant and most diverse mechanisms of Anti-Microbial Resistance (AMR) in the dust samples were antibiotic target alteration and antibiotic efflux, accounting for ∼70% of cumulative RPKMs detected, potentially representing a compromise between the certainty of working and energy investment required. Despite the core home microbiome previously detected in diverse house dust samples, there was only limited evidence for a core resistome, with only two AMR genes present in all samples.
Additional Links: PMID-42576818
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@article {pmid42576818,
year = {2025},
author = {Pearce, DA and Crown, M and Nelson, A and Jabeen, K and Thompson, JR and Argyraki, A and Hursthouse, AS and Bashton, M and Entwistle, JA},
title = {House dust-a Pandora's box of antimicrobial resistance (AMR) activity?.},
journal = {Sustainable microbiology},
volume = {2},
number = {4},
pages = {qvaf022},
pmid = {42576818},
issn = {2755-1970},
abstract = {The presence and spread of Antibiotic Resistant Bacteria (ARB) and Antibiotic Resistant Genes (ARGs) in the environment is now recognised as one of the top ten global public health threats to humanity. In a previous study, we used citizen science and MiSeq to target 16S rRNA gene amplicons to investigate house dust microbiomes across diverse households and found a core microbiome. In this study, we used shotgun metagenomics to target antimicrobial resistance (AMR) genes in order to investigate the potential for functional differences and to test the hypothesis that there was a core resistome associated with this core microbiome, including any patterns in a core resistome in terms of likely origin and mechanisms of action. In this study we did not find a core resistome, but found that the predominant and most diverse mechanisms of Anti-Microbial Resistance (AMR) in the dust samples were antibiotic target alteration and antibiotic efflux, accounting for ∼70% of cumulative RPKMs detected, potentially representing a compromise between the certainty of working and energy investment required. Despite the core home microbiome previously detected in diverse house dust samples, there was only limited evidence for a core resistome, with only two AMR genes present in all samples.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
Bridging research gaps and advancing policy for healthy soils.
Sustainable microbiology, 2(3):qvaf017.
The policy framework previously presented by Neale and colleagues in Sustainable Microbiology highlights the central role of soil microorganisms in sustainable agriculture and global food security, offering actionable interventions grounded in emerging scientific advances. However, the translation of soil science and ecology into impactful policy and practice remains limited. This opinion article revisits the longstanding concept of soil biotechnology, and regulatory/societal barriers to progress. We emphasize that the soil microbiome holds untapped potential for improving plant health, reducing agrochemical reliance, and promoting sustainable food systems through continued research. Interkingdom microbial interactions, especially those involving root exudation as a mechanism for microbial recruitment, are proposed as pivotal but underexplored areas of study. Phenotype-driven, trait-based approaches are advocated over traditional phylogenetic methods to better identify functionally relevant microbial consortia and intervention strategies. Furthermore, we stress the need to integrate ecological, agronomic, and economic insights to develop soil-centric food systems. This includes monetizing ecosystem services provided by healthy soils and implementing incentivized conservation schemes. Unlocking the potential of soil microbial ecology requires coordinated, interdisciplinary efforts and a paradigm shift in policy, funding, and public perception.
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@article {pmid42576819,
year = {2025},
author = {Williams, A and Lynch, J},
title = {Bridging research gaps and advancing policy for healthy soils.},
journal = {Sustainable microbiology},
volume = {2},
number = {3},
pages = {qvaf017},
pmid = {42576819},
issn = {2755-1970},
abstract = {The policy framework previously presented by Neale and colleagues in Sustainable Microbiology highlights the central role of soil microorganisms in sustainable agriculture and global food security, offering actionable interventions grounded in emerging scientific advances. However, the translation of soil science and ecology into impactful policy and practice remains limited. This opinion article revisits the longstanding concept of soil biotechnology, and regulatory/societal barriers to progress. We emphasize that the soil microbiome holds untapped potential for improving plant health, reducing agrochemical reliance, and promoting sustainable food systems through continued research. Interkingdom microbial interactions, especially those involving root exudation as a mechanism for microbial recruitment, are proposed as pivotal but underexplored areas of study. Phenotype-driven, trait-based approaches are advocated over traditional phylogenetic methods to better identify functionally relevant microbial consortia and intervention strategies. Furthermore, we stress the need to integrate ecological, agronomic, and economic insights to develop soil-centric food systems. This includes monetizing ecosystem services provided by healthy soils and implementing incentivized conservation schemes. Unlocking the potential of soil microbial ecology requires coordinated, interdisciplinary efforts and a paradigm shift in policy, funding, and public perception.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
Exploring overlooked growth-promoting mechanisms by plant-associated bacteria.
