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ESP: PubMed Auto Bibliography 10 Oct 2026 at 01:55 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: 2026-10-08
Gut Microbiota-Mediated Biotransformation of Coumarins.
Xenobiotica; the fate of foreign compounds in biological systems [Epub ahead of print].
1. Coumarins are plant-derived secondary metabolites widely present in foods, spices, and medicinal plants. Their limited intestinal absorption and extensive host metabolism allow a variable fraction to reach the colon, where gut microorganisms can transform them into metabolites with distinct physicochemical and biological properties.2. This review synthesizes current evidence on gut microbiota-mediated coumarin biotransformation, focusing on microbial taxa, metabolic reactions, structural determinants, and consequences for biological activity. Reported transformations include deglycosylation, reduction, O-demethylation, hydroxylation, deprenylation, and lactone ring opening. Recent studies have identified multiple human gut bacteria capable of coumarin reduction and implicated the NADPH-dependent reductase NemA in this process. Gut bacteria may also generate simple coumarins from dietary phenolic precursors. These transformations can modify biological activity, while coumarins and their metabolites may reciprocally influence microbial composition and metabolism.3. Current evidence supports gut microbiota as an important determinant of coumarin metabolism, but its physiological relevance in humans remains uncertain. Key gaps include interindividual variability, specific microbial enzymes and taxa, enterohepatic recycling, and the contribution of the gut mycobiome. Integrated microbiome, metabolomic, and pharmacokinetic approaches are needed to establish the contribution of microbiota-derived metabolites to coumarin bioactivity and safety.
Additional Links: PMID-42848816
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@article {pmid42848816,
year = {2026},
author = {Flores Iglesias, JC and Méndez López, LF},
title = {Gut Microbiota-Mediated Biotransformation of Coumarins.},
journal = {Xenobiotica; the fate of foreign compounds in biological systems},
volume = {},
number = {},
pages = {1-22},
doi = {10.1080/00498254.2026.2747088},
pmid = {42848816},
issn = {1366-5928},
abstract = {1. Coumarins are plant-derived secondary metabolites widely present in foods, spices, and medicinal plants. Their limited intestinal absorption and extensive host metabolism allow a variable fraction to reach the colon, where gut microorganisms can transform them into metabolites with distinct physicochemical and biological properties.2. This review synthesizes current evidence on gut microbiota-mediated coumarin biotransformation, focusing on microbial taxa, metabolic reactions, structural determinants, and consequences for biological activity. Reported transformations include deglycosylation, reduction, O-demethylation, hydroxylation, deprenylation, and lactone ring opening. Recent studies have identified multiple human gut bacteria capable of coumarin reduction and implicated the NADPH-dependent reductase NemA in this process. Gut bacteria may also generate simple coumarins from dietary phenolic precursors. These transformations can modify biological activity, while coumarins and their metabolites may reciprocally influence microbial composition and metabolism.3. Current evidence supports gut microbiota as an important determinant of coumarin metabolism, but its physiological relevance in humans remains uncertain. Key gaps include interindividual variability, specific microbial enzymes and taxa, enterohepatic recycling, and the contribution of the gut mycobiome. Integrated microbiome, metabolomic, and pharmacokinetic approaches are needed to establish the contribution of microbiota-derived metabolites to coumarin bioactivity and safety.},
}
RevDate: 2026-10-09
CmpDate: 2026-10-08
The human gut microbiome primes fever after vaccination.
Science (New York, N.Y.), 394(6820):eaea7733.
Fever is a common adverse reaction to vaccination, contributing to vaccine hesitancy and reduced uptake. To understand variation in fever risk, we longitudinally profiled fecal microbiota, oral temperature, and serological markers in 171 healthy adults receiving Severe acute respiratory syndrome coronavirus 2 mRNA vaccines. Fever risk correlated with low-grade intestinal inflammation, increased abundance of flagellated Lachnospiraceae bacteria, and increased flagellin expression prevaccine. Microbiomes from fever-high donors triggered stronger inflammation in human intestinal organoids and drove flagellin-dependent vaccine reactions in gnotobiotic mice. Moreover, microbiome flagellin phenotypes and murine vaccine reactions were modifiable by diet. Consistent with this, human fever risk was associated with self-reported diet and metabolic markers. These findings identify the gut microbiome as a driver of vaccine-induced fever, suggesting that microbiome-targeting strategies could modulate immune tone and improve vaccine side effects.
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@article {pmid42848888,
year = {2026},
author = {Huus, KE and , and Abo, H and Tan, YH and Atay, E and Rytter, H and Keller, R and Dauser, S and Vu, DL and Azad, MB and Knight, R and Ke, A and Lotoski, L and Langlois, MA and Liu, R and Tyakht, AV and Youngblut, N and Kang, SM and Parsonnet, J and Maier, L and Chassaing, B and Kremsner, PG and Gewirtz, AT and Esen, M and Ley, RE and Gabor, JJ and Gaile, JM and Fleischmann, WA and Siebner, AS and Smeenk, G and Flügge, J and De Moraes, RA and Jakob, D and Prokipchuk, A and Wilhelm, C},
title = {The human gut microbiome primes fever after vaccination.},
journal = {Science (New York, N.Y.)},
volume = {394},
number = {6820},
pages = {eaea7733},
doi = {10.1126/science.aea7733},
pmid = {42848888},
issn = {1095-9203},
mesh = {Adult ; Animals ; Female ; Humans ; Male ; Mice ; Diet ; Feces/microbiology ; *Fever/etiology/immunology/microbiology ; Flagellin/immunology/metabolism/genetics ; *Gastrointestinal Microbiome/immunology ; Germ-Free Life ; Inflammation ; SARS-CoV-2/immunology ; *Vaccination/adverse effects ; *Viral Vaccines/adverse effects ; Organoids ; *Eubacteriales/immunology ; *BNT162 Vaccine/adverse effects/immunology ; Mice, Inbred C57BL ; Mice, Knockout ; Toll-Like Receptor 5/genetics ; Calcium-Binding Proteins/genetics ; Apoptosis Regulatory Proteins/genetics ; },
abstract = {Fever is a common adverse reaction to vaccination, contributing to vaccine hesitancy and reduced uptake. To understand variation in fever risk, we longitudinally profiled fecal microbiota, oral temperature, and serological markers in 171 healthy adults receiving Severe acute respiratory syndrome coronavirus 2 mRNA vaccines. Fever risk correlated with low-grade intestinal inflammation, increased abundance of flagellated Lachnospiraceae bacteria, and increased flagellin expression prevaccine. Microbiomes from fever-high donors triggered stronger inflammation in human intestinal organoids and drove flagellin-dependent vaccine reactions in gnotobiotic mice. Moreover, microbiome flagellin phenotypes and murine vaccine reactions were modifiable by diet. Consistent with this, human fever risk was associated with self-reported diet and metabolic markers. These findings identify the gut microbiome as a driver of vaccine-induced fever, suggesting that microbiome-targeting strategies could modulate immune tone and improve vaccine side effects.},
}
MeSH Terms:
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hide MeSH Terms
Adult
Animals
Female
Humans
Male
Mice
Diet
Feces/microbiology
*Fever/etiology/immunology/microbiology
Flagellin/immunology/metabolism/genetics
*Gastrointestinal Microbiome/immunology
Germ-Free Life
Inflammation
SARS-CoV-2/immunology
*Vaccination/adverse effects
*Viral Vaccines/adverse effects
Organoids
*Eubacteriales/immunology
*BNT162 Vaccine/adverse effects/immunology
Mice, Inbred C57BL
Mice, Knockout
Toll-Like Receptor 5/genetics
Calcium-Binding Proteins/genetics
Apoptosis Regulatory Proteins/genetics
RevDate: 2026-10-09
CmpDate: 2026-10-08
Before the immunological Big Bang.
Science (New York, N.Y.), 394(6820):170-171.
The nature of the gut microbiome before vaccination influences later inflammatory reactions and fever.
Additional Links: PMID-42848904
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@article {pmid42848904,
year = {2026},
author = {Pulendran, B},
title = {Before the immunological Big Bang.},
journal = {Science (New York, N.Y.)},
volume = {394},
number = {6820},
pages = {170-171},
doi = {10.1126/science.ael7318},
pmid = {42848904},
issn = {1095-9203},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Vaccination/adverse effects ; Fever/immunology ; Inflammation/immunology ; Animals ; },
abstract = {The nature of the gut microbiome before vaccination influences later inflammatory reactions and fever.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/immunology
*Vaccination/adverse effects
Fever/immunology
Inflammation/immunology
Animals
RevDate: 2026-10-08
Nutritional interventions' impacts on human milk: Three trials in low-resource settings.
Science (New York, N.Y.) [Epub ahead of print].
Human milk (HM) composition is variable to support changing infant needs and is influenced by maternal diet and health. We harmonized HM data from three randomized trials in Burkina Faso (MISAME-III), Pakistan (Mumta-LW), and Tanzania (ELICIT) within the International Milk Composition (IMiC) Consortium to test how maternal nutrition affects HM composition. Balanced energy-protein (BEP) supplements or nicotinamide given to lactating mothers increased milk B-vitamins, while macronutrients, oligosaccharides, bioactive proteins, and microbiome composition were physiologically buffered. Metabolomic and proteomic analyses revealed shifts in vitamin-related metabolites, triglyceride profiles, and intracellular protein representation. In a MISAME-III subset, maternal and infant blood showed concordant changes. Postnatal BEP improved infant growth only in the more undernourished cohort. Improved milk micronutrient quality across settings supports extending maternal supplementation into lactation.
Additional Links: PMID-42848938
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@article {pmid42848938,
year = {2026},
author = {Dailey-Chwalibóg, T and Mertens, A and Fehr, K and Shu, CH and Jauhal, A and Manus, MB and Deng, L and Toe, LC and Muhammed, A and Pasha, A and Shafiq, Y and Iqbal, N and Khan, W and Nisar, MI and Baxter, JB and Beggs, MR and Sundararaman, N and Van Eyk, JE and Bode, L and Hubbard, A and Lagerborg, KA and Jain, M and Hampel, D and Shahab-Ferdows, S and Allen, LH and Lachat, C and DeBoer, MD and Jehan, F and Aghaeepour, N and Shenhav, L and McDermid, JM and Azad, MB},
title = {Nutritional interventions' impacts on human milk: Three trials in low-resource settings.},
journal = {Science (New York, N.Y.)},
volume = {},
number = {},
pages = {},
doi = {10.1126/science.aee9284},
pmid = {42848938},
issn = {1095-9203},
abstract = {Human milk (HM) composition is variable to support changing infant needs and is influenced by maternal diet and health. We harmonized HM data from three randomized trials in Burkina Faso (MISAME-III), Pakistan (Mumta-LW), and Tanzania (ELICIT) within the International Milk Composition (IMiC) Consortium to test how maternal nutrition affects HM composition. Balanced energy-protein (BEP) supplements or nicotinamide given to lactating mothers increased milk B-vitamins, while macronutrients, oligosaccharides, bioactive proteins, and microbiome composition were physiologically buffered. Metabolomic and proteomic analyses revealed shifts in vitamin-related metabolites, triglyceride profiles, and intracellular protein representation. In a MISAME-III subset, maternal and infant blood showed concordant changes. Postnatal BEP improved infant growth only in the more undernourished cohort. Improved milk micronutrient quality across settings supports extending maternal supplementation into lactation.},
}
RevDate: 2026-10-08
An eco-evolutionary consumer-resource theory of host-microbe symbioses.
Journal of evolutionary biology pii:8885813 [Epub ahead of print].
Symbiotic associations between microorganisms and hosts are universal, diverse, and dynamic. Yet, our ability to represent this complexity mathematically remains limited. We propose extending consumer-resource theory to incorporate evolutionary processes to advance our understanding of symbioses, from pairwise interactions to complex host-microbe assemblages. The resulting eco-evolutionary framework captures feedbacks between host-microbe interaction structure, biotic resource availability, and selection acting across biological scales. Importantly, this approach relaxes the assumption of separated ecological and evolutionary timescales, so that both processes unfold simultaneously. The coupling between ecological and evolutionary dynamics allows key properties of symbioses, such as ecological dependence and functional integration, to emerge from evolving resource-mediated interactions, rather than being imposed a priori. We illustrate the framework with a mathematical model of mycorrhizal symbiosis. The proposed consumer-resource formulation provides a unified basis for linking ecological and evolutionary dynamics in host-microbe symbioses, with implications for both basic theory and applied management.
Additional Links: PMID-42849016
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@article {pmid42849016,
year = {2026},
author = {Martignoni, MM and Bordenstein, SR and Karakoç, C and Tyson, RC and Brown, SP and Garnier, J},
title = {An eco-evolutionary consumer-resource theory of host-microbe symbioses.},
journal = {Journal of evolutionary biology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jeb/voag100},
pmid = {42849016},
issn = {1420-9101},
abstract = {Symbiotic associations between microorganisms and hosts are universal, diverse, and dynamic. Yet, our ability to represent this complexity mathematically remains limited. We propose extending consumer-resource theory to incorporate evolutionary processes to advance our understanding of symbioses, from pairwise interactions to complex host-microbe assemblages. The resulting eco-evolutionary framework captures feedbacks between host-microbe interaction structure, biotic resource availability, and selection acting across biological scales. Importantly, this approach relaxes the assumption of separated ecological and evolutionary timescales, so that both processes unfold simultaneously. The coupling between ecological and evolutionary dynamics allows key properties of symbioses, such as ecological dependence and functional integration, to emerge from evolving resource-mediated interactions, rather than being imposed a priori. We illustrate the framework with a mathematical model of mycorrhizal symbiosis. The proposed consumer-resource formulation provides a unified basis for linking ecological and evolutionary dynamics in host-microbe symbioses, with implications for both basic theory and applied management.},
}
RevDate: 2026-10-08
Seasonal dynamics of plastic-degradation-associated microbiomes in an anthropogenically impacted Pearl River Estuary: A genome-resolved metagenomic study.
Marine pollution bulletin, 233(Pt 3):120421 pii:S0025-326X(26)01208-7 [Epub ahead of print].
Estuarine sediments are important sinks for plastic debris and potential reservoirs of microbial functions involved in plastic transformation. Here, metagenomic sequencing and genome-resolved analyses were used to characterize the seasonal distribution and environmental associations of microbial taxa and genes potentially associated with plastic degradation in the Pearl River Estuary. The screened taxa differed between wet and dry seasons, with Priestia and Staphylococcus showing higher relative abundances in the dry season, whereas Vibrio, Photobacterium, Methylobacterium, and Ralstonia were more abundant in the wet season. Microbial community dynamics were associated with variation in organic matter, pH, temperature, and nitrogen variables, with the leading environmental predictors differing between microbial communities and seasons. Genome-resolved analysis recovered 150 non-redundant medium- to high-quality metagenome-assembled genomes (MAGs), of which 42 carried putative plastic-degradation-associated gene homologs identified through comparison with PlasticDB. Approximately 60% of these 42 MAGs belonged to Pseudomonadota, and three Burkholderiaceae MAGs harbored multiple candidate homologs. KEGG annotations further identified genes related to alkane oxidation, fatty acid degradation, ester hydrolysis, and aromatic-compound metabolism, providing a broader metabolic context for these genomes. Together, these findings characterize seasonal variation in the screened microbial communities and identify candidate microbial hosts and genes for investigating plastic transformation in estuarine sediments.
Additional Links: PMID-42849098
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@article {pmid42849098,
year = {2026},
author = {Wen, Y and Huang, X and Zhang, L and Zhang, S and Li, M and Zou, K},
title = {Seasonal dynamics of plastic-degradation-associated microbiomes in an anthropogenically impacted Pearl River Estuary: A genome-resolved metagenomic study.},
journal = {Marine pollution bulletin},
volume = {233},
number = {Pt 3},
pages = {120421},
doi = {10.1016/j.marpolbul.2026.120421},
pmid = {42849098},
issn = {1879-3363},
abstract = {Estuarine sediments are important sinks for plastic debris and potential reservoirs of microbial functions involved in plastic transformation. Here, metagenomic sequencing and genome-resolved analyses were used to characterize the seasonal distribution and environmental associations of microbial taxa and genes potentially associated with plastic degradation in the Pearl River Estuary. The screened taxa differed between wet and dry seasons, with Priestia and Staphylococcus showing higher relative abundances in the dry season, whereas Vibrio, Photobacterium, Methylobacterium, and Ralstonia were more abundant in the wet season. Microbial community dynamics were associated with variation in organic matter, pH, temperature, and nitrogen variables, with the leading environmental predictors differing between microbial communities and seasons. Genome-resolved analysis recovered 150 non-redundant medium- to high-quality metagenome-assembled genomes (MAGs), of which 42 carried putative plastic-degradation-associated gene homologs identified through comparison with PlasticDB. Approximately 60% of these 42 MAGs belonged to Pseudomonadota, and three Burkholderiaceae MAGs harbored multiple candidate homologs. KEGG annotations further identified genes related to alkane oxidation, fatty acid degradation, ester hydrolysis, and aromatic-compound metabolism, providing a broader metabolic context for these genomes. Together, these findings characterize seasonal variation in the screened microbial communities and identify candidate microbial hosts and genes for investigating plastic transformation in estuarine sediments.},
}
RevDate: 2026-10-08
Deciphering the heterogeneity of prodromal α-synucleinopathy: linking brain biotyping and gut dysbiosis in isolated REM sleep behaviour disorder.
EBioMedicine, 133:106503 pii:S2352-3964(26)00387-7 [Epub ahead of print].
BACKGROUND: Isolated/idiopathic REM sleep behaviour disorder (iRBD) is a specific prodrome of α-synucleinopathies. We previously identified two distinct clinical-neuroimaging biotypes in iRBD: Biotype 1, marked by widespread cortical-subcortical-cerebellar atrophy with motor and cognitive deficits, and Biotype 2, with preserved brain structure and neurocognition. Converging evidence implicates the gut-brain axis in early α-synucleinopathy, yet its role in these divergent iRBD phenotypes remains unexplored.
METHODS: We analysed faecal microbiota using shotgun metagenomic sequencing and structural neuroimaging data from 167 participants (42 Biotype 1, 50 Biotype 2, 75 controls). Microbial features and brain structure were compared across groups. Gut-brain associations were assessed using sparse partial least squares regression to link microbiome features with neuroanatomical patterns.
FINDINGS: Overall microbial composition did not significantly differ between Biotype 1 and Biotype 2, and both biotypes showed depletion of short-chain fatty acid-producing bacteria. Relative to the shared dysbiotic background, Biotype 1 displayed more pronounced taxon- and pathway-level alterations, including enrichment of Collinsella aerofaciens, Cloacibacillus evryensis, and Mogibacterium sp. BX12, which were associated with Biotype 1-specific brain atrophy. Biotype 2 showed milder dysbiosis with fewer differentially abundant species. These patterns were consistent in sensitivity analyses and fully adjusted models.
INTERPRETATION: Beyond a shared depletion of short-chain fatty acid-producing bacteria, iRBD biotypes exhibit differences in taxonomic and functional profiles, with these differences being more pronounced in Biotype 1. These findings support a role for the gut-brain axis in early α-synucleinopathy and its phenotypic heterogeneity.
FUNDING: This study was funded by the Health and Medical Research Fund of the Food and Health Bureau (Ref No.: 05162876 and 10210686) and Research Grants Council (RGC-CRF Ref No.: C4044-21G) of Hong Kong.
Additional Links: PMID-42849177
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PubMed:
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@article {pmid42849177,
year = {2026},
author = {Tang, S and Yang, Y and Wang, Y and Gong, S and Li, N and He, Z and Ni, J and Wang, J and Liu, Y and Chan, JWY and Chu, WCW and Mok, VCT and Chen, Z and Huang, B and Wing, YK},
title = {Deciphering the heterogeneity of prodromal α-synucleinopathy: linking brain biotyping and gut dysbiosis in isolated REM sleep behaviour disorder.},
journal = {EBioMedicine},
volume = {133},
number = {},
pages = {106503},
doi = {10.1016/j.ebiom.2026.106503},
pmid = {42849177},
issn = {2352-3964},
abstract = {BACKGROUND: Isolated/idiopathic REM sleep behaviour disorder (iRBD) is a specific prodrome of α-synucleinopathies. We previously identified two distinct clinical-neuroimaging biotypes in iRBD: Biotype 1, marked by widespread cortical-subcortical-cerebellar atrophy with motor and cognitive deficits, and Biotype 2, with preserved brain structure and neurocognition. Converging evidence implicates the gut-brain axis in early α-synucleinopathy, yet its role in these divergent iRBD phenotypes remains unexplored.
METHODS: We analysed faecal microbiota using shotgun metagenomic sequencing and structural neuroimaging data from 167 participants (42 Biotype 1, 50 Biotype 2, 75 controls). Microbial features and brain structure were compared across groups. Gut-brain associations were assessed using sparse partial least squares regression to link microbiome features with neuroanatomical patterns.
FINDINGS: Overall microbial composition did not significantly differ between Biotype 1 and Biotype 2, and both biotypes showed depletion of short-chain fatty acid-producing bacteria. Relative to the shared dysbiotic background, Biotype 1 displayed more pronounced taxon- and pathway-level alterations, including enrichment of Collinsella aerofaciens, Cloacibacillus evryensis, and Mogibacterium sp. BX12, which were associated with Biotype 1-specific brain atrophy. Biotype 2 showed milder dysbiosis with fewer differentially abundant species. These patterns were consistent in sensitivity analyses and fully adjusted models.
INTERPRETATION: Beyond a shared depletion of short-chain fatty acid-producing bacteria, iRBD biotypes exhibit differences in taxonomic and functional profiles, with these differences being more pronounced in Biotype 1. These findings support a role for the gut-brain axis in early α-synucleinopathy and its phenotypic heterogeneity.
FUNDING: This study was funded by the Health and Medical Research Fund of the Food and Health Bureau (Ref No.: 05162876 and 10210686) and Research Grants Council (RGC-CRF Ref No.: C4044-21G) of Hong Kong.},
}
RevDate: 2026-10-08
Dietary Cupplant (Silphium perfoliatum L.) flavonoid supplementation is associated with changes in cecal microbial diversity and community structure in broiler chickens.
Poultry science, 105(12):107876 pii:S0032-5791(26)01510-5 [Epub ahead of print].
Cupplant (Silphium perfoliatum L.) contains flavonoids that may influence the intestinal microbiota, but their effects in broilers remain poorly defined. We examined cecal microbial responses to dietary Cupplant flavonoids. Two hundred forty one-day-old broilers were assigned to four diets containing 0 (CH), 100 (S1), 200 (S2), or 300 (S3) mg/kg flavonoid extract, with five replicate cages per treatment. At day 42, cecal digesta from six birds per treatment were characterized using 16S rRNA gene amplicon sequencing; one cage per treatment contributed two sampled birds. QIIME2/DADA2 processing yielded 1,601,918 retained reads and 2,735 amplicon sequence variants. Observed ASVs, Chao1 richness, and Shannon diversity were higher in S3 than CH (adjusted P < 0.05), although responses were non-monotonic. Global Bray-Curtis PERMANOVA showed treatment-associated differences in community composition (pseudo-F(3,20) = 2.997, R[2] = 0.310, P = 0.001), while PERMDISP was non-significant (P = 0.168). All pairwise PERMANOVA comparisons remained significant after multiplicity correction. False-discovery-rate (FDR)-controlled metagenomeSeq identified six genera in the CH-S1 comparison and three in CH-S3, with Escherichia-Shigella, Desulfovibrio, and Anaerotignum recurring in both contrasts; CH-S2 had no FDR-significant genera. Reconstructed FDR-controlled networks retained only 6.8-12.0 % of nominal edges, and βNTI, NST, and iCAMP results did not support a monotonic dose-dependent shift in community assembly. Descriptive final body weight and average daily gain values were similar across treatments, but cage-level growth inference was not possible from the archived data. Cupplant flavonoid supplementation was associated with non-linear changes in cecal microbial diversity and composition, warranting confirmation in cage-aware, adequately powered studies.
Additional Links: PMID-42849234
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PubMed:
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@article {pmid42849234,
year = {2026},
author = {Makatjane, KA and Xu, J and Guo, W and Liu, G and Wang, Y and Lin, H and Fang, Z and Li, T and Zhou, H},
title = {Dietary Cupplant (Silphium perfoliatum L.) flavonoid supplementation is associated with changes in cecal microbial diversity and community structure in broiler chickens.},
journal = {Poultry science},
volume = {105},
number = {12},
pages = {107876},
doi = {10.1016/j.psj.2026.107876},
pmid = {42849234},
issn = {1525-3171},
abstract = {Cupplant (Silphium perfoliatum L.) contains flavonoids that may influence the intestinal microbiota, but their effects in broilers remain poorly defined. We examined cecal microbial responses to dietary Cupplant flavonoids. Two hundred forty one-day-old broilers were assigned to four diets containing 0 (CH), 100 (S1), 200 (S2), or 300 (S3) mg/kg flavonoid extract, with five replicate cages per treatment. At day 42, cecal digesta from six birds per treatment were characterized using 16S rRNA gene amplicon sequencing; one cage per treatment contributed two sampled birds. QIIME2/DADA2 processing yielded 1,601,918 retained reads and 2,735 amplicon sequence variants. Observed ASVs, Chao1 richness, and Shannon diversity were higher in S3 than CH (adjusted P < 0.05), although responses were non-monotonic. Global Bray-Curtis PERMANOVA showed treatment-associated differences in community composition (pseudo-F(3,20) = 2.997, R[2] = 0.310, P = 0.001), while PERMDISP was non-significant (P = 0.168). All pairwise PERMANOVA comparisons remained significant after multiplicity correction. False-discovery-rate (FDR)-controlled metagenomeSeq identified six genera in the CH-S1 comparison and three in CH-S3, with Escherichia-Shigella, Desulfovibrio, and Anaerotignum recurring in both contrasts; CH-S2 had no FDR-significant genera. Reconstructed FDR-controlled networks retained only 6.8-12.0 % of nominal edges, and βNTI, NST, and iCAMP results did not support a monotonic dose-dependent shift in community assembly. Descriptive final body weight and average daily gain values were similar across treatments, but cage-level growth inference was not possible from the archived data. Cupplant flavonoid supplementation was associated with non-linear changes in cecal microbial diversity and composition, warranting confirmation in cage-aware, adequately powered studies.},
}
RevDate: 2026-10-08
Genotype-dependent phosphorus acquisition responses of two soybean genotypes under combined low phosphorus and salt stress: evidence from root traits, exudates and rhizosphere microbiome.
Plant physiology and biochemistry : PPB, 239:111810 pii:S0981-9428(26)00796-5 [Epub ahead of print].
Soil salinization and phosphorus (P) deficiency often co-occur in coastal saline-alkali soils, severely limiting crop productivity. Although root exudates are known to mediate rhizosphere microbiome assembly, the coordinated associations among root exudates, rhizosphere microbes, and P acquisition under combined salinity stress and phosphate deficiency remain unclear. In this study, we used two salt-tolerant soybean genotypes differing in P efficiency (A74, P-efficient; A6, P-inefficient) as materials. In a controlled pot experiment, four treatments were established: control (CK), low P (LP), salt (S), and combined stress (LPS). By integrating root phenotypes, P acquisition traits, root exudate metabolomics, and rhizosphere metagenomics, the genotype-dependent rhizosphere responses were investigated. Results showed that, compared to A6, A74 maintained a more extensive root-soil interface and superior P nutritional status under LP and LPS, exhibiting more robust P acquisition responses. Metabolomics and metagenomics identified 16 candidate metabolites and 12 candidate microbial taxa, respectively. Effect-size and correlation analyses prioritized naringenin and Sinorhizobium as candidate components associated with genotype-dependent P acquisition responses. KO annotation identified Sinorhizobium-associated genes with potential roles in phosphonate and phosphinate metabolism and benzoate degradation (e.g., phnJ, pcaC, and mhpD). In summary, these results support a genotype-dependent rhizosphere response pattern involving naringenin and Sinorhizobium, in which coordinated changes in root traits, exudate profiles, and microbial functional potential were associated with the stronger P acquisition response of A74 under combined stress. These findings identify candidate relationships for future functional validation under saline conditions.
Additional Links: PMID-42849293
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@article {pmid42849293,
year = {2026},
author = {Zhou, X and Cui, G and Dong, H and Wen, S and Li, Y and Han, M and Wang, G},
title = {Genotype-dependent phosphorus acquisition responses of two soybean genotypes under combined low phosphorus and salt stress: evidence from root traits, exudates and rhizosphere microbiome.},
journal = {Plant physiology and biochemistry : PPB},
volume = {239},
number = {},
pages = {111810},
doi = {10.1016/j.plaphy.2026.111810},
pmid = {42849293},
issn = {1873-2690},
abstract = {Soil salinization and phosphorus (P) deficiency often co-occur in coastal saline-alkali soils, severely limiting crop productivity. Although root exudates are known to mediate rhizosphere microbiome assembly, the coordinated associations among root exudates, rhizosphere microbes, and P acquisition under combined salinity stress and phosphate deficiency remain unclear. In this study, we used two salt-tolerant soybean genotypes differing in P efficiency (A74, P-efficient; A6, P-inefficient) as materials. In a controlled pot experiment, four treatments were established: control (CK), low P (LP), salt (S), and combined stress (LPS). By integrating root phenotypes, P acquisition traits, root exudate metabolomics, and rhizosphere metagenomics, the genotype-dependent rhizosphere responses were investigated. Results showed that, compared to A6, A74 maintained a more extensive root-soil interface and superior P nutritional status under LP and LPS, exhibiting more robust P acquisition responses. Metabolomics and metagenomics identified 16 candidate metabolites and 12 candidate microbial taxa, respectively. Effect-size and correlation analyses prioritized naringenin and Sinorhizobium as candidate components associated with genotype-dependent P acquisition responses. KO annotation identified Sinorhizobium-associated genes with potential roles in phosphonate and phosphinate metabolism and benzoate degradation (e.g., phnJ, pcaC, and mhpD). In summary, these results support a genotype-dependent rhizosphere response pattern involving naringenin and Sinorhizobium, in which coordinated changes in root traits, exudate profiles, and microbial functional potential were associated with the stronger P acquisition response of A74 under combined stress. These findings identify candidate relationships for future functional validation under saline conditions.},
}
RevDate: 2026-10-08
Lactobacillus apisdorsatae sp. nov. from the giant honeybee (Apis dorsata), Lactobacillus pollinatoris sp. nov. and Lactobacillus xylocopae sp. nov., from the carpenter bee (Xylocopa violacea).
Systematic and applied microbiology, 49(6):126776 pii:S0723-2020(26)00084-6 [Epub ahead of print].
Insects host diverse and distinctive communities of gut mutualistic bacteria, including lactic acid bacteria of the Lactobacillus genus. Recently, most research in the insect microbial taxonomy has focused on identifying novel Lactobacillaceae species in managed insects such as Apis mellifera and few species of Bombus spp. from North America, Europe, and China. However, the gut microbiota of wild insects remains largely unexplored. Yet, insects represent the largest animal class and a vast, untouched source of novel microbial symbionts, especially in wild populations. This study focuses on the isolation and characterization of novel Lactobacillaceae strains from wild and solitary insects, such as the carpenter bee (Xylocopa violacea), the strawberry seed beetle (Harpalus rufipes), and the giant honeybee (Apis dorsata). Full-genome sequencing and annotation, including investigation of distinctive functional traits, were performed for these strains, along with phenotypic characterization of sugar fermentation, enzymatic activity, cellular fatty acid profiles and G + C content. Phylogenetic relationships were determined using 16S rRNA gene sequences and core genome computation, which confirmed the classification of novel taxa within the Lactobacillus genus. From the aforementioned insect species, three novel Lactobacillus species were isolated and characterized: Lactobacillus xylocopae XV31L (= DSM 120036[T] = MSCL 1776[T]) and Lactobacillus pollinatoris XV13L (= DSM 104957 [T] = LMG 30141[T]) from X. violacea, and CA30L (= DSM 119968[R] = MSCL 1777[R]) from H. rufipes, and Lactobacillus apisdorsatae C449L (= VTT E-263657 [T] = MSCL 1775[T] = NCCB 101125[T]) from A. dorsata.
Additional Links: PMID-42849303
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PubMed:
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@article {pmid42849303,
year = {2026},
author = {Baffoni, L and Fernandez de Landa, G and Braglia, C and Braschi, G and Siroli, L and Di Gioia, D and Alberoni, D},
title = {Lactobacillus apisdorsatae sp. nov. from the giant honeybee (Apis dorsata), Lactobacillus pollinatoris sp. nov. and Lactobacillus xylocopae sp. nov., from the carpenter bee (Xylocopa violacea).},
journal = {Systematic and applied microbiology},
volume = {49},
number = {6},
pages = {126776},
doi = {10.1016/j.syapm.2026.126776},
pmid = {42849303},
issn = {1618-0984},
abstract = {Insects host diverse and distinctive communities of gut mutualistic bacteria, including lactic acid bacteria of the Lactobacillus genus. Recently, most research in the insect microbial taxonomy has focused on identifying novel Lactobacillaceae species in managed insects such as Apis mellifera and few species of Bombus spp. from North America, Europe, and China. However, the gut microbiota of wild insects remains largely unexplored. Yet, insects represent the largest animal class and a vast, untouched source of novel microbial symbionts, especially in wild populations. This study focuses on the isolation and characterization of novel Lactobacillaceae strains from wild and solitary insects, such as the carpenter bee (Xylocopa violacea), the strawberry seed beetle (Harpalus rufipes), and the giant honeybee (Apis dorsata). Full-genome sequencing and annotation, including investigation of distinctive functional traits, were performed for these strains, along with phenotypic characterization of sugar fermentation, enzymatic activity, cellular fatty acid profiles and G + C content. Phylogenetic relationships were determined using 16S rRNA gene sequences and core genome computation, which confirmed the classification of novel taxa within the Lactobacillus genus. From the aforementioned insect species, three novel Lactobacillus species were isolated and characterized: Lactobacillus xylocopae XV31L (= DSM 120036[T] = MSCL 1776[T]) and Lactobacillus pollinatoris XV13L (= DSM 104957 [T] = LMG 30141[T]) from X. violacea, and CA30L (= DSM 119968[R] = MSCL 1777[R]) from H. rufipes, and Lactobacillus apisdorsatae C449L (= VTT E-263657 [T] = MSCL 1775[T] = NCCB 101125[T]) from A. dorsata.},
}
RevDate: 2026-10-08
Microbiome oncolytic virus interactions in cancer: emerging evidence and therapeutic implications for immunotherapy.
Seminars in oncology, 53(6):152564 pii:S0093-7754(26)00109-0 [Epub ahead of print].
The tumor microenvironment (TME) is essential for the regulation of tumor progression, immune responses, and therapeutic outcomes. The importance of the tumor microbiome, a complex ecosystem of microorganisms that reside within the TME, in shaping tumor dynamics and modulating treatment responses has been underscored by recent advancements in cancer research. Oncolytic viruses (OVs) have been recognized as promising treatment options in cancer immunotherapy due to their ability to selectively target and eliminate tumor cells while protecting normal tissue. Recent preclinical studies suggest a bidirectional relationship between OVs and the microbiome, although direct evidence that OVs remodel tumor-resident microbial communities remains limited. Most available data concern the gut microbiome, where OV treatment has been associated with changes in microbial composition, while baseline or experimentally manipulated microbiota can, in turn, influence virotherapy efficacy. This review examines these emerging interactions, distinguishes direct experimental evidence from proposed mechanisms, and discusses how microbiome-informed strategies may complement OV-based immunotherapy. We also highlight the scarcity of longitudinal intratumoral and clinical microbiome data and identify the experimental steps required to establish causality.
Additional Links: PMID-42849380
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PubMed:
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@article {pmid42849380,
year = {2026},
author = {Khamidov, F and Jalolov, O and Ne'matov, U and Ilmira, U and Mavlyuda, Q and Malohat, S and Alkhawaja, AS and Gulkhayyo, J and Siahmansouri, H},
title = {Microbiome oncolytic virus interactions in cancer: emerging evidence and therapeutic implications for immunotherapy.},
journal = {Seminars in oncology},
volume = {53},
number = {6},
pages = {152564},
doi = {10.1016/j.seminoncol.2026.152564},
pmid = {42849380},
issn = {1532-8708},
abstract = {The tumor microenvironment (TME) is essential for the regulation of tumor progression, immune responses, and therapeutic outcomes. The importance of the tumor microbiome, a complex ecosystem of microorganisms that reside within the TME, in shaping tumor dynamics and modulating treatment responses has been underscored by recent advancements in cancer research. Oncolytic viruses (OVs) have been recognized as promising treatment options in cancer immunotherapy due to their ability to selectively target and eliminate tumor cells while protecting normal tissue. Recent preclinical studies suggest a bidirectional relationship between OVs and the microbiome, although direct evidence that OVs remodel tumor-resident microbial communities remains limited. Most available data concern the gut microbiome, where OV treatment has been associated with changes in microbial composition, while baseline or experimentally manipulated microbiota can, in turn, influence virotherapy efficacy. This review examines these emerging interactions, distinguishes direct experimental evidence from proposed mechanisms, and discusses how microbiome-informed strategies may complement OV-based immunotherapy. We also highlight the scarcity of longitudinal intratumoral and clinical microbiome data and identify the experimental steps required to establish causality.},
}
RevDate: 2026-10-08
Microbiota-mediated naringenin release limits postoperative acute gastrointestinal injury by suppressing ferroptosis.