Sustainable microbiology, 1(1):qvae011.
Agriculture-oriented microbiome studies try to develop microbiota beneficial to their plant hosts. This positive goal extends to the soil quality driving plant growth and disease resistance. In research aimed at identifying the causes of this beneficial action, a common interpretation is that microbes will synthesize metabolites useful to their hosts. This view assumes that important microbial metabolites are exported for use by their hosts. Yet, this seems unlikely for essential metabolites, without a counterpart imported from the plants, as the corresponding syntheses would often involve the consumption of resources without explicit benefit to the microbes. Illustrating this function with the example of Bacilli of the Subtilis clade, we emphasize here that the most direct access to the contents of microbial cells is through cell lysis, a phenomenon often linked to the process of sporulation. This process also releases macromolecules that are digested in the environment, releasing key metabolites such as queuine, an important base analog present in the anticodon of some transfer RNAs. This overlooked importance of cell lysis could also be a major cause of the ubiquitous presence of bacteriophages in microbiota.
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@article {pmid42576846,
year = {2024},
author = {Danchin, A},
title = {Exploring overlooked growth-promoting mechanisms by plant-associated bacteria.},
journal = {Sustainable microbiology},
volume = {1},
number = {1},
pages = {qvae011},
pmid = {42576846},
issn = {2755-1970},
abstract = {Agriculture-oriented microbiome studies try to develop microbiota beneficial to their plant hosts. This positive goal extends to the soil quality driving plant growth and disease resistance. In research aimed at identifying the causes of this beneficial action, a common interpretation is that microbes will synthesize metabolites useful to their hosts. This view assumes that important microbial metabolites are exported for use by their hosts. Yet, this seems unlikely for essential metabolites, without a counterpart imported from the plants, as the corresponding syntheses would often involve the consumption of resources without explicit benefit to the microbes. Illustrating this function with the example of Bacilli of the Subtilis clade, we emphasize here that the most direct access to the contents of microbial cells is through cell lysis, a phenomenon often linked to the process of sporulation. This process also releases macromolecules that are digested in the environment, releasing key metabolites such as queuine, an important base analog present in the anticodon of some transfer RNAs. This overlooked importance of cell lysis could also be a major cause of the ubiquitous presence of bacteriophages in microbiota.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
Microbiome interventions combined with artificial humic acid treatments for restoring soil bacterial diversity.
Sustainable microbiology, 3(2):qvag012.
Soil health is under threat worldwide and technologies for soil restoration are urgently needed. Here we study the effect of artificial humic acids (A-HA) and soil transplants fo one restoration of depleted soil microbiomes. We used a controlled microcosm experiment with gradients of microbial diversity, with and without A-HA, across three soil types. Microbial abundance, diversity, and composition were assessed using qPCR and 16S rRNA gene amplicon sequencing, complemented by metabolomic profiling of water-extractable compounds and the growth characterization of bacterial isolates. A-HA treatment had a stronger effect on bacterial richness and community structure in degraded than in the original soil. Soil microbiome transplants could partially regenerate microbial abundances and increased bacterial richness and diversity in the degraded soils. Interestingly, the combination of A-HAs with addition of 10% soil transplants yielded the best restoration effect. The effect of individual as well as combined treatments strongly depended on the composition of the native soil microbiome. From a mechanistic point of view, A-HA treatment inhibited fast-growing bacteria, which allowed slow-growing bacteria to recover. By combined treatment, depending on the soil type and its native soil microbiome, we can synergistically restore the soil microbiome to resemble its original composition.
Additional Links: PMID-42576847
PubMed:
Citation:
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@article {pmid42576847,
year = {2026},
author = {Wicaksono, WA and Bickel, S and Peissl, J and Marzban, N and Hoefle, D and Abdelfattah, A and Antonietti, M and Berg, G},
title = {Microbiome interventions combined with artificial humic acid treatments for restoring soil bacterial diversity.},
journal = {Sustainable microbiology},
volume = {3},
number = {2},
pages = {qvag012},
pmid = {42576847},
issn = {2755-1970},
abstract = {Soil health is under threat worldwide and technologies for soil restoration are urgently needed. Here we study the effect of artificial humic acids (A-HA) and soil transplants fo one restoration of depleted soil microbiomes. We used a controlled microcosm experiment with gradients of microbial diversity, with and without A-HA, across three soil types. Microbial abundance, diversity, and composition were assessed using qPCR and 16S rRNA gene amplicon sequencing, complemented by metabolomic profiling of water-extractable compounds and the growth characterization of bacterial isolates. A-HA treatment had a stronger effect on bacterial richness and community structure in degraded than in the original soil. Soil microbiome transplants could partially regenerate microbial abundances and increased bacterial richness and diversity in the degraded soils. Interestingly, the combination of A-HAs with addition of 10% soil transplants yielded the best restoration effect. The effect of individual as well as combined treatments strongly depended on the composition of the native soil microbiome. From a mechanistic point of view, A-HA treatment inhibited fast-growing bacteria, which allowed slow-growing bacteria to recover. By combined treatment, depending on the soil type and its native soil microbiome, we can synergistically restore the soil microbiome to resemble its original composition.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
From dysbiosis to dysfunction: specific gut microbes and metabolites in the pathogenesis of Parkinson's disease.
Sustainable microbiology, 3(1):qvag002.
Parkinson's disease (PD) involves a complex interplay between the gut microbiota, their metabolites, and host neurophysiology. Studies across independent cohorts have begun to reveal reproducible microbial signatures, with taxa such as Desulfovibrio spp., Akkermansia, and Bifidobacterium repeatedly enriched, whereas Prevotellaceae and Faecalibacterium are consistently reduced. Beyond these broad compositional patterns, several species and strains-including Helicobacter pylori, curli-producing Escherichia coli, and Desulfovibrio spp.-have been linked to processes such as α-synuclein aggregation, immune activation, and dopaminergic vulnerability. Microbial metabolites including short-chain fatty acids, hydrogen sulfide, lipopolysaccharides, bile acids, and iron-related compounds provide additional mechanistic connections, influencing gut barrier function, inflammatory responses, and neuronal homeostasis. In this review, we bring together findings from taxonomic, metabolic, and mechanistic studies, evaluate the therapeutic potential of microbiota-targeted interventions. Future research should pivot from descriptive microbiome profiling toward mechanistic studies that delineate causal relationships between defined microbes, their metabolites, and PD pathology. Such efforts are essential for identifying early diagnostic biomarkers and developing targeted microbiota-based therapies that could alter the clinical course of PD.
Additional Links: PMID-42576849
PubMed:
Citation:
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@article {pmid42576849,
year = {2026},
author = {Chi, F and Chen, K and Yin, Y and Hakovirta, JR and Saris, PEJ},
title = {From dysbiosis to dysfunction: specific gut microbes and metabolites in the pathogenesis of Parkinson's disease.},
journal = {Sustainable microbiology},
volume = {3},
number = {1},
pages = {qvag002},
pmid = {42576849},
issn = {2755-1970},
abstract = {Parkinson's disease (PD) involves a complex interplay between the gut microbiota, their metabolites, and host neurophysiology. Studies across independent cohorts have begun to reveal reproducible microbial signatures, with taxa such as Desulfovibrio spp., Akkermansia, and Bifidobacterium repeatedly enriched, whereas Prevotellaceae and Faecalibacterium are consistently reduced. Beyond these broad compositional patterns, several species and strains-including Helicobacter pylori, curli-producing Escherichia coli, and Desulfovibrio spp.-have been linked to processes such as α-synuclein aggregation, immune activation, and dopaminergic vulnerability. Microbial metabolites including short-chain fatty acids, hydrogen sulfide, lipopolysaccharides, bile acids, and iron-related compounds provide additional mechanistic connections, influencing gut barrier function, inflammatory responses, and neuronal homeostasis. In this review, we bring together findings from taxonomic, metabolic, and mechanistic studies, evaluate the therapeutic potential of microbiota-targeted interventions. Future research should pivot from descriptive microbiome profiling toward mechanistic studies that delineate causal relationships between defined microbes, their metabolites, and PD pathology. Such efforts are essential for identifying early diagnostic biomarkers and developing targeted microbiota-based therapies that could alter the clinical course of PD.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
Improving soil health in the UK: why a microbial approach is indispensable in attaining sustainable soils.
Sustainable microbiology, 1(1):qvae026.
Current agricultural approaches in the UK-and across much of the world-are unsustainable, particularly due to their impacts on soil health. With evidence already showing diminishing returns in productivity, which are only predicted to get worse with the climate crisis, restoring the health of soils and soil-dwelling microbes is an essential prerequisite for a thriving planet. This report proposes taking a new approach to soil health based on the soil microbiome. The complex community of soil microbes and their interactions are known to underpin soil health and consequently food security, resilience to climate change, global health, biodiversity, and more. As such, an approach that holistically takes soil into account is needed, rather than the siloed approaches used to date. This report therefore highlights the opportunity to take a microbiome approach to soil and how such an approach could be implemented in the UK going forward, whilst also recommending microbial solutions that can be deployed to improve the UK's soils now.