Cell reports. Medicine pii:S2666-3791(26)00518-5 [Epub ahead of print].
Acute gastrointestinal injury (AGI) remains a major complication after cardiopulmonary bypass, yet its microbiome-related determinants are unclear. We identify microbiota-mediated naringenin (NAR) release as a candidate modulator of AGI susceptibility. Patients who subsequently develop AGI have lower preoperative fecal NAR levels and β-glucuronidase (GUS) activity, accompanied by reduced abundance of Bacteroides vulgatus (B. vulgatus). In germ-free and conventional mice, B. vulgatus alleviates intestinal ischemia-reperfusion injury through GUS-dependent release of NAR from its glucuronide conjugate. Mechanistically, NAR engages the TLR4/MyD88-SPRR2A axis to suppress CHAC1-driven ferroptosis, thereby maintaining epithelial integrity and promoting mucosal repair in vivo and in organoids. Clinically, preoperative fecal NAR concentration and GUS activity show exploratory value as noninvasive markers for postoperative AGI risk stratification. Collectively, these findings support a microbiota-host metabolic model in which microbial NAR release may mitigate postoperative gastrointestinal injury by restricting ferroptosis, with potential implications for risk assessment and therapeutic modulation.
Additional Links: PMID-42849446
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PubMed:
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@article {pmid42849446,
year = {2026},
author = {Deng, F and Hu, J and Min, Y and Xie, S and Lin, Z and Sun, Q and Liu, H and He, S and Feng, S and Wu, L and Chen, X and Xu, L and Zhang, Z and Tang, W and Li, Z and Zhou, H and Liu, K},
title = {Microbiota-mediated naringenin release limits postoperative acute gastrointestinal injury by suppressing ferroptosis.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {103101},
doi = {10.1016/j.xcrm.2026.103101},
pmid = {42849446},
issn = {2666-3791},
abstract = {Acute gastrointestinal injury (AGI) remains a major complication after cardiopulmonary bypass, yet its microbiome-related determinants are unclear. We identify microbiota-mediated naringenin (NAR) release as a candidate modulator of AGI susceptibility. Patients who subsequently develop AGI have lower preoperative fecal NAR levels and β-glucuronidase (GUS) activity, accompanied by reduced abundance of Bacteroides vulgatus (B. vulgatus). In germ-free and conventional mice, B. vulgatus alleviates intestinal ischemia-reperfusion injury through GUS-dependent release of NAR from its glucuronide conjugate. Mechanistically, NAR engages the TLR4/MyD88-SPRR2A axis to suppress CHAC1-driven ferroptosis, thereby maintaining epithelial integrity and promoting mucosal repair in vivo and in organoids. Clinically, preoperative fecal NAR concentration and GUS activity show exploratory value as noninvasive markers for postoperative AGI risk stratification. Collectively, these findings support a microbiota-host metabolic model in which microbial NAR release may mitigate postoperative gastrointestinal injury by restricting ferroptosis, with potential implications for risk assessment and therapeutic modulation.},
}
RevDate: 2026-10-08
The Gut-Lumbar Axis: A Comprehensive Review of Mechanisms, Clinical Evidence, and Future Therapeutic Perspectives.
Pharmacological research pii:S1043-6618(26)01582-3 [Epub ahead of print].
Low back pain (LBP) affects approximately 619 million people globally and is the leading cause of years lived with disability, yet the pathogenesis of chronic LBP remains incompletely understood despite extensive research into structural and biomechanical factors. Emerging evidence suggests that the gut microbiota, through its influence on systemic inflammation, immune regulation, metabolic homeostasis, and neuromodulation, plays a previously unrecognized role in lumbar spine pathology. While prior frameworks such as the "gut-disc axis" and "gut-spine axis" have addressed intervertebral disc degeneration or vertebral bone metabolism in relative isolation, we propose the "gut-lumbar axis" as an integrative framework that systematically unifies the intervertebral discs, vertebrae, paraspinal musculature, and neural structures of the lumbar spine within a single physiological and pathological continuum. This review synthesizes current evidence on the bidirectional communication between intestinal microbiota and lumbar spine health, covering intervertebral disc degeneration, chronic LBP, lumbar spinal stenosis, and vertebral osteoporosis. Multiple pathways linking gut dysbiosis to lumbar pathology are identified, supporting the gut-lumbar axis as a paradigm-shifting framework. However, large-scale longitudinal cohorts and well-designed randomized controlled trials are urgently needed to translate these findings into clinical practice. Microbiome-targeted therapies, including probiotics, dietary interventions, and fecal microbiota transplantation, hold promise as novel adjunctive strategies for managing chronic lumbar spine disorders, and key knowledge gaps for future investigation are highlighted.
Additional Links: PMID-42849550
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PubMed:
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@article {pmid42849550,
year = {2026},
author = {Wang, Z and Zhang, H and Tian, P and Li, S and Li, L and Tian, K and Shi, X and Wu, C and Fan, Y and Lv, YE},
title = {The Gut-Lumbar Axis: A Comprehensive Review of Mechanisms, Clinical Evidence, and Future Therapeutic Perspectives.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {109667},
doi = {10.1016/j.phrs.2026.109667},
pmid = {42849550},
issn = {1096-1186},
abstract = {Low back pain (LBP) affects approximately 619 million people globally and is the leading cause of years lived with disability, yet the pathogenesis of chronic LBP remains incompletely understood despite extensive research into structural and biomechanical factors. Emerging evidence suggests that the gut microbiota, through its influence on systemic inflammation, immune regulation, metabolic homeostasis, and neuromodulation, plays a previously unrecognized role in lumbar spine pathology. While prior frameworks such as the "gut-disc axis" and "gut-spine axis" have addressed intervertebral disc degeneration or vertebral bone metabolism in relative isolation, we propose the "gut-lumbar axis" as an integrative framework that systematically unifies the intervertebral discs, vertebrae, paraspinal musculature, and neural structures of the lumbar spine within a single physiological and pathological continuum. This review synthesizes current evidence on the bidirectional communication between intestinal microbiota and lumbar spine health, covering intervertebral disc degeneration, chronic LBP, lumbar spinal stenosis, and vertebral osteoporosis. Multiple pathways linking gut dysbiosis to lumbar pathology are identified, supporting the gut-lumbar axis as a paradigm-shifting framework. However, large-scale longitudinal cohorts and well-designed randomized controlled trials are urgently needed to translate these findings into clinical practice. Microbiome-targeted therapies, including probiotics, dietary interventions, and fecal microbiota transplantation, hold promise as novel adjunctive strategies for managing chronic lumbar spine disorders, and key knowledge gaps for future investigation are highlighted.},
}
RevDate: 2026-10-08
Genetic risk for dystonia reprograms host-microbiome interactions and gut-brain communication.
Experimental neurology pii:S0014-4886(26)00421-8 [Epub ahead of print].
Dystonia is a neurological movement disorder characterized by involuntary, sustained, or intermittent muscle contractions that result in twisting movements, repetitive motor patterns, or abnormal postures. While genetic mutations such as TOR1A[+/∆GAG] are known contributors, the environmental and peripheral factors influencing disease onset and progression remain poorly understood. Emerging evidence implicates the gut microbiome in shaping neurodevelopment and host behavioral function, yet its contribution to dystonia pathobiology is largely unexplored. Here, we longitudinally profiled the gut microbiome of a Tor1a[+/∆GAG] mouse model using 16S rRNA gene sequencing and uncovered early emerging, persistent disruptions in microbial diversity and community composition that coincided with progressive motor impairment. Mutant mice exhibited alterations in key commensal taxa, and molecular signatures indicative of compromised gut-barrier integrity. Parallel transcriptomic profiling of colonic tissues revealed coordinated dysregulation of pathways governing epithelial stress responses, endoplasmic reticulum homeostasis, lipid signaling, autophagy, and DNA damage and repair, suggesting a previously unrecognized epithelial stress state in Tor1a[+/∆GAG] mouse model. Integrative microbial-host interaction correlation analyses uncovered associations between specific dysbiotic taxa and host signaling pathways. These peripheral perturbations coincided with longitudinal motor deficits, identifying an age-dependent association between gut dysbiosis and neurobehavioral dysfunction. Together, our findings provide an experimental framework for investigating the relationship among microbiome perturbations, gut-barrier disruption, and neuronal vulnerability in a genetic model of dystonia. These findings reveal a previously underexplored peripheral dimension of DYT1 dystonia and provide a foundation for future studies to determine whether microbiome and intestinal alterations functionally contribute to disease pathobiology.
Additional Links: PMID-42849604
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PubMed:
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@article {pmid42849604,
year = {2026},
author = {Xiao, J and Khan, S and Shukla, PK and Johnson, D and LeDoux, MS and Khan, MM},
title = {Genetic risk for dystonia reprograms host-microbiome interactions and gut-brain communication.},
journal = {Experimental neurology},
volume = {},
number = {},
pages = {116054},
doi = {10.1016/j.expneurol.2026.116054},
pmid = {42849604},
issn = {1090-2430},
abstract = {Dystonia is a neurological movement disorder characterized by involuntary, sustained, or intermittent muscle contractions that result in twisting movements, repetitive motor patterns, or abnormal postures. While genetic mutations such as TOR1A[+/∆GAG] are known contributors, the environmental and peripheral factors influencing disease onset and progression remain poorly understood. Emerging evidence implicates the gut microbiome in shaping neurodevelopment and host behavioral function, yet its contribution to dystonia pathobiology is largely unexplored. Here, we longitudinally profiled the gut microbiome of a Tor1a[+/∆GAG] mouse model using 16S rRNA gene sequencing and uncovered early emerging, persistent disruptions in microbial diversity and community composition that coincided with progressive motor impairment. Mutant mice exhibited alterations in key commensal taxa, and molecular signatures indicative of compromised gut-barrier integrity. Parallel transcriptomic profiling of colonic tissues revealed coordinated dysregulation of pathways governing epithelial stress responses, endoplasmic reticulum homeostasis, lipid signaling, autophagy, and DNA damage and repair, suggesting a previously unrecognized epithelial stress state in Tor1a[+/∆GAG] mouse model. Integrative microbial-host interaction correlation analyses uncovered associations between specific dysbiotic taxa and host signaling pathways. These peripheral perturbations coincided with longitudinal motor deficits, identifying an age-dependent association between gut dysbiosis and neurobehavioral dysfunction. Together, our findings provide an experimental framework for investigating the relationship among microbiome perturbations, gut-barrier disruption, and neuronal vulnerability in a genetic model of dystonia. These findings reveal a previously underexplored peripheral dimension of DYT1 dystonia and provide a foundation for future studies to determine whether microbiome and intestinal alterations functionally contribute to disease pathobiology.},
}
RevDate: 2026-10-08
Synbiotic to Attenuate Resorption of the Skeleton (STARS): Design and participant recruitment of a randomized, double-blind, placebo-controlled trial to test the efficacy of SBD111 medical food in older women.
Contemporary clinical trials pii:S1551-7144(26)00287-9 [Epub ahead of print].
Osteoporosis and related fractures pose a costly public health challenge. Primary prevention of bone loss is largely limited to non-pharmacologic options without consistent guidelines. Prior studies have demonstrated that modification of the gut microbiome can influence bone homeostasis. The Synbiotic To Attenuate Resorption of the Skeleton (STARS) trial aimed to evaluate the efficacy, safety, and mechanistic effects of daily intake of SBD111, a fruit and vegetable-derived synbiotic medical food on the skeleton, gut microbiome, and inflammation biomarkers in women aged ≥60 years. This 18-month, investigator-initiated, single-site, randomized, double-blind, placebo-controlled trial had an enrollment goal of 220 women, a primary endpoint of proportionate change in lumbar spine bone mineral density (BMD) relative to baseline, and secondary outcomes including Quantitative Computed Tomography derived volumetric BMD and vertebral compressive strength, gut microbiome function, and bone and inflammatory biomarkers. Recruitment approaches included simultaneous digital and traditional methods beginning August 2024. As of July 2025, there were 42 enrolled participants (32 via digital, 10 via traditional); baseline demographics, eligibility, and enrollment rates were similar across recruitment strategies. Digital recruitment achieved over three times faster enrollment (2.9 vs. 0.9 enrollments/month) and was nearly 10 times more staff-efficient (0.05 vs. 0.48 cumulative weekly full-time equivalent) despite greater cost per enrollment ($548 vs. $173). These findings demonstrate the feasibility and efficiency of digital recruitment of older adults, offering valuable insights for future nutrition and microbiome clinical trials. The STARS trial is positioned to provide high-quality evidence for skeletal health maintenance in older women using SBD111.
Additional Links: PMID-42849708
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PubMed:
Citation:
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@article {pmid42849708,
year = {2026},
author = {Ford, JG and O'Neill, E and Tolland, C and Travison, TG and Singer, K and Charbonneau, MR and Easson, DD and Jacques, PF and Toledo, GV and Rosen, CJ and Schott, EM and Kiel, DP and Sahni, S},
title = {Synbiotic to Attenuate Resorption of the Skeleton (STARS): Design and participant recruitment of a randomized, double-blind, placebo-controlled trial to test the efficacy of SBD111 medical food in older women.},
journal = {Contemporary clinical trials},
volume = {},
number = {},
pages = {108501},
doi = {10.1016/j.cct.2026.108501},
pmid = {42849708},
issn = {1559-2030},
abstract = {Osteoporosis and related fractures pose a costly public health challenge. Primary prevention of bone loss is largely limited to non-pharmacologic options without consistent guidelines. Prior studies have demonstrated that modification of the gut microbiome can influence bone homeostasis. The Synbiotic To Attenuate Resorption of the Skeleton (STARS) trial aimed to evaluate the efficacy, safety, and mechanistic effects of daily intake of SBD111, a fruit and vegetable-derived synbiotic medical food on the skeleton, gut microbiome, and inflammation biomarkers in women aged ≥60 years. This 18-month, investigator-initiated, single-site, randomized, double-blind, placebo-controlled trial had an enrollment goal of 220 women, a primary endpoint of proportionate change in lumbar spine bone mineral density (BMD) relative to baseline, and secondary outcomes including Quantitative Computed Tomography derived volumetric BMD and vertebral compressive strength, gut microbiome function, and bone and inflammatory biomarkers. Recruitment approaches included simultaneous digital and traditional methods beginning August 2024. As of July 2025, there were 42 enrolled participants (32 via digital, 10 via traditional); baseline demographics, eligibility, and enrollment rates were similar across recruitment strategies. Digital recruitment achieved over three times faster enrollment (2.9 vs. 0.9 enrollments/month) and was nearly 10 times more staff-efficient (0.05 vs. 0.48 cumulative weekly full-time equivalent) despite greater cost per enrollment ($548 vs. $173). These findings demonstrate the feasibility and efficiency of digital recruitment of older adults, offering valuable insights for future nutrition and microbiome clinical trials. The STARS trial is positioned to provide high-quality evidence for skeletal health maintenance in older women using SBD111.},
}
RevDate: 2026-10-08
Comment on "Breastfeeding, early-life feeding practices and adolescent gut microbiota: Long-term associations in a birth cohort".
Additional Links: PMID-42849840
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PubMed:
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@article {pmid42849840,
year = {2026},
author = {Chelladurai, and Premkumar, R and Jenivi, A and Mohanapriya, },
title = {Comment on "Breastfeeding, early-life feeding practices and adolescent gut microbiota: Long-term associations in a birth cohort".},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105176},
doi = {10.1016/j.clnesp.2026.105176},
pmid = {42849840},
issn = {2405-4577},
}
RevDate: 2026-10-08
Gut Microbiota and nutrition as Emerging Modulators of Immune Checkpoint Inhibitor Therapy: Current Evidence, Challenges, and Future Perspectives.
Clinical nutrition ESPEN pii:S2405-4577(26)02265-5 [Epub ahead of print].
Immune checkpoint inhibitors (ICIs), a major class of cancer immunotherapies, have transformed the treatment of advanced cancers, yet durable benefit remains limited by primary or acquired resistance and immune-related adverse events (irAEs). Increasing evidence implicates the gut microbiome and nutritional state as modifiable host factors that may shape both therapeutic efficacy and toxicity. Here, we critically review the emerging evidence linking microbial ecology, dietary exposure, immunonutrition and ICI outcomes, with particular emphasis on the diet-microbiome-metabolite-immune axis. Clinical cohorts and preclinical models indicate that microbiome composition and, increasingly, microbial function and metabolic cross-talk are associated with ICI responsiveness, while microbiome perturbations may also influence susceptibility to irAEs. Dietary patterns and nutritional status likewise correlate with treatment outcomes, with dietary fibre and Mediterranean-style dietary patterns providing early clinical signals, whereas evidence for specific immunonutrients and restrictive dietary strategies remains inconsistent or insufficient. Mechanistically, dietary substrates can reshape microbial communities and metabolite production, thereby modulating immune-cell states and antitumour responses. However, these effects are highly context dependent and cannot be inferred from individual taxa or metabolites alone. We further examine emerging strategies that integrate nutritional optimization with microbiome modulation as a potential means of simultaneously improving efficacy and therapeutic tolerability. Despite substantial mechanistic progress, clinical evidence remains predominantly observational or early phase, and no microbiome-informed dietary intervention has yet established a reproducible benefit in prospective trials. Future studies should therefore move beyond descriptive associations towards evaluating causal, biomarker-guided and patient-stratified interventions integrating longitudinal dietary, microbiome, metabolomic and immune profiling.
Additional Links: PMID-42849841
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PubMed:
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@article {pmid42849841,
year = {2026},
author = {Qi, YL and Yan, Y and Li, XM and Li, YL and Liao, LZ and Liu, J and Ma, JW and Ma, JH and Chen, H},
title = {Gut Microbiota and nutrition as Emerging Modulators of Immune Checkpoint Inhibitor Therapy: Current Evidence, Challenges, and Future Perspectives.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105168},
doi = {10.1016/j.clnesp.2026.105168},
pmid = {42849841},
issn = {2405-4577},
abstract = {Immune checkpoint inhibitors (ICIs), a major class of cancer immunotherapies, have transformed the treatment of advanced cancers, yet durable benefit remains limited by primary or acquired resistance and immune-related adverse events (irAEs). Increasing evidence implicates the gut microbiome and nutritional state as modifiable host factors that may shape both therapeutic efficacy and toxicity. Here, we critically review the emerging evidence linking microbial ecology, dietary exposure, immunonutrition and ICI outcomes, with particular emphasis on the diet-microbiome-metabolite-immune axis. Clinical cohorts and preclinical models indicate that microbiome composition and, increasingly, microbial function and metabolic cross-talk are associated with ICI responsiveness, while microbiome perturbations may also influence susceptibility to irAEs. Dietary patterns and nutritional status likewise correlate with treatment outcomes, with dietary fibre and Mediterranean-style dietary patterns providing early clinical signals, whereas evidence for specific immunonutrients and restrictive dietary strategies remains inconsistent or insufficient. Mechanistically, dietary substrates can reshape microbial communities and metabolite production, thereby modulating immune-cell states and antitumour responses. However, these effects are highly context dependent and cannot be inferred from individual taxa or metabolites alone. We further examine emerging strategies that integrate nutritional optimization with microbiome modulation as a potential means of simultaneously improving efficacy and therapeutic tolerability. Despite substantial mechanistic progress, clinical evidence remains predominantly observational or early phase, and no microbiome-informed dietary intervention has yet established a reproducible benefit in prospective trials. Future studies should therefore move beyond descriptive associations towards evaluating causal, biomarker-guided and patient-stratified interventions integrating longitudinal dietary, microbiome, metabolomic and immune profiling.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Mining Impacts on a Threatened and Burnt Swamp Ecosystem: Responses of the Microbial Soil Community.
Environmental microbiology reports, 18(5):e70397.
Peatlands are globally important carbon reservoirs that mitigate global warming while regulating biogeochemical cycles. However, these ecosystems are highly vulnerable to environmental disturbances, such as fire and mining. Despite the key ecological roles of soil microbes, descriptions of microbial assemblages in many peatland systems, and how they may shift under the dual disturbances of fire and mining, remain poorly addressed. Here, we assessed the composition and diversity of soil microbial communities in three mined and three unmined swamps in southeastern Australia, all affected by the unprecedented summer bushfires during 2019-2020. Bacterial and eukaryotic communities were analysed alongside soil chemical properties across a moisture gradient within each swamp. Our results revealed significant differences in communities due to mining activities, with the most pronounced differences observed within swamp communities rather than other sites along the moisture gradient. The eukaryotic community was significantly influenced by the combined effects of mining activity and fire history. The bacterial community was significantly correlated with pH. Our findings suggest that mining was associated with changes in eukaryotic diversity and bacterial community structure and functionality, with fire history potentially contributing to the observed patterns. This study underscores the critical, detrimental impacts that mining can have on peatland microbial composition.
Additional Links: PMID-42850030
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PubMed:
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@article {pmid42850030,
year = {2026},
author = {de Lima, NM and Vázquez-Campos, X and Thomsen, A and Ooi, M and Muñoz-Rojas, M},
title = {Mining Impacts on a Threatened and Burnt Swamp Ecosystem: Responses of the Microbial Soil Community.},
journal = {Environmental microbiology reports},
volume = {18},
number = {5},
pages = {e70397},
doi = {10.1111/1758-2229.70397},
pmid = {42850030},
issn = {1758-2229},
support = {PID2021-123097OA-I00//Ministerio de Ciencia e Innovación/ ; PID2024-161692OB-C33//Ministerio de Ciencia e Innovación/ ; LP180100741//Australian Research Council/ ; },
mesh = {*Soil Microbiology ; Bacteria/classification/isolation & purification/genetics ; *Mining ; *Wetlands ; Soil/chemistry ; *Microbiota ; Biodiversity ; Australia ; Ecosystem ; Eukaryota/classification/isolation & purification/genetics ; Fires ; },
abstract = {Peatlands are globally important carbon reservoirs that mitigate global warming while regulating biogeochemical cycles. However, these ecosystems are highly vulnerable to environmental disturbances, such as fire and mining. Despite the key ecological roles of soil microbes, descriptions of microbial assemblages in many peatland systems, and how they may shift under the dual disturbances of fire and mining, remain poorly addressed. Here, we assessed the composition and diversity of soil microbial communities in three mined and three unmined swamps in southeastern Australia, all affected by the unprecedented summer bushfires during 2019-2020. Bacterial and eukaryotic communities were analysed alongside soil chemical properties across a moisture gradient within each swamp. Our results revealed significant differences in communities due to mining activities, with the most pronounced differences observed within swamp communities rather than other sites along the moisture gradient. The eukaryotic community was significantly influenced by the combined effects of mining activity and fire history. The bacterial community was significantly correlated with pH. Our findings suggest that mining was associated with changes in eukaryotic diversity and bacterial community structure and functionality, with fire history potentially contributing to the observed patterns. This study underscores the critical, detrimental impacts that mining can have on peatland microbial composition.},
}
MeSH Terms:
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*Soil Microbiology
Bacteria/classification/isolation & purification/genetics
*Mining
*Wetlands
Soil/chemistry
*Microbiota
Biodiversity
Australia
Ecosystem
Eukaryota/classification/isolation & purification/genetics
Fires
RevDate: 2026-10-08
What's New Is Old: "Cultural Lag" and Governance of Risk in the Life Sciences.
Cold Spring Harbor perspectives in medicine pii:cshperspect.a041953 [Epub ahead of print].
As advancement in the life sciences quickens, management of risks remains reactive, creating problematic delays in risk mitigation and difficulties for development of a holistic risk governance strategy. A reactive posture for addressing risk undermines biosecurity and contributes to public distrust in science. This problem is not new. A temporal offset between scientific advancement and oversight of associated risks was described more than a century ago. In 1922, the American sociologist, William Ogburn, coined the term, "cultural lag." Cultural lag was premised on the interconnectedness of technology and society and referred to a period of maladjustment between the introduction of a new technology and societal responses to mitigate its downsides. We examine the consequences of cultural lag for risk governance in the life sciences by looking at three recently introduced technologies, CRISPR-Cas9 gene editing, the proposed creation of mirror life, and microbiome engineering. Our observations lead to three recommendations for addressing cultural lag. The first recommendation is structural, namely, consolidation of governmental oversight on emerging technologies; the second is goal-oriented, that is, a call for a holistic form of horizon scanning; and the third concerns process and calls for implementation of deliberative democratic principles and practices. By pursuing an anticipatory governance regime, with policymaking closely aligned to and coordinated with technology breakthroughs, we enhance research safety and security while promoting innovation, and as a secondary benefit, help to restore public trust in science.
Additional Links: PMID-42850034
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@article {pmid42850034,
year = {2026},
author = {Arunachalam, JC and Relman, DA},
title = {What's New Is Old: "Cultural Lag" and Governance of Risk in the Life Sciences.},
journal = {Cold Spring Harbor perspectives in medicine},
volume = {},
number = {},
pages = {},
doi = {10.1101/cshperspect.a041953},
pmid = {42850034},
issn = {2157-1422},
abstract = {As advancement in the life sciences quickens, management of risks remains reactive, creating problematic delays in risk mitigation and difficulties for development of a holistic risk governance strategy. A reactive posture for addressing risk undermines biosecurity and contributes to public distrust in science. This problem is not new. A temporal offset between scientific advancement and oversight of associated risks was described more than a century ago. In 1922, the American sociologist, William Ogburn, coined the term, "cultural lag." Cultural lag was premised on the interconnectedness of technology and society and referred to a period of maladjustment between the introduction of a new technology and societal responses to mitigate its downsides. We examine the consequences of cultural lag for risk governance in the life sciences by looking at three recently introduced technologies, CRISPR-Cas9 gene editing, the proposed creation of mirror life, and microbiome engineering. Our observations lead to three recommendations for addressing cultural lag. The first recommendation is structural, namely, consolidation of governmental oversight on emerging technologies; the second is goal-oriented, that is, a call for a holistic form of horizon scanning; and the third concerns process and calls for implementation of deliberative democratic principles and practices. By pursuing an anticipatory governance regime, with policymaking closely aligned to and coordinated with technology breakthroughs, we enhance research safety and security while promoting innovation, and as a secondary benefit, help to restore public trust in science.},
}
RevDate: 2026-10-08
Context-dependent roles of ketone metabolism in intestinal inflammation.
Trends in immunology pii:S1471-4906(26)00260-7 [Epub ahead of print].
Ketone metabolism is traditionally viewed as an alternative metabolic pathway providing energy during carbohydrate deprivation through the production and utilization of ketone bodies. Ketone bodies also function as signaling molecules regulating immune and metabolic processes. Accumulating evidence shows that ketone metabolism influences diverse diseases and immune responses, including inflammation, autoimmunity, and infection. Recently, ketone metabolism has been associated with inflammatory bowel disease (IBD), a chronic inflammatory disorder of the intestine, although reported effects are heterogeneous and context-dependent. In this review, we synthesize current evidence on ketone metabolism in IBD and intestinal inflammation, highlighting its roles in barrier integrity, immune regulation, and microbiota interactions. We also discuss potential mechanisms underlying divergent outcomes and outline key questions for future research.
Additional Links: PMID-42850154
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PubMed:
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@article {pmid42850154,
year = {2026},
author = {Dong, W and Yan, C and Korwin-Mihavics, B and Alexander, M},
title = {Context-dependent roles of ketone metabolism in intestinal inflammation.},
journal = {Trends in immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.it.2026.09.005},
pmid = {42850154},
issn = {1471-4981},
abstract = {Ketone metabolism is traditionally viewed as an alternative metabolic pathway providing energy during carbohydrate deprivation through the production and utilization of ketone bodies. Ketone bodies also function as signaling molecules regulating immune and metabolic processes. Accumulating evidence shows that ketone metabolism influences diverse diseases and immune responses, including inflammation, autoimmunity, and infection. Recently, ketone metabolism has been associated with inflammatory bowel disease (IBD), a chronic inflammatory disorder of the intestine, although reported effects are heterogeneous and context-dependent. In this review, we synthesize current evidence on ketone metabolism in IBD and intestinal inflammation, highlighting its roles in barrier integrity, immune regulation, and microbiota interactions. We also discuss potential mechanisms underlying divergent outcomes and outline key questions for future research.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Hydrothermal regimes regulate microbiome patterns across vertical profile and their responses to alpine permafrost degradation.
Nature communications, 17(1):.
Deciphering microbiomes across vertical profiles is critical for understanding biogeochemical cycling and potential biosafety hazards associated with permafrost degradation under climate warming. However, knowledge about microbiome patterns over key profile layers in response to degradation remains limited in the Qinghai-Tibet Plateau. Using metagenomic data obtained from 150 samples of six 15 m-depth alpine permafrost cores along a degradation gradient, we analyzed microbial community structure and functional potential across different main-layers, including the active, frozen fringe, and frozen layers. We found the recovered microbial and functional diversity decreased with profile depth, and declined only in the active layer as permafrost degraded. Interestingly, Pithoviridae, Caulimoviridae, and virulence factors related to adhesion, biofilm formation, and immune regulation were enriched in the frozen fringe layer, along with increasing relative abundance of Lavidaviridae under the degradation. Along the degradation gradient, carbohydrate-active enzymes diversity decreased in the active layer, while the ratio of nitrite reductase genes to nitrous oxide reductase genes increased in the active and the frozen fringe layers. Hydrothermal regimes emerged as the primary controls shaping microbiome distributions across the vertical profile and along the degradation gradient. Notably, hydrothermal and microbiome attributes jointly regulated carbon/nitrogen loss during the degradation. Taken together, these findings offer crucial insights into microbiome patterns, carbon/nitrogen loss and biosecurity concerning permafrost degradation under global warming.
Additional Links: PMID-42850249
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Citation:
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@article {pmid42850249,
year = {2026},
author = {Chen, S and Bahadur, A and Zhu, J and Liu, E and Gu, Y and Liang, H and Zhang, W and Li, S and Li, A and Wei, P and Liu, Q and Wu, T and Yang, P and Zou, Y and Han, M and Malard, LA},
title = {Hydrothermal regimes regulate microbiome patterns across vertical profile and their responses to alpine permafrost degradation.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42850249},
issn = {2041-1723},
support = {U23A2062//National Natural Science Foundation of China (National Science Foundation of China)/ ; U24A20586//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {*Permafrost/microbiology ; *Microbiota/genetics/physiology ; Bacteria/genetics/classification ; Soil Microbiology ; Tibet ; Metagenome ; Nitrogen/metabolism ; },
abstract = {Deciphering microbiomes across vertical profiles is critical for understanding biogeochemical cycling and potential biosafety hazards associated with permafrost degradation under climate warming. However, knowledge about microbiome patterns over key profile layers in response to degradation remains limited in the Qinghai-Tibet Plateau. Using metagenomic data obtained from 150 samples of six 15 m-depth alpine permafrost cores along a degradation gradient, we analyzed microbial community structure and functional potential across different main-layers, including the active, frozen fringe, and frozen layers. We found the recovered microbial and functional diversity decreased with profile depth, and declined only in the active layer as permafrost degraded. Interestingly, Pithoviridae, Caulimoviridae, and virulence factors related to adhesion, biofilm formation, and immune regulation were enriched in the frozen fringe layer, along with increasing relative abundance of Lavidaviridae under the degradation. Along the degradation gradient, carbohydrate-active enzymes diversity decreased in the active layer, while the ratio of nitrite reductase genes to nitrous oxide reductase genes increased in the active and the frozen fringe layers. Hydrothermal regimes emerged as the primary controls shaping microbiome distributions across the vertical profile and along the degradation gradient. Notably, hydrothermal and microbiome attributes jointly regulated carbon/nitrogen loss during the degradation. Taken together, these findings offer crucial insights into microbiome patterns, carbon/nitrogen loss and biosecurity concerning permafrost degradation under global warming.},
}
MeSH Terms:
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*Permafrost/microbiology
*Microbiota/genetics/physiology
Bacteria/genetics/classification
Soil Microbiology
Tibet
Metagenome
Nitrogen/metabolism
RevDate: 2026-10-08
CmpDate: 2026-10-08
Metabolic immune checkpoints (MICs) in cancer: from molecular mechanisms to challenges and opportunities in clinical translation.
Signal transduction and targeted therapy, 11(1):.
Metabolic reprogramming is a core feature of tumor cells in adapting to microenvironmental stress and acquiring malignant phenotypes. It not only supports rapid proliferation but also mediates immune escape by reshaping the immune microenvironment. In recent years, the "metabolism-immune axis", serving as a central hub for the crosstalk between metabolic regulation and immune suppression, has provided a new perspective for understanding tumor immune evasion. This review systematically discusses how metabolic pathways, including glucose, lipid, and amino acid metabolism, along with mitochondrial function and other related processes, shape the immunosuppressive tumor microenvironment by regulating immune cell function, immune checkpoint expression, and immune signaling networks, thereby promoting tumor immune escape. The concept of "metabolic immune checkpoints (MICs)" is innovatively proposed and classified into three categories based on their mechanisms of action: (1) MIC-I: metabolic modification-type immune checkpoints, exemplified by posttranslational modifications of immune checkpoint molecules such as PD-L1 lactylation, acetylation and glycosylation, etc.; (2) MIC-II: metabolic enzyme-dependent immune regulatory nodes, represented by enzymes such as indoleamine 2,3-dioxygenase 1 and others that directly influence immune cell function; and (3) MIC-III: microbial metabolite-coupled immune regulatory targets, including receptors for microbe-derived metabolites such as short-chain fatty acid receptors. By integrating molecular interaction networks of key targets such as lactate dehydrogenase A and ATP citrate lyase, this review explores synergistic therapeutic strategies that combine small-molecule inhibitors targeting MICs with immune checkpoint blockade. This highlights how metabolic intervention can restore immune cell function and reverse exhaustion. Current key challenges in clinical translation include limitations in metabolic dynamic monitoring technologies, lack of patient stratification biomarkers and insufficient specificity in microbiome regulation. Future directions will focus on personalized treatment guided by multiomics, integrating single-cell metabolic flux analysis, deep learning-driven target prediction, and synthetic microbiome engineering, driving tumor immunotherapy into the era of precision metabolic regulation. By integrating the fundamental mechanisms of MICs with translational medical research, this review not only provides a systematic paradigm but also establishes a foundation for the development of new-generation precision combination therapies.
Additional Links: PMID-42850252
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Citation:
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@article {pmid42850252,
year = {2026},
author = {Yang, J and Cai, X and He, F and Zhang, J and Zhang, Z and Yi, Z and Xie, C and Xu, B},
title = {Metabolic immune checkpoints (MICs) in cancer: from molecular mechanisms to challenges and opportunities in clinical translation.},
journal = {Signal transduction and targeted therapy},
volume = {11},
number = {1},
pages = {},
pmid = {42850252},
issn = {2059-3635},
support = {320.6750.2023-11-21//Ministry of Health of China | Wu Jieping Medical Foundation/ ; 82473253//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {Humans ; *Neoplasms/immunology/therapy/genetics/pathology/metabolism ; Metabolic Reprogramming ; *Tumor Microenvironment/immunology/genetics ; *Immune Checkpoint Proteins/immunology/genetics ; Animals ; },
abstract = {Metabolic reprogramming is a core feature of tumor cells in adapting to microenvironmental stress and acquiring malignant phenotypes. It not only supports rapid proliferation but also mediates immune escape by reshaping the immune microenvironment. In recent years, the "metabolism-immune axis", serving as a central hub for the crosstalk between metabolic regulation and immune suppression, has provided a new perspective for understanding tumor immune evasion. This review systematically discusses how metabolic pathways, including glucose, lipid, and amino acid metabolism, along with mitochondrial function and other related processes, shape the immunosuppressive tumor microenvironment by regulating immune cell function, immune checkpoint expression, and immune signaling networks, thereby promoting tumor immune escape. The concept of "metabolic immune checkpoints (MICs)" is innovatively proposed and classified into three categories based on their mechanisms of action: (1) MIC-I: metabolic modification-type immune checkpoints, exemplified by posttranslational modifications of immune checkpoint molecules such as PD-L1 lactylation, acetylation and glycosylation, etc.; (2) MIC-II: metabolic enzyme-dependent immune regulatory nodes, represented by enzymes such as indoleamine 2,3-dioxygenase 1 and others that directly influence immune cell function; and (3) MIC-III: microbial metabolite-coupled immune regulatory targets, including receptors for microbe-derived metabolites such as short-chain fatty acid receptors. By integrating molecular interaction networks of key targets such as lactate dehydrogenase A and ATP citrate lyase, this review explores synergistic therapeutic strategies that combine small-molecule inhibitors targeting MICs with immune checkpoint blockade. This highlights how metabolic intervention can restore immune cell function and reverse exhaustion. Current key challenges in clinical translation include limitations in metabolic dynamic monitoring technologies, lack of patient stratification biomarkers and insufficient specificity in microbiome regulation. Future directions will focus on personalized treatment guided by multiomics, integrating single-cell metabolic flux analysis, deep learning-driven target prediction, and synthetic microbiome engineering, driving tumor immunotherapy into the era of precision metabolic regulation. By integrating the fundamental mechanisms of MICs with translational medical research, this review not only provides a systematic paradigm but also establishes a foundation for the development of new-generation precision combination therapies.},
}
MeSH Terms:
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Humans
*Neoplasms/immunology/therapy/genetics/pathology/metabolism
Metabolic Reprogramming
*Tumor Microenvironment/immunology/genetics
*Immune Checkpoint Proteins/immunology/genetics
Animals
RevDate: 2026-10-08
CmpDate: 2026-10-08
Expanded proinflammatory CD4 T cells expressing toll like receptor 4 in trauma associated acute lung injury.
Communications biology, 9(1):.
Acute lung injury (ALI) is characterised by hypoxia and inflammation that derives from diverse aetiologies. Delineating the molecular pathogeneses may identify treatable subgroups and inform clinical trials. Using a multi-omics approach, we analysed trauma-associated ALI (n = 9), COVID-19 ALI (n = 11), ICU controls (n = 13) using scRNA-seq, serum cytokine profiling, and bronchoalveolar lavage (BAL) microbiome analysis. We identified a population of activated CD4[+] T cells expressing Toll-like receptor 4 (TLR4) and downstream NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome complex, predominantly in trauma-associated ALI (23% of CD45[+] Cells) compared to COVID-19 ALI (14%) and ICU controls (15%). Serum IL-1RA and IL-6 were upregulated in trauma ALI, along with TLR4-binding ligand hyaluronan. TLR4 expression on CD4[+] T cells was confirmed by spectral cytometry. Lung microbiome analysis revealed distinct diversity in trauma-associated ALI compared to COVID-19 ALI. These findings highlight TLR4-mediated inflammation in trauma-associated ALI and suggest potential precision medicine approaches for ALI management.
Additional Links: PMID-42850295
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Citation:
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@article {pmid42850295,
year = {2026},
author = {Hastak, P and Andersen, CR and Crammond, P and Zhang, ZH and Phetsouphanh, C and van Bockel, D and Walsh, C and Judd, LM and Stinear, TP and Lohani, A and Shrestha, S and Louie, R and Bass, F and Delaney, A and Hammond, N and Venkatesh, B and Finfer, S and Tedla, N and Kelleher, AD and Sasson, SC},
title = {Expanded proinflammatory CD4 T cells expressing toll like receptor 4 in trauma associated acute lung injury.},
journal = {Communications biology},
volume = {9},
number = {1},
pages = {},
pmid = {42850295},
issn = {2399-3642},
mesh = {*Acute Lung Injury/immunology/etiology/metabolism ; *Toll-Like Receptor 4/metabolism/genetics ; *CD4-Positive T-Lymphocytes/metabolism/immunology ; Humans ; *Wounds and Injuries/complications/immunology ; COVID-19/immunology/complications ; Male ; Female ; Bronchoalveolar Lavage Fluid/microbiology ; SARS-CoV-2 ; Cytokines/blood ; Inflammation ; Microbiota ; },
abstract = {Acute lung injury (ALI) is characterised by hypoxia and inflammation that derives from diverse aetiologies. Delineating the molecular pathogeneses may identify treatable subgroups and inform clinical trials. Using a multi-omics approach, we analysed trauma-associated ALI (n = 9), COVID-19 ALI (n = 11), ICU controls (n = 13) using scRNA-seq, serum cytokine profiling, and bronchoalveolar lavage (BAL) microbiome analysis. We identified a population of activated CD4[+] T cells expressing Toll-like receptor 4 (TLR4) and downstream NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome complex, predominantly in trauma-associated ALI (23% of CD45[+] Cells) compared to COVID-19 ALI (14%) and ICU controls (15%). Serum IL-1RA and IL-6 were upregulated in trauma ALI, along with TLR4-binding ligand hyaluronan. TLR4 expression on CD4[+] T cells was confirmed by spectral cytometry. Lung microbiome analysis revealed distinct diversity in trauma-associated ALI compared to COVID-19 ALI. These findings highlight TLR4-mediated inflammation in trauma-associated ALI and suggest potential precision medicine approaches for ALI management.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Acute Lung Injury/immunology/etiology/metabolism
*Toll-Like Receptor 4/metabolism/genetics
*CD4-Positive T-Lymphocytes/metabolism/immunology
Humans
*Wounds and Injuries/complications/immunology
COVID-19/immunology/complications
Male
Female
Bronchoalveolar Lavage Fluid/microbiology
SARS-CoV-2
Cytokines/blood
Inflammation
Microbiota
RevDate: 2026-10-09
CmpDate: 2026-10-09
The core taxa connectivity in leaf microbiomes in ash trees stands is modulated by host-related and environmental factors.
Environmental microbiome, 21(1):.
BACKGROUND: Forests cover large areas of the terrestrial land surface and play a key role in climate regulation and biodiversity conservation. Tree-associated microbial communities are integral components of forest ecosystems and contribute to plant functioning, stress tolerance, and interactions with the environment. However, the factors shaping the phyllosphere microbiome of forest trees across large environmental gradients remain less explored. Here, we investigated the bacterial leaf microbiome of Fraxinus excelsior across different climatic regions in Germany to identify its core microbiome and determine the relative importance of environmental and host-related factors shaping the phyllosphere microbiome of forest trees across large environmental gradients assembly. Therefore, 30 ash trees were sampled at each of the 12 sites across Germany, at which we assessed their leaf microbiome, leaf physio-chemical properties and a set of site parameters.
RESULTS: In total, 755 genera were detected. Only three genera Hymenobacter, Massilia and Sphingomonas were predominant across all sites. Geographical position, precipitation, tree age and the leaf and soil chemistry parameters were significant factors that explained 22.1% of variance between microbiome structures between the different sites. Seven genera were identified as the core leave microbiome of F. excelsior. The core microbiome assessed for each sampling site was mostly more diverse and differed between sites. Complex co-occurrence networks separated by sites with the identified six hub bacterial taxa proved that they were essential for the local core microbiomes. However, the network complexity differed significantly between the sampling sites.
CONCLUSION: Our findings clearly indicate the existence of an ash core microbiome on leaves that occurred at all sites but was locally differently interconnected to further microbiome members. The network analyses revealed that less frequent genera play important roles as hub taxa. Furthermore, we were also able to prove the modulating role of biotic and abiotic factors on the ash phyllosphere microbiome. An optimized core microbiome may be considered crucial for improving tolerance against plant diseases, such as ash dieback, in future.
Additional Links: PMID-42850677
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Citation:
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@article {pmid42850677,
year = {2026},
author = {Burghard, V and Wende, S and Kahlenberg, G and Häuser, H and Kätzel, R and Kolb, S and Ulrich, A},
title = {The core taxa connectivity in leaf microbiomes in ash trees stands is modulated by host-related and environmental factors.},
journal = {Environmental microbiome},
volume = {21},
number = {1},
pages = {},
pmid = {42850677},
issn = {2524-6372},
support = {2219WK22I4//Fachagentur Nachwachsende Rohstoffe/ ; },
abstract = {BACKGROUND: Forests cover large areas of the terrestrial land surface and play a key role in climate regulation and biodiversity conservation. Tree-associated microbial communities are integral components of forest ecosystems and contribute to plant functioning, stress tolerance, and interactions with the environment. However, the factors shaping the phyllosphere microbiome of forest trees across large environmental gradients remain less explored. Here, we investigated the bacterial leaf microbiome of Fraxinus excelsior across different climatic regions in Germany to identify its core microbiome and determine the relative importance of environmental and host-related factors shaping the phyllosphere microbiome of forest trees across large environmental gradients assembly. Therefore, 30 ash trees were sampled at each of the 12 sites across Germany, at which we assessed their leaf microbiome, leaf physio-chemical properties and a set of site parameters.
RESULTS: In total, 755 genera were detected. Only three genera Hymenobacter, Massilia and Sphingomonas were predominant across all sites. Geographical position, precipitation, tree age and the leaf and soil chemistry parameters were significant factors that explained 22.1% of variance between microbiome structures between the different sites. Seven genera were identified as the core leave microbiome of F. excelsior. The core microbiome assessed for each sampling site was mostly more diverse and differed between sites. Complex co-occurrence networks separated by sites with the identified six hub bacterial taxa proved that they were essential for the local core microbiomes. However, the network complexity differed significantly between the sampling sites.
CONCLUSION: Our findings clearly indicate the existence of an ash core microbiome on leaves that occurred at all sites but was locally differently interconnected to further microbiome members. The network analyses revealed that less frequent genera play important roles as hub taxa. Furthermore, we were also able to prove the modulating role of biotic and abiotic factors on the ash phyllosphere microbiome. An optimized core microbiome may be considered crucial for improving tolerance against plant diseases, such as ash dieback, in future.},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
Salinity-adapted and core microbiota along the soil salinity gradients encircling the Tarim Basin.
Environmental microbiome, 21(1):.
BACKGROUND: Soil salinization affects nearly one-tenth of global drylands and imposes strong environmental filters on microbial communities. The Tarim Basin in Xinjiang, China, is one of the world's largest inland basins and an extreme saline-arid ecosystem, yet a basin-scale understanding of its microbiota remains lacking. In this study, we collected 132 soil samples along a salinity gradient spanning more than 3,000 km encircling the Tarim Basin. By combining amplicon sequencing with measurements of soil physicochemical properties, we aimed to unravel the salinity-adapted microbiota and core microbial taxa characteristic of this extreme environment.
RESULTS: Our results showed that bacterial communities, rather than fungal communities, were strongly shaped by soil salinity. Extremely saline soils exhibited reduced bacterial diversity and were enriched in halophilic and halotolerant taxa, including Natronomonas, Salinimicrobium, Stenotrophomonas, Salinibacter, Halorussus, and Halomicrobium. In contrast, taxa such as Arthrobacter, Rubrobacter, Rubellimicrobium, and Fusarium declined with increasing salinity. Soil cation concentrations (Na[+], K[+], Ca[2+], Mg[2+]), major anions (Cl[-], SO4[2-]), and electrical conductivity all increased significantly along the salinity gradient. Despite this strong environmental filtering, we identified a set of potential core microbiota consistently present across all soils, dominated by Halomonas, Salinimicrobium, Natronomonas, Rubrobacter, and members of the Palleronia-Pseudomaribius group. Their persistent occurrence across the basin suggests that these taxa play key roles in sustaining ecosystem functions within the extreme saline-arid environments of the Tarim Basin.
CONCLUSIONS: Our basin-scale analysis reveals that soil salinity significantly contributes to microbial community assembly in the Tarim Basin, selecting for specialized halophilic and halotolerant taxa while reducing overall bacterial diversity. The discovery of core microbiota with known salt-adaptation mechanisms highlights the presence of a stable microbial backbone across heterogeneous saline landscapes. These findings provide new ecological insights into how extreme salinity shapes microbiome structure and identify candidate microbial groups potentially contributing to ecosystem stability and plant stress resilience in arid saline environments.
Additional Links: PMID-42850678
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@article {pmid42850678,
year = {2026},
author = {Liu, X and Jia, Q and Tang, Q and Ding, Y and Zhang, Z and Gu, M and Huang, W and Wang, N and Zhang, L and Zhu, J},
title = {Salinity-adapted and core microbiota along the soil salinity gradients encircling the Tarim Basin.},
journal = {Environmental microbiome},
volume = {21},
number = {1},
pages = {},
pmid = {42850678},
issn = {2524-6372},
support = {32360033//The National Natural Science Foundation of China/ ; 2024TSYCJU0007//Tianshan Talent Training Program of Xinjiang Uygur Autonomous Region/ ; },
abstract = {BACKGROUND: Soil salinization affects nearly one-tenth of global drylands and imposes strong environmental filters on microbial communities. The Tarim Basin in Xinjiang, China, is one of the world's largest inland basins and an extreme saline-arid ecosystem, yet a basin-scale understanding of its microbiota remains lacking. In this study, we collected 132 soil samples along a salinity gradient spanning more than 3,000 km encircling the Tarim Basin. By combining amplicon sequencing with measurements of soil physicochemical properties, we aimed to unravel the salinity-adapted microbiota and core microbial taxa characteristic of this extreme environment.
RESULTS: Our results showed that bacterial communities, rather than fungal communities, were strongly shaped by soil salinity. Extremely saline soils exhibited reduced bacterial diversity and were enriched in halophilic and halotolerant taxa, including Natronomonas, Salinimicrobium, Stenotrophomonas, Salinibacter, Halorussus, and Halomicrobium. In contrast, taxa such as Arthrobacter, Rubrobacter, Rubellimicrobium, and Fusarium declined with increasing salinity. Soil cation concentrations (Na[+], K[+], Ca[2+], Mg[2+]), major anions (Cl[-], SO4[2-]), and electrical conductivity all increased significantly along the salinity gradient. Despite this strong environmental filtering, we identified a set of potential core microbiota consistently present across all soils, dominated by Halomonas, Salinimicrobium, Natronomonas, Rubrobacter, and members of the Palleronia-Pseudomaribius group. Their persistent occurrence across the basin suggests that these taxa play key roles in sustaining ecosystem functions within the extreme saline-arid environments of the Tarim Basin.
CONCLUSIONS: Our basin-scale analysis reveals that soil salinity significantly contributes to microbial community assembly in the Tarim Basin, selecting for specialized halophilic and halotolerant taxa while reducing overall bacterial diversity. The discovery of core microbiota with known salt-adaptation mechanisms highlights the presence of a stable microbial backbone across heterogeneous saline landscapes. These findings provide new ecological insights into how extreme salinity shapes microbiome structure and identify candidate microbial groups potentially contributing to ecosystem stability and plant stress resilience in arid saline environments.},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
Modeling complex measurement error in microbiome experiments to estimate relative abundances and detection effects.
Biostatistics (Oxford, England), 27(1):.
Accurate estimates of microbial species abundances are needed to advance our understanding of the role that microbiomes play in human and environmental health. However, laboratory-constructed microbiomes demonstrate that intuitive estimators of microbial relative abundances are biased. To address this, we propose a method to estimate relative abundances, species detection effects, and/or cross-sample contamination in microbiome experiments. We show that certain experimental designs result in identifiable model parameters, and present consistent estimators and asymptotically valid inference procedures that are robust to misspecification of the working likelihood. Notably, our procedure can estimate relative abundances on the boundary of the simplex. We demonstrate the utility of the method for comparing experimental protocols, removing cross-sample contamination, and estimating species' detectability.
Additional Links: PMID-42850765
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@article {pmid42850765,
year = {2026},
author = {Clausen, DS and Willis, AD},
title = {Modeling complex measurement error in microbiome experiments to estimate relative abundances and detection effects.},
journal = {Biostatistics (Oxford, England)},
volume = {27},
number = {1},
pages = {},
doi = {10.1093/biostatistics/kxag036},
pmid = {42850765},
issn = {1468-4357},
support = {R35 GM133420/NH/NIH HHS/United States ; },
mesh = {*Microbiota ; *Models, Statistical ; Humans ; *Biostatistics/methods ; },
abstract = {Accurate estimates of microbial species abundances are needed to advance our understanding of the role that microbiomes play in human and environmental health. However, laboratory-constructed microbiomes demonstrate that intuitive estimators of microbial relative abundances are biased. To address this, we propose a method to estimate relative abundances, species detection effects, and/or cross-sample contamination in microbiome experiments. We show that certain experimental designs result in identifiable model parameters, and present consistent estimators and asymptotically valid inference procedures that are robust to misspecification of the working likelihood. Notably, our procedure can estimate relative abundances on the boundary of the simplex. We demonstrate the utility of the method for comparing experimental protocols, removing cross-sample contamination, and estimating species' detectability.},
}
MeSH Terms:
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*Microbiota
*Models, Statistical
Humans
*Biostatistics/methods
RevDate: 2026-10-09
Towards Personalised Therapeutics for Epidermal Differentiation Disorders: Integrating Host Genetics, Immuno-Endotypes and the Skin Microbiome.
The British journal of dermatology pii:8891555 [Epub ahead of print].
Epidermal differentiation disorders (EDDs), are a rare, heterogeneous grouping of monogenic disorders. EDDs, comprising the previously termed congenital ichthyosis, are characterised by epidermal barrier dysfunction, cutaneous inflammation, and associated morbidity. Immunomodulatory therapies, particularly repurposed biologics, are an emerging approach for management. However, clinical implementation has been impeded by a variable and unpredictable response rate, reflecting the genetic and immunological heterogeneity of EDD as well as raising questions over other contributory pathogenic mechanisms. Patient genotyping and immune profiling have revealed a shared immune polarisation across EDD subtypes, predominantly Th17, with some subtypes demonstrating a mixed immuno-endotype with contribution from Th2 or lL-36 mediated signalling. This improved immunological understanding has informed the repurposing of established biologics targeting IL-4R, IL-17, IL-12/23, alongside emerging interest in JAK inhibitors. Metagenomic microbiome profiling has revealed a homeostatic disruption across EDD subtypes with depleted commensal organisms, including Cutibacterium acnes and Malassezia species, and enrichment of pathobiont Staphylococcus and Corynebacterium species. Patients may be further stratified into dysbiotic groupings, with pathogenic variant and phenotypic severity influencing microbial composition. Ecological dysbiosis may contribute to immune polarisation through an "outside-inside-outside" model of host-microbe interactions, potentially underlying the variable response rates to repurposed biologics. In this review, we propose a "host genome and microbiome" framework for personalised EDD clinical management, integrating the EDD genotype and immuno-endotype ("Host genome"), and cutaneous microbiome as candidate simultaneous stratifiable elements. Genomic diagnosis, spurred by recent EDD reclassification, provides mechanistic context. Immuno-endotyping may enable a rational biologic selection but requires prospective validation. Microbiome profiling may guide emerging therapeutics or serve as a biomarker. We propose that a route to therapeutic restoration in EDD may require simultaneous targeting of the host-microbe axis. Delineation of the complex interplay between host genetics, immuno-endotypes, epidermal barrier dysfunction, and skin microbiome is a key priority for future research to bring this approach to the clinic.
Additional Links: PMID-42850800
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@article {pmid42850800,
year = {2026},
author = {Sharkey, T and Eisner, M and Common, J and Rajan, N},
title = {Towards Personalised Therapeutics for Epidermal Differentiation Disorders: Integrating Host Genetics, Immuno-Endotypes and the Skin Microbiome.},
journal = {The British journal of dermatology},
volume = {},
number = {},
pages = {},
doi = {10.1093/bjd/ljag447},
pmid = {42850800},
issn = {1365-2133},
abstract = {Epidermal differentiation disorders (EDDs), are a rare, heterogeneous grouping of monogenic disorders. EDDs, comprising the previously termed congenital ichthyosis, are characterised by epidermal barrier dysfunction, cutaneous inflammation, and associated morbidity. Immunomodulatory therapies, particularly repurposed biologics, are an emerging approach for management. However, clinical implementation has been impeded by a variable and unpredictable response rate, reflecting the genetic and immunological heterogeneity of EDD as well as raising questions over other contributory pathogenic mechanisms. Patient genotyping and immune profiling have revealed a shared immune polarisation across EDD subtypes, predominantly Th17, with some subtypes demonstrating a mixed immuno-endotype with contribution from Th2 or lL-36 mediated signalling. This improved immunological understanding has informed the repurposing of established biologics targeting IL-4R, IL-17, IL-12/23, alongside emerging interest in JAK inhibitors. Metagenomic microbiome profiling has revealed a homeostatic disruption across EDD subtypes with depleted commensal organisms, including Cutibacterium acnes and Malassezia species, and enrichment of pathobiont Staphylococcus and Corynebacterium species. Patients may be further stratified into dysbiotic groupings, with pathogenic variant and phenotypic severity influencing microbial composition. Ecological dysbiosis may contribute to immune polarisation through an "outside-inside-outside" model of host-microbe interactions, potentially underlying the variable response rates to repurposed biologics. In this review, we propose a "host genome and microbiome" framework for personalised EDD clinical management, integrating the EDD genotype and immuno-endotype ("Host genome"), and cutaneous microbiome as candidate simultaneous stratifiable elements. Genomic diagnosis, spurred by recent EDD reclassification, provides mechanistic context. Immuno-endotyping may enable a rational biologic selection but requires prospective validation. Microbiome profiling may guide emerging therapeutics or serve as a biomarker. We propose that a route to therapeutic restoration in EDD may require simultaneous targeting of the host-microbe axis. Delineation of the complex interplay between host genetics, immuno-endotypes, epidermal barrier dysfunction, and skin microbiome is a key priority for future research to bring this approach to the clinic.},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
C. butyricum Combined With Resmetirom Provides Therapeutic Benefits in MASH Associated With Gut-Liver-Brain Axis Modulation.
Liver international : official journal of the International Association for the Study of the Liver, 46(11):e70905.
BACKGROUND AND AIMS: Resmetirom has emerged as a major advance in MASH pharmacotherapy as the first approved liver-targeted THR-β agonist; however, variable therapeutic efficacy and adverse responses may limit its clinical benefits. This study investigated whether C. butyricum could provide additional therapeutic benefits when combined with resmetirom and attenuate nausea/vomiting-like responses in association with changes across the gut-liver-brain axis.
METHODS: In this study, we established a high-fat diet-induced MASH mouse model and administered C. butyricum, resmetirom, or their combination. Comprehensive biochemical, histological, molecular, 16S rRNA sequencing-based microbiome profiling, and gut-brain axis-related analyses were performed to evaluate the effects of combination therapy on hepatic metabolism, inflammation, fibrosis, intestinal barrier integrity, gut microbiota remodelling, microbial metabolites, and resmetirom-associated adverse responses.
RESULTS: Combined treatment with C. butyricum and resmetirom produced additional therapeutic benefits compared with either monotherapy, markedly improving hepatic steatosis, lipid accumulation, insulin resistance, inflammation, oxidative stress, and fibrosis in MASH mice. At the molecular level, combination treatment was associated with increased hepatic THR-β expression and coordinated changes in AMPK-related lipid metabolism, NRF2/HO-1 antioxidant, and TLR4/MyD88/NF-κB inflammatory markers. Furthermore, combination therapy restored intestinal barrier integrity, alleviated MASH-associated gut microbial dysbiosis, increased beneficial bacterial taxa, and increased faecal butyrate levels. Notably, C. butyricum attenuated resmetirom-induced nausea/vomiting-like responses, accompanied by reduced colonic and cerebral 5-HT/SP signalling, decreased brain Htr3a and Tacr1 mRNA expression, and suppressed neuronal FOS activation. Faecal butyrate levels were inversely associated with hepatic lipid burden and brain 5-HT/SP levels.
CONCLUSIONS: C. butyricum combined with resmetirom provides additional therapeutic benefits and attenuates nausea/vomiting-like responses in MASH, accompanied by coordinated changes across the gut-liver-brain axis. This combination strategy provides a potential microbiota-based adjunctive approach for optimizing the therapeutic benefits of resmetirom in MASH.
Additional Links: PMID-42850916
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PubMed:
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@article {pmid42850916,
year = {2026},
author = {Zhang, K and Zeng, Y and Wu, J and Liu, Y and Zhang, Y and Liao, Z and Li, Y and Zhong, J and Xie, Z and Chen, T},
title = {C. butyricum Combined With Resmetirom Provides Therapeutic Benefits in MASH Associated With Gut-Liver-Brain Axis Modulation.},
journal = {Liver international : official journal of the International Association for the Study of the Liver},
volume = {46},
number = {11},
pages = {e70905},
doi = {10.1111/liv.70905},
pmid = {42850916},
issn = {1478-3231},
mesh = {Animals ; Mice ; *Liver/metabolism/drug effects/pathology ; *Gastrointestinal Microbiome/drug effects ; Male ; Diet, High-Fat ; Disease Models, Animal ; *Clostridium butyricum ; Mice, Inbred C57BL ; Brain/metabolism/drug effects ; *Brain-Gut Axis/drug effects ; Intestinal Barrier Function ; *Probiotics ; },
abstract = {BACKGROUND AND AIMS: Resmetirom has emerged as a major advance in MASH pharmacotherapy as the first approved liver-targeted THR-β agonist; however, variable therapeutic efficacy and adverse responses may limit its clinical benefits. This study investigated whether C. butyricum could provide additional therapeutic benefits when combined with resmetirom and attenuate nausea/vomiting-like responses in association with changes across the gut-liver-brain axis.
METHODS: In this study, we established a high-fat diet-induced MASH mouse model and administered C. butyricum, resmetirom, or their combination. Comprehensive biochemical, histological, molecular, 16S rRNA sequencing-based microbiome profiling, and gut-brain axis-related analyses were performed to evaluate the effects of combination therapy on hepatic metabolism, inflammation, fibrosis, intestinal barrier integrity, gut microbiota remodelling, microbial metabolites, and resmetirom-associated adverse responses.
RESULTS: Combined treatment with C. butyricum and resmetirom produced additional therapeutic benefits compared with either monotherapy, markedly improving hepatic steatosis, lipid accumulation, insulin resistance, inflammation, oxidative stress, and fibrosis in MASH mice. At the molecular level, combination treatment was associated with increased hepatic THR-β expression and coordinated changes in AMPK-related lipid metabolism, NRF2/HO-1 antioxidant, and TLR4/MyD88/NF-κB inflammatory markers. Furthermore, combination therapy restored intestinal barrier integrity, alleviated MASH-associated gut microbial dysbiosis, increased beneficial bacterial taxa, and increased faecal butyrate levels. Notably, C. butyricum attenuated resmetirom-induced nausea/vomiting-like responses, accompanied by reduced colonic and cerebral 5-HT/SP signalling, decreased brain Htr3a and Tacr1 mRNA expression, and suppressed neuronal FOS activation. Faecal butyrate levels were inversely associated with hepatic lipid burden and brain 5-HT/SP levels.
CONCLUSIONS: C. butyricum combined with resmetirom provides additional therapeutic benefits and attenuates nausea/vomiting-like responses in MASH, accompanied by coordinated changes across the gut-liver-brain axis. This combination strategy provides a potential microbiota-based adjunctive approach for optimizing the therapeutic benefits of resmetirom in MASH.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Mice
*Liver/metabolism/drug effects/pathology
*Gastrointestinal Microbiome/drug effects
Male
Diet, High-Fat
Disease Models, Animal
*Clostridium butyricum
Mice, Inbred C57BL
Brain/metabolism/drug effects
*Brain-Gut Axis/drug effects
Intestinal Barrier Function
*Probiotics
RevDate: 2026-10-09
CmpDate: 2026-10-09
Amplicon Characterization of Fungal Diversity and Functional Prediction of Glycine max L. Rhizosphere Microbiome Under Different Organic Fertilization.
MicrobiologyOpen, 15(5):e70437.
The rhizosphere microbiome is extremely important for soil health and plant productivity, with fungi primarily acting as the drivers of soil ecosystem functions. This study explores the fungal diversity and predicted functional potential of the soybean (Glycine max L.) rhizosphere under different organic fertilization treatments, including cattle dung, poultry waste, untreated control, and bulk. Fungal communities were profiled using ITS rRNA gene amplicon sequencing on the Illumina NovaSeq. 6000 platform following DNA extraction from rhizosphere soil. Raw sequences were processed and analyzed using QIIME 2 version 2019.1. Significant differences in fungal richness were observed among treatments. Bulk soil and cattle dung-amended soils showed the highest richness (Chao1 = 1603.33 and 1456.64, respectively), whereas poultry waste-amended soil exhibited the lowest richness (Chao1 = 957.93) and the lowest evenness (Pielou's index = 0.560), and the untreated control showed intermediate richness (Chao1 = 1242.11). The dominant phyla include Ascomycota, Basidiomycota, and Zygomycota, with enrichment in organic matter degradation and plant symbiosis. Beta-diversity analysis showed the greatest compositional divergence between cattle dung and poultry waste (ANOSIM R = 0.74), none of the pairwise comparisons reached conventional statistical significance (p > 0.05), indicating ecologically relevant but statistically subtle shifts in community structure. LEfSe identified Hypocreales as a significant biomarker of cattle dung and Onygenales of poultry waste, consistent with FUNGuild predictions of enriched dung/wood-saprotrophic and keratinolytic functions, respectively. FUNGuild predictions showed increased saprotroph and symbiotroph diversity in organically amended soils. Organic fertilizers enrich beneficial fungi, enhancing ecosystem functions in sustainable soybean cultivation.
Additional Links: PMID-42850929
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@article {pmid42850929,
year = {2026},
author = {Osuji, IE and Akanmu, AO and Babalola, OO},
title = {Amplicon Characterization of Fungal Diversity and Functional Prediction of Glycine max L. Rhizosphere Microbiome Under Different Organic Fertilization.},
journal = {MicrobiologyOpen},
volume = {15},
number = {5},
pages = {e70437},
doi = {10.1002/mbo3.70437},
pmid = {42850929},
issn = {2045-8827},
support = {CRP/ZAF22-93//International Centre for Genetic Engineering and Biotechnology/ ; },
mesh = {*Rhizosphere ; *Glycine max/microbiology ; *Fungi/classification/genetics/isolation & purification ; *Soil Microbiology ; Animals ; *Fertilizers/analysis ; Cattle ; DNA, Fungal/genetics ; Manure/microbiology ; Biodiversity ; *Mycobiome ; Phylogeny ; Soil/chemistry ; DNA, Ribosomal Spacer/genetics ; Sequence Analysis, DNA ; *Microbiota ; },
abstract = {The rhizosphere microbiome is extremely important for soil health and plant productivity, with fungi primarily acting as the drivers of soil ecosystem functions. This study explores the fungal diversity and predicted functional potential of the soybean (Glycine max L.) rhizosphere under different organic fertilization treatments, including cattle dung, poultry waste, untreated control, and bulk. Fungal communities were profiled using ITS rRNA gene amplicon sequencing on the Illumina NovaSeq. 6000 platform following DNA extraction from rhizosphere soil. Raw sequences were processed and analyzed using QIIME 2 version 2019.1. Significant differences in fungal richness were observed among treatments. Bulk soil and cattle dung-amended soils showed the highest richness (Chao1 = 1603.33 and 1456.64, respectively), whereas poultry waste-amended soil exhibited the lowest richness (Chao1 = 957.93) and the lowest evenness (Pielou's index = 0.560), and the untreated control showed intermediate richness (Chao1 = 1242.11). The dominant phyla include Ascomycota, Basidiomycota, and Zygomycota, with enrichment in organic matter degradation and plant symbiosis. Beta-diversity analysis showed the greatest compositional divergence between cattle dung and poultry waste (ANOSIM R = 0.74), none of the pairwise comparisons reached conventional statistical significance (p > 0.05), indicating ecologically relevant but statistically subtle shifts in community structure. LEfSe identified Hypocreales as a significant biomarker of cattle dung and Onygenales of poultry waste, consistent with FUNGuild predictions of enriched dung/wood-saprotrophic and keratinolytic functions, respectively. FUNGuild predictions showed increased saprotroph and symbiotroph diversity in organically amended soils. Organic fertilizers enrich beneficial fungi, enhancing ecosystem functions in sustainable soybean cultivation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Rhizosphere
*Glycine max/microbiology
*Fungi/classification/genetics/isolation & purification
*Soil Microbiology
Animals
*Fertilizers/analysis
Cattle
DNA, Fungal/genetics
Manure/microbiology
Biodiversity
*Mycobiome
Phylogeny
Soil/chemistry
DNA, Ribosomal Spacer/genetics
Sequence Analysis, DNA
*Microbiota
RevDate: 2026-10-09
gutMDisorder v3.0: an updated database for dysbiosis of the gut and oral microbiota in phenotypes and interventions.
Nucleic acids research pii:8892720 [Epub ahead of print].
Microbiota plays an essential role in host health, and dysbiosis of microbial communities has been widely associated with diverse phenotypes and intervention responses. With the rapid development of microbiome research, microbiome studies are no longer restricted to gut-derived samples, and the oral microbiota has emerged as another important microbial habitat closely connected with both local and systemic conditions. To meet the growing need for integrative resources across body sites, we updated gutMDisorder to version 3.0. In this version, the scope was expanded from gut microbiota to both gut and oral microbiota in humans and mice. We extensively reviewed previous publications and newly published studies, resulting in 13 402 manually curated literature-based associations under diverse comparison conditions. In addition, raw sequencing datasets from gut and oral samples were collected and reprocessed using standardized workflows, yielding 22 241 raw data-based associations, and corresponding host metadata were manually curated. To facilitate data exploration, gutMDisorder v3.0 provides sample-source-aware browsing, improved filtering options, interactive visualizations for raw data-based associations, and downloadable resources. The backend processing and frontend rendering logic were also optimized to improve page responsiveness and user experience. The database is freely available at https://bio-computing.hrbmu.edu.cn/gutMDisorder/.
Additional Links: PMID-42850991
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PubMed:
Citation:
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@article {pmid42850991,
year = {2026},
author = {Guan, S and Qi, C and Liu, X and Li, B and Zhang, Y and Gao, H and Chen, Q and Cheng, L and Zhang, X},
title = {gutMDisorder v3.0: an updated database for dysbiosis of the gut and oral microbiota in phenotypes and interventions.},
journal = {Nucleic acids research},
volume = {},
number = {},
pages = {},
doi = {10.1093/nar/gkag985},
pmid = {42850991},
issn = {1362-4962},
support = {62531007//National Natural Science Foundation of China/ ; },
abstract = {Microbiota plays an essential role in host health, and dysbiosis of microbial communities has been widely associated with diverse phenotypes and intervention responses. With the rapid development of microbiome research, microbiome studies are no longer restricted to gut-derived samples, and the oral microbiota has emerged as another important microbial habitat closely connected with both local and systemic conditions. To meet the growing need for integrative resources across body sites, we updated gutMDisorder to version 3.0. In this version, the scope was expanded from gut microbiota to both gut and oral microbiota in humans and mice. We extensively reviewed previous publications and newly published studies, resulting in 13 402 manually curated literature-based associations under diverse comparison conditions. In addition, raw sequencing datasets from gut and oral samples were collected and reprocessed using standardized workflows, yielding 22 241 raw data-based associations, and corresponding host metadata were manually curated. To facilitate data exploration, gutMDisorder v3.0 provides sample-source-aware browsing, improved filtering options, interactive visualizations for raw data-based associations, and downloadable resources. The backend processing and frontend rendering logic were also optimized to improve page responsiveness and user experience. The database is freely available at https://bio-computing.hrbmu.edu.cn/gutMDisorder/.},
}
RevDate: 2026-10-09
Harnessing bacterial symbionts of beetles for the valorization of lignin into value-added byproducts: Recent advances and future perspectives.
Insect science [Epub ahead of print].
Lignin is the most abundant renewable aromatic heteropolymer in nature and is highly recalcitrant due to its complex structure. The gut systems of beetles function as an evolutionarily optimized microreactor wherein mechanical pretreatment, physicochemical gradients, and selectively maintained microbial consortia act synergistically to transform, mineralize, and metabolize lignin as an energy source. Beetle-associated bacterial symbionts represent a promising yet underexploited resource for lignin valorization into value-added products. This review provides emerging evidence of lignin degradation by beetles in association with their gut symbionts and indicates the diversity of gut bacteria involved in lignin depolymerization. We further discuss the mechanisms by which beetles and their gut bacteria metabolize lignin, the lignin-transforming capacities of the bacterial symbionts and their potential application in the valorization of waste lignin into added-value byproducts. Finally, we assess the emerging research trends on the bioprospection of lignin-degrading bacteria from underexplored beetle species. Despite significant advantages, several key challenges remain unresolved, including difficulties in isolation and culturing of key gut bacteria in vitro, limited biochemical validation of candidate enzymes and the unresolved linking of specific genes or taxa to in situ lignin transformation. Future studies should integrate discovery-driven microbial ecology, multi-omics, predictive modeling and precision genome engineering to convert the complexity of beetle gut bacterial communities into a practical blueprint for scalable lignin valorization, and the biomanufacturing of high-value products from lignin-based waste.
Additional Links: PMID-42851078
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PubMed:
Citation:
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@article {pmid42851078,
year = {2026},
author = {Doumbia, B and Luo, S and Yang, S and Wang, C and Jia, Y and Kuprin, AV and Geng, A and Zhu, D and Sun, J and Ezenwanne, BC and Xie, R and Dar, MA},
title = {Harnessing bacterial symbionts of beetles for the valorization of lignin into value-added byproducts: Recent advances and future perspectives.},
journal = {Insect science},
volume = {},
number = {},
pages = {},
doi = {10.1111/1744-7917.70378},
pmid = {42851078},
issn = {1744-7917},
support = {32250410285//National Natural Science Foundation of China/ ; 2023YFC3403600//National Key R&D Program of China/ ; WGXZ2023020L//Foreign Expert Program, of Ministry of Science and Technology (MoST) of China/ ; 124012400285-7//Ministry of Science and Higher Education of the Russian Federation/ ; },
abstract = {Lignin is the most abundant renewable aromatic heteropolymer in nature and is highly recalcitrant due to its complex structure. The gut systems of beetles function as an evolutionarily optimized microreactor wherein mechanical pretreatment, physicochemical gradients, and selectively maintained microbial consortia act synergistically to transform, mineralize, and metabolize lignin as an energy source. Beetle-associated bacterial symbionts represent a promising yet underexploited resource for lignin valorization into value-added products. This review provides emerging evidence of lignin degradation by beetles in association with their gut symbionts and indicates the diversity of gut bacteria involved in lignin depolymerization. We further discuss the mechanisms by which beetles and their gut bacteria metabolize lignin, the lignin-transforming capacities of the bacterial symbionts and their potential application in the valorization of waste lignin into added-value byproducts. Finally, we assess the emerging research trends on the bioprospection of lignin-degrading bacteria from underexplored beetle species. Despite significant advantages, several key challenges remain unresolved, including difficulties in isolation and culturing of key gut bacteria in vitro, limited biochemical validation of candidate enzymes and the unresolved linking of specific genes or taxa to in situ lignin transformation. Future studies should integrate discovery-driven microbial ecology, multi-omics, predictive modeling and precision genome engineering to convert the complexity of beetle gut bacterial communities into a practical blueprint for scalable lignin valorization, and the biomanufacturing of high-value products from lignin-based waste.},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
Harnessing probiotics against candidiasis: a systematic review of experimental and mechanistic evidence.
Frontiers in cellular and infection microbiology, 16:1894309.
BACKGROUND: Candida species are among the most important opportunistic fungal pathogens responsible for superficial mucosal infections and life-threatening invasive candidiasis, particularly in immunocompromised individuals. The increasing prevalence of antifungal resistance, biofilm-associated tolerance, and the emergence of multidrug-resistant species such as Candida auris have highlighted the need for alternative or adjunctive therapeutic strategies. Probiotics have emerged as promising microbiome-based interventions owing to their ability to inhibit Candida growth, suppress virulence traits, restore microbial homeostasis, and modulate host immune responses.
METHODS: This systematic review comprehensively evaluated the experimental and mechanistic evidence regarding the anti-Candida activity of probiotics and probiotic-derived products. A systematic literature search was conducted in PubMed, Scopus, and Web of Science for studies published between 1 January 2015 and 5 January 2026 in accordance with PRISMA 2020 guidelines. Studies meeting the predefined eligibility criteria were included in the qualitative synthesis.
RESULTS: Eighteen studies met the predefined eligibility criteria. Most studies investigated Lactobacillus species, followed by Bifidobacterium, Saccharomyces, and probiotic-derived metabolites or postbiotics, using predominantly in vitro models with limited in vivo evidence. Across studies, probiotics consistently demonstrated anti-Candida activity through inhibition of fungal growth, adhesion, yeast-to-hyphal transition, biofilm formation, and virulence-associated gene expression. Additional mechanisms included the production of antimicrobial metabolites, competitive exclusion, immune modulation, enhancement of epithelial barrier function, and restoration of microbial homeostasis. Emerging evidence also supports the antifungal potential of postbiotics and activity against non-albicans Candida species and Candida auris, although available evidence remains limited. Considerable heterogeneity in probiotic strains, experimental models, methodologies, and outcome measures precluded quantitative meta-analysis.
CONCLUSIONS: Current evidence supports probiotics and postbiotics as promising microbiome-based strategies for reducing Candida pathogenicity; however, the available evidence remains predominantly preclinical. Well-designed clinical studies are required to establish strain-specific efficacy, optimal formulations, dosing strategies, safety, and therapeutic applicability before routine clinical implementation.
https://www.crd.york.ac.uk/prospero/view/CRD420261278363, identifier CRD420261278363.
Additional Links: PMID-42851311
PubMed:
Citation:
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@article {pmid42851311,
year = {2026},
author = {Saloni, T and Chaithra, N and Umamaheshwari, S},
title = {Harnessing probiotics against candidiasis: a systematic review of experimental and mechanistic evidence.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1894309},
pmid = {42851311},
issn = {2235-2988},
mesh = {*Probiotics/therapeutic use/pharmacology ; Humans ; Biofilms/drug effects/growth & development ; *Candidiasis/therapy/microbiology ; Animals ; *Candida/drug effects/growth & development ; Antifungal Agents/pharmacology/therapeutic use ; Microbiota ; Virulence ; Lactobacillus ; },
abstract = {BACKGROUND: Candida species are among the most important opportunistic fungal pathogens responsible for superficial mucosal infections and life-threatening invasive candidiasis, particularly in immunocompromised individuals. The increasing prevalence of antifungal resistance, biofilm-associated tolerance, and the emergence of multidrug-resistant species such as Candida auris have highlighted the need for alternative or adjunctive therapeutic strategies. Probiotics have emerged as promising microbiome-based interventions owing to their ability to inhibit Candida growth, suppress virulence traits, restore microbial homeostasis, and modulate host immune responses.
METHODS: This systematic review comprehensively evaluated the experimental and mechanistic evidence regarding the anti-Candida activity of probiotics and probiotic-derived products. A systematic literature search was conducted in PubMed, Scopus, and Web of Science for studies published between 1 January 2015 and 5 January 2026 in accordance with PRISMA 2020 guidelines. Studies meeting the predefined eligibility criteria were included in the qualitative synthesis.
RESULTS: Eighteen studies met the predefined eligibility criteria. Most studies investigated Lactobacillus species, followed by Bifidobacterium, Saccharomyces, and probiotic-derived metabolites or postbiotics, using predominantly in vitro models with limited in vivo evidence. Across studies, probiotics consistently demonstrated anti-Candida activity through inhibition of fungal growth, adhesion, yeast-to-hyphal transition, biofilm formation, and virulence-associated gene expression. Additional mechanisms included the production of antimicrobial metabolites, competitive exclusion, immune modulation, enhancement of epithelial barrier function, and restoration of microbial homeostasis. Emerging evidence also supports the antifungal potential of postbiotics and activity against non-albicans Candida species and Candida auris, although available evidence remains limited. Considerable heterogeneity in probiotic strains, experimental models, methodologies, and outcome measures precluded quantitative meta-analysis.
CONCLUSIONS: Current evidence supports probiotics and postbiotics as promising microbiome-based strategies for reducing Candida pathogenicity; however, the available evidence remains predominantly preclinical. Well-designed clinical studies are required to establish strain-specific efficacy, optimal formulations, dosing strategies, safety, and therapeutic applicability before routine clinical implementation.
https://www.crd.york.ac.uk/prospero/view/CRD420261278363, identifier CRD420261278363.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Probiotics/therapeutic use/pharmacology
Humans
Biofilms/drug effects/growth & development
*Candidiasis/therapy/microbiology
Animals
*Candida/drug effects/growth & development
Antifungal Agents/pharmacology/therapeutic use
Microbiota
Virulence
Lactobacillus
RevDate: 2026-10-09
CmpDate: 2026-10-09
From microbiome signatures to precision oncology in colorectal cancer.
Frontiers in oncology, 16:1926171.
Additional Links: PMID-42851327
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Citation:
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@article {pmid42851327,
year = {2026},
author = {Langellotti, L and Schena, CA and Covino, M and Alfieri, S and Rosa, F},
title = {From microbiome signatures to precision oncology in colorectal cancer.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1926171},
pmid = {42851327},
issn = {2234-943X},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
Transient short-chain fatty acid exposure and the temporal question of epithelial barrier immunity.
Frontiers in immunology, 17:1930311.
Studies of microbiome-targeted interventions often use persistence of an administered organism or endpoint metabolite abundance as markers of biological consequence, but host barriers may be altered by microbial chemistry after the initiating exposure has disappeared. Short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate, provide a tractable model for this temporal problem because they connect microbial fermentation to epithelial metabolism, G protein-coupled receptor signaling, tight-junction regulation, immune tone, and chromatin-associated gene regulation. This Perspective argues that SCFA biology should be used to distinguish three outcomes at the host-microbial interface: exposure-dependent modulation, reversible epithelial reprogramming, and durable barrier imprint. Current evidence supports robust epithelial responses to SCFAs and makes persistence biologically plausible through chromatin-associated regulation and epithelial immune memory, but it does not yet establish whether brief adult SCFA exposure can alter later barrier behavior after withdrawal. Clarifying this conversion step will provide a common temporal framework for dietary, prebiotic, probiotic, postbiotic, and microbiota-transfer studies by distinguishing intervention delivery and engraftment from epithelial persistence.
Additional Links: PMID-42851354
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@article {pmid42851354,
year = {2026},
author = {Lewandowski, R},
title = {Transient short-chain fatty acid exposure and the temporal question of epithelial barrier immunity.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1930311},
pmid = {42851354},
issn = {1664-3224},
mesh = {*Fatty Acids, Volatile/metabolism/immunology ; Humans ; Animals ; Intestinal Barrier Function ; *Intestinal Mucosa/immunology/metabolism/microbiology ; *Immunity, Mucosal ; *Gastrointestinal Microbiome/immunology ; },
abstract = {Studies of microbiome-targeted interventions often use persistence of an administered organism or endpoint metabolite abundance as markers of biological consequence, but host barriers may be altered by microbial chemistry after the initiating exposure has disappeared. Short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate, provide a tractable model for this temporal problem because they connect microbial fermentation to epithelial metabolism, G protein-coupled receptor signaling, tight-junction regulation, immune tone, and chromatin-associated gene regulation. This Perspective argues that SCFA biology should be used to distinguish three outcomes at the host-microbial interface: exposure-dependent modulation, reversible epithelial reprogramming, and durable barrier imprint. Current evidence supports robust epithelial responses to SCFAs and makes persistence biologically plausible through chromatin-associated regulation and epithelial immune memory, but it does not yet establish whether brief adult SCFA exposure can alter later barrier behavior after withdrawal. Clarifying this conversion step will provide a common temporal framework for dietary, prebiotic, probiotic, postbiotic, and microbiota-transfer studies by distinguishing intervention delivery and engraftment from epithelial persistence.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Fatty Acids, Volatile/metabolism/immunology
Humans
Animals
Intestinal Barrier Function
*Intestinal Mucosa/immunology/metabolism/microbiology
*Immunity, Mucosal
*Gastrointestinal Microbiome/immunology
RevDate: 2026-10-09
CmpDate: 2026-10-09
Engineered bacteria and engineered probiotics for intestinal disease therapy: a bibliometric and knowledge mapping analysis.
Frontiers in microbiology, 17:1970221.
OBJECTIVE: Engineered bacteria and engineered probiotics are emerging living therapeutic platforms for intestinal diseases, supported by advances in synthetic biology, genetic engineering, and microbiome technologies. This study aimed to characterize the research landscape, knowledge structure, research hotspots, and emerging trends of engineered bacteria and engineered probiotics for intestinal disease therapy using bibliometric and knowledge mapping approaches.
METHODS: Publications were retrieved from the Web of Science Core Collection and Scopus databases. After publication type restriction, thematic relevance screening, database merging, and duplicate removal, 499 publications published between 2015 and 2026 were included. The search was completed on July 3, 2026; therefore, records from 2026 represent a partial-year dataset. R, Python, VOSviewer, and CiteSpace were used to analyze annual publication trends, country/region, institution, author and journal distributions, keyword co-occurrence and bursts, co-cited references, and research frontiers.
RESULTS: Publication output increased markedly over the study period, reaching 109 publications in 2025; 64 records were retrieved for 2026 by the cutoff date. China had the highest publication output, whereas the United States had the highest total link strength, and Asia contributed 361 publications. Keyword analysis identified inflammatory bowel disease, gut microbiota, probiotics, engineered bacteria, engineered probiotics, synthetic biology, intestinal barrier, drug delivery, colorectal cancer, and immunotherapy as major research hotspots. Co-cited reference and timeline analyses indicated a shift in research attention from conventional probiotic-mediated anti-inflammatory effects, mucosal immune regulation, and intestinal barrier protection toward bacterial chassis selection, enhanced colonization, self-regulated genetic circuits, probiotic-based biomaterials, sustained-release delivery systems, and engineered bacteria-mediated antitumor therapy.
CONCLUSION: The bibliometric evidence indicates that recent research attention is increasingly focused on programmable living therapeutic strategies. Environmental sensing, local therapeutic delivery, sustained activity, and multifunctional design features are capabilities reported in the underlying literature and represented among the emerging themes identified in this analysis, rather than therapeutic performance directly established by the bibliometric data. Future research should further address biosafety, genetic stability, spatiotemporal controllability, intestinal colonization, delivery efficiency, and clinical translation.
Additional Links: PMID-42851468
PubMed:
Citation:
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@article {pmid42851468,
year = {2026},
author = {Sun, W and Liu, H and Shao, A and Li, R and Ma, W and Zheng, M and Yan, S and Liu, S and Wu, M and Sun, D},
title = {Engineered bacteria and engineered probiotics for intestinal disease therapy: a bibliometric and knowledge mapping analysis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1970221},
pmid = {42851468},
issn = {1664-302X},
abstract = {OBJECTIVE: Engineered bacteria and engineered probiotics are emerging living therapeutic platforms for intestinal diseases, supported by advances in synthetic biology, genetic engineering, and microbiome technologies. This study aimed to characterize the research landscape, knowledge structure, research hotspots, and emerging trends of engineered bacteria and engineered probiotics for intestinal disease therapy using bibliometric and knowledge mapping approaches.
METHODS: Publications were retrieved from the Web of Science Core Collection and Scopus databases. After publication type restriction, thematic relevance screening, database merging, and duplicate removal, 499 publications published between 2015 and 2026 were included. The search was completed on July 3, 2026; therefore, records from 2026 represent a partial-year dataset. R, Python, VOSviewer, and CiteSpace were used to analyze annual publication trends, country/region, institution, author and journal distributions, keyword co-occurrence and bursts, co-cited references, and research frontiers.
RESULTS: Publication output increased markedly over the study period, reaching 109 publications in 2025; 64 records were retrieved for 2026 by the cutoff date. China had the highest publication output, whereas the United States had the highest total link strength, and Asia contributed 361 publications. Keyword analysis identified inflammatory bowel disease, gut microbiota, probiotics, engineered bacteria, engineered probiotics, synthetic biology, intestinal barrier, drug delivery, colorectal cancer, and immunotherapy as major research hotspots. Co-cited reference and timeline analyses indicated a shift in research attention from conventional probiotic-mediated anti-inflammatory effects, mucosal immune regulation, and intestinal barrier protection toward bacterial chassis selection, enhanced colonization, self-regulated genetic circuits, probiotic-based biomaterials, sustained-release delivery systems, and engineered bacteria-mediated antitumor therapy.
CONCLUSION: The bibliometric evidence indicates that recent research attention is increasingly focused on programmable living therapeutic strategies. Environmental sensing, local therapeutic delivery, sustained activity, and multifunctional design features are capabilities reported in the underlying literature and represented among the emerging themes identified in this analysis, rather than therapeutic performance directly established by the bibliometric data. Future research should further address biosafety, genetic stability, spatiotemporal controllability, intestinal colonization, delivery efficiency, and clinical translation.},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
The microbiome-nitric oxide axis in cancer immunotherapy: a targeted qualitative systematic review of mechanistic and translational evidence.
Frontiers in immunology, 17:1904698.
BACKGROUND: Immune checkpoint inhibitors (ICIs) have transformed cancer treatment, but responses vary substantially among patients. Clinical studies have associated features of the gut microbiome with ICI outcomes, while experimental evidence suggests that microbial metabolites and nitric oxide (NO)-related pathways may influence antitumor immunity and tumor vascular biology. This qualitative systematic review evaluated the evidence supporting a proposed microbiome-NO-ICI framework.
METHODS: Five databases were searched for peer-reviewed studies published between January 2000 and August 2025. Fifty-four distinct primary studies met the eligibility criteria, comprising 21 clinical studies, 19 animal studies and 14 in vitro mechanistic studies. Evidence was synthesized narratively according to study type and thematic domain.
RESULTS: Several clinical cohorts associated enrichment of Akkermansia muciniphila, Faecalibacterium prausnitzii, Bifidobacterium species and other short-chain fatty acid-producing taxa with favorable ICI outcomes; however, the reported microbial signatures varied across cohorts and analytical platforms. Microbial-transfer experiments and early non-randomized fecal microbiota transplantation studies provide proof-of-concept evidence that microbiome composition can influence antitumor immune responses, although the clinical intervention evidence remains preliminary. Animal and cellular studies indicate that microbial metabolites, host nitric oxide synthase pathways and reactive nitrogen signaling can affect immune-cell function, vascular regulation and tumor hypoxia. Direct clinical evidence linking microbiota-mediated nitrate reduction or dietary nitrate supplementation to improved ICI outcomes is lacking. Human dietary nitrate studies conducted outside oncology demonstrate increased circulating nitrate and nitrite and measurable vascular effects but do not establish anticancer or ICI efficacy.
CONCLUSION: The microbiome-NO-ICI axis should be regarded as a testable integrative model linking microbial ecology, immune regulation and tumor vascular biology. Current evidence supports biological plausibility but is insufficient to establish NO- or microbiome-directed interventions as effective adjuncts to ICI therapy. Prospective mechanistic studies and biomarker-driven clinical trials are required before therapeutic translation.
Additional Links: PMID-42851568
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Citation:
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@article {pmid42851568,
year = {2026},
author = {Enwere, M and Bryan, NS and Onu, A and Neufeld, M and El-Hussein, MT and Yakub, I and Omale, C and Onyedike, O and Atim, T and Agbeyomi, O and Davies, E and Okeke, UE and Holmes, L},
title = {The microbiome-nitric oxide axis in cancer immunotherapy: a targeted qualitative systematic review of mechanistic and translational evidence.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1904698},
pmid = {42851568},
issn = {1664-3224},
mesh = {Humans ; *Neoplasms/therapy/immunology/metabolism/microbiology ; *Nitric Oxide/metabolism/immunology ; Animals ; *Gastrointestinal Microbiome/immunology ; *Immunotherapy/methods ; *Immune Checkpoint Inhibitors/therapeutic use ; Fecal Microbiota Transplantation ; Translational Research, Biomedical ; },
abstract = {BACKGROUND: Immune checkpoint inhibitors (ICIs) have transformed cancer treatment, but responses vary substantially among patients. Clinical studies have associated features of the gut microbiome with ICI outcomes, while experimental evidence suggests that microbial metabolites and nitric oxide (NO)-related pathways may influence antitumor immunity and tumor vascular biology. This qualitative systematic review evaluated the evidence supporting a proposed microbiome-NO-ICI framework.
METHODS: Five databases were searched for peer-reviewed studies published between January 2000 and August 2025. Fifty-four distinct primary studies met the eligibility criteria, comprising 21 clinical studies, 19 animal studies and 14 in vitro mechanistic studies. Evidence was synthesized narratively according to study type and thematic domain.
RESULTS: Several clinical cohorts associated enrichment of Akkermansia muciniphila, Faecalibacterium prausnitzii, Bifidobacterium species and other short-chain fatty acid-producing taxa with favorable ICI outcomes; however, the reported microbial signatures varied across cohorts and analytical platforms. Microbial-transfer experiments and early non-randomized fecal microbiota transplantation studies provide proof-of-concept evidence that microbiome composition can influence antitumor immune responses, although the clinical intervention evidence remains preliminary. Animal and cellular studies indicate that microbial metabolites, host nitric oxide synthase pathways and reactive nitrogen signaling can affect immune-cell function, vascular regulation and tumor hypoxia. Direct clinical evidence linking microbiota-mediated nitrate reduction or dietary nitrate supplementation to improved ICI outcomes is lacking. Human dietary nitrate studies conducted outside oncology demonstrate increased circulating nitrate and nitrite and measurable vascular effects but do not establish anticancer or ICI efficacy.
CONCLUSION: The microbiome-NO-ICI axis should be regarded as a testable integrative model linking microbial ecology, immune regulation and tumor vascular biology. Current evidence supports biological plausibility but is insufficient to establish NO- or microbiome-directed interventions as effective adjuncts to ICI therapy. Prospective mechanistic studies and biomarker-driven clinical trials are required before therapeutic translation.},
}
MeSH Terms:
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Humans
*Neoplasms/therapy/immunology/metabolism/microbiology
*Nitric Oxide/metabolism/immunology
Animals
*Gastrointestinal Microbiome/immunology
*Immunotherapy/methods
*Immune Checkpoint Inhibitors/therapeutic use
Fecal Microbiota Transplantation
Translational Research, Biomedical
RevDate: 2026-10-09
CmpDate: 2026-10-09
Editorial: Rodent model organisms: therapeutic treatments and drugs interaction with the gut microbiome, volume II.
Frontiers in microbiology, 17:1962495.
Additional Links: PMID-42851677
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@article {pmid42851677,
year = {2026},
author = {Plaza-Diaz, J and Voidarou, CC and Bezirtzoglou, E and Stavropoulou, E},
title = {Editorial: Rodent model organisms: therapeutic treatments and drugs interaction with the gut microbiome, volume II.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1962495},
doi = {10.3389/fmicb.2026.1962495},
pmid = {42851677},
issn = {1664-302X},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
Structured succession of a cross-kingdom microbiome drives degradation and detoxification of oolong tea waste.
Frontiers in microbiomes, 5:1871476.
The spontaneous aerobic degradation of oolong tea waste offers a promising but underexplored route for sustainable waste valorization. In this study, we used whole-genome metagenomic sequencing to examine microbial succession and functional gene dynamics over a 35-day degradation period. Our results uncovered a three-phase ecological progression: an initial mesophilic phase (Days 0-7) dominated by Pseudomonadota, which reached 93.4% relative abundance and specialized in simple substrate utilization; a thermotolerant transition (Days 8-15, 30-33°C) characterized by increased abundance of glycoside hydrolases (GH5, GH13); and a maturation phase (Days 16-35) marked by the emergence of lignocellulose-degrading taxa such as Cellulomonas and Microbacterium, accompanied by a 78% reduction in antibiotic resistance genes. Profiling of carbohydrate-active enzymes revealed a sequential shift from pectinases (GH28) to hemicellulases (GH43), while mobile genetic elements declined substantially during the maturation phase. These results indicate that tea waste degradation follows structured microbial succession patterns influenced by abiotic factors and suggests a potential self-purification capacity through the attenuation of antibiotic resistance genes. This study establishes a foundation for optimizing composting processes and designing targeted bioaugmentation strategies to enhance tea waste valorization.
Additional Links: PMID-42851762
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@article {pmid42851762,
year = {2026},
author = {Ye, G and Yu, X and Ismaiah, MJ and Ke, R and Zeng, Z and Wang, J and Lan, S and Yu, H and Liu, H and Xie, S and Leung, KS and Zhang, L and Lee, JC and Habimana, O},
title = {Structured succession of a cross-kingdom microbiome drives degradation and detoxification of oolong tea waste.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1871476},
pmid = {42851762},
issn = {2813-4338},
abstract = {The spontaneous aerobic degradation of oolong tea waste offers a promising but underexplored route for sustainable waste valorization. In this study, we used whole-genome metagenomic sequencing to examine microbial succession and functional gene dynamics over a 35-day degradation period. Our results uncovered a three-phase ecological progression: an initial mesophilic phase (Days 0-7) dominated by Pseudomonadota, which reached 93.4% relative abundance and specialized in simple substrate utilization; a thermotolerant transition (Days 8-15, 30-33°C) characterized by increased abundance of glycoside hydrolases (GH5, GH13); and a maturation phase (Days 16-35) marked by the emergence of lignocellulose-degrading taxa such as Cellulomonas and Microbacterium, accompanied by a 78% reduction in antibiotic resistance genes. Profiling of carbohydrate-active enzymes revealed a sequential shift from pectinases (GH28) to hemicellulases (GH43), while mobile genetic elements declined substantially during the maturation phase. These results indicate that tea waste degradation follows structured microbial succession patterns influenced by abiotic factors and suggests a potential self-purification capacity through the attenuation of antibiotic resistance genes. This study establishes a foundation for optimizing composting processes and designing targeted bioaugmentation strategies to enhance tea waste valorization.},
}
RevDate: 2026-10-09
Characterization of the Middle Ear Microbiome in Meniere's Disease by 16S rRNA Gene Sequencing Compared to Chronic Suppurative Otitis Media.
World journal of otorhinolaryngology - head and neck surgery [Epub ahead of print].
OBJECTIVE: To investigate the middle ear microbiome in Meniere's disease (MD) patients.
METHODS: Middle ear smears from 10 MD patients (ME group) and 10 chronic suppurative otitis patients (OE group) were collected during surgery and processed via 16S rRNA gene sequencing.
RESULTS: The ME group demonstrated significant differences in alpha diversity (Shannon/Simpson index, p < 0.01) and beta diversity (ANOSIM/PERMANOVA, the Bray-Curtis distance matrix, R = 0.144, p < 0.05; R [2] = 0.107, p < 0.05) compared to OE group, and the PERMDISP showed lower heterogeneity in the ME group (p < 0.01). Ruminococcus, Ochrobactrum, and Halomonas at the genus level were enriched in the ME group, and the difference reached marginal significance. The linear discriminant analysis effect size analysis (LefSe) identified Bacteroides, Halomonas, and Prevotella as significantly enriched in ME, while Neisseriales was downregulated (|LDA| > 2, p < 0.05). BugBase phenotype analysis revealed that facultatively anaerobic bacteria and bacteria containing mobile genetic elements were significantly reduced in the ME group compared to the OE group (p < 0.05). The proportion of anaerobes was higher in the ME group (p = 0.123). Nine KEGG metabolic pathways were enriched in the ME group, though the difference was not significant after correction.
CONCLUSION: These findings suggested that inner ear inflammation resulted from middle ear dysbiosis may contribute to MD pathogenesis, offering novel perspectives for MD etiology and therapies.
Additional Links: PMID-42851936
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Citation:
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@article {pmid42851936,
year = {2026},
author = {Tao, YT and Wang, L and Zheng, HW and Yu, LS},
title = {Characterization of the Middle Ear Microbiome in Meniere's Disease by 16S rRNA Gene Sequencing Compared to Chronic Suppurative Otitis Media.},
journal = {World journal of otorhinolaryngology - head and neck surgery},
volume = {},
number = {},
pages = {},
pmid = {42851936},
issn = {2589-1081},
abstract = {OBJECTIVE: To investigate the middle ear microbiome in Meniere's disease (MD) patients.
METHODS: Middle ear smears from 10 MD patients (ME group) and 10 chronic suppurative otitis patients (OE group) were collected during surgery and processed via 16S rRNA gene sequencing.
RESULTS: The ME group demonstrated significant differences in alpha diversity (Shannon/Simpson index, p < 0.01) and beta diversity (ANOSIM/PERMANOVA, the Bray-Curtis distance matrix, R = 0.144, p < 0.05; R [2] = 0.107, p < 0.05) compared to OE group, and the PERMDISP showed lower heterogeneity in the ME group (p < 0.01). Ruminococcus, Ochrobactrum, and Halomonas at the genus level were enriched in the ME group, and the difference reached marginal significance. The linear discriminant analysis effect size analysis (LefSe) identified Bacteroides, Halomonas, and Prevotella as significantly enriched in ME, while Neisseriales was downregulated (|LDA| > 2, p < 0.05). BugBase phenotype analysis revealed that facultatively anaerobic bacteria and bacteria containing mobile genetic elements were significantly reduced in the ME group compared to the OE group (p < 0.05). The proportion of anaerobes was higher in the ME group (p = 0.123). Nine KEGG metabolic pathways were enriched in the ME group, though the difference was not significant after correction.
CONCLUSION: These findings suggested that inner ear inflammation resulted from middle ear dysbiosis may contribute to MD pathogenesis, offering novel perspectives for MD etiology and therapies.},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
Intermittent fasting-associated microbiome remodeling and functional modulation by Lacticaseibacillus rhamnosus HN001.
Frontiers in nutrition, 13:1947132.
OBJECTIVE: The gut microbiome is a critical regulator of host metabolism, yet how intermittent fasting (IF) remodels the gut ecosystem independent of dietary composition remains unclear. This study aimed to isolate the effect of feeding rhythm on the gut microbiome and identify specific microbial taxa mediating IF-induced metabolic changes.
METHODS: We employed a family-based 'shared meal' model that strictly standardized dietary composition across all participants. Five healthy adults (3 males, 2 females) from a single family participated in a pilot, hypothesis-generating 4-week 16:8 IF intervention with longitudinal fecal sampling for 16S rRNA sequencing and untargeted metabolomics. To functionally test a candidate Lacticaseibacillus-associated mechanism, C57BL/6 J mice were subjected to a 1-week 16:8 IF protocol with or without daily oral supplementation of Lacticaseibacillus rhamnosus HN001. Plasma beta-hydroxybutyrate (betaOHB) and peptide YY (PYY) were measured by ELISA.
RESULTS: IF was associated with body weight loss in humans (2.1 +/- 0.4 kg, 95% CI: 1.3 to 2.9 kg, p < 0.05) without a significant reduction in caloric intake. In the primary paired genus-level DESeq2 analysis accounting for participant identity, no genus remained significant after false-discovery-rate correction, although Lacticaseibacillus showed a directional decrease after IF, consistent in direction with the original exploratory unpaired analysis. Predicted microbial functional and fecal metabolomic changes were consistent with altered microbial energy metabolism. In mice, IF significantly elevated plasma betaOHB (p = 0.0046) and reduced body weight, whereas HN001 supplementation reversed these IF-associated effects under the conditions tested.
CONCLUSION: In this pilot, hypothesis-generating human cohort, IF was associated with coordinated microbiome and metabolomic remodeling, including a directional Lacticaseibacillus signal that motivated subsequent functional testing. In mice, L. rhamnosus HN001 supplementation reversed IF-associated weight loss and ketosis, supporting the functional plausibility of a Lacticaseibacillus-associated mechanism. The human observations require confirmation in larger, independent cohorts with time-matched non-fasting controls and species-resolved microbiome measurements.
Additional Links: PMID-42852269
PubMed:
Citation:
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@article {pmid42852269,
year = {2026},
author = {Shao, T and Liu, JM},
title = {Intermittent fasting-associated microbiome remodeling and functional modulation by Lacticaseibacillus rhamnosus HN001.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1947132},
pmid = {42852269},
issn = {2296-861X},
abstract = {OBJECTIVE: The gut microbiome is a critical regulator of host metabolism, yet how intermittent fasting (IF) remodels the gut ecosystem independent of dietary composition remains unclear. This study aimed to isolate the effect of feeding rhythm on the gut microbiome and identify specific microbial taxa mediating IF-induced metabolic changes.
METHODS: We employed a family-based 'shared meal' model that strictly standardized dietary composition across all participants. Five healthy adults (3 males, 2 females) from a single family participated in a pilot, hypothesis-generating 4-week 16:8 IF intervention with longitudinal fecal sampling for 16S rRNA sequencing and untargeted metabolomics. To functionally test a candidate Lacticaseibacillus-associated mechanism, C57BL/6 J mice were subjected to a 1-week 16:8 IF protocol with or without daily oral supplementation of Lacticaseibacillus rhamnosus HN001. Plasma beta-hydroxybutyrate (betaOHB) and peptide YY (PYY) were measured by ELISA.
RESULTS: IF was associated with body weight loss in humans (2.1 +/- 0.4 kg, 95% CI: 1.3 to 2.9 kg, p < 0.05) without a significant reduction in caloric intake. In the primary paired genus-level DESeq2 analysis accounting for participant identity, no genus remained significant after false-discovery-rate correction, although Lacticaseibacillus showed a directional decrease after IF, consistent in direction with the original exploratory unpaired analysis. Predicted microbial functional and fecal metabolomic changes were consistent with altered microbial energy metabolism. In mice, IF significantly elevated plasma betaOHB (p = 0.0046) and reduced body weight, whereas HN001 supplementation reversed these IF-associated effects under the conditions tested.
CONCLUSION: In this pilot, hypothesis-generating human cohort, IF was associated with coordinated microbiome and metabolomic remodeling, including a directional Lacticaseibacillus signal that motivated subsequent functional testing. In mice, L. rhamnosus HN001 supplementation reversed IF-associated weight loss and ketosis, supporting the functional plausibility of a Lacticaseibacillus-associated mechanism. The human observations require confirmation in larger, independent cohorts with time-matched non-fasting controls and species-resolved microbiome measurements.},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
Correction: Clinical evidence for microbial-derived polyphenol metabolites in health and disease: a scoping review.
Frontiers in nutrition, 13:1993867.
[This corrects the article DOI: 10.3389/fnut.2026.1859472.].
Additional Links: PMID-42852270
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@article {pmid42852270,
year = {2026},
author = {Brown, J and Norby-Adams, L and Ghanem, N and Lewis, A and Goldenberg, JZ and Weir, T and Vita, AA},
title = {Correction: Clinical evidence for microbial-derived polyphenol metabolites in health and disease: a scoping review.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1993867},
doi = {10.3389/fnut.2026.1993867},
pmid = {42852270},
issn = {2296-861X},
abstract = {[This corrects the article DOI: 10.3389/fnut.2026.1859472.].},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
Maternal obesity, diet, and the gut microbiome: implications for offspring cardiometabolic programming.
Frontiers in nutrition, 13:1909112.
Maternal obesity is associated with adverse pregnancy and long-term offspring outcomes. The maternal gut microbiome may contribute through altered microbial functions, barrier integrity, immune signaling, and metabolite production. Pregnancy itself entails microbial and metabolic remodeling, but obesity and obesogenic dietary patterns may modify these adaptations. Evidence from human cohorts and animal models links maternal obesity with context-dependent differences in microbial composition and function, reduced butyrate-producing capacity, altered bile acid and short-chain fatty acid profiles, and heightened inflammation. These changes may influence placental function and early-life microbial assembly through delivery-related exposures, breastfeeding, human milk oligosaccharides, and shared environmental and dietary factors. Maternal diets high in saturated fat and refined carbohydrate tend to be associated with less favorable microbial and cardiometabolic profiles, whereas fiber-rich, plant-diverse dietary patterns may support short-chain fatty acid production and metabolic resilience. However, causal inference is limited by heterogeneity, confounding, and inconsistent findings. Probiotic, prebiotic, and synbiotic interventions show potential, but clinical results-particularly for gestational diabetes prevention-remain mixed. This narrative review integrates evidence on diet-microbiome interactions in maternal obesity, microbial metabolites and immune pathways, early-life colonization, and implications for offspring obesity and cardiometabolic risk. Overall, the maternal microbiome is a plausible but incompletely validated target; well-powered longitudinal studies and pregnancy-specific randomized trials are needed before precision microbiome strategies can be incorporated into routine care.
Additional Links: PMID-42852271
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@article {pmid42852271,
year = {2026},
author = {Jahan-Mihan, A and Salamat, S and Nodarse, R and Shangraw, R and Labyak, C and Snyder, J and Berg, K and Leftwich, J},
title = {Maternal obesity, diet, and the gut microbiome: implications for offspring cardiometabolic programming.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1909112},
pmid = {42852271},
issn = {2296-861X},
abstract = {Maternal obesity is associated with adverse pregnancy and long-term offspring outcomes. The maternal gut microbiome may contribute through altered microbial functions, barrier integrity, immune signaling, and metabolite production. Pregnancy itself entails microbial and metabolic remodeling, but obesity and obesogenic dietary patterns may modify these adaptations. Evidence from human cohorts and animal models links maternal obesity with context-dependent differences in microbial composition and function, reduced butyrate-producing capacity, altered bile acid and short-chain fatty acid profiles, and heightened inflammation. These changes may influence placental function and early-life microbial assembly through delivery-related exposures, breastfeeding, human milk oligosaccharides, and shared environmental and dietary factors. Maternal diets high in saturated fat and refined carbohydrate tend to be associated with less favorable microbial and cardiometabolic profiles, whereas fiber-rich, plant-diverse dietary patterns may support short-chain fatty acid production and metabolic resilience. However, causal inference is limited by heterogeneity, confounding, and inconsistent findings. Probiotic, prebiotic, and synbiotic interventions show potential, but clinical results-particularly for gestational diabetes prevention-remain mixed. This narrative review integrates evidence on diet-microbiome interactions in maternal obesity, microbial metabolites and immune pathways, early-life colonization, and implications for offspring obesity and cardiometabolic risk. Overall, the maternal microbiome is a plausible but incompletely validated target; well-powered longitudinal studies and pregnancy-specific randomized trials are needed before precision microbiome strategies can be incorporated into routine care.},
}
RevDate: 2026-10-09
CmpDate: 2026-10-09
Associations of Urinary Triclosan Concentrations Across Gestation and Childhood with the Adolescent Gut Microbiome.
Environmental health perspectives, 134(6):672-687.
Research on the influence of repeated exposure to antimicrobial chemicals, such as triclosan, on the microbiome is lacking. The goal of this study was to elucidate the associations of time-varying urinary triclosan concentrations with the adolescent gut microbiome. We used data from a prospective cohort based in Cincinnati, OH (enrolled 2003-2006, n = 146), to assess the time-varying associations of urinary triclosan concentrations with adolescent (age ∼ 12 years) gut microbiome diversity and composition. Individuals ≥ 18-years-old were recruited during the second trimester of pregnancy, and urinary triclosan concentrations were measured in pregnant women up to 2 times in pregnancy and up to 7 times in the child from ages 1 through 12 years. At age ∼ 12 years, fecal microbiome diversity and composition was characterized with metagenomic sequencing. We estimated differences in the relative abundance of prevalent (≥50%) bacterial species and gene pathways using linear regression and generalized estimating equations to assess windows of heightened susceptibility adjusted for sociodemographic characteristics. Additionally, we examined sex-specific associations by including an interaction term. The adolescent median Shannon diversity was 3.5 (IQR: 3.3, 3.5). Higher gestational triclosan concentrations with lower gut microbiome diversity [β = -0.13 per 10-fold increase (95%CI: -0.24, -0.02)]. Triclosan concentrations were also positively associated with higher abundance of antibiotic resistance genes and differential abundance of some bacterial species, with the strongest associations observed in early life and at age 12 years. We also found differences depending on sex, with more significant associations observed among males. Our findings provide insight into windows of triclosan exposure that are relevant to gut microbiome composition and the impacts of antimicrobial agents.
Additional Links: PMID-42852388
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@article {pmid42852388,
year = {2026},
author = {Laue, HE and Fleisch, AF and Calafat, AM and Lanphear, BP and Cecil, KM and Yolton, K and Buckley, JP and Karagas, MR and Madan, JC and Willis, AD and Braun, JM},
title = {Associations of Urinary Triclosan Concentrations Across Gestation and Childhood with the Adolescent Gut Microbiome.},
journal = {Environmental health perspectives},
volume = {134},
number = {6},
pages = {672-687},
pmid = {42852388},
issn = {1552-9924},
mesh = {*Triclosan/urine ; Humans ; Female ; Pregnancy ; Adolescent ; Child ; *Gastrointestinal Microbiome/drug effects ; Child, Preschool ; Male ; Infant ; *Anti-Infective Agents, Local/urine ; Ohio ; Prospective Studies ; Feces/microbiology ; },
abstract = {Research on the influence of repeated exposure to antimicrobial chemicals, such as triclosan, on the microbiome is lacking. The goal of this study was to elucidate the associations of time-varying urinary triclosan concentrations with the adolescent gut microbiome. We used data from a prospective cohort based in Cincinnati, OH (enrolled 2003-2006, n = 146), to assess the time-varying associations of urinary triclosan concentrations with adolescent (age ∼ 12 years) gut microbiome diversity and composition. Individuals ≥ 18-years-old were recruited during the second trimester of pregnancy, and urinary triclosan concentrations were measured in pregnant women up to 2 times in pregnancy and up to 7 times in the child from ages 1 through 12 years. At age ∼ 12 years, fecal microbiome diversity and composition was characterized with metagenomic sequencing. We estimated differences in the relative abundance of prevalent (≥50%) bacterial species and gene pathways using linear regression and generalized estimating equations to assess windows of heightened susceptibility adjusted for sociodemographic characteristics. Additionally, we examined sex-specific associations by including an interaction term. The adolescent median Shannon diversity was 3.5 (IQR: 3.3, 3.5). Higher gestational triclosan concentrations with lower gut microbiome diversity [β = -0.13 per 10-fold increase (95%CI: -0.24, -0.02)]. Triclosan concentrations were also positively associated with higher abundance of antibiotic resistance genes and differential abundance of some bacterial species, with the strongest associations observed in early life and at age 12 years. We also found differences depending on sex, with more significant associations observed among males. Our findings provide insight into windows of triclosan exposure that are relevant to gut microbiome composition and the impacts of antimicrobial agents.},
}
MeSH Terms:
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*Triclosan/urine
Humans
Female
Pregnancy
Adolescent
Child
*Gastrointestinal Microbiome/drug effects
Child, Preschool
Male
Infant
*Anti-Infective Agents, Local/urine
Ohio
Prospective Studies
Feces/microbiology
RevDate: 2026-10-09
Gut microbiota-derived tryptophan metabolite attenuates calcium oxalate nephropathy by suppressing renal tubular cell apoptosis through the AhR-SOCS3-STAT1 axis.
The Journal of pathology [Epub ahead of print].
Calcium oxalate (CaOx) nephropathy is a highly prevalent urological disease worldwide. Gut microbiota dysbiosis and host metabolic dysregulation are recognized as pivotal drivers in disease pathogenesis, yet the underlying mechanisms remain incompletely understood. In this study, by integrating metagenomics and metabolomics, we identified dysregulation of tryptophan metabolites in patients with CaOx nephrolithiasis, with microbiota-derived indole-3-propionic acid (IPA) as the most discriminatory differential metabolite. Oral IPA supplementation markedly reduced renal CaOx crystal deposition and tubular injury in a CaOx nephropathy murine model. Mechanistically, IPA activated the aryl hydrocarbon receptor (AhR), which translocated to the nucleus and transcriptionally upregulated suppressor of cytokine signaling 3 (SOCS3)-a negative regulator of signal transducer and activator of transcription 1 (STAT1)-thereby suppressing STAT1 phosphorylation, alleviating oxalate-induced tubular cell injury and apoptosis, and inhibiting CaOx crystal deposition. Our findings identify tryptophan metabolite alteration as a critical metabolic signature of CaOx nephropathy and demonstrate that microbiota-derived IPA attenuates oxalate-induced renal tubular cell injury and apoptosis via the AhR-SOCS3-STAT1 axis. © 2026 The Pathological Society of Great Britain and Ireland.
Additional Links: PMID-42852494
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@article {pmid42852494,
year = {2026},
author = {Li, Y and Chen, J and Lin, L and Jian, Z and Liu, L and Wang, M and Wei, J and Chen, X and Yang, M and Li, T and Xiang, L and Liao, B and Jin, X and Wang, K},
title = {Gut microbiota-derived tryptophan metabolite attenuates calcium oxalate nephropathy by suppressing renal tubular cell apoptosis through the AhR-SOCS3-STAT1 axis.},
journal = {The Journal of pathology},
volume = {},
number = {},
pages = {},
doi = {10.1002/path.70135},
pmid = {42852494},
issn = {1096-9896},
support = {82570894//National Natural Science Foundation of China/ ; 82270799//National Natural Science Foundation of China/ ; 2023SCUH0054//Sichuan University/ ; CZ2026001//Project of National Outstanding Medical Doctors/ ; 2023HXFH014//Clinical Research Incubation Project of West China Hospital of Sichuan University/ ; },
abstract = {Calcium oxalate (CaOx) nephropathy is a highly prevalent urological disease worldwide. Gut microbiota dysbiosis and host metabolic dysregulation are recognized as pivotal drivers in disease pathogenesis, yet the underlying mechanisms remain incompletely understood. In this study, by integrating metagenomics and metabolomics, we identified dysregulation of tryptophan metabolites in patients with CaOx nephrolithiasis, with microbiota-derived indole-3-propionic acid (IPA) as the most discriminatory differential metabolite. Oral IPA supplementation markedly reduced renal CaOx crystal deposition and tubular injury in a CaOx nephropathy murine model. Mechanistically, IPA activated the aryl hydrocarbon receptor (AhR), which translocated to the nucleus and transcriptionally upregulated suppressor of cytokine signaling 3 (SOCS3)-a negative regulator of signal transducer and activator of transcription 1 (STAT1)-thereby suppressing STAT1 phosphorylation, alleviating oxalate-induced tubular cell injury and apoptosis, and inhibiting CaOx crystal deposition. Our findings identify tryptophan metabolite alteration as a critical metabolic signature of CaOx nephropathy and demonstrate that microbiota-derived IPA attenuates oxalate-induced renal tubular cell injury and apoptosis via the AhR-SOCS3-STAT1 axis. © 2026 The Pathological Society of Great Britain and Ireland.},
}
RevDate: 2026-10-09
Core microbial populations drive longitudinal development of the hindgut bacterial microbiota in Jersey calve.
Microbiology spectrum [Epub ahead of print].
The early-life gut microbiome represents a critical window during which microbial succession may exert lasting effects on host metabolism and productivity. While gut microbiome-host phenotypic associations have been extensively studied in Holstein calves, such relationships are rarely reported in alternative breeds, including Jersey calves. We hypothesized that Jersey calves would exhibit age-dependent community shifts characterized by core microbial populations and breed-associated bacterial networks that may contribute to metabolic phenotype. Fecal samples were collected from dams post-calving, and Jersey calves (n = 12) were sampled longitudinally at 24-48 h and weekly through 12 weeks. Bacterial communities were profiled using the V1-V2 region of the 16S rRNA gene. The number of observed ASVs and Shannon diversity increased with age (P < 0.001), and Beta diversity revealed age-dependent structuring (weighted R[2] =0.12, P = 0.023; unweighted R[2] =0.37, P = 0.001), with calf communities gradually converging toward dams. Taxonomic analyses revealed a conserved core microbiome comprising 34 taxa accounting for over 90% of total community abundance. Neonatal samples were dominated by facultative anaerobes, including Escherichia and Streptococcus, with early colonization by Blautia and Collinsella. Calves then exhibited transient enrichment of milk-glycan-associated taxa, including Lactobacillus and Bacteroides. Weeks 3-7 stages saw preeminence of acetogens (Blautia, Dorea, Collinsella), followed by later enrichment of adult-associated fiber-degrading taxa. Collectively, these findings demonstrate a consistent age-dependent pattern of hindgut microbiome maturation among Jersey calves. The taxonomic patterns provide a foundation for investigating potential links between early-life microbial ecology and breed-specific metabolic phenotypes.IMPORTANCEThe neonatal period represents a critical window for microbial community assembly and interaction with the host. While microbial succession in Holstein calves has been studied extensively, little is known about microbiome assembly in Jersey calves. Herein, we performed longitudinal profiling of the hindgut microbiome of Jersey calves from birth through twelve weeks of age. Microbial communities underwent a structured succession broadly resembling patterns reported previously in Holsteins, with network analyses revealing microbial assemblages that shift with diet throughout the pre- and postweaning periods. Jersey calves also exhibited a notably elevated abundance of several acetate-associated taxa during early life. These findings provide the first detailed characterization of hindgut microbiome assembly in Jersey calves and identify microbial community structures potentially linked to breed-specific metabolic phenotypes. Such information is critical for designing microbiome-targeted strategies to improve calf growth, health, and feed efficiency, and for influencing milk components.
Additional Links: PMID-42852572
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@article {pmid42852572,
year = {2026},
author = {Post, A and Yadlapalli, A and Webb, T and Zhang, A and Yelampalli, A and Challa, K and Indugu, N and Pitta, DW},
title = {Core microbial populations drive longitudinal development of the hindgut bacterial microbiota in Jersey calve.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0187826},
doi = {10.1128/spectrum.01878-26},
pmid = {42852572},
issn = {2165-0497},
abstract = {The early-life gut microbiome represents a critical window during which microbial succession may exert lasting effects on host metabolism and productivity. While gut microbiome-host phenotypic associations have been extensively studied in Holstein calves, such relationships are rarely reported in alternative breeds, including Jersey calves. We hypothesized that Jersey calves would exhibit age-dependent community shifts characterized by core microbial populations and breed-associated bacterial networks that may contribute to metabolic phenotype. Fecal samples were collected from dams post-calving, and Jersey calves (n = 12) were sampled longitudinally at 24-48 h and weekly through 12 weeks. Bacterial communities were profiled using the V1-V2 region of the 16S rRNA gene. The number of observed ASVs and Shannon diversity increased with age (P < 0.001), and Beta diversity revealed age-dependent structuring (weighted R[2] =0.12, P = 0.023; unweighted R[2] =0.37, P = 0.001), with calf communities gradually converging toward dams. Taxonomic analyses revealed a conserved core microbiome comprising 34 taxa accounting for over 90% of total community abundance. Neonatal samples were dominated by facultative anaerobes, including Escherichia and Streptococcus, with early colonization by Blautia and Collinsella. Calves then exhibited transient enrichment of milk-glycan-associated taxa, including Lactobacillus and Bacteroides. Weeks 3-7 stages saw preeminence of acetogens (Blautia, Dorea, Collinsella), followed by later enrichment of adult-associated fiber-degrading taxa. Collectively, these findings demonstrate a consistent age-dependent pattern of hindgut microbiome maturation among Jersey calves. The taxonomic patterns provide a foundation for investigating potential links between early-life microbial ecology and breed-specific metabolic phenotypes.IMPORTANCEThe neonatal period represents a critical window for microbial community assembly and interaction with the host. While microbial succession in Holstein calves has been studied extensively, little is known about microbiome assembly in Jersey calves. Herein, we performed longitudinal profiling of the hindgut microbiome of Jersey calves from birth through twelve weeks of age. Microbial communities underwent a structured succession broadly resembling patterns reported previously in Holsteins, with network analyses revealing microbial assemblages that shift with diet throughout the pre- and postweaning periods. Jersey calves also exhibited a notably elevated abundance of several acetate-associated taxa during early life. These findings provide the first detailed characterization of hindgut microbiome assembly in Jersey calves and identify microbial community structures potentially linked to breed-specific metabolic phenotypes. Such information is critical for designing microbiome-targeted strategies to improve calf growth, health, and feed efficiency, and for influencing milk components.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Impact of Antibiotic Therapy in Patients with Cholangiocarcinoma Treated with Chemoimmunotherapy.
Oncology, 104(5):575-591.
INTRODUCTION: Patients with biliary tract cancers (BTCs) often require antibiotic therapy before starting systemic treatment that includes an immune checkpoint inhibitor. This study aimed to evaluate the prognostic impact of antibiotic therapy administered in the 15 days prior to the start of chemoimmunotherapy in patients with BTC.
METHODS: The study population included patients with metastatic or locally advanced BTC from Western and Eastern populations treated with first-line chemoimmunotherapy. The aim of the study was to evaluate the impact of antibiotic therapy in the 15 days prior to starting oncological treatment (AT population) compared to patients who did not receive antibiotic therapy (NAT). Univariate and multivariate analyses were used to evaluate predictive factors for overall survival (OS) and progression-free survival (PFS), while prognostic factors were analyzed by univariate and multivariate analysis using Cox regression model.
RESULTS: A total of 666 patients were enrolled in the study: 93 (14%) in AT cohort and 573 (86%) in NAT cohort. In the AT population, the incidence of cholangitis (p = 0.0017), alanine aminotransferase elevation (p = 0.0009), fever (p = 0.0021), decreased appetite (p = 0.0007), itching (p = 0.0081), and rash (p = 0.012) was significantly higher compared to the NAT. The median OS was 15.9 months (95% confidence interval [CI]: 13.8-18.3) in NAT cohort versus 10.1 months (95% CI: 7.9-12.4) in AT cohort (NAT vs. AT, hazard ratio [HR]: 0.43, 95% CI: 0.27-0.70, p = 0.0006), while median PFS was 8.5 months in NAT cohort versus 5.4 months in AT cohort (NAT vs. AT, HR: 0.49, 95% CI: 0.34-0.71, p = 0.0001). Multivariate analysis confirmed the prognostic role of antibiotic for OS and PFS. Finally, NAT cohort showed better overall response rate compared with AT cohort (31.4% vs. 20.4%, p = 0.03).
CONCLUSIONS: The use of antibiotic therapy in the 15 days prior to starting chemoimmunotherapy is an independent unfavorable prognostic factor for survival in our cohort of patients with advanced BTC treated with cisplatin, gemcitabine and durvalumab.
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@article {pmid40815107,
year = {2026},
author = {Vitiello, F and Vivaldi, C and Rimini, M and Prinzi, FL and Rizzato, MD and Saborowski, A and Antonuzzo, L and Rossari, F and Satake, T and Peeters, F and Salani, F and Pressiani, T and Lucchetti, J and Kim, JW and Abidoye, O and Rapposelli, IG and Gallio, C and Tamberi, S and Finkelmeier, F and Giordano, G and Pircher, C and Chon, HJ and Braconi, C and Qaisar, A and Pastorino, A and Castet, F and Tamburini, E and Yoo, C and Parisi, A and Diana, A and Scartozzi, M and Prager, GW and Avallone, A and Schirripa, M and Kim, IH and Perkhofer, L and Oneda, E and Verrico, M and Couto, N and Adeva, J and Chan, SL and Spinelli, GP and Personeni, N and Garajova, I and Rodriguez, MG and Leo, S and Alvim, CM and Roque, R and Farinea, G and Genovesi, V and De Rosa, A and Lavacchi, D and Camera, S and Ikeda, M and Dekervel, J and Niger, M and Balsano, R and Tonini, G and Kang, M and Tesini, G and Esposito, L and Boccancino, A and Himmelsbach, V and Landriscina, M and Ahcene Djaballah, S and Bekaii-Saab, T and Masi, G and Vogel, A and Lonardi, S and Fornaro, L and Rimassa, L and Casadei-Gardini, A},
title = {Impact of Antibiotic Therapy in Patients with Cholangiocarcinoma Treated with Chemoimmunotherapy.},
journal = {Oncology},
volume = {104},
number = {5},
pages = {575-591},
doi = {10.1159/000546856},
pmid = {40815107},
issn = {1423-0232},
mesh = {Humans ; Female ; Male ; Aged ; Middle Aged ; *Anti-Bacterial Agents/therapeutic use/administration & dosage ; *Cholangiocarcinoma/drug therapy/mortality/pathology ; Prognosis ; *Bile Duct Neoplasms/drug therapy/mortality/pathology ; Immunotherapy/methods ; Aged, 80 and over ; Progression-Free Survival ; Retrospective Studies ; Immune Checkpoint Inhibitors/therapeutic use ; Adult ; },
abstract = {INTRODUCTION: Patients with biliary tract cancers (BTCs) often require antibiotic therapy before starting systemic treatment that includes an immune checkpoint inhibitor. This study aimed to evaluate the prognostic impact of antibiotic therapy administered in the 15 days prior to the start of chemoimmunotherapy in patients with BTC.
METHODS: The study population included patients with metastatic or locally advanced BTC from Western and Eastern populations treated with first-line chemoimmunotherapy. The aim of the study was to evaluate the impact of antibiotic therapy in the 15 days prior to starting oncological treatment (AT population) compared to patients who did not receive antibiotic therapy (NAT). Univariate and multivariate analyses were used to evaluate predictive factors for overall survival (OS) and progression-free survival (PFS), while prognostic factors were analyzed by univariate and multivariate analysis using Cox regression model.
RESULTS: A total of 666 patients were enrolled in the study: 93 (14%) in AT cohort and 573 (86%) in NAT cohort. In the AT population, the incidence of cholangitis (p = 0.0017), alanine aminotransferase elevation (p = 0.0009), fever (p = 0.0021), decreased appetite (p = 0.0007), itching (p = 0.0081), and rash (p = 0.012) was significantly higher compared to the NAT. The median OS was 15.9 months (95% confidence interval [CI]: 13.8-18.3) in NAT cohort versus 10.1 months (95% CI: 7.9-12.4) in AT cohort (NAT vs. AT, hazard ratio [HR]: 0.43, 95% CI: 0.27-0.70, p = 0.0006), while median PFS was 8.5 months in NAT cohort versus 5.4 months in AT cohort (NAT vs. AT, HR: 0.49, 95% CI: 0.34-0.71, p = 0.0001). Multivariate analysis confirmed the prognostic role of antibiotic for OS and PFS. Finally, NAT cohort showed better overall response rate compared with AT cohort (31.4% vs. 20.4%, p = 0.03).
CONCLUSIONS: The use of antibiotic therapy in the 15 days prior to starting chemoimmunotherapy is an independent unfavorable prognostic factor for survival in our cohort of patients with advanced BTC treated with cisplatin, gemcitabine and durvalumab.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
Male
Aged
Middle Aged
*Anti-Bacterial Agents/therapeutic use/administration & dosage
*Cholangiocarcinoma/drug therapy/mortality/pathology
Prognosis
*Bile Duct Neoplasms/drug therapy/mortality/pathology
Immunotherapy/methods
Aged, 80 and over
Progression-Free Survival
Retrospective Studies
Immune Checkpoint Inhibitors/therapeutic use
Adult
RevDate: 2026-10-07
CmpDate: 2026-10-07
Myeloid cell reprogramming drives enhanced defense against Streptococcus pneumoniae lung infection following exposure to commensal Prevotella.
Proceedings of the National Academy of Sciences of the United States of America, 123(41):e2623525123.
Clinical data link the prevalent respiratory tract anaerobe Prevotella with reduced pneumonia mortality, but the mechanisms directing Prevotella regulation of lung immune homeostasis are unclear. Here, single-cell RNA sequencing was employed to define the transcriptional immune signatures underlying improved clearance of Streptococcus pneumoniae following lung exposure to Prevotella melaninogenica. Overall, we observed a substantial shift in myeloid cell transcriptional programming from interferon-dominant to a more antibacterial profile in S. pneumoniae-infected mice after pre-exposure to P. melaninogenica, correlating with increased macrophage and neutrophil phagocytosis of S. pneumoniae and improved pathogen clearance. In neutrophils, tumor necrosis factor (TNF) signaling through TNFR2 was essential for increased antimicrobial function. Moreover, improved defense required CCR2-dependent monocyte-derived macrophages, with selective enrichment of more a mature Cxcl3+ population which was distinct from the hallmark S. pneumoniae-associated C1qa+ population enriched in the absence of effective clearance. Together, these findings inform the myeloid cell transcriptional changes associated with natural infection resistance mediated by pulmonary microbial exposures.
Additional Links: PMID-42842405
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PubMed:
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@article {pmid42842405,
year = {2026},
author = {Stoner, SN and Larson, ED and Fulte, S and Shaw, SC and Fish, ER and Janoff, EN and Mack, M and Clark, SE},
title = {Myeloid cell reprogramming drives enhanced defense against Streptococcus pneumoniae lung infection following exposure to commensal Prevotella.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {41},
pages = {e2623525123},
doi = {10.1073/pnas.2623525123},
pmid = {42842405},
issn = {1091-6490},
support = {R01AI172958//HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; T32DC012280//HHS | NIH | National Institute on Deafness and Other Communication Disorders (NIDCD)/ ; T32AI007405//HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; },
mesh = {Animals ; *Streptococcus pneumoniae/immunology ; Mice ; *Myeloid Cells/immunology ; *Prevotella/immunology ; Lung/microbiology/immunology ; *Pneumonia, Pneumococcal/immunology/microbiology ; Neutrophils/immunology ; Macrophages/immunology ; Mice, Inbred C57BL ; Phagocytosis ; },
abstract = {Clinical data link the prevalent respiratory tract anaerobe Prevotella with reduced pneumonia mortality, but the mechanisms directing Prevotella regulation of lung immune homeostasis are unclear. Here, single-cell RNA sequencing was employed to define the transcriptional immune signatures underlying improved clearance of Streptococcus pneumoniae following lung exposure to Prevotella melaninogenica. Overall, we observed a substantial shift in myeloid cell transcriptional programming from interferon-dominant to a more antibacterial profile in S. pneumoniae-infected mice after pre-exposure to P. melaninogenica, correlating with increased macrophage and neutrophil phagocytosis of S. pneumoniae and improved pathogen clearance. In neutrophils, tumor necrosis factor (TNF) signaling through TNFR2 was essential for increased antimicrobial function. Moreover, improved defense required CCR2-dependent monocyte-derived macrophages, with selective enrichment of more a mature Cxcl3+ population which was distinct from the hallmark S. pneumoniae-associated C1qa+ population enriched in the absence of effective clearance. Together, these findings inform the myeloid cell transcriptional changes associated with natural infection resistance mediated by pulmonary microbial exposures.},
}
MeSH Terms:
show MeSH Terms
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Animals
*Streptococcus pneumoniae/immunology
Mice
*Myeloid Cells/immunology
*Prevotella/immunology
Lung/microbiology/immunology
*Pneumonia, Pneumococcal/immunology/microbiology
Neutrophils/immunology
Macrophages/immunology
Mice, Inbred C57BL
Phagocytosis
RevDate: 2026-10-07
CmpDate: 2026-10-07
Exploring Blastocystis: hidden complexity in a common intestinal microbe.
Journal of medical microbiology, 75(10):.
Blastocystis is an anaerobic stramenopile that colonizes the large intestine of humans and many animals worldwide. Small-subunit rRNA-based typing reveals deep genetic diversity: at least 44 genetic variants, namely, subtypes (STs), are recognized, with ST1-ST4 accounting for most human carriage. Its medical relevance remains contested. Blastocystis carriage is frequently asymptomatic, and while associations with non-specific gastrointestinal symptoms (e.g. diarrhoea, abdominal pain and bloating), irritable bowel syndrome and extraintestinal manifestations such as urticaria have been proposed. In parallel, multiple microbiome studies, including a recent population-scale analysis, link Blastocystis carriage to higher bacterial diversity, healthier diets and favourable cardiometabolic profiles, suggesting that in many settings, it may be a marker of a resilient gut ecosystem rather than a primary pathogen. Transmission is primarily faecal-oral, most likely via environmentally resilient cysts, with potential for zoonotic and waterborne spread. Diagnosis using quantitative PCR is the most sensitive method; microscopy has limited sensitivity and can be confounded by morphological plasticity, though its diagnostic accuracy varies considerably according to the experience of the microscopist. Treatment is typically based on excluding alternative causes rather than confirmed causality; while metronidazole is commonly used, clinical outcomes are highly variable due to potential co-infections, inconsistent links between parasite eradication and symptom relief and reports of reduced drug susceptibility.
Additional Links: PMID-42842449
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@article {pmid42842449,
year = {2026},
author = {Guadano-Procesi, I and García Ramos, A and Gentekaki, E and Tsaousis, AD},
title = {Exploring Blastocystis: hidden complexity in a common intestinal microbe.},
journal = {Journal of medical microbiology},
volume = {75},
number = {10},
pages = {},
pmid = {42842449},
issn = {1473-5644},
mesh = {Humans ; *Blastocystis/genetics/classification/isolation & purification ; *Blastocystis Infections/parasitology/diagnosis/drug therapy/transmission ; Animals ; Genetic Variation ; *Gastrointestinal Microbiome ; Carrier State/parasitology ; },
abstract = {Blastocystis is an anaerobic stramenopile that colonizes the large intestine of humans and many animals worldwide. Small-subunit rRNA-based typing reveals deep genetic diversity: at least 44 genetic variants, namely, subtypes (STs), are recognized, with ST1-ST4 accounting for most human carriage. Its medical relevance remains contested. Blastocystis carriage is frequently asymptomatic, and while associations with non-specific gastrointestinal symptoms (e.g. diarrhoea, abdominal pain and bloating), irritable bowel syndrome and extraintestinal manifestations such as urticaria have been proposed. In parallel, multiple microbiome studies, including a recent population-scale analysis, link Blastocystis carriage to higher bacterial diversity, healthier diets and favourable cardiometabolic profiles, suggesting that in many settings, it may be a marker of a resilient gut ecosystem rather than a primary pathogen. Transmission is primarily faecal-oral, most likely via environmentally resilient cysts, with potential for zoonotic and waterborne spread. Diagnosis using quantitative PCR is the most sensitive method; microscopy has limited sensitivity and can be confounded by morphological plasticity, though its diagnostic accuracy varies considerably according to the experience of the microscopist. Treatment is typically based on excluding alternative causes rather than confirmed causality; while metronidazole is commonly used, clinical outcomes are highly variable due to potential co-infections, inconsistent links between parasite eradication and symptom relief and reports of reduced drug susceptibility.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Blastocystis/genetics/classification/isolation & purification
*Blastocystis Infections/parasitology/diagnosis/drug therapy/transmission
Animals
Genetic Variation
*Gastrointestinal Microbiome
Carrier State/parasitology
RevDate: 2026-10-07
CmpDate: 2026-10-07
Lower 24-hour urinary 6-sulfatoxymelatonin and exploratory bile-acid and microbiome associations in adults with dyslipidemia: a prospectively enrolled cross-sectional study.
Annals of medicine, 58(1):2743367.
BACKGROUND: We tested the primary hypothesis that lower continuous 24-hour urinary 6-sulfatoxymelatonin (6-SMT) is associated with an adverse lipid and inflammatory profile in adults with dyslipidemia. Associations with FGF19, bile-acid composition, and gut microbiome features were secondary and exploratory.
METHODS: This prospectively enrolled, single-center cross-sectional study included 577 consecutive adults evaluated at the Institute for Personalized Medicine, Tbilisi, Georgia, during 2020-2025. Each participant completed three non-consecutive 24-hour urine collections. Validity required a measured-to-predicted creatinine-excretion ratio of 0.80-1.20, and the participant-level 6-SMT value was the arithmetic mean of three valid collections. Fasting lipids, hs-CRP, FGF19, bile-acid profiles, and 16S rRNA taxonomic composition were assessed. An internal method-matched but unmatched normolipidemic reference comparator (n = 120) was used only for descriptive analyses.
RESULTS: Median 6-SMT was 8.4 μg/24 h (IQR 5.2-12.1). Lower 6-SMT was associated with higher LDL-C (Spearman ρ = -0.38; approximate 95% CI -0.45 to -0.31), triglycerides (ρ = -0.31; -0.38 to -0.23), and hs-CRP (ρ = -0.35; -0.42 to -0.28), and with lower HDL-C (ρ = 0.29; 0.21 to 0.36). FGF19 was above the stated fasting reference range in 489/577 participants (85%; median 312 pg/mL) and correlated inversely with 6-SMT (ρ=-0.42; -0.48 to -0.35). The emphasized microbial taxa correlated positively with 6-SMT. In a post hoc unadjusted statin-stratified sensitivity analysis, the mean difference in 6-SMT for statin users versus non-users was -0.30 μg/24 h (95% CI -0.83 to 0.23; p = 0.26). False-discovery-rate sensitivity analysis across the 14 reported reference-comparator microbiome tests retained q < 0.05 for each reported comparison; this does not resolve comparator confounding. The exploratory complete-case multivariable model had adjusted R[2]=0.40 but was not interpreted causally.
CONCLUSIONS: Lower 24-hour urinary 6-SMT clustered with adverse lipid and inflammatory measures and with exploratory enterohepatic and taxonomic microbiome features. The findings are hypothesis-generating and do not establish a coordinated biological axis, directionality, diagnostic utility, incremental predictive value, or treatment effect.
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Citation:
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@article {pmid42842454,
year = {2026},
author = {Tavartkiladze, A and Tavartkiladze, L and Reiter, RJ and Burnier, M and Ulukaya, E and Simonia, G and Kasradze, D and Nozadze, P and Revazishvili, P and Andronikashvili, I and Maisuradze, M},
title = {Lower 24-hour urinary 6-sulfatoxymelatonin and exploratory bile-acid and microbiome associations in adults with dyslipidemia: a prospectively enrolled cross-sectional study.},
journal = {Annals of medicine},
volume = {58},
number = {1},
pages = {2743367},
pmid = {42842454},
issn = {1365-2060},
mesh = {Humans ; Male ; Female ; Cross-Sectional Studies ; Prospective Studies ; Middle Aged ; *Dyslipidemias/urine/microbiology/blood ; *Melatonin/analogs & derivatives/urine ; Adult ; *Bile Acids and Salts/metabolism ; Fibroblast Growth Factors/blood ; *Gastrointestinal Microbiome/physiology ; Aged ; Biomarkers/urine ; },
abstract = {BACKGROUND: We tested the primary hypothesis that lower continuous 24-hour urinary 6-sulfatoxymelatonin (6-SMT) is associated with an adverse lipid and inflammatory profile in adults with dyslipidemia. Associations with FGF19, bile-acid composition, and gut microbiome features were secondary and exploratory.
METHODS: This prospectively enrolled, single-center cross-sectional study included 577 consecutive adults evaluated at the Institute for Personalized Medicine, Tbilisi, Georgia, during 2020-2025. Each participant completed three non-consecutive 24-hour urine collections. Validity required a measured-to-predicted creatinine-excretion ratio of 0.80-1.20, and the participant-level 6-SMT value was the arithmetic mean of three valid collections. Fasting lipids, hs-CRP, FGF19, bile-acid profiles, and 16S rRNA taxonomic composition were assessed. An internal method-matched but unmatched normolipidemic reference comparator (n = 120) was used only for descriptive analyses.
RESULTS: Median 6-SMT was 8.4 μg/24 h (IQR 5.2-12.1). Lower 6-SMT was associated with higher LDL-C (Spearman ρ = -0.38; approximate 95% CI -0.45 to -0.31), triglycerides (ρ = -0.31; -0.38 to -0.23), and hs-CRP (ρ = -0.35; -0.42 to -0.28), and with lower HDL-C (ρ = 0.29; 0.21 to 0.36). FGF19 was above the stated fasting reference range in 489/577 participants (85%; median 312 pg/mL) and correlated inversely with 6-SMT (ρ=-0.42; -0.48 to -0.35). The emphasized microbial taxa correlated positively with 6-SMT. In a post hoc unadjusted statin-stratified sensitivity analysis, the mean difference in 6-SMT for statin users versus non-users was -0.30 μg/24 h (95% CI -0.83 to 0.23; p = 0.26). False-discovery-rate sensitivity analysis across the 14 reported reference-comparator microbiome tests retained q < 0.05 for each reported comparison; this does not resolve comparator confounding. The exploratory complete-case multivariable model had adjusted R[2]=0.40 but was not interpreted causally.
CONCLUSIONS: Lower 24-hour urinary 6-SMT clustered with adverse lipid and inflammatory measures and with exploratory enterohepatic and taxonomic microbiome features. The findings are hypothesis-generating and do not establish a coordinated biological axis, directionality, diagnostic utility, incremental predictive value, or treatment effect.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Male
Female
Cross-Sectional Studies
Prospective Studies
Middle Aged
*Dyslipidemias/urine/microbiology/blood
*Melatonin/analogs & derivatives/urine
Adult
*Bile Acids and Salts/metabolism
Fibroblast Growth Factors/blood
*Gastrointestinal Microbiome/physiology
Aged
Biomarkers/urine
RevDate: 2026-10-07
A Narrative Review of Integrating Artificial Intelligence and Omics in Food Science and Nutrition: Current Uses, Issues, and Future Perspectives.
Nutrition reviews pii:8875930 [Epub ahead of print].
This narrative review examines how artificial intelligence (AI) and omics are being integrated in food science and nutrition, with particular attention to current applications, practical limitations, and challenges that are specific to foods and dietary exposure. Foods are complex, multicomponent matrices whose composition and biological effects can change during processing, cooking, storage, and consumption. Dietary exposure also varies over time and across individuals. These features make food and nutrition fundamentally more difficult to model than many domains in which AI has advanced rapidly. Relevant literature was identified through searches of PubMed, Google Scholar, and Web of Science. For studies applying AI to foods, reports published in 2023 or later were preferentially selected unless suitable recent studies were unavailable. Selected publications were independently evaluated by the authors and subsequently discussed. The integration of AI and omics approaches are being applied to data integration, feature selection, predictive modeling, network analysis, clustering, interpretation, flavor and taste design, discovery of bioactive ingredients, functional food development, and prediction of dietary responses involving metabolites and the gut microbiome. Across these applications, food- and nutrition-specific difficulties emerged repeatedly, including the partial observability of food composition, changes caused by processing and cooking, mismatches between short-term measurements and long-term health outcomes, nonlinear dose-response relationships, and inter-individual variation. These challenges add to general issues such as data quality, multi-omics integration, model interpretability, and external validation. The integration of AI and omics is expanding the capacity to analyze complex data in food science and nutrition, but reliable translation will require methods adapted to the dynamic and partly observable nature of foods and diets. Improved standardization, exposure assessment, validation, study design, and interpretability will be essential for future research and practical application.
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@article {pmid42842487,
year = {2026},
author = {Miyazawa, T and Toda, M and Hatakeyama, N and Sogame, R and Huang, CY and Yoshioka, T and Nakano, Y and Maejima, D and Ohta, S and Tsuda, T and Iimura, J and Ashida, K and Omae, Y and Ochi, H and Nakada, H and Kusama, K and Matsuda, T and Hattori, K and Aida, T and Sugimoto, K and Miyazawa, T},
title = {A Narrative Review of Integrating Artificial Intelligence and Omics in Food Science and Nutrition: Current Uses, Issues, and Future Perspectives.},
journal = {Nutrition reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/nutrit/nuag143},
pmid = {42842487},
issn = {1753-4887},
support = {//the Tohoku University Fund, Tohoku University, Sendai, Japan/ ; },
abstract = {This narrative review examines how artificial intelligence (AI) and omics are being integrated in food science and nutrition, with particular attention to current applications, practical limitations, and challenges that are specific to foods and dietary exposure. Foods are complex, multicomponent matrices whose composition and biological effects can change during processing, cooking, storage, and consumption. Dietary exposure also varies over time and across individuals. These features make food and nutrition fundamentally more difficult to model than many domains in which AI has advanced rapidly. Relevant literature was identified through searches of PubMed, Google Scholar, and Web of Science. For studies applying AI to foods, reports published in 2023 or later were preferentially selected unless suitable recent studies were unavailable. Selected publications were independently evaluated by the authors and subsequently discussed. The integration of AI and omics approaches are being applied to data integration, feature selection, predictive modeling, network analysis, clustering, interpretation, flavor and taste design, discovery of bioactive ingredients, functional food development, and prediction of dietary responses involving metabolites and the gut microbiome. Across these applications, food- and nutrition-specific difficulties emerged repeatedly, including the partial observability of food composition, changes caused by processing and cooking, mismatches between short-term measurements and long-term health outcomes, nonlinear dose-response relationships, and inter-individual variation. These challenges add to general issues such as data quality, multi-omics integration, model interpretability, and external validation. The integration of AI and omics is expanding the capacity to analyze complex data in food science and nutrition, but reliable translation will require methods adapted to the dynamic and partly observable nature of foods and diets. Improved standardization, exposure assessment, validation, study design, and interpretability will be essential for future research and practical application.},
}
RevDate: 2026-10-07
A joint mixture Tobit method with latent microbial abundance improves detection of microbiome-disease associations in zero-inflated data.
PLoS computational biology, 22(10):e1014844 pii:PCOMPBIOL-D-26-00012 [Epub ahead of print].
Zero inflation remains a major challenge in microbiome differential abundance analysis, often resulting in inflated type I error rates or reduced statistical power. Although numerous methods have been proposed to address excess zeros, many existing approaches do not explicitly distinguish between distinct zero-generating mechanisms, and censoring-based modeling perspectives remain relatively underexplored in microbiome data analysis. To advance methodological development in this area, we introduce a novel censoring-based modeling perspective for microbiome differential abundance analysis. Specifically, we develop a joint mixture Tobit (joint mTobit) method for zero-inflated microbiome data. Building on a mixture Tobit formulation, the model incorporates a point-mass component to represent structural zeros, while modeling latent microbial abundance via a Tobit regression component. The proposed framework jointly links disease status, latent true microbial abundance, and relevant covariates within a unified probabilistic model, allowing appropriate adjustment for confounding factors and facilitating more reliable statistical inference. By explicitly modeling the latent abundance underlying observed counts, the joint mTobit method improves estimation stability and enhances detection power under zero inflation. Extensive simulation studies demonstrate that the joint mTobit method achieves effective type I error control while maintaining high statistical power and stable coefficient estimation across a wide range of settings. Application to a real-world colorectal cancer and adenoma microbiome dataset further illustrates its ability to identify biologically meaningful differentially abundant taxa. Overall, this work develops a joint mTobit modeling framework for zero-inflated microbiome data, enabling inference on latent microbial abundance and providing a censoring-based statistical framework for investigating disease-microbiome associations in differential abundance analysis.
Additional Links: PMID-42842625
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@article {pmid42842625,
year = {2026},
author = {Deng, J and Chen, D and Shen, S and Zhou, Y and Cui, H and Qiu, Y and Li, Q and Hu, YQ},
title = {A joint mixture Tobit method with latent microbial abundance improves detection of microbiome-disease associations in zero-inflated data.},
journal = {PLoS computational biology},
volume = {22},
number = {10},
pages = {e1014844},
doi = {10.1371/journal.pcbi.1014844},
pmid = {42842625},
issn = {1553-7358},
abstract = {Zero inflation remains a major challenge in microbiome differential abundance analysis, often resulting in inflated type I error rates or reduced statistical power. Although numerous methods have been proposed to address excess zeros, many existing approaches do not explicitly distinguish between distinct zero-generating mechanisms, and censoring-based modeling perspectives remain relatively underexplored in microbiome data analysis. To advance methodological development in this area, we introduce a novel censoring-based modeling perspective for microbiome differential abundance analysis. Specifically, we develop a joint mixture Tobit (joint mTobit) method for zero-inflated microbiome data. Building on a mixture Tobit formulation, the model incorporates a point-mass component to represent structural zeros, while modeling latent microbial abundance via a Tobit regression component. The proposed framework jointly links disease status, latent true microbial abundance, and relevant covariates within a unified probabilistic model, allowing appropriate adjustment for confounding factors and facilitating more reliable statistical inference. By explicitly modeling the latent abundance underlying observed counts, the joint mTobit method improves estimation stability and enhances detection power under zero inflation. Extensive simulation studies demonstrate that the joint mTobit method achieves effective type I error control while maintaining high statistical power and stable coefficient estimation across a wide range of settings. Application to a real-world colorectal cancer and adenoma microbiome dataset further illustrates its ability to identify biologically meaningful differentially abundant taxa. Overall, this work develops a joint mTobit modeling framework for zero-inflated microbiome data, enabling inference on latent microbial abundance and providing a censoring-based statistical framework for investigating disease-microbiome associations in differential abundance analysis.},
}
RevDate: 2026-10-07
Recurrence is not the same as robustness: Refining reproducibility in the multiple sclerosis gut microbiome.
Multiple sclerosis and related disorders, 115:107964 pii:S2211-0348(26)00999-5 [Epub ahead of print].
Additional Links: PMID-42843190
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@article {pmid42843190,
year = {2026},
author = {Chan, CWK},
title = {Recurrence is not the same as robustness: Refining reproducibility in the multiple sclerosis gut microbiome.},
journal = {Multiple sclerosis and related disorders},
volume = {115},
number = {},
pages = {107964},
doi = {10.1016/j.msard.2026.107964},
pmid = {42843190},
issn = {2211-0356},
}
RevDate: 2026-10-07
From boron symbiotaxis to symbiogenic nutrients: extending the concept of ecological essentiality.
Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS), 98:127974 pii:S0946-672X(26)00160-4 [Epub ahead of print].
Nutritional science has traditionally interpreted the biological functions of nutrients according to their metabolic roles within the host organism. Microbiome-oriented concepts, including prebiotics, probiotics, synbiotics, and postbiotics, have substantially expanded this perspective by recognizing the biological importance of microbial communities. However, existing nutritional classifications remain largely centered on either the host or the microbiota, without explicitly considering the functional organization emerging from their continuous interaction. In this review, we propose the concept of symbiogenic nutrients (SNs) as a complementary functional classification of nutrients defined according to their demonstrated capacity to preserve, restore, or enhance host-microbiome functional organization (HMFO). Building upon the concepts of ecological essentiality and boron (B) symbiotaxis, we introduce a systems-oriented framework in which nutritional function is interpreted not only through direct metabolic activities or microbial modulation but also through preservation of the structural, communicative, ecological, and metabolic processes that collectively sustain functional symbiosis. To facilitate operational implementation, we propose explicit principles and criteria for the classification of SNs and illustrate their application using B as the first experimentally supported prototype. Current evidence indicates that B contributes to biological interface integrity, microbial communication, ecological regulation, and host metabolic integration, thereby fulfilling the proposed operational framework. The concept is further extended from individual SNs to symbiogenic compositions, interface-active compositions, and symbiogenic nutrition, as a systems-oriented nutritional strategy aimed at preserving HMFO. This framework provides new perspectives for healthy longevity, metabolic health, chronic inflammation, and precision nutrition, establishing a conceptual foundation for future interface-targeted nutritional interventions.
Additional Links: PMID-42843232
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@article {pmid42843232,
year = {2026},
author = {Biţă, A and Scorei, IR and Mogoşanu, GD and Gheonea, DI},
title = {From boron symbiotaxis to symbiogenic nutrients: extending the concept of ecological essentiality.},
journal = {Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)},
volume = {98},
number = {},
pages = {127974},
doi = {10.1016/j.jtemb.2026.127974},
pmid = {42843232},
issn = {1878-3252},
abstract = {Nutritional science has traditionally interpreted the biological functions of nutrients according to their metabolic roles within the host organism. Microbiome-oriented concepts, including prebiotics, probiotics, synbiotics, and postbiotics, have substantially expanded this perspective by recognizing the biological importance of microbial communities. However, existing nutritional classifications remain largely centered on either the host or the microbiota, without explicitly considering the functional organization emerging from their continuous interaction. In this review, we propose the concept of symbiogenic nutrients (SNs) as a complementary functional classification of nutrients defined according to their demonstrated capacity to preserve, restore, or enhance host-microbiome functional organization (HMFO). Building upon the concepts of ecological essentiality and boron (B) symbiotaxis, we introduce a systems-oriented framework in which nutritional function is interpreted not only through direct metabolic activities or microbial modulation but also through preservation of the structural, communicative, ecological, and metabolic processes that collectively sustain functional symbiosis. To facilitate operational implementation, we propose explicit principles and criteria for the classification of SNs and illustrate their application using B as the first experimentally supported prototype. Current evidence indicates that B contributes to biological interface integrity, microbial communication, ecological regulation, and host metabolic integration, thereby fulfilling the proposed operational framework. The concept is further extended from individual SNs to symbiogenic compositions, interface-active compositions, and symbiogenic nutrition, as a systems-oriented nutritional strategy aimed at preserving HMFO. This framework provides new perspectives for healthy longevity, metabolic health, chronic inflammation, and precision nutrition, establishing a conceptual foundation for future interface-targeted nutritional interventions.},
}
RevDate: 2026-10-07
Prediction of age using shotgun metagenomic sequencing and random forest algorithm based on cadaveric colon.
Forensic science international, 390:113154 pii:S0379-0738(26)00342-7 [Epub ahead of print].
Age estimation is important for the identification of unknown cadavers in forensic practice. Previous studies have shown that gut microbiota is associated with host age, but most evidence has been derived from fecal samples of living individuals. In this study, shotgun metagenomic sequencing was performed on mid-colon tissue samples from 76 cadavers to explore age-associated taxonomic and predicted functional patterns in cadaveric colon microbiota and to evaluate their potential value for forensic age estimation. After quality control and taxonomic annotation, 3980 microbial species were identified. Descriptive differences among age groups were observed in microbial composition, alpha diversity, species-enrichment patterns, co-occurrence network structure, and KEGG functional profiles; however, a multivariable PERMANOVA did not detect a statistically significant association between age group and overall species-level community composition after accounting for postmortem sampling interval, cause-of-death category, and sex. The complete random forest pipeline was re-evaluated using repeated nested five-fold cross-validation, with all data-dependent filtering, transformation, feature selection, and hyperparameter tuning restricted to the outer training data. The resulting out-of-fold performance was limited (R[2] = 0.005, MAE = 13.686 years, and RMSE = 17.741 years), and predictions showed regression toward the cohort mean. Overall, this study provides preliminary evidence that cadaveric colon microbiota contains age-associated microbial signals, but these findings should be interpreted as exploratory. Larger cohorts and independent external validation are needed before microbiome-based age prediction can be applied in forensic practice.
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@article {pmid42843234,
year = {2026},
author = {Su, K and Wu, D and Xia, Y and Tian, S and Li, C and Ji, J and Guo, Y and Zhao, X and Huang, J and Hu, S and Ye, J},
title = {Prediction of age using shotgun metagenomic sequencing and random forest algorithm based on cadaveric colon.},
journal = {Forensic science international},
volume = {390},
number = {},
pages = {113154},
doi = {10.1016/j.forsciint.2026.113154},
pmid = {42843234},
issn = {1872-6283},
abstract = {Age estimation is important for the identification of unknown cadavers in forensic practice. Previous studies have shown that gut microbiota is associated with host age, but most evidence has been derived from fecal samples of living individuals. In this study, shotgun metagenomic sequencing was performed on mid-colon tissue samples from 76 cadavers to explore age-associated taxonomic and predicted functional patterns in cadaveric colon microbiota and to evaluate their potential value for forensic age estimation. After quality control and taxonomic annotation, 3980 microbial species were identified. Descriptive differences among age groups were observed in microbial composition, alpha diversity, species-enrichment patterns, co-occurrence network structure, and KEGG functional profiles; however, a multivariable PERMANOVA did not detect a statistically significant association between age group and overall species-level community composition after accounting for postmortem sampling interval, cause-of-death category, and sex. The complete random forest pipeline was re-evaluated using repeated nested five-fold cross-validation, with all data-dependent filtering, transformation, feature selection, and hyperparameter tuning restricted to the outer training data. The resulting out-of-fold performance was limited (R[2] = 0.005, MAE = 13.686 years, and RMSE = 17.741 years), and predictions showed regression toward the cohort mean. Overall, this study provides preliminary evidence that cadaveric colon microbiota contains age-associated microbial signals, but these findings should be interpreted as exploratory. Larger cohorts and independent external validation are needed before microbiome-based age prediction can be applied in forensic practice.},
}
RevDate: 2026-10-07
Biogenic maturation of mineral-encrusted plastispheres overrides ecological drift to orchestrate multi-kingdom assembly and nitrogen reprogramming in agroecosystems.
Journal of hazardous materials, 517:143809 pii:S0304-3894(26)02790-1 [Epub ahead of print].
The quantitative assembly rules and multi-kingdom functional gateways of the soil plastisphere remain poorly resolved. We integrated multi-omics with high-resolution surface deconvolution to decode the ecological signatures of weathered polyethylene (PE) films in intensive agroecosystems. Surface characterization revealed an interfacial metamorphosis where biogenic maturation facilitated the formation of a dense mineral organic crust, transforming inert polymers into reactive metabolic islands. Ecological modeling identifies a distinct departure from neutral assembly, demonstrating that niche-based selection driven by polymer surface remodeling overrides ecological drift in shaping microbial consortia. Machine learning and structural equation modeling identify ammonia oxidizing archaea as the primary functional keystone taxa orchestrating the global interactome. This archaeal-bacterial axis, regulated by protistan assemblages that exhibit significant topological densification, catalyzes a cross-kingdom metabolic relay synchronized with nitrogenous biomarker accumulation and intensified enzymatic mineralization. Functional decoupling across taxonomic domains reveals a metabolic lag where rapid deterministic recruitment outpaces steady-state nutrient stabilization. While promoting local alpha-diversity, the bacterial core exhibits structural fragmentation and elevated antagonistic interactions, signaling an asynchronous regime shift that may trigger positive priming effects on native soil organic carbon. These findings establish a mechanistic blueprint for how weathered PE residues redirect terrestrial nutrient fluxes via deterministic multi-kingdom assembly, pinpointing specific organo-mineral signatures and archaeal keystone taxa as critical targets for precision microbiome engineering in the Anthropocene.
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@article {pmid42843243,
year = {2026},
author = {Pu, G and Han, Q and Liu, Y and Zheng, M and Shang, J and Shao, J and Yun, K and Yan, J and Guo, Z},
title = {Biogenic maturation of mineral-encrusted plastispheres overrides ecological drift to orchestrate multi-kingdom assembly and nitrogen reprogramming in agroecosystems.},
journal = {Journal of hazardous materials},
volume = {517},
number = {},
pages = {143809},
doi = {10.1016/j.jhazmat.2026.143809},
pmid = {42843243},
issn = {1873-3336},
abstract = {The quantitative assembly rules and multi-kingdom functional gateways of the soil plastisphere remain poorly resolved. We integrated multi-omics with high-resolution surface deconvolution to decode the ecological signatures of weathered polyethylene (PE) films in intensive agroecosystems. Surface characterization revealed an interfacial metamorphosis where biogenic maturation facilitated the formation of a dense mineral organic crust, transforming inert polymers into reactive metabolic islands. Ecological modeling identifies a distinct departure from neutral assembly, demonstrating that niche-based selection driven by polymer surface remodeling overrides ecological drift in shaping microbial consortia. Machine learning and structural equation modeling identify ammonia oxidizing archaea as the primary functional keystone taxa orchestrating the global interactome. This archaeal-bacterial axis, regulated by protistan assemblages that exhibit significant topological densification, catalyzes a cross-kingdom metabolic relay synchronized with nitrogenous biomarker accumulation and intensified enzymatic mineralization. Functional decoupling across taxonomic domains reveals a metabolic lag where rapid deterministic recruitment outpaces steady-state nutrient stabilization. While promoting local alpha-diversity, the bacterial core exhibits structural fragmentation and elevated antagonistic interactions, signaling an asynchronous regime shift that may trigger positive priming effects on native soil organic carbon. These findings establish a mechanistic blueprint for how weathered PE residues redirect terrestrial nutrient fluxes via deterministic multi-kingdom assembly, pinpointing specific organo-mineral signatures and archaeal keystone taxa as critical targets for precision microbiome engineering in the Anthropocene.},
}
RevDate: 2026-10-07
Oral microbial nitrate metabolism is associated with lower prevalence of prediabetes.
Cell reports. Medicine pii:S2666-3791(26)00509-4 [Epub ahead of print].
The oral microbiome is a key microbial interface for dietary or oral nitrate metabolism, yet its role in early glycemic dysregulation remains poorly defined. In a population-based cohort (n = 472), we perform metagenomic profiling of tongue dorsum microbiomes and identify 11 taxa and nine microbial pathways associated with prediabetes. Among these, Rothia mucilaginosa and microbial nitrate reduction emerge as the only taxon and the strongest pathway associated with lower prediabetes prevalence. Individuals without prediabetes show higher salivary nitrate and nitrite concentrations, supporting enhanced oral nitrate bioavailability. Functional characterization of an isolated Rothia mucilaginosa strain demonstrates its capacity to mediate both nitrate-nitrite-NO and nitrate-nitrite-NH4[+] pathways under oxygen-limited conditions. Incorporating nitrate metabolism-associated microbial features into clinical risk factors improves risk stratification for progression to prediabetes. These findings support oral nitrate metabolism as a microbial pathway linking oral ecology to systemic metabolic health and suggest that tongue cleaning may modulate microbial functions involved in this pathway.
Additional Links: PMID-42843345
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@article {pmid42843345,
year = {2026},
author = {Zhao, S and Haryono, MAS and Lai, CWM and Seah, F and Tang, YL and Lim, M and Febriana, E and Lee, MH and Tan, KS and Fu, JH and Yip, JK and Preshaw, PM and Williams, RBH and Toh, SA and Lee, JWJ and Goh, CE},
title = {Oral microbial nitrate metabolism is associated with lower prevalence of prediabetes.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {103092},
doi = {10.1016/j.xcrm.2026.103092},
pmid = {42843345},
issn = {2666-3791},
abstract = {The oral microbiome is a key microbial interface for dietary or oral nitrate metabolism, yet its role in early glycemic dysregulation remains poorly defined. In a population-based cohort (n = 472), we perform metagenomic profiling of tongue dorsum microbiomes and identify 11 taxa and nine microbial pathways associated with prediabetes. Among these, Rothia mucilaginosa and microbial nitrate reduction emerge as the only taxon and the strongest pathway associated with lower prediabetes prevalence. Individuals without prediabetes show higher salivary nitrate and nitrite concentrations, supporting enhanced oral nitrate bioavailability. Functional characterization of an isolated Rothia mucilaginosa strain demonstrates its capacity to mediate both nitrate-nitrite-NO and nitrate-nitrite-NH4[+] pathways under oxygen-limited conditions. Incorporating nitrate metabolism-associated microbial features into clinical risk factors improves risk stratification for progression to prediabetes. These findings support oral nitrate metabolism as a microbial pathway linking oral ecology to systemic metabolic health and suggest that tongue cleaning may modulate microbial functions involved in this pathway.},
}
RevDate: 2026-10-07
CmpDate: 2026-10-07
Fecal Microbiota Transplantation Beyond Clostridioides difficile Infection: Expanding Indications, Mechanisms, and Future Directions.
Journal of Korean medical science, 41(38):e335.
Fecal microbiota transplantation (FMT) has emerged as a transformative therapeutic approach to restore gut microbial homeostasis. The most established indication is recurrent Clostridioides difficile infection (CDI), demonstrating that restoring ecosystem-level microbiota has substantial clinical benefits. Building on this success, FMT is now being investigated across a broader range of indications associated with gut dysbiosis and altered microbiome-host signaling, including inflammatory bowel disease, irritable bowel syndrome, metabolic, and neurological disorders. Mechanistic insights into the gut-organ axes provide biological plausibility for this expansion; gut dysbiosis can function as a modifiable upstream driver of host metabolism, immune-neural signaling, and barrier function. However, the clinical benefits beyond CDI remain heterogeneous and often modest, highlighting the need for further research on patient stratification, standardized protocols, and mechanistic biomarkers. Furthermore, regulatory frameworks remain heterogeneous worldwide, and recent approvals of standardized microbiota-based products for recurrent CDI represent a transition toward treating microbiome therapeutics as regulated biologics. This review synthesizes the mechanistic rationale and current evidence for FMT beyond CDI and outlines future directions for personalized and next-generation microbiome therapeutics.
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@article {pmid42843354,
year = {2026},
author = {Hasanuzzaman, M and Bang, CS and Lee, JJ and Gong, EJ},
title = {Fecal Microbiota Transplantation Beyond Clostridioides difficile Infection: Expanding Indications, Mechanisms, and Future Directions.},
journal = {Journal of Korean medical science},
volume = {41},
number = {38},
pages = {e335},
pmid = {42843354},
issn = {1598-6357},
support = {RS-2023-00223501/NRF/National Research Foundation of Korea/Korea ; /Hallym/Hallym University/Korea ; },
mesh = {*Fecal Microbiota Transplantation ; Humans ; *Clostridium Infections/therapy/microbiology ; Inflammatory Bowel Diseases/therapy ; Clostridioides difficile ; Irritable Bowel Syndrome/therapy ; Dysbiosis/therapy ; Gastrointestinal Microbiome ; Nervous System Diseases/therapy ; Metabolic Diseases/therapy ; Animals ; },
abstract = {Fecal microbiota transplantation (FMT) has emerged as a transformative therapeutic approach to restore gut microbial homeostasis. The most established indication is recurrent Clostridioides difficile infection (CDI), demonstrating that restoring ecosystem-level microbiota has substantial clinical benefits. Building on this success, FMT is now being investigated across a broader range of indications associated with gut dysbiosis and altered microbiome-host signaling, including inflammatory bowel disease, irritable bowel syndrome, metabolic, and neurological disorders. Mechanistic insights into the gut-organ axes provide biological plausibility for this expansion; gut dysbiosis can function as a modifiable upstream driver of host metabolism, immune-neural signaling, and barrier function. However, the clinical benefits beyond CDI remain heterogeneous and often modest, highlighting the need for further research on patient stratification, standardized protocols, and mechanistic biomarkers. Furthermore, regulatory frameworks remain heterogeneous worldwide, and recent approvals of standardized microbiota-based products for recurrent CDI represent a transition toward treating microbiome therapeutics as regulated biologics. This review synthesizes the mechanistic rationale and current evidence for FMT beyond CDI and outlines future directions for personalized and next-generation microbiome therapeutics.},
}
MeSH Terms:
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*Fecal Microbiota Transplantation
Humans
*Clostridium Infections/therapy/microbiology
Inflammatory Bowel Diseases/therapy
Clostridioides difficile
Irritable Bowel Syndrome/therapy
Dysbiosis/therapy
Gastrointestinal Microbiome
Nervous System Diseases/therapy
Metabolic Diseases/therapy
Animals
RevDate: 2026-10-07
Nanoparticle-based senolytic and senomorphic therapies for healthy aging: design principles, translational evidence, and challenges.
Ageing research reviews pii:S1568-1637(26)00390-9 [Epub ahead of print].
Cellular senescence contributes to age-associated tissue dysfunction through persistent growth arrest, metabolic remodeling, and altered communication with immune and stromal cells. Senolytic therapies preferentially eliminate susceptible senescent cells, while senomorphic therapies modulate harmful senescence-associated activities. Nanoparticle engineering can improve the delivery of these agents through cargo protection, surface functionalization, and controlled release. Surface ligands can promote cellular uptake, and components responsive to lysosomal β-galactosidase, acidic pH, reactive oxygen species, or protease activity can regulate cargo release. The selectivity of these mechanisms depends on biological features that vary among senescent populations and also occur in other cellular states. This review examines how material composition and physicochemical properties influence target recognition, intracellular transport, therapeutic activity, and safety. Representative platforms are evaluated across fibrotic, musculoskeletal, metabolic, oncologic, and neurodegenerative disease models, with particular attention to mitochondrial delivery, immune-mediated clearance, nucleic-acid modulation, and microbiome interactions. Preclinical findings are considered alongside human senotherapy studies, which have primarily evaluated small-molecule drug regimens and yielded preliminary or mixed outcomes. Clinical development requires reproducible manufacturing, pharmacokinetic characterization of both carrier and cargo, and assessment of immunotoxicity and delayed organ injury in older hosts. Progress depends on matching a defined pathological cell population to an appropriate delivery strategy and demonstrating an advantage in therapeutic index or sustained functional outcomes against relevant comparators, including clinically feasible non-nanoparticle treatments where available.
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@article {pmid42843466,
year = {2026},
author = {Huang, J and Ji, L and Jin, H and Shi, Z and Song, X and Cai, Y and Tong, X},
title = {Nanoparticle-based senolytic and senomorphic therapies for healthy aging: design principles, translational evidence, and challenges.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {103398},
doi = {10.1016/j.arr.2026.103398},
pmid = {42843466},
issn = {1872-9649},
abstract = {Cellular senescence contributes to age-associated tissue dysfunction through persistent growth arrest, metabolic remodeling, and altered communication with immune and stromal cells. Senolytic therapies preferentially eliminate susceptible senescent cells, while senomorphic therapies modulate harmful senescence-associated activities. Nanoparticle engineering can improve the delivery of these agents through cargo protection, surface functionalization, and controlled release. Surface ligands can promote cellular uptake, and components responsive to lysosomal β-galactosidase, acidic pH, reactive oxygen species, or protease activity can regulate cargo release. The selectivity of these mechanisms depends on biological features that vary among senescent populations and also occur in other cellular states. This review examines how material composition and physicochemical properties influence target recognition, intracellular transport, therapeutic activity, and safety. Representative platforms are evaluated across fibrotic, musculoskeletal, metabolic, oncologic, and neurodegenerative disease models, with particular attention to mitochondrial delivery, immune-mediated clearance, nucleic-acid modulation, and microbiome interactions. Preclinical findings are considered alongside human senotherapy studies, which have primarily evaluated small-molecule drug regimens and yielded preliminary or mixed outcomes. Clinical development requires reproducible manufacturing, pharmacokinetic characterization of both carrier and cargo, and assessment of immunotoxicity and delayed organ injury in older hosts. Progress depends on matching a defined pathological cell population to an appropriate delivery strategy and demonstrating an advantage in therapeutic index or sustained functional outcomes against relevant comparators, including clinically feasible non-nanoparticle treatments where available.},
}
RevDate: 2026-10-08
Glycosylation in colorectal cancer: From tumor-intrinsic signaling to the host-microbiome glyco-interface.
Biochimica et biophysica acta. Reviews on cancer, 1881(6):189735 pii:S0304-419X(26)00207-6 [Epub ahead of print].
Aberrant glycosylation is increasingly recognized as a key regulatory layer in colorectal cancer (CRC), extending beyond tumor-cell-intrinsic signaling to shape the tumor microenvironment and host-microbiome interactions. In the immune compartment, glycosylation modulates the stability and activity of classical checkpoints, including PD-L1, while tumor-associated glycans engage MGL, DC-SIGN, Siglecs, and galectins to form glyco-immune checkpoints that influence T-cell dysfunction, macrophage polarization, dendritic-cell tolerance, and NK-cell activity. These mechanisms support emerging glyco-immunotherapeutic strategies such as targeted desialylation, glycoform-specific targeting, and combination with immune checkpoint blockade. Glycosylation also functions as a molecular language at the host-microbiome interface. Site-specific epithelial glycoproteins, mucin O-glycoforms, bidirectional host-bacterial fucosylation, IgA-associated glycan recognition, and microbial glycan utilization may collectively shape CRC-associated dysbiosis and mucosal inflammation. Integrating stool glycoproteomics with microbiome profiling may further enable noninvasive screening and patient stratification. This review highlights glycosylation as a multidimensional interface linking tumor biology, antitumor immunity, and microbiome ecology, with implications for biomarker development and precision therapy in CRC.
Additional Links: PMID-42843574
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@article {pmid42843574,
year = {2026},
author = {Wen, Y and Sun, H and Xiong, N and Xu, X and Ye, Y and Shen, Z and Wang, C},
title = {Glycosylation in colorectal cancer: From tumor-intrinsic signaling to the host-microbiome glyco-interface.},
journal = {Biochimica et biophysica acta. Reviews on cancer},
volume = {1881},
number = {6},
pages = {189735},
doi = {10.1016/j.bbcan.2026.189735},
pmid = {42843574},
issn = {1879-2561},
abstract = {Aberrant glycosylation is increasingly recognized as a key regulatory layer in colorectal cancer (CRC), extending beyond tumor-cell-intrinsic signaling to shape the tumor microenvironment and host-microbiome interactions. In the immune compartment, glycosylation modulates the stability and activity of classical checkpoints, including PD-L1, while tumor-associated glycans engage MGL, DC-SIGN, Siglecs, and galectins to form glyco-immune checkpoints that influence T-cell dysfunction, macrophage polarization, dendritic-cell tolerance, and NK-cell activity. These mechanisms support emerging glyco-immunotherapeutic strategies such as targeted desialylation, glycoform-specific targeting, and combination with immune checkpoint blockade. Glycosylation also functions as a molecular language at the host-microbiome interface. Site-specific epithelial glycoproteins, mucin O-glycoforms, bidirectional host-bacterial fucosylation, IgA-associated glycan recognition, and microbial glycan utilization may collectively shape CRC-associated dysbiosis and mucosal inflammation. Integrating stool glycoproteomics with microbiome profiling may further enable noninvasive screening and patient stratification. This review highlights glycosylation as a multidimensional interface linking tumor biology, antitumor immunity, and microbiome ecology, with implications for biomarker development and precision therapy in CRC.},
}
RevDate: 2026-10-07
The Immunomodulatory Landscape of Anesthetic Agents: Mechanisms, Clinical Implications, and Therapeutic Potential.
European journal of pharmacology pii:S0014-2999(26)00883-6 [Epub ahead of print].
The pharmacological actions of anesthetic agents extend far beyond neurodepression, encompassing complex immunomodulatory effects with implications for perioperative immune function, surgical outcomes, infection risk, and cancer biology. This review critically evaluates current evidence on how different anesthetic classes influence innate and adaptive immunity, examining cellular targets and signaling mechanisms. Rather than viewing anesthesia as monolithically immunosuppressive, current evidence supports a nuanced understanding in which immunological effects vary according to anesthetic agent, dose, timing, and clinical context. Volatile anesthetics (isoflurane, sevoflurane) attenuate natural killer cell cytotoxicity and neutrophil function, promote lymphocyte apoptosis with T helper 2 cell skewing, and exhibit context-dependent anti-inflammatory properties. Propofol preserves immune function by attenuating ROS-mediated cellular damage and maintaining Th1/Th2 balance. Ketamine exerts concentration-dependent immunomodulatory effects including anti-inflammatory actions on macrophages and biphasic lymphocyte modulation. We discuss clinical implications in oncological surgery, sepsis, and autoimmune disorders, emphasizing strengths and limitations of current evidence. Emerging frontiers include personalized anesthesia guided by immune phenotyping, novel targeted agents, and the gut microbiome as a modulator of anesthetic-immune interactions, though these remain promising directions rather than established practice. This review integrates mechanistic insights with clinical evidence and identifies priorities for translational research.
Additional Links: PMID-42843699
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PubMed:
Citation:
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@article {pmid42843699,
year = {2026},
author = {Ye, J and Deng, M and Liao, Y and Li, J and Jia, X and Li, C and Wu, K},
title = {The Immunomodulatory Landscape of Anesthetic Agents: Mechanisms, Clinical Implications, and Therapeutic Potential.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {179401},
doi = {10.1016/j.ejphar.2026.179401},
pmid = {42843699},
issn = {1879-0712},
abstract = {The pharmacological actions of anesthetic agents extend far beyond neurodepression, encompassing complex immunomodulatory effects with implications for perioperative immune function, surgical outcomes, infection risk, and cancer biology. This review critically evaluates current evidence on how different anesthetic classes influence innate and adaptive immunity, examining cellular targets and signaling mechanisms. Rather than viewing anesthesia as monolithically immunosuppressive, current evidence supports a nuanced understanding in which immunological effects vary according to anesthetic agent, dose, timing, and clinical context. Volatile anesthetics (isoflurane, sevoflurane) attenuate natural killer cell cytotoxicity and neutrophil function, promote lymphocyte apoptosis with T helper 2 cell skewing, and exhibit context-dependent anti-inflammatory properties. Propofol preserves immune function by attenuating ROS-mediated cellular damage and maintaining Th1/Th2 balance. Ketamine exerts concentration-dependent immunomodulatory effects including anti-inflammatory actions on macrophages and biphasic lymphocyte modulation. We discuss clinical implications in oncological surgery, sepsis, and autoimmune disorders, emphasizing strengths and limitations of current evidence. Emerging frontiers include personalized anesthesia guided by immune phenotyping, novel targeted agents, and the gut microbiome as a modulator of anesthetic-immune interactions, though these remain promising directions rather than established practice. This review integrates mechanistic insights with clinical evidence and identifies priorities for translational research.},
}
RevDate: 2026-10-07
Microbial Metabolic Messengers from Fermented Foods: Multi-Organ Regulation of Energy Homeostasis and Obesity.
Nutrition reviews pii:8876170 [Epub ahead of print].
Mechanistic evidence was systematically reviewed on how major metabolites produced during fermentation of foods modulate obesity through gut microbiota remodeling and multiorgan metabolic regulation, with emphasis on the gut-brain axis, immunometabolic pathways, and epigenetic mechanisms. Obesity remains a major global public health challenge, and conventional management strategies are frequently limited by poor long-term efficacy, low adherence, and undesirable side effects. Increasing evidence positions the gut microbiome as a central metabolic organ that profoundly influences host energy homeostasis and adiposity. Individuals with obesity commonly have a disrupted intestinal microbial ecosystem characterized by reduced microbial diversity, depletion of health-promoting taxa, and enrichment of facultative pathogens, which compromise intestinal barrier function, promote chronic low-grade inflammation, and disturb systemic metabolic regulation. Fermented foods, integral to traditional diets, provide a rich source of live microorganisms and a diverse repertoire of bioactive metabolites produced through fermentation. A narrative review was conducted by synthesizing evidence from experimental, mechanistic, and preclinical studies on fermented foods, gut microbial ecology, fermentation-derived metabolites, and obesity-related metabolic pathways. Current evidence indicates that the anti-obesity effects of fermented foods are mediated not only by transient microbial colonization but, more importantly, by fermentation-derived metabolites such as short-chain fatty acids, conjugated linoleic acid, and indole derivatives (eg, indole-3-propionic acid). These metabolites exert multiorgan physiological effects through the gut-brain axis, immunometabolic pathways, and epigenetic regulation. Collectively, they modulate key processes, including enteroendocrine hormone secretion, hepatic glucose and lipid metabolism, browning of white adipose tissue, and central appetite control, ultimately contributing to metabolic restoration. This review provides a systematic and mechanistic evaluation of how major fermentation-derived metabolites counteract obesity by reshaping gut microbiota composition and functional activity across interconnected organ systems. The insights provide a strengthened conceptual framework for designing microbiota-directed nutritional strategies to sustain body-weight regulation.
Additional Links: PMID-42843892
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PubMed:
Citation:
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@article {pmid42843892,
year = {2026},
author = {Hu, B and Liu, Y and Zhang, X and Manickam, S},
title = {Microbial Metabolic Messengers from Fermented Foods: Multi-Organ Regulation of Energy Homeostasis and Obesity.},
journal = {Nutrition reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/nutrit/nuag146},
pmid = {42843892},
issn = {1753-4887},
support = {2025S075//Ningbo Public Welfare Research/ ; Y202557618//General Scientific Research Project of Zhejiang Provincial Department of Education/ ; UTB/GSR/2/2025 (5)//Universiti Teknologi Brunei (UTB)/ ; },
abstract = {Mechanistic evidence was systematically reviewed on how major metabolites produced during fermentation of foods modulate obesity through gut microbiota remodeling and multiorgan metabolic regulation, with emphasis on the gut-brain axis, immunometabolic pathways, and epigenetic mechanisms. Obesity remains a major global public health challenge, and conventional management strategies are frequently limited by poor long-term efficacy, low adherence, and undesirable side effects. Increasing evidence positions the gut microbiome as a central metabolic organ that profoundly influences host energy homeostasis and adiposity. Individuals with obesity commonly have a disrupted intestinal microbial ecosystem characterized by reduced microbial diversity, depletion of health-promoting taxa, and enrichment of facultative pathogens, which compromise intestinal barrier function, promote chronic low-grade inflammation, and disturb systemic metabolic regulation. Fermented foods, integral to traditional diets, provide a rich source of live microorganisms and a diverse repertoire of bioactive metabolites produced through fermentation. A narrative review was conducted by synthesizing evidence from experimental, mechanistic, and preclinical studies on fermented foods, gut microbial ecology, fermentation-derived metabolites, and obesity-related metabolic pathways. Current evidence indicates that the anti-obesity effects of fermented foods are mediated not only by transient microbial colonization but, more importantly, by fermentation-derived metabolites such as short-chain fatty acids, conjugated linoleic acid, and indole derivatives (eg, indole-3-propionic acid). These metabolites exert multiorgan physiological effects through the gut-brain axis, immunometabolic pathways, and epigenetic regulation. Collectively, they modulate key processes, including enteroendocrine hormone secretion, hepatic glucose and lipid metabolism, browning of white adipose tissue, and central appetite control, ultimately contributing to metabolic restoration. This review provides a systematic and mechanistic evaluation of how major fermentation-derived metabolites counteract obesity by reshaping gut microbiota composition and functional activity across interconnected organ systems. The insights provide a strengthened conceptual framework for designing microbiota-directed nutritional strategies to sustain body-weight regulation.},
}
RevDate: 2026-10-07
Early nutrition and the infant microbiome: Implications for atopy.
The journal of allergy and clinical immunology. In practice, 14(10):2437.
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@article {pmid42843943,
year = {2026},
author = {Daulat, S},
title = {Early nutrition and the infant microbiome: Implications for atopy.},
journal = {The journal of allergy and clinical immunology. In practice},
volume = {14},
number = {10},
pages = {2437},
doi = {10.1016/j.jaip.2026.07.029},
pmid = {42843943},
issn = {2213-2201},
}
RevDate: 2026-10-07
Reply to "Early nutrition and the infant microbiome: implications for atopy".
The journal of allergy and clinical immunology. In practice, 14(10):2437-2438.
Additional Links: PMID-42843944
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PubMed:
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@article {pmid42843944,
year = {2026},
author = {Robbins, E and Koueik, J and Singh, AM and Frischmeyer-Guerrerio, PA and Hourigan, SK},
title = {Reply to "Early nutrition and the infant microbiome: implications for atopy".},
journal = {The journal of allergy and clinical immunology. In practice},
volume = {14},
number = {10},
pages = {2437-2438},
doi = {10.1016/j.jaip.2026.07.030},
pmid = {42843944},
issn = {2213-2201},
}
RevDate: 2026-10-07
CmpDate: 2026-10-07
Landscape-associated pesticide contamination shapes pollen provision microbiomes in Osmia cornifrons (Hymenoptera: Megachilidae).
Journal of insect science (Online), 26(5):.
Bees live and forage across a landscape increasingly altered by human activity, collecting pollen, nectar, and an essential microbiome from the local environment as well as chemical contamination from surrounding human activities. The increasing frequency and intensity of antimicrobial chemical use in agricultural systems disrupts the environmental microbial community and has been linked to bee declines. However, it remains largely unknown how pesticides and antimicrobial agents vary across the landscape, and in turn, cascade to alter microbiome assembly in solitary bees. To evaluate landscape-level effects of pesticide contamination on the pollen microbiome of solitary bees, we surveyed Osmia cornifrons (Hymenoptera: Megachilidae Radoszkowski, 1887) pollen provisions across 3 contrasting land use types in central upstate New York: forest, urban, and orchard habitats. Pollen provisions were screened for 94 common pesticides and sequenced to characterize their bacterial community. We found pesticide concentrations and risk varied significantly across land use types and was highest at orchard sites. Microbial communities also differed across landscapes, with increased surrounding forest cover corresponding to higher abundances of Apilactobacillus, a beneficial bee-associated genus in the family Lactobacilliacea. We found a significant correlation between increased pesticide concentration and decreased pollen-associated microbial diversity. These results indicate links between land use, pesticide exposure, and the microbiome of solitary bees.
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Citation:
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@article {pmid42843978,
year = {2026},
author = {Mueller, T and Kueneman, J and Fordyce, R and McArt, S and Danforth, B},
title = {Landscape-associated pesticide contamination shapes pollen provision microbiomes in Osmia cornifrons (Hymenoptera: Megachilidae).},
journal = {Journal of insect science (Online)},
volume = {26},
number = {5},
pages = {},
pmid = {42843978},
issn = {1536-2442},
support = {NSF-DEB 1929499//National Science Foundation/ ; },
mesh = {Animals ; *Pollen/microbiology ; Bees/microbiology ; *Microbiota/drug effects ; *Pesticides/analysis/adverse effects ; New York ; Bacteria ; Ecosystem ; },
abstract = {Bees live and forage across a landscape increasingly altered by human activity, collecting pollen, nectar, and an essential microbiome from the local environment as well as chemical contamination from surrounding human activities. The increasing frequency and intensity of antimicrobial chemical use in agricultural systems disrupts the environmental microbial community and has been linked to bee declines. However, it remains largely unknown how pesticides and antimicrobial agents vary across the landscape, and in turn, cascade to alter microbiome assembly in solitary bees. To evaluate landscape-level effects of pesticide contamination on the pollen microbiome of solitary bees, we surveyed Osmia cornifrons (Hymenoptera: Megachilidae Radoszkowski, 1887) pollen provisions across 3 contrasting land use types in central upstate New York: forest, urban, and orchard habitats. Pollen provisions were screened for 94 common pesticides and sequenced to characterize their bacterial community. We found pesticide concentrations and risk varied significantly across land use types and was highest at orchard sites. Microbial communities also differed across landscapes, with increased surrounding forest cover corresponding to higher abundances of Apilactobacillus, a beneficial bee-associated genus in the family Lactobacilliacea. We found a significant correlation between increased pesticide concentration and decreased pollen-associated microbial diversity. These results indicate links between land use, pesticide exposure, and the microbiome of solitary bees.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Pollen/microbiology
Bees/microbiology
*Microbiota/drug effects
*Pesticides/analysis/adverse effects
New York
Bacteria
Ecosystem
RevDate: 2026-10-07
Engineering anaerobic fungal-bacterial consortia for direct conversion of lignocellulosic biomass into medium-chain fatty acids.
Trends in biotechnology pii:S0167-7799(26)00383-5 [Epub ahead of print].
Lignocellulosic biomass is a renewable feedstock for sustainable fuels and chemicals, yet industrial conversion remains constrained by carbohydrate solubilization. Inspired by herbivore rumen microbiomes, we engineered an anaerobic fungal-bacterial consortium thatconverts native lignocellulose into medium-chain fatty acids (MCFAs) without pretreatment. Systematic screening identified the anaerobic fungus isolated here, Neocallimastix sp. FC1, togetherwith Megasphaerahexanoica, as a top-performing consortium, achieving a lignocellulose-to-MCFA yield of 21.0% (carbon-to-carbon basis) through tight lactate cross-feeding without competition for soluble sugars. Fungal lactate production limited the growth of M. hexanoica in co-culture, and the bacterium reallocated protein from growth toward chain elongation, resulting in increased MCFA production. These findings identify fungal lactate production as the primary biological constraint, and balancing lactate production and consumption as a key engineering strategy for improving lignocellulose-to-MCFA conversion. Techno-economic analysis identified high cultivation medium costs as the primary economic constraint and established quantitative cost-yield targets for profitable MCFA production.
Additional Links: PMID-42844060
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PubMed:
Citation:
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@article {pmid42844060,
year = {2026},
author = {Kim, BR and Blair, EM and Howard, JP and Gois, IM and Flick, R and Lankiewicz, TS and Mondo, S and Pangilinan, J and Lipzen, A and Guo, J and Hundley, H and Lee, R and Talag, J and Bunting, V and Rajasekar, S and Barry, K and Grigoriev, IV and O'Malley, MA and Lawson, CE},
title = {Engineering anaerobic fungal-bacterial consortia for direct conversion of lignocellulosic biomass into medium-chain fatty acids.},
journal = {Trends in biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tibtech.2026.09.013},
pmid = {42844060},
issn = {1879-3096},
abstract = {Lignocellulosic biomass is a renewable feedstock for sustainable fuels and chemicals, yet industrial conversion remains constrained by carbohydrate solubilization. Inspired by herbivore rumen microbiomes, we engineered an anaerobic fungal-bacterial consortium thatconverts native lignocellulose into medium-chain fatty acids (MCFAs) without pretreatment. Systematic screening identified the anaerobic fungus isolated here, Neocallimastix sp. FC1, togetherwith Megasphaerahexanoica, as a top-performing consortium, achieving a lignocellulose-to-MCFA yield of 21.0% (carbon-to-carbon basis) through tight lactate cross-feeding without competition for soluble sugars. Fungal lactate production limited the growth of M. hexanoica in co-culture, and the bacterium reallocated protein from growth toward chain elongation, resulting in increased MCFA production. These findings identify fungal lactate production as the primary biological constraint, and balancing lactate production and consumption as a key engineering strategy for improving lignocellulose-to-MCFA conversion. Techno-economic analysis identified high cultivation medium costs as the primary economic constraint and established quantitative cost-yield targets for profitable MCFA production.},
}
RevDate: 2026-10-07
CmpDate: 2026-10-07
Recent Advances in Autism Spectrum Disorder Research on Epigenetics and Personalised Medicine.
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 86(6):e70184.
BACKGROUND: Autism spectrum disorder (ASD) is a multifaceted neurodevelopmental condition characterised by impairments in social interaction and communication, repetitive and restricted patterns of behaviour and atypical sensory processing. Although genetic susceptibility accounts for a substantial proportion of ASD risk, increasing evidence indicates that epigenetic modifications and environmental exposures play pivotal roles in disease development and progression.
PURPOSE: This review provides an updated overview of the current understanding of ASD pathogenesis, focusing on the interplay between epigenetic regulation, maternal health and the gut microbiome. It also highlights emerging diagnostic biomarkers and therapeutic strategies that have the potential to enhance early diagnosis and improve clinical management.
MAIN FINDINGS: Recent studies indicate that maternal immune dysregulation, nutritional status, metabolic disorders and alterations in the maternal gut microbiota during pregnancy may contribute to ASD risk by inducing epigenetic changes and disrupting neurodevelopmental pathways. At the same time, novel pharmacological interventions aimed at alleviating behavioural symptoms and targeting epigenetic mechanisms are being actively explored. Advances in diagnostic technologies, including saliva-based microRNA profiling and epigenetic biomarkers, offer promising opportunities for earlier and more accurate ASD detection. Furthermore, genome-wide analyses and multi-omics approaches are facilitating the development of personalised diagnostic and therapeutic strategies.
CONCLUSION: Despite considerable progress in elucidating the genetic and environmental factors associated with ASD, the disorder remains highly heterogeneous and biologically complex. Future research integrating epigenetic insights, microbiome investigations and precision medicine approaches will be crucial for uncovering the underlying molecular mechanisms and translating these discoveries into more effective diagnostic tools and targeted therapies.
Additional Links: PMID-42844155
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PubMed:
Citation:
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@article {pmid42844155,
year = {2026},
author = {Khosrofar, R and Morshedi, I and Behzadpour, M and Afzali, N and Hosseini, RS and Aghili, A},
title = {Recent Advances in Autism Spectrum Disorder Research on Epigenetics and Personalised Medicine.},
journal = {International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience},
volume = {86},
number = {6},
pages = {e70184},
doi = {10.1002/jdn.70184},
pmid = {42844155},
issn = {1873-474X},
mesh = {Humans ; *Autism Spectrum Disorder/genetics/therapy/diagnosis ; *Epigenesis, Genetic ; *Precision Medicine/methods ; Pregnancy ; Animals ; Female ; },
abstract = {BACKGROUND: Autism spectrum disorder (ASD) is a multifaceted neurodevelopmental condition characterised by impairments in social interaction and communication, repetitive and restricted patterns of behaviour and atypical sensory processing. Although genetic susceptibility accounts for a substantial proportion of ASD risk, increasing evidence indicates that epigenetic modifications and environmental exposures play pivotal roles in disease development and progression.
PURPOSE: This review provides an updated overview of the current understanding of ASD pathogenesis, focusing on the interplay between epigenetic regulation, maternal health and the gut microbiome. It also highlights emerging diagnostic biomarkers and therapeutic strategies that have the potential to enhance early diagnosis and improve clinical management.
MAIN FINDINGS: Recent studies indicate that maternal immune dysregulation, nutritional status, metabolic disorders and alterations in the maternal gut microbiota during pregnancy may contribute to ASD risk by inducing epigenetic changes and disrupting neurodevelopmental pathways. At the same time, novel pharmacological interventions aimed at alleviating behavioural symptoms and targeting epigenetic mechanisms are being actively explored. Advances in diagnostic technologies, including saliva-based microRNA profiling and epigenetic biomarkers, offer promising opportunities for earlier and more accurate ASD detection. Furthermore, genome-wide analyses and multi-omics approaches are facilitating the development of personalised diagnostic and therapeutic strategies.
CONCLUSION: Despite considerable progress in elucidating the genetic and environmental factors associated with ASD, the disorder remains highly heterogeneous and biologically complex. Future research integrating epigenetic insights, microbiome investigations and precision medicine approaches will be crucial for uncovering the underlying molecular mechanisms and translating these discoveries into more effective diagnostic tools and targeted therapies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Autism Spectrum Disorder/genetics/therapy/diagnosis
*Epigenesis, Genetic
*Precision Medicine/methods
Pregnancy
Animals
Female
RevDate: 2026-10-07
Revealed: how this common gut microbe protects against heart disease.
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Citation:
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@article {pmid42844446,
year = {2026},
author = {Kozlov, M},
title = {Revealed: how this common gut microbe protects against heart disease.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42844446},
issn = {1476-4687},
}
RevDate: 2026-10-07
Prehistoric global migration of vanishing gut microbes with humans.
Nature [Epub ahead of print].
The gut microbiome is crucial for health and is affected strongly by lifestyle[1]. Many microorganisms commonly found in non-industrialized populations are disappearing or have become extinct in industrialized populations[2-6]. Studying which microorganisms have been long-term residents of the human gut and may have co-evolved with humans[2,7,8] could provide insights into how microbial biodiversity loss affects human health. However, the genetic complexities of microbial evolution and the plasticity of gut microbiome composition have made it challenging to resolve the evolutionary history of these long-term associations. Here we performed deep metagenomic sequencing of the Tsimane horticulturalists of Bolivia and compared their gut microbiomes with those of the Hadza hunter-gatherers of Tanzania[3]. These two populations, whose ancestors have been separated for tens of thousands of years, share 1,231 microbial species, most of which are rare in or absent from industrialized populations. Population genetic analyses of 636 of the shared species revealed patterns of microbial divergence and gene flow consistent with prehistoric human co-migration, with estimated split times that approximately align with human migration out of Africa and into the Americas. Our findings indicate that a diverse gut microbiome co-migrated with humans worldwide and has persisted over millennia. However, many of these species are now vanishing from industrialized populations and the consequences for human health remain uncertain.
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@article {pmid42844483,
year = {2026},
author = {Carter, MM and Liu, Z and Olm, MR and Martin, M and Sprockett, DD and Ghadermazi, P and Trumble, BC and Kaplan, H and Stieglitz, J and Rodriguez, DE and Relman, DA and Sonnenburg, ED and Gurven, M and Good, BH and Sonnenburg, JL},
title = {Prehistoric global migration of vanishing gut microbes with humans.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42844483},
issn = {1476-4687},
abstract = {The gut microbiome is crucial for health and is affected strongly by lifestyle[1]. Many microorganisms commonly found in non-industrialized populations are disappearing or have become extinct in industrialized populations[2-6]. Studying which microorganisms have been long-term residents of the human gut and may have co-evolved with humans[2,7,8] could provide insights into how microbial biodiversity loss affects human health. However, the genetic complexities of microbial evolution and the plasticity of gut microbiome composition have made it challenging to resolve the evolutionary history of these long-term associations. Here we performed deep metagenomic sequencing of the Tsimane horticulturalists of Bolivia and compared their gut microbiomes with those of the Hadza hunter-gatherers of Tanzania[3]. These two populations, whose ancestors have been separated for tens of thousands of years, share 1,231 microbial species, most of which are rare in or absent from industrialized populations. Population genetic analyses of 636 of the shared species revealed patterns of microbial divergence and gene flow consistent with prehistoric human co-migration, with estimated split times that approximately align with human migration out of Africa and into the Americas. Our findings indicate that a diverse gut microbiome co-migrated with humans worldwide and has persisted over millennia. However, many of these species are now vanishing from industrialized populations and the consequences for human health remain uncertain.},
}
RevDate: 2026-10-07
The Gut-Insulin Axis in Polycystic Ovary Syndrome: A Narrative Review of Gut Dysbiosis, Inflammation, and Emerging Therapeutic Strategies.
Reproductive sciences (Thousand Oaks, Calif.) [Epub ahead of print].
Polycystic ovary syndrome (PCOS) is a complicated, endocrine-endemic disorder with a prevalence rate of 8-13% in reproductive-age women in the world, which manifests through insulin resistance, hyperandrogenism, and reproductive dysfunction. Despite its high global prevalence, existing therapeutic interventions focus predominantly on symptom management rather than targeting the heterogeneous and multifactorial pathophysiology of the syndrome. Intestinal barrier integrity is destroyed by dysbiosis of the gut microbiota and induces endotoxemia and chronic low-grade inflammation through signalling pathways, such as LPS-TLR4-NF-kB signalling, which contribute to increased insulin resistance and androgen excess. These mechanistic pathways we dissect include changes in short-chain fatty acids (SCFAs), bile acid metabolism, involvement of FXR and TGR5 receptors, neuroendocrine regulation of the gut-brain axis, and microbial metabolites (tryptophan and agmatine), which altogether alter metabolic and reproductive abnormalities in PCOS. The preclinical evidence in the area of fecal microbiota transplantation proves the causal component of microbiota imbalance in the phenotype of PCOS. Dietary interventions that have been reviewed are fiber and resistant starch modulation, probiotics, prebiotics, synbiotics, fecal microbiota transplantation, and pharmacotherapies like metformin, which also alter the microbiome. They are heading towards individualized microbiome-based therapies and diagnostics, aided by artificial intelligence and standardized biomarkers. This review explains the emerging role of the gut-insulin axis as an important factor in the pathogenesis of PCOS and uses a novel way of combining them as a radical intervention for personalized and innovative PCOS treatment, which has the potential to enhance metabolic and endocrine health, as well as reproductive outcomes.
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@article {pmid42844513,
year = {2026},
author = {Shruti, and Bala, K},
title = {The Gut-Insulin Axis in Polycystic Ovary Syndrome: A Narrative Review of Gut Dysbiosis, Inflammation, and Emerging Therapeutic Strategies.},
journal = {Reproductive sciences (Thousand Oaks, Calif.)},
volume = {},
number = {},
pages = {},
pmid = {42844513},
issn = {1933-7205},
abstract = {Polycystic ovary syndrome (PCOS) is a complicated, endocrine-endemic disorder with a prevalence rate of 8-13% in reproductive-age women in the world, which manifests through insulin resistance, hyperandrogenism, and reproductive dysfunction. Despite its high global prevalence, existing therapeutic interventions focus predominantly on symptom management rather than targeting the heterogeneous and multifactorial pathophysiology of the syndrome. Intestinal barrier integrity is destroyed by dysbiosis of the gut microbiota and induces endotoxemia and chronic low-grade inflammation through signalling pathways, such as LPS-TLR4-NF-kB signalling, which contribute to increased insulin resistance and androgen excess. These mechanistic pathways we dissect include changes in short-chain fatty acids (SCFAs), bile acid metabolism, involvement of FXR and TGR5 receptors, neuroendocrine regulation of the gut-brain axis, and microbial metabolites (tryptophan and agmatine), which altogether alter metabolic and reproductive abnormalities in PCOS. The preclinical evidence in the area of fecal microbiota transplantation proves the causal component of microbiota imbalance in the phenotype of PCOS. Dietary interventions that have been reviewed are fiber and resistant starch modulation, probiotics, prebiotics, synbiotics, fecal microbiota transplantation, and pharmacotherapies like metformin, which also alter the microbiome. They are heading towards individualized microbiome-based therapies and diagnostics, aided by artificial intelligence and standardized biomarkers. This review explains the emerging role of the gut-insulin axis as an important factor in the pathogenesis of PCOS and uses a novel way of combining them as a radical intervention for personalized and innovative PCOS treatment, which has the potential to enhance metabolic and endocrine health, as well as reproductive outcomes.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Novel Antarctic chemolithotroph drives iron biomineralization.
Microbiome, 14(1):.
BACKGROUND: Iron, the most abundant redox-active metal in the Earth's crust, is coupled to numerous biogeochemical cycles. However, the mechanisms of iron oxidation and the organisms involved remain incompletely understood. Banded iron formations (BIFs) are a major reservoir of iron ore in the Precambrian sedimentary record, yet the biological contribution to their genesis remains a subject of unresolved debate. While large-scale BIF deposition largely ceased after the Proterozoic, microbial activity in modern Holocene sediments under fluctuating redox conditions provides a unique opportunity to examine mechanisms reminiscent of ancient iron cycling. Here, we report the stratigraphic sequence of microbiome profiles recorded in laminated facies with iron-containing crystalline illite in the embayment sediments beneath the Larsen C Ice Shelf (LCIS) in Antarctica during the Holocene.
RESULTS: LCIS sediments record microbial community shifts tightly coupled to environmental changes throughout the Holocene. Metagenomic analyses revealed three dominant microbial phases corresponding to geological facies boundaries. The open marine setting (phase A) showed higher taxonomic richness, whereas the sub-ice shelf sediments (phases B and C) were largely anoxic and characterized by diverse chemolithoautotrophic metabolisms. Keystone taxa including uncultured members of Thermodesulfovibrionia, as well as unique microbial communities and metabolisms, were evident in the aphotic, anoxic seawater; metagenomic analyses further revealed chemolithotrophy. The Thermodesulfovibrionia bacterium, visualized using fluorescence in situ hybridization and designated as "Candidatus Mariimomonas ferrooxydans", formed a novel clade in the phylum Nitrospirota. Metagenome-assembled genome analysis identified a putative outer-membrane Fe(II) oxidase, Cyc2, whose Fe(II)-oxidation activity was experimentally confirmed.
CONCLUSION: Our findings document the interaction between microbiome and environment, illustrating how LCIS sediments preserve a dynamic record of microbial community responses to environmental transitions. These results provide critical insights into microbial iron mineralization, echoing the biogeochemistry of the geologic past, particularly synglacial iron formation during the Neoproterozoic Snowball Earth. Video Abstract.
Additional Links: PMID-42844624
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@article {pmid42844624,
year = {2026},
author = {Yoon, J and Lee, B and Yoo, KC and Kwak, MJ and Song, HJ and Hwang, CY and Chung, Y and Kim, K and Kwon, SK and Song, JY and Yoon, HS and Kim, JF},
title = {Novel Antarctic chemolithotroph drives iron biomineralization.},
journal = {Microbiome},
volume = {14},
number = {1},
pages = {},
pmid = {42844624},
issn = {2049-2618},
mesh = {*Iron/metabolism ; *Geologic Sediments/microbiology/chemistry ; Antarctic Regions ; *Biomineralization ; Oxidation-Reduction ; *Bacteria/classification/genetics/metabolism/isolation & purification ; *Microbiota ; *Chemoautotrophic Growth ; RNA, Ribosomal, 16S/genetics ; Phylogeny ; Metagenomics/methods ; Seawater/microbiology ; },
abstract = {BACKGROUND: Iron, the most abundant redox-active metal in the Earth's crust, is coupled to numerous biogeochemical cycles. However, the mechanisms of iron oxidation and the organisms involved remain incompletely understood. Banded iron formations (BIFs) are a major reservoir of iron ore in the Precambrian sedimentary record, yet the biological contribution to their genesis remains a subject of unresolved debate. While large-scale BIF deposition largely ceased after the Proterozoic, microbial activity in modern Holocene sediments under fluctuating redox conditions provides a unique opportunity to examine mechanisms reminiscent of ancient iron cycling. Here, we report the stratigraphic sequence of microbiome profiles recorded in laminated facies with iron-containing crystalline illite in the embayment sediments beneath the Larsen C Ice Shelf (LCIS) in Antarctica during the Holocene.
RESULTS: LCIS sediments record microbial community shifts tightly coupled to environmental changes throughout the Holocene. Metagenomic analyses revealed three dominant microbial phases corresponding to geological facies boundaries. The open marine setting (phase A) showed higher taxonomic richness, whereas the sub-ice shelf sediments (phases B and C) were largely anoxic and characterized by diverse chemolithoautotrophic metabolisms. Keystone taxa including uncultured members of Thermodesulfovibrionia, as well as unique microbial communities and metabolisms, were evident in the aphotic, anoxic seawater; metagenomic analyses further revealed chemolithotrophy. The Thermodesulfovibrionia bacterium, visualized using fluorescence in situ hybridization and designated as "Candidatus Mariimomonas ferrooxydans", formed a novel clade in the phylum Nitrospirota. Metagenome-assembled genome analysis identified a putative outer-membrane Fe(II) oxidase, Cyc2, whose Fe(II)-oxidation activity was experimentally confirmed.
CONCLUSION: Our findings document the interaction between microbiome and environment, illustrating how LCIS sediments preserve a dynamic record of microbial community responses to environmental transitions. These results provide critical insights into microbial iron mineralization, echoing the biogeochemistry of the geologic past, particularly synglacial iron formation during the Neoproterozoic Snowball Earth. Video Abstract.},
}
MeSH Terms:
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*Iron/metabolism
*Geologic Sediments/microbiology/chemistry
Antarctic Regions
*Biomineralization
Oxidation-Reduction
*Bacteria/classification/genetics/metabolism/isolation & purification
*Microbiota
*Chemoautotrophic Growth
RNA, Ribosomal, 16S/genetics
Phylogeny
Metagenomics/methods
Seawater/microbiology
RevDate: 2026-10-08
Source tracking and transmission of antibiotic resistance genes mediated by core microbiota in black soldier fly larvae bioconversion of doxycycline-contaminated hen manure.
Insect science [Epub ahead of print].
Black soldier fly larvae (BSFL) bioconversion of doxycycline-contaminated hen manure raises concerns about antibiotic resistance gene (ARG) transmission. Although core microbiota in gut may participate in ARG dynamics, the relative contributions of microbiota from manure and baseline larval gut to the BSFL gut resistome remain unclear. Using metagenomics, amplicon sequencing, and cultivable bacteria analysis, we found that: (1) Providencia, Klebsiella, Enterococcus, and Escherichia-Shigella dominated the BSFL gut and served as primary ARG hosts; (2) Fecal filtrate intervention drastically altered gut microbiota and ARG profiles, suppressing Klebsiella (by 95.56%) and Escherichia-Shigella (to < 0.5%) while enriching Providencia (3.53 fold increase) and Enterococcus, with increased ARGs such as tet(59) and qnrD1. Long-read metagenomic analysis indicated that viable manure-borne bacteria, rather than cell-free fecal filtrate, delivered structurally intact ARG-MGE units as key carrier of mobile resistance cassettes; (3) Source tracking (FEAST) assigned the majority of ARBs (> 90%) and their ARGs in the BSFL gut to the baseline BSFL gut source, with manure-derived ARBs contributing 4.80%. Culture-based 16S rRNA gene homology provided evidence consistent with possible manure-to-gut transfer of selected Escherichia-Shigella and Enterococcus. The BSFL gut resistome was more strongly associated with the baseline BSFL microbiota than with manure, but manure still represented a detectable source of ARB and ARG introduction. FEAST source assignments should be interpreted as composition-based bioinformatic estimates rather than definitive proof of origin, due to lack of direct functional tracing. These findings have critical implications for assessing the ecological safety of BSFL-based waste valorization.
Additional Links: PMID-42844853
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PubMed:
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@article {pmid42844853,
year = {2026},
author = {Chen, J and Deng, W and He, J and Niu, S and Xing, S and Liao, X},
title = {Source tracking and transmission of antibiotic resistance genes mediated by core microbiota in black soldier fly larvae bioconversion of doxycycline-contaminated hen manure.},
journal = {Insect science},
volume = {},
number = {},
pages = {},
doi = {10.1111/1744-7917.70366},
pmid = {42844853},
issn = {1744-7917},
support = {32072783//National Natural Science Foundation of China/ ; 2020B1212060060//Science and Technology Program of Guangdong Province, China/ ; CARS-40//Modern Agro-industry Technology Research System/ ; },
abstract = {Black soldier fly larvae (BSFL) bioconversion of doxycycline-contaminated hen manure raises concerns about antibiotic resistance gene (ARG) transmission. Although core microbiota in gut may participate in ARG dynamics, the relative contributions of microbiota from manure and baseline larval gut to the BSFL gut resistome remain unclear. Using metagenomics, amplicon sequencing, and cultivable bacteria analysis, we found that: (1) Providencia, Klebsiella, Enterococcus, and Escherichia-Shigella dominated the BSFL gut and served as primary ARG hosts; (2) Fecal filtrate intervention drastically altered gut microbiota and ARG profiles, suppressing Klebsiella (by 95.56%) and Escherichia-Shigella (to < 0.5%) while enriching Providencia (3.53 fold increase) and Enterococcus, with increased ARGs such as tet(59) and qnrD1. Long-read metagenomic analysis indicated that viable manure-borne bacteria, rather than cell-free fecal filtrate, delivered structurally intact ARG-MGE units as key carrier of mobile resistance cassettes; (3) Source tracking (FEAST) assigned the majority of ARBs (> 90%) and their ARGs in the BSFL gut to the baseline BSFL gut source, with manure-derived ARBs contributing 4.80%. Culture-based 16S rRNA gene homology provided evidence consistent with possible manure-to-gut transfer of selected Escherichia-Shigella and Enterococcus. The BSFL gut resistome was more strongly associated with the baseline BSFL microbiota than with manure, but manure still represented a detectable source of ARB and ARG introduction. FEAST source assignments should be interpreted as composition-based bioinformatic estimates rather than definitive proof of origin, due to lack of direct functional tracing. These findings have critical implications for assessing the ecological safety of BSFL-based waste valorization.},
}
RevDate: 2026-10-08
The Gut-Brain Axis in Parkinson's Disease: From Clinical Observation toward Mechanism-Based Precision Medicine.
Movement disorders : official journal of the Movement Disorder Society [Epub ahead of print].
Gastrointestinal dysfunction is increasingly recognized as a core feature of Parkinson's disease (PD), affecting quality of life, nutrition, medication response, and potentially the earliest stages of pathogenesis. This perspective traces the evolution of the gut from a neglected source of non-motor symptoms to a central component of biological models of PD. Gastrointestinal manifestations are physiologically heterogeneous and require objective phenotyping to distinguish dysphagia, gastroparesis, slow transit, defecatory dysfunction, and overlapping mechanisms. The body-first/brain-first framework further suggests that Lewy pathology may follow distinct anatomical trajectories, with early enteric and autonomic involvement defining a subgroup in which gut-directed biomarkers and therapies may be especially relevant. Alterations of the gut microbiome are reproducibly associated with PD, although geography, constipation, medication, diet, disease stage, and reverse causation complicate interpretation. Emerging work is shifting from taxonomy toward microbial functions and host pathways, including barrier integrity, immune and enteroendocrine signaling, short-chain fatty acids, glucagon-like peptide-1 (GLP-1), host genetic susceptibility, α-synuclein aggregation and propagation, and microbial levodopa metabolism. Trials of probiotics, fecal microbiota transplantation, and dietary interventions remain heterogeneous and have not established disease-modifying efficacy. Progress will require longitudinal studies in prodromal and subtype-defined populations, objective gastrointestinal measurements, integrated microbial, host-genetic and other multi-omics, mechanistic human and animal models, and clinical trials combining target-engagement markers with meaningful outcomes. Such an approach may enable precision gut-brain medicine for appropriately selected patients with PD. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
Additional Links: PMID-42845110
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PubMed:
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@article {pmid42845110,
year = {2026},
author = {Scheperjans, F and Borghammer, P and Pfeiffer, RF and Appel-Cresswell, S and Keshavarzian, A},
title = {The Gut-Brain Axis in Parkinson's Disease: From Clinical Observation toward Mechanism-Based Precision Medicine.},
journal = {Movement disorders : official journal of the Movement Disorder Society},
volume = {},
number = {},
pages = {},
doi = {10.1002/mds.70566},
pmid = {42845110},
issn = {1531-8257},
support = {//Sigrid Juséliuksen Säätiö/ ; 1U01DK140923-01/NH/NIH HHS/United States ; //Pacific Parkinson's Research Institute/ ; },
abstract = {Gastrointestinal dysfunction is increasingly recognized as a core feature of Parkinson's disease (PD), affecting quality of life, nutrition, medication response, and potentially the earliest stages of pathogenesis. This perspective traces the evolution of the gut from a neglected source of non-motor symptoms to a central component of biological models of PD. Gastrointestinal manifestations are physiologically heterogeneous and require objective phenotyping to distinguish dysphagia, gastroparesis, slow transit, defecatory dysfunction, and overlapping mechanisms. The body-first/brain-first framework further suggests that Lewy pathology may follow distinct anatomical trajectories, with early enteric and autonomic involvement defining a subgroup in which gut-directed biomarkers and therapies may be especially relevant. Alterations of the gut microbiome are reproducibly associated with PD, although geography, constipation, medication, diet, disease stage, and reverse causation complicate interpretation. Emerging work is shifting from taxonomy toward microbial functions and host pathways, including barrier integrity, immune and enteroendocrine signaling, short-chain fatty acids, glucagon-like peptide-1 (GLP-1), host genetic susceptibility, α-synuclein aggregation and propagation, and microbial levodopa metabolism. Trials of probiotics, fecal microbiota transplantation, and dietary interventions remain heterogeneous and have not established disease-modifying efficacy. Progress will require longitudinal studies in prodromal and subtype-defined populations, objective gastrointestinal measurements, integrated microbial, host-genetic and other multi-omics, mechanistic human and animal models, and clinical trials combining target-engagement markers with meaningful outcomes. Such an approach may enable precision gut-brain medicine for appropriately selected patients with PD. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.},
}
RevDate: 2026-10-08
Tissue Level and Intratumoral Microbiome: A Missing Piece in the Prostate Cancer Microbiome Landscape.
Additional Links: PMID-42845171
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PubMed:
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@article {pmid42845171,
year = {2026},
author = {Lee, HY and Kim, JH},
title = {Tissue Level and Intratumoral Microbiome: A Missing Piece in the Prostate Cancer Microbiome Landscape.},
journal = {The world journal of men's health},
volume = {},
number = {},
pages = {},
doi = {10.5534/wjmh.260229},
pmid = {42845171},
issn = {2287-4208},
support = {/SCH/Soonchunhyang University/Korea ; },
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Gut Microbiota Modulation by Abelmoschus manihot (L.) Improves Circulating Metabolites and Alleviates Diabetic Nephropathy in db/db Mice.
BioMed research international, 2026(1):e5630909.
BACKGROUND: Huangkui capsule (HKC), derived from the ethanol extract of Abelmoschus manihot (L.) flowers, is widely used in China for treating kidney diseases, including diabetic nephropathy (DN). Our previous study demonstrated that HKC modulates the intestinal microbiota and circulating metabolites in non-obese diabetic mice, a type 1 diabetes model. To further explore its efficacy, we evaluated HKC in db/db mice, a well-established type 2 diabetes and DN model.
METHODS: An HKC cohort studied in 2022 was compared with historical Ctrl and DN cohorts studied in 2021. Shotgun metagenomic sequencing was performed to characterize intestinal microbiota changes, while liquid chromatography-mass spectrometry (LC-MS)-based plasma metabolomics was used to identify alterations in circulating metabolites. The biological functions of the altered microbiota and plasma metabolites were analyzed, and the potential association between the intestinal microbiome and plasma metabolome was evaluated.
RESULTS: Compared with the historical DN cohort, the HKC cohort had higher abundances of Streptococcaceae, Streptococcus, and Massilimaliae and lower abundances of Alloprevotella and Prevotellamassilia in exploratory comparisons. In the HKC-versus-DN comparison, the archived gene set enrichment analysis reported 15 pathways with nominal positive enrichment. Additionally, 12 plasma metabolites were upregulated and 14 downregulated, including branched-chain amino acids (DL-leucine, DL-valine, D-isoleucine), organic acids (N-methyl-α-aminoisobutyric acid, guanidineacetic acid), and choline.
CONCLUSION: In db/db mice, the cohort receiving A. manihot (L.)-derived HKC had lower urinary albumin-to-creatinine ratio (UACR) and different intestinal microbiota and plasma metabolite profiles than the historical DN cohort, highlighting its therapeutic potential for DN.
Additional Links: PMID-42845172
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Citation:
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@article {pmid42845172,
year = {2026},
author = {Xu, Q and Song, Y and Yu, H and Wang, Y and Gu, HF},
title = {Gut Microbiota Modulation by Abelmoschus manihot (L.) Improves Circulating Metabolites and Alleviates Diabetic Nephropathy in db/db Mice.},
journal = {BioMed research international},
volume = {2026},
number = {1},
pages = {e5630909},
pmid = {42845172},
issn = {2314-6141},
support = {CPU20200228//Suzhong Pharmaceutical Group Co. Ltd/ ; },
mesh = {Animals ; *Diabetic Nephropathies/drug therapy/microbiology/blood/metabolism ; Mice ; *Gastrointestinal Microbiome/drug effects ; *Abelmoschus/chemistry ; Male ; Metabolomics ; Metabolome/drug effects ; Diabetes Mellitus, Experimental/drug therapy ; *Plant Extracts/pharmacology ; Diabetes Mellitus, Type 2/drug therapy ; Disease Models, Animal ; Mice, Inbred C57BL ; *Drugs, Chinese Herbal/pharmacology ; },
abstract = {BACKGROUND: Huangkui capsule (HKC), derived from the ethanol extract of Abelmoschus manihot (L.) flowers, is widely used in China for treating kidney diseases, including diabetic nephropathy (DN). Our previous study demonstrated that HKC modulates the intestinal microbiota and circulating metabolites in non-obese diabetic mice, a type 1 diabetes model. To further explore its efficacy, we evaluated HKC in db/db mice, a well-established type 2 diabetes and DN model.
METHODS: An HKC cohort studied in 2022 was compared with historical Ctrl and DN cohorts studied in 2021. Shotgun metagenomic sequencing was performed to characterize intestinal microbiota changes, while liquid chromatography-mass spectrometry (LC-MS)-based plasma metabolomics was used to identify alterations in circulating metabolites. The biological functions of the altered microbiota and plasma metabolites were analyzed, and the potential association between the intestinal microbiome and plasma metabolome was evaluated.
RESULTS: Compared with the historical DN cohort, the HKC cohort had higher abundances of Streptococcaceae, Streptococcus, and Massilimaliae and lower abundances of Alloprevotella and Prevotellamassilia in exploratory comparisons. In the HKC-versus-DN comparison, the archived gene set enrichment analysis reported 15 pathways with nominal positive enrichment. Additionally, 12 plasma metabolites were upregulated and 14 downregulated, including branched-chain amino acids (DL-leucine, DL-valine, D-isoleucine), organic acids (N-methyl-α-aminoisobutyric acid, guanidineacetic acid), and choline.
CONCLUSION: In db/db mice, the cohort receiving A. manihot (L.)-derived HKC had lower urinary albumin-to-creatinine ratio (UACR) and different intestinal microbiota and plasma metabolite profiles than the historical DN cohort, highlighting its therapeutic potential for DN.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Diabetic Nephropathies/drug therapy/microbiology/blood/metabolism
Mice
*Gastrointestinal Microbiome/drug effects
*Abelmoschus/chemistry
Male
Metabolomics
Metabolome/drug effects
Diabetes Mellitus, Experimental/drug therapy
*Plant Extracts/pharmacology
Diabetes Mellitus, Type 2/drug therapy
Disease Models, Animal
Mice, Inbred C57BL
*Drugs, Chinese Herbal/pharmacology
RevDate: 2026-10-08
CmpDate: 2026-10-08
Gut-Skin Axis Revisited: A Nationwide Cohort Study on the Bi-directional Relationship Between Rosacea and Irritable Bowel Syndrome.
Annals of dermatology, 38(5):388-396.
BACKGROUND: The gut-skin axis has emerged as a key concept linking cutaneous and gastrointestinal inflammation. Although prior studies have reported an increased risk of irritable bowel syndrome (IBS) among patients with rosacea, the reverse association remains unclear.
OBJECTIVE: To examine the bidirectional association between rosacea and IBS using a nationwide cohort database, clarifying whether IBS increases the risk of rosacea as well as the reverse relationship.
METHODS: We conducted a retrospective cohort study using the Korean National Health Insurance Service-National Sample Cohort (NHIS-NSC), including adults aged ≥20 years from 2002 to 2013. Incident cases of rosacea and IBS were identified using International Classification of Diseases, 10th Revision codes and matched to controls by age, sex, and index year. Cox proportional hazards models were applied to estimate adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs), controlling for sociodemographic and clinical covariates.
RESULTS: During follow-up, patients with rosacea showed a higher incidence of IBS than matched controls (56.3 vs. 36.9 per 1,000 person-years), with a significantly increased risk in the fully adjusted Cox model (aHR, 1.30; 95% CI, 1.11-1.52). Conversely, patients with IBS had a higher incidence of rosacea compared with matched controls (0.37 vs. 0.21 per 1,000 person-years), corresponding to an elevated adjusted risk (aHR, 1.61; 95% CI, 1.39-1.87). These bidirectional associations remained consistent across sensitivity and subgroup analyses.
CONCLUSION: This nationwide study demonstrates a reciprocal relationship between rosacea and IBS, underscoring shared inflammatory and neuroimmune mechanisms underlying the gut-skin axis.
Additional Links: PMID-42845202
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PubMed:
Citation:
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@article {pmid42845202,
year = {2026},
author = {Min, JH and Jo, YW and Her, Y and Kwon, JW},
title = {Gut-Skin Axis Revisited: A Nationwide Cohort Study on the Bi-directional Relationship Between Rosacea and Irritable Bowel Syndrome.},
journal = {Annals of dermatology},
volume = {38},
number = {5},
pages = {388-396},
doi = {10.5021/ad.25.210},
pmid = {42845202},
issn = {2005-3894},
support = {KNUH_2024-02-04//Institute of Medical Sciences, Kangwon National University/Korea ; RS-2025-24535069/KHIDI/Korea Health Industry Development Institute/Korea ; KNUH_2025-01-01//Kangwon National University Hospital/Korea ; },
abstract = {BACKGROUND: The gut-skin axis has emerged as a key concept linking cutaneous and gastrointestinal inflammation. Although prior studies have reported an increased risk of irritable bowel syndrome (IBS) among patients with rosacea, the reverse association remains unclear.
OBJECTIVE: To examine the bidirectional association between rosacea and IBS using a nationwide cohort database, clarifying whether IBS increases the risk of rosacea as well as the reverse relationship.
METHODS: We conducted a retrospective cohort study using the Korean National Health Insurance Service-National Sample Cohort (NHIS-NSC), including adults aged ≥20 years from 2002 to 2013. Incident cases of rosacea and IBS were identified using International Classification of Diseases, 10th Revision codes and matched to controls by age, sex, and index year. Cox proportional hazards models were applied to estimate adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs), controlling for sociodemographic and clinical covariates.
RESULTS: During follow-up, patients with rosacea showed a higher incidence of IBS than matched controls (56.3 vs. 36.9 per 1,000 person-years), with a significantly increased risk in the fully adjusted Cox model (aHR, 1.30; 95% CI, 1.11-1.52). Conversely, patients with IBS had a higher incidence of rosacea compared with matched controls (0.37 vs. 0.21 per 1,000 person-years), corresponding to an elevated adjusted risk (aHR, 1.61; 95% CI, 1.39-1.87). These bidirectional associations remained consistent across sensitivity and subgroup analyses.
CONCLUSION: This nationwide study demonstrates a reciprocal relationship between rosacea and IBS, underscoring shared inflammatory and neuroimmune mechanisms underlying the gut-skin axis.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Longitudinal microneedle sampling resolves tissue-restricted immune-microbiome dynamics in skin.
medRxiv : the preprint server for health sciences pii:2026.04.24.26351513.
The skin microbiome shapes local immunity, but the mechanisms of microbiome-immune crosstalk remain poorly understood. A major barrier to discovery is the lack of approaches that enable simultaneous, longitudinal measurement of microbes and immune cells from the same tissue without disrupting barrier integrity. Here we present a hydrogel-coated microneedle (MN) patch that enables minimally invasive co-sampling of viable microbes, immune cells, and interstitial fluid from skin. In humans, the patches were well tolerated and preserved inter-individual microbial signatures. Murine models colonized with commensal Staphylococcus epidermidis and the opportunistic pathogen Staphylococcus aureus , revealed distinct immune trajectories during commensal colonization, pathogen challenge, and commensal-pathogen co-colonization. Pathogen colonization drives progressive inflammatory amplification, whereas commensal exposure induces controlled immune activation that stabilizes over time. Notably, S. epidermidis reshapes pathogen-induced responses, producing a transient immune activation followed by attenuation of inflammation. These results establish MN sampling as a strategy to resolve immune-microbiome dynamics in barrier tissues and provide a framework for mechanistic studies of host-microbe interactions in health and disease.
Additional Links: PMID-42845278
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@article {pmid42845278,
year = {2026},
author = {Dhinakaran, AK and Voigt, AY and Szacik, A and Kang, SY and Giarratana, S and Oh, J and Jalili, S},
title = {Longitudinal microneedle sampling resolves tissue-restricted immune-microbiome dynamics in skin.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.04.24.26351513},
pmid = {42845278},
abstract = {The skin microbiome shapes local immunity, but the mechanisms of microbiome-immune crosstalk remain poorly understood. A major barrier to discovery is the lack of approaches that enable simultaneous, longitudinal measurement of microbes and immune cells from the same tissue without disrupting barrier integrity. Here we present a hydrogel-coated microneedle (MN) patch that enables minimally invasive co-sampling of viable microbes, immune cells, and interstitial fluid from skin. In humans, the patches were well tolerated and preserved inter-individual microbial signatures. Murine models colonized with commensal Staphylococcus epidermidis and the opportunistic pathogen Staphylococcus aureus , revealed distinct immune trajectories during commensal colonization, pathogen challenge, and commensal-pathogen co-colonization. Pathogen colonization drives progressive inflammatory amplification, whereas commensal exposure induces controlled immune activation that stabilizes over time. Notably, S. epidermidis reshapes pathogen-induced responses, producing a transient immune activation followed by attenuation of inflammation. These results establish MN sampling as a strategy to resolve immune-microbiome dynamics in barrier tissues and provide a framework for mechanistic studies of host-microbe interactions in health and disease.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Gut community-level analysis reveals an altered balance between Phocaeicola vulgatus and Bacteroides fragilis in Alzheimer's disease.
bioRxiv : the preprint server for biology pii:2026.08.12.743985.
Gut microbiome differences in Alzheimer's disease (AD) are typically cataloged taxon by taxon, yet bacterial competition and cross-feeding make species' roles dependent on the entire community. We analyzed 274 stool metagenomes from 119 older adults (18 with AD) as communities, retaining 22 recurring across 1,000 runs. Using our AI framework, we identified 15 species differing in abundance in AD, particularly the commensal Phocaeicola vulgatus (Cohen's d -0.91, 95% CI [-1.23, -0.59]), a finding robust to repeated sampling. It correlated negatively with its sister species, Phocaeicola dorei (r -0.57), suggesting possible niche competition; this replicated in an independent cohort (r -0.43). P. vulgatus was depleted in AD and the opportunistic pathogen Bacteroides fragilis enriched, shifting their balance toward B. fragilis (d -0.70), a modestly reproduced AD-associated pattern (d -0.24). Our findings suggest that AD-associated gut microbiome variation extends beyond taxon-specific abundance to the balance between specific species within a community matrix.
Additional Links: PMID-42845384
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@article {pmid42845384,
year = {2026},
author = {Huang, Z and McGrath, PM and Ferdinand, DC and McCormick, BA and Ward, DV and Bucci, V and Haran, JP},
title = {Gut community-level analysis reveals an altered balance between Phocaeicola vulgatus and Bacteroides fragilis in Alzheimer's disease.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.12.743985},
pmid = {42845384},
issn = {2692-8205},
abstract = {Gut microbiome differences in Alzheimer's disease (AD) are typically cataloged taxon by taxon, yet bacterial competition and cross-feeding make species' roles dependent on the entire community. We analyzed 274 stool metagenomes from 119 older adults (18 with AD) as communities, retaining 22 recurring across 1,000 runs. Using our AI framework, we identified 15 species differing in abundance in AD, particularly the commensal Phocaeicola vulgatus (Cohen's d -0.91, 95% CI [-1.23, -0.59]), a finding robust to repeated sampling. It correlated negatively with its sister species, Phocaeicola dorei (r -0.57), suggesting possible niche competition; this replicated in an independent cohort (r -0.43). P. vulgatus was depleted in AD and the opportunistic pathogen Bacteroides fragilis enriched, shifting their balance toward B. fragilis (d -0.70), a modestly reproduced AD-associated pattern (d -0.24). Our findings suggest that AD-associated gut microbiome variation extends beyond taxon-specific abundance to the balance between specific species within a community matrix.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Mining Microbial Transcriptomes to Engineer Cell-Based Bacterial Biosensors in Gut-Resident Bacteroidaceae.
bioRxiv : the preprint server for biology pii:2026.08.10.744002.
The gastrointestinal tract is rich in metabolic, immune, and microbiome-derived signals that can inform the design of live biotherapeutics and diagnosis of intestinal disorders. Engineered cell-based biosensors can tap into this molecular information and report on their environment, yet their development in gut-resident symbionts has been limited by a lack of validated sensor systems. Here, we present a generalizable pipeline that leverages bacterial transcriptional profiling to identify environment-responsive systems for biosensor engineering. Candidate Sensors Systems (CSSs) mined from healthy, disease, and in vitro transcriptomes were assembled into a barcoded library in Bacteroidaceae chassis and screened in high-throughput in vivo to identify responsive promoters. A unique Bacteroidales ECF-type sigma factor operon with ties to sphingolipid metabolism and flux was highly responsive in chemically-induced colitis models. The biosensor responded robustly to disease and returned to baseline upon recovery, establishing an in vivo -driven strategy for discovering functional biosensors in non-model gut-resident bacteria.
Additional Links: PMID-42845408
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@article {pmid42845408,
year = {2026},
author = {Glazier, J and Villegas, D and McClure, S and Ghali, J and Fuerte-Stone, J and Mimee, M},
title = {Mining Microbial Transcriptomes to Engineer Cell-Based Bacterial Biosensors in Gut-Resident Bacteroidaceae.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.10.744002},
pmid = {42845408},
issn = {2692-8205},
abstract = {The gastrointestinal tract is rich in metabolic, immune, and microbiome-derived signals that can inform the design of live biotherapeutics and diagnosis of intestinal disorders. Engineered cell-based biosensors can tap into this molecular information and report on their environment, yet their development in gut-resident symbionts has been limited by a lack of validated sensor systems. Here, we present a generalizable pipeline that leverages bacterial transcriptional profiling to identify environment-responsive systems for biosensor engineering. Candidate Sensors Systems (CSSs) mined from healthy, disease, and in vitro transcriptomes were assembled into a barcoded library in Bacteroidaceae chassis and screened in high-throughput in vivo to identify responsive promoters. A unique Bacteroidales ECF-type sigma factor operon with ties to sphingolipid metabolism and flux was highly responsive in chemically-induced colitis models. The biosensor responded robustly to disease and returned to baseline upon recovery, establishing an in vivo -driven strategy for discovering functional biosensors in non-model gut-resident bacteria.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
A microproteome screen identifies immunomodulatory bacterial microproteins encoded in expanded gene arrays in Leptotrichia.
bioRxiv : the preprint server for biology pii:2026.08.11.744246.
The human microbiome exerts broad influence in health and disease with associative studies implicating the microbiome in influencing immunity, cancer outcomes, and neurodegeneration. However, the molecular mediators of microbe-host communication remain poorly defined. Bacterial microproteins from the microbiome represent a largely uncharacterized class of potential regulators of host immunity. Here, we utilize functional genomics to interrogate 3,552 microproteins in order to identify novel microbial-immune interactions. We constructed a microproteome library from microbial metagenomic datasets, expressed it in macrophages and assayed for immunomodulatory activity. We identify several bacterial microproteins that drive macrophage M1 polarization. Among the strongest hits are a cluster of structurally related microproteins from Leptotrichia species, which are oral Gram-negative commensals associated with differential cancer outcomes. Genomic analysis reveals that Leptotrichia species encode these putative immunomodulatory microproteins in tandem arrays of up to 44 copies. These genes encode microproteins with varying sequences but conserved predicted structures. In an orthogonal approach, we demonstrate that bacterial expression of Leptotrichia microproteins influences macrophage cell state and function. As a whole, our findings identify novel microbial microproteins with immunomodulatory activity and provide a framework for future discovery of host-microbe interactions that influence human health.
Additional Links: PMID-42845442
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@article {pmid42845442,
year = {2026},
author = {Ragheb, M and Kiguchi, Y and Lin, JD and Hoffman, FT and Daigh, L and Chakraborty, M and Doyle, B and Grieshop, MP and Lin, A and Maghini, D and Spees, K and Bintu, L and Bassik, MC and Bhatt, AS},
title = {A microproteome screen identifies immunomodulatory bacterial microproteins encoded in expanded gene arrays in Leptotrichia.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.11.744246},
pmid = {42845442},
issn = {2692-8205},
abstract = {The human microbiome exerts broad influence in health and disease with associative studies implicating the microbiome in influencing immunity, cancer outcomes, and neurodegeneration. However, the molecular mediators of microbe-host communication remain poorly defined. Bacterial microproteins from the microbiome represent a largely uncharacterized class of potential regulators of host immunity. Here, we utilize functional genomics to interrogate 3,552 microproteins in order to identify novel microbial-immune interactions. We constructed a microproteome library from microbial metagenomic datasets, expressed it in macrophages and assayed for immunomodulatory activity. We identify several bacterial microproteins that drive macrophage M1 polarization. Among the strongest hits are a cluster of structurally related microproteins from Leptotrichia species, which are oral Gram-negative commensals associated with differential cancer outcomes. Genomic analysis reveals that Leptotrichia species encode these putative immunomodulatory microproteins in tandem arrays of up to 44 copies. These genes encode microproteins with varying sequences but conserved predicted structures. In an orthogonal approach, we demonstrate that bacterial expression of Leptotrichia microproteins influences macrophage cell state and function. As a whole, our findings identify novel microbial microproteins with immunomodulatory activity and provide a framework for future discovery of host-microbe interactions that influence human health.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Marine nematodes exhibit widespread symbiosis, novel chemoautotrophy, and evolutionary conservation of holobiont taxa.
bioRxiv : the preprint server for biology pii:2026.08.12.744518.
Microbial symbioses drive the evolutionary and functional diversification of eukaryotic clades, from single-celled protists to large invertebrates. However, our knowledge of host-associated assemblages (the "holobiont") is limited in microscopic animal phyla with a body size <1mm, due to practical challenges such as low biomass and difficult taxonomy of host species. Marine nematodes represent an ideal case study for rapidly advancing our knowledge of bacterial-animal symbioses, representing a globally abundant invertebrate group with strong links to terrestrial and model organism species within the same phylum. Here, we sequenced the holobionts of 220 marine nematodes and generated 815 metagenome-assembled genomes (MAGs) of host-associated bacteria/archaea. Our data indicates that 20-34% of marine nematodes harbor an obligate intracellular symbiont, often with multiple endosymbionts co-occurring within the same host. Three bacterial phyla (Pseudomonadota Bacteroidota, and Verrucomicrobiota) account for three-quarters of all nematode-associated MAGs, and the majority of these holobiont MAGs represent deeply divergent lineages in the prokaryotic tree of life. The Flavobacteriaceae (a core microbiome taxon in C. elegans and other terrestrial nematodes), were consistently recovered across phylogenetically diverse marine nematode lineages, suggesting evolutionary conservation of holobiont taxa across marine and terrestrial environments. We also report a novel chemoautotroph family (Ca. Thionematobacter) recovered from nematode hosts in both deep-sea and shallow-water habitats, and report the first confirmed instance of Cardinium endosymbionts from marine invertebrates. Finally, ∼65% of nematode-associated MAGs are able to degrade chitin, via hexosaminidase, implying that benthic invertebrate holobionts make significant contributions to global carbon cycling. These results underline the importance of evaluating symbiosis in microscopic marine invertebrates, and accelerating our understanding of animal evolution and ecosystem dynamics in vast benthic habitats.
Additional Links: PMID-42845486
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@article {pmid42845486,
year = {2026},
author = {De Santiago, A and Han, MK and Hargadon, SB and Marcellino Barros, M and Brito De Jesus, S and Pereira, TJ and Bik, HM},
title = {Marine nematodes exhibit widespread symbiosis, novel chemoautotrophy, and evolutionary conservation of holobiont taxa.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.12.744518},
pmid = {42845486},
issn = {2692-8205},
abstract = {Microbial symbioses drive the evolutionary and functional diversification of eukaryotic clades, from single-celled protists to large invertebrates. However, our knowledge of host-associated assemblages (the "holobiont") is limited in microscopic animal phyla with a body size <1mm, due to practical challenges such as low biomass and difficult taxonomy of host species. Marine nematodes represent an ideal case study for rapidly advancing our knowledge of bacterial-animal symbioses, representing a globally abundant invertebrate group with strong links to terrestrial and model organism species within the same phylum. Here, we sequenced the holobionts of 220 marine nematodes and generated 815 metagenome-assembled genomes (MAGs) of host-associated bacteria/archaea. Our data indicates that 20-34% of marine nematodes harbor an obligate intracellular symbiont, often with multiple endosymbionts co-occurring within the same host. Three bacterial phyla (Pseudomonadota Bacteroidota, and Verrucomicrobiota) account for three-quarters of all nematode-associated MAGs, and the majority of these holobiont MAGs represent deeply divergent lineages in the prokaryotic tree of life. The Flavobacteriaceae (a core microbiome taxon in C. elegans and other terrestrial nematodes), were consistently recovered across phylogenetically diverse marine nematode lineages, suggesting evolutionary conservation of holobiont taxa across marine and terrestrial environments. We also report a novel chemoautotroph family (Ca. Thionematobacter) recovered from nematode hosts in both deep-sea and shallow-water habitats, and report the first confirmed instance of Cardinium endosymbionts from marine invertebrates. Finally, ∼65% of nematode-associated MAGs are able to degrade chitin, via hexosaminidase, implying that benthic invertebrate holobionts make significant contributions to global carbon cycling. These results underline the importance of evaluating symbiosis in microscopic marine invertebrates, and accelerating our understanding of animal evolution and ecosystem dynamics in vast benthic habitats.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Systematic quantification and removal of host DNA contamination in 16S rRNA gene sequencing.
Quantitative biology (Beijing, China), 14(4):e70055.
16S ribosomal RNA (rRNA) gene sequencing is a standard tool for microbial community analysis. Challenges can occur, particularly in low-biomass samples, when host DNA triggers off-target amplification. Low-biomass microbiome studies are particularly vulnerable to contamination from host DNA, which can obscure microbial signals and bias interpretation. This contamination presents a significant barrier to accurately characterizing microbial communities, especially in clinical or environmental samples with limited bacterial DNA. To systematically quantify and mitigate host DNA interference, we constructed a bacterial mock community dilution series spiked with controlled proportions of human DNA. Using 16S rRNA gene sequencing, we assessed how increasing host DNA affects microbial community profiles and evaluated several computational approaches for removing host-derived sequences, including pre-clustering filtering, post-clustering operational taxonomic unit (OTU) filtering, and the R package Decontam. We found that off-target amplification was more prevalent when the bacterial content was less than 10% relative to host DNA. Total DNA concentration induced minimal bias. Post-clustering OTU filtering and reference genome mapping effectively reduced host contamination. Among the tested correction strategies, post-clustering OTU filtering proved most effective and computationally sustainable, achieving nearly complete removal of host-derived reads with minimal effect on microbial diversity estimates. Although 16S rRNA gene sequencing remains a cost-effective and high-throughput technology, it requires rigorous methodological controls in low-biomass contexts. Our study offers a systematic evaluation of off-target amplification effects and practical mitigation strategies to improve the accuracy of microbial community analysis. The presented framework provides a robust and scalable approach for identifying and removing host contamination from low-biomass 16S rRNA sequencing data.
Additional Links: PMID-42845678
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@article {pmid42845678,
year = {2026},
author = {Birkner, T and Patricia Bartolomaeus, TU and McParland, V and Forslund-Startceva, SK and Löber, U},
title = {Systematic quantification and removal of host DNA contamination in 16S rRNA gene sequencing.},
journal = {Quantitative biology (Beijing, China)},
volume = {14},
number = {4},
pages = {e70055},
pmid = {42845678},
issn = {2095-4697},
abstract = {16S ribosomal RNA (rRNA) gene sequencing is a standard tool for microbial community analysis. Challenges can occur, particularly in low-biomass samples, when host DNA triggers off-target amplification. Low-biomass microbiome studies are particularly vulnerable to contamination from host DNA, which can obscure microbial signals and bias interpretation. This contamination presents a significant barrier to accurately characterizing microbial communities, especially in clinical or environmental samples with limited bacterial DNA. To systematically quantify and mitigate host DNA interference, we constructed a bacterial mock community dilution series spiked with controlled proportions of human DNA. Using 16S rRNA gene sequencing, we assessed how increasing host DNA affects microbial community profiles and evaluated several computational approaches for removing host-derived sequences, including pre-clustering filtering, post-clustering operational taxonomic unit (OTU) filtering, and the R package Decontam. We found that off-target amplification was more prevalent when the bacterial content was less than 10% relative to host DNA. Total DNA concentration induced minimal bias. Post-clustering OTU filtering and reference genome mapping effectively reduced host contamination. Among the tested correction strategies, post-clustering OTU filtering proved most effective and computationally sustainable, achieving nearly complete removal of host-derived reads with minimal effect on microbial diversity estimates. Although 16S rRNA gene sequencing remains a cost-effective and high-throughput technology, it requires rigorous methodological controls in low-biomass contexts. Our study offers a systematic evaluation of off-target amplification effects and practical mitigation strategies to improve the accuracy of microbial community analysis. The presented framework provides a robust and scalable approach for identifying and removing host contamination from low-biomass 16S rRNA sequencing data.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Precise assessment of facial skin based on multimodal data fusion of the microbiome.
Quantitative biology (Beijing, China), 14(3):e70046.
The skin microecology plays a vital role in maintaining cutaneous health and is intricately linked to host skin phenotypes. However, there remains a lack of precise and quantitative biomarkers for evaluating skin health conditions, making it challenging to identify individuals at potential risk of microecological imbalance. In this study, we collected facial skin microbiomes from 242 female volunteers aged 16-50 years in Shanghai, China. Microbial communities were surveyed using 16S rRNA gene sequencing and integrated with high-resolution facial images and host skin phenotypes for comprehensive analysis. Our findings reveal that although the community complexity of the facial microbiome is comparable between individuals with "ideal" and "non-ideal" skin conditions, the composition and structure of key microbes varied significantly between the two groups. Differential abundance analysis further emphasized the role of interactions between the skin microbiome and host phenotypic traits in skin aging and status transitions. To enable a more holistic and quantitative assessment of facial skin status, we developed a novel multimodal skin index (MSI) that fuses multiple modal data from facial images, microbiome profiles, and host skin phenotype features through a deep learning-based framework. Importantly, MSI identified individuals with an outwardly healthy facial appearance but significant underlying microbial dysbiosis that conventional diagnostic approaches often overlook. This work enables the detection of such hidden risks, offering new avenues for individualized facial skin health assessment, precision dermatology, and microbiome-informed esthetic interventions.
Additional Links: PMID-42845732
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@article {pmid42845732,
year = {2026},
author = {Meng, F and Zhang, J and Yuan, C and Li, R and Sun, Y and Jiang, H and Yang, S and Li, Y and Su, X},
title = {Precise assessment of facial skin based on multimodal data fusion of the microbiome.},
journal = {Quantitative biology (Beijing, China)},
volume = {14},
number = {3},
pages = {e70046},
pmid = {42845732},
issn = {2095-4697},
abstract = {The skin microecology plays a vital role in maintaining cutaneous health and is intricately linked to host skin phenotypes. However, there remains a lack of precise and quantitative biomarkers for evaluating skin health conditions, making it challenging to identify individuals at potential risk of microecological imbalance. In this study, we collected facial skin microbiomes from 242 female volunteers aged 16-50 years in Shanghai, China. Microbial communities were surveyed using 16S rRNA gene sequencing and integrated with high-resolution facial images and host skin phenotypes for comprehensive analysis. Our findings reveal that although the community complexity of the facial microbiome is comparable between individuals with "ideal" and "non-ideal" skin conditions, the composition and structure of key microbes varied significantly between the two groups. Differential abundance analysis further emphasized the role of interactions between the skin microbiome and host phenotypic traits in skin aging and status transitions. To enable a more holistic and quantitative assessment of facial skin status, we developed a novel multimodal skin index (MSI) that fuses multiple modal data from facial images, microbiome profiles, and host skin phenotype features through a deep learning-based framework. Importantly, MSI identified individuals with an outwardly healthy facial appearance but significant underlying microbial dysbiosis that conventional diagnostic approaches often overlook. This work enables the detection of such hidden risks, offering new avenues for individualized facial skin health assessment, precision dermatology, and microbiome-informed esthetic interventions.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Gut-brain axis dysfunction in Parkinson's disease: a meta-analysis of microbiome dysbiosis and intestinal barrier markers.
Frontiers in medicine, 13:1909087.
BACKGROUND: Parkinson's disease (PD) has traditionally been conceptualized as a neurodegenerative disorder centered within the central nervous system. However, growing evidence suggests that gastrointestinal dysfunction, intestinal permeability abnormalities, and gut microbiome dysbiosis may contribute to disease initiation and progression in a subset of patients. While several studies have characterized microbial alterations in PD, the integration of dysbiosis with intestinal barrier dysfunction and emerging phenotype-oriented models remains incompletely synthesized.
METHODS: A systematic review and meta-analysis was conducted according to PRISMA 2020 guidelines. PubMed, Embase, Scopus, Web of Science, and Cochrane Library databases were searched from inception to January 2025 for studies evaluating gut microbiota composition and/or intestinal permeability markers in Parkinson's disease. Random-effects meta-analysis was performed using standardized mean differences (SMDs) with subgroup and sensitivity analyses exploring geographic variation, sequencing methodology, disease duration, and phenotype-specific findings.
RESULTS: Thirty-four studies were identified; one (an experimental fecal-microbiota-transfer study in mice) was reclassified as preclinical mechanistic evidence rather than a primary human dataset. The remaining 33 human studies comprised 1,588 PD patients and 1,449 healthy controls. Consistent microbial alterations were identified across studies, characterized by depletion of short-chain fatty acid-producing taxa including Prevotellaceae, Faecalibacterium, and Lachnospiraceae, alongside enrichment of Akkermansia, Bifidobacteriaceae, and Christensenellaceae. Elevated fecal calprotectin and zonulin levels suggested concomitant low-grade intestinal inflammation and impaired epithelial barrier integrity. In limited phenotype-stratified subgroup analyses, gut-first PD phenotypes showed potentially more pronounced dysbiosis patterns than brain-first phenotypes; this preliminary observation is based on very few phenotype-stratified studies and requires validation in larger, prospective cohorts. Functional interpretation of the included literature suggested potential alterations in butyrate metabolism, mucosal barrier maintenance, inflammatory signaling, and microbial-host immune interactions.
CONCLUSION: Parkinson's disease is associated with reproducible alterations in gut microbial composition together with evidence of intestinal barrier dysfunction. Although causality cannot be established from predominantly observational studies, the findings support a biologically plausible role for gut-related mechanisms in disease pathophysiology, with a preliminary signal for more pronounced involvement in gut-first PD phenotypes that remains to be confirmed. Future longitudinal and mechanistic studies integrating microbiome, metabolomic, and permeability data are required to clarify therapeutic and biomarker implications.
https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD420251078511, CRD420251078511.
Additional Links: PMID-42845985
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@article {pmid42845985,
year = {2026},
author = {Mehrotra, P and Vengadakrishnan, K and Mehrotra, P and Dan, S},
title = {Gut-brain axis dysfunction in Parkinson's disease: a meta-analysis of microbiome dysbiosis and intestinal barrier markers.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1909087},
pmid = {42845985},
issn = {2296-858X},
abstract = {BACKGROUND: Parkinson's disease (PD) has traditionally been conceptualized as a neurodegenerative disorder centered within the central nervous system. However, growing evidence suggests that gastrointestinal dysfunction, intestinal permeability abnormalities, and gut microbiome dysbiosis may contribute to disease initiation and progression in a subset of patients. While several studies have characterized microbial alterations in PD, the integration of dysbiosis with intestinal barrier dysfunction and emerging phenotype-oriented models remains incompletely synthesized.
METHODS: A systematic review and meta-analysis was conducted according to PRISMA 2020 guidelines. PubMed, Embase, Scopus, Web of Science, and Cochrane Library databases were searched from inception to January 2025 for studies evaluating gut microbiota composition and/or intestinal permeability markers in Parkinson's disease. Random-effects meta-analysis was performed using standardized mean differences (SMDs) with subgroup and sensitivity analyses exploring geographic variation, sequencing methodology, disease duration, and phenotype-specific findings.
RESULTS: Thirty-four studies were identified; one (an experimental fecal-microbiota-transfer study in mice) was reclassified as preclinical mechanistic evidence rather than a primary human dataset. The remaining 33 human studies comprised 1,588 PD patients and 1,449 healthy controls. Consistent microbial alterations were identified across studies, characterized by depletion of short-chain fatty acid-producing taxa including Prevotellaceae, Faecalibacterium, and Lachnospiraceae, alongside enrichment of Akkermansia, Bifidobacteriaceae, and Christensenellaceae. Elevated fecal calprotectin and zonulin levels suggested concomitant low-grade intestinal inflammation and impaired epithelial barrier integrity. In limited phenotype-stratified subgroup analyses, gut-first PD phenotypes showed potentially more pronounced dysbiosis patterns than brain-first phenotypes; this preliminary observation is based on very few phenotype-stratified studies and requires validation in larger, prospective cohorts. Functional interpretation of the included literature suggested potential alterations in butyrate metabolism, mucosal barrier maintenance, inflammatory signaling, and microbial-host immune interactions.
CONCLUSION: Parkinson's disease is associated with reproducible alterations in gut microbial composition together with evidence of intestinal barrier dysfunction. Although causality cannot be established from predominantly observational studies, the findings support a biologically plausible role for gut-related mechanisms in disease pathophysiology, with a preliminary signal for more pronounced involvement in gut-first PD phenotypes that remains to be confirmed. Future longitudinal and mechanistic studies integrating microbiome, metabolomic, and permeability data are required to clarify therapeutic and biomarker implications.
https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD420251078511, CRD420251078511.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Gut microbiome diversity, genus-level variation, and associations with clinical features in critically ill patients.
Frontiers in medicine, 13:1903736.
BACKGROUND: Gut microbiota alterations are common in critical illness, but differences between critically ill patients with and without sepsis and their clinical relevance remain incompletely understood. We investigated gut microbial diversity, genus-level differences and their associations with inflammatory profiles and clinical outcomes in critically ill patients.
METHODS: This single-centre case-control study enrolled adult critically ill patients grouped by Sepsis-3 criteria. Gut microbiota was profiled by 16S rRNA sequencing. The primary M2 model, adjusted for age, intra-abdominal infection, pre-sampling anti-anaerobic antibiotic exposure, APACHE II score, and chronic kidney disease, was used for all adjusted analyses. Alpha diversity was analyzed with HC3-robust linear regression; beta diversity with PERMANOVA, PERMDISP, and dbRDA. Genus-level primary discovery used Wilcoxon rank-sum with Benjamini-Hochberg FDR and |log2 fold change| threshold. Complementary sensitivity analyses used fully adjusted MaAsLin2 and ANCOM-BC2 with pseudo-count sensitivity. Associations of the four Wilcoxon-identified genera with clinical variables were assessed via partial Spearman correlations, logistic regression, and longitudinal mixed-effects models.
RESULTS: Of 103 participants, 68 had sepsis and 35 did not. After M2 adjustment, Shannon, Simpson, and Pielou evenness were lower in sepsis (β = -0.60, -0.54, -0.60; all q = 0.025), whereas Chao1 richness and observed species did not differ. Bray-Curtis and Jaccard group effects did not meet FDR threshold. Wilcoxon identified higher Lactococcus_A and lower Ezakiella, Fenollaria, Peptoniphilus_B in sepsis. ANCOM-BC2 signals were not robust to pseudo-count sensitivity, and MaAsLin2 identified no significant genus (min q = 0.333), indicating genus-level findings inconsistent across methods. No cross-sectional clinical association met significance after FDR correction. Longitudinal analyses found time-by-genus interactions: Fenollaria with CRP (q = 0.010), Peptoniphilus_B with PCT (q = 0.042) and CRP (q = 0.010).
CONCLUSIONS: Sepsis was associated with lower values for selected alpha-diversity measures, whereas differences in overall community composition were modest. Four genera met the primary FDR- and effect-size-adjusted Wilcoxon criteria, but genus-level differences were not consistently supported across Wilcoxon, ANCOM-BC2 and MaAsLin2, indicating these are exploratory signals rather than confirmed candidates. Associations with clinical features and inflammatory markers were limited; therefore, these findings should be considered exploratory and validated using multiple analytical approaches in independent cohorts.
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@article {pmid42846293,
year = {2026},
author = {Wang, Y and Guo, P and Shen, J},
title = {Gut microbiome diversity, genus-level variation, and associations with clinical features in critically ill patients.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1903736},
doi = {10.3389/fmed.2026.1903736},
pmid = {42846293},
issn = {2296-858X},
abstract = {BACKGROUND: Gut microbiota alterations are common in critical illness, but differences between critically ill patients with and without sepsis and their clinical relevance remain incompletely understood. We investigated gut microbial diversity, genus-level differences and their associations with inflammatory profiles and clinical outcomes in critically ill patients.
METHODS: This single-centre case-control study enrolled adult critically ill patients grouped by Sepsis-3 criteria. Gut microbiota was profiled by 16S rRNA sequencing. The primary M2 model, adjusted for age, intra-abdominal infection, pre-sampling anti-anaerobic antibiotic exposure, APACHE II score, and chronic kidney disease, was used for all adjusted analyses. Alpha diversity was analyzed with HC3-robust linear regression; beta diversity with PERMANOVA, PERMDISP, and dbRDA. Genus-level primary discovery used Wilcoxon rank-sum with Benjamini-Hochberg FDR and |log2 fold change| threshold. Complementary sensitivity analyses used fully adjusted MaAsLin2 and ANCOM-BC2 with pseudo-count sensitivity. Associations of the four Wilcoxon-identified genera with clinical variables were assessed via partial Spearman correlations, logistic regression, and longitudinal mixed-effects models.
RESULTS: Of 103 participants, 68 had sepsis and 35 did not. After M2 adjustment, Shannon, Simpson, and Pielou evenness were lower in sepsis (β = -0.60, -0.54, -0.60; all q = 0.025), whereas Chao1 richness and observed species did not differ. Bray-Curtis and Jaccard group effects did not meet FDR threshold. Wilcoxon identified higher Lactococcus_A and lower Ezakiella, Fenollaria, Peptoniphilus_B in sepsis. ANCOM-BC2 signals were not robust to pseudo-count sensitivity, and MaAsLin2 identified no significant genus (min q = 0.333), indicating genus-level findings inconsistent across methods. No cross-sectional clinical association met significance after FDR correction. Longitudinal analyses found time-by-genus interactions: Fenollaria with CRP (q = 0.010), Peptoniphilus_B with PCT (q = 0.042) and CRP (q = 0.010).
CONCLUSIONS: Sepsis was associated with lower values for selected alpha-diversity measures, whereas differences in overall community composition were modest. Four genera met the primary FDR- and effect-size-adjusted Wilcoxon criteria, but genus-level differences were not consistently supported across Wilcoxon, ANCOM-BC2 and MaAsLin2, indicating these are exploratory signals rather than confirmed candidates. Associations with clinical features and inflammatory markers were limited; therefore, these findings should be considered exploratory and validated using multiple analytical approaches in independent cohorts.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Understanding the regulatory mechanisms of nanomaterials on carbon metabolism in plants.
Fundamental research, 6(5):2974-2985 pii:S2667-3258(26)00245-1.
Agricultural nanotechnology offers innovative strategies to enhance crop productivity by modulating fundamental physiological processes in plants. Despite growing evidence that nanomaterials (NMs) can significantly promote crop growth, a standardized theoretical framework explaining the underlying mechanisms remains elusive. This review proposes a systematic framework to elucidate how NMs positively regulate plant carbon assimilation and partitioning to ultimately enhance crop yield. We categorize internal carbon flow into three interconnected modules:(1) inorganic-organic carbon inter-conversion (photosynthesis and respiration), (2) organic carbon intra-conversion (sucrose and starch metabolism, alongside amino acid and fatty acid metabolism), and (3) supporting metabolic processes (nitrogen and secondary metabolism) that supply essential substrates and energy. To enhance carbon assimilation, NMs must be strategically selected to improve photosynthetic light conversion efficiency, electron transport, and enzyme activities, promote fatty acid metabolism, and bolster the glutamine synthetase-glutamate synthase (GS-GOGAT) cycle in nitrogen metabolism. Furthermore, NMs can modulate root exudates and reshape the structure and function of the rhizosphere microbiome, which in turn establishes a feedback loop that influences plant carbon assimilation and partitioning. This review also addresses the critical trade-offs between the economic potential and environmental risks of NMs, providing essential insights for their sustainable implementation in agriculture. Collectively, it provides a mechanistic