Additional Links: PMID-42576854
PubMed:
Citation:
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@article {pmid42576854,
year = {2024},
author = {Neale, D and Cullen, L and Ranout, AS},
title = {Improving soil health in the UK: why a microbial approach is indispensable in attaining sustainable soils.},
journal = {Sustainable microbiology},
volume = {1},
number = {1},
pages = {qvae026},
pmid = {42576854},
issn = {2755-1970},
abstract = {Current agricultural approaches in the UK-and across much of the world-are unsustainable, particularly due to their impacts on soil health. With evidence already showing diminishing returns in productivity, which are only predicted to get worse with the climate crisis, restoring the health of soils and soil-dwelling microbes is an essential prerequisite for a thriving planet. This report proposes taking a new approach to soil health based on the soil microbiome. The complex community of soil microbes and their interactions are known to underpin soil health and consequently food security, resilience to climate change, global health, biodiversity, and more. As such, an approach that holistically takes soil into account is needed, rather than the siloed approaches used to date. This report therefore highlights the opportunity to take a microbiome approach to soil and how such an approach could be implemented in the UK going forward, whilst also recommending microbial solutions that can be deployed to improve the UK's soils now.},
}
RevDate: 2026-08-11
CmpDate: 2026-08-11
Towards sustainable antimicrobial therapies for Staphylococcus aureus skin infections.
Sustainable microbiology, 1(1):qvae023.
Skin and soft tissue infections (SSTIs) are a major economic and clinical burden. With the emergence of increasing antimicrobial resistance, novel treatment options, as well as advanced drug delivery systems will be essential to fight these infections and meet the UN Sustainability Development Goals (SDGs). SSTIs are commonly caused by Staphylococcus aureus, including the infamous MRSA (methicillin-resistant S. aureus). In this short review, we discuss new antimicrobial therapies with potential to combat skin infections caused by S. aureus. This includes discussion of antimicrobial strategies originating from both the host and microbiota. Adapting immunotherapy-type approaches to infection is also discussed, giving examples of cellular targets of interest. We examine the difficulties of therapeutic delivery into a barrier tissue such as skin and discuss exciting new developments in interdisciplinary approaches that may help overcome these challenges.
Additional Links: PMID-42576857
PubMed:
Citation:
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@article {pmid42576857,
year = {2024},
author = {Lang, JC and Shahata, M and Melican, K},
title = {Towards sustainable antimicrobial therapies for Staphylococcus aureus skin infections.},
journal = {Sustainable microbiology},
volume = {1},
number = {1},
pages = {qvae023},
pmid = {42576857},
issn = {2755-1970},
abstract = {Skin and soft tissue infections (SSTIs) are a major economic and clinical burden. With the emergence of increasing antimicrobial resistance, novel treatment options, as well as advanced drug delivery systems will be essential to fight these infections and meet the UN Sustainability Development Goals (SDGs). SSTIs are commonly caused by Staphylococcus aureus, including the infamous MRSA (methicillin-resistant S. aureus). In this short review, we discuss new antimicrobial therapies with potential to combat skin infections caused by S. aureus. This includes discussion of antimicrobial strategies originating from both the host and microbiota. Adapting immunotherapy-type approaches to infection is also discussed, giving examples of cellular targets of interest. We examine the difficulties of therapeutic delivery into a barrier tissue such as skin and discuss exciting new developments in interdisciplinary approaches that may help overcome these challenges.},
}
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
ESP Goal
In reading the early works of classical genetics, one is drawn, almost inexorably, into ever more complex models, until molecular explanations begin to seem both necessary and natural. At that point, the tools for understanding genome research are at hand. Assisting readers reach this point was the original goal of The Electronic Scholarly Publishing Project.
ESP Usage
Usage of the site grew rapidly and has remained high. Faculty began to use the site for their assigned readings. Other on-line publishers, ranging from The New York Times to Nature referenced ESP materials in their own publications. Nobel laureates (e.g., Joshua Lederberg) regularly used the site and even wrote to suggest changes and improvements.
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When the site began, no journals were making their early content available in digital format. As a result, ESP was obliged to digitize classic literature before it could be made available. For many important papers — such as Mendel's original paper or the first genetic map — ESP had to produce entirely new typeset versions of the works, if they were to be available in a high-quality format.
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Early support from the DOE component of the Human Genome Project was critically important for getting the ESP project on a firm foundation. Since that funding ended (nearly 20 years ago), the project has been operated as a purely volunteer effort. Anyone wishing to assist in these efforts should send an email to Robbins.
ESP Plans
With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
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Dinosaur tail, complete with feathers, found preserved in amber.
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Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
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Hacking the genome: Identifying anonymized human subjects using publicly available data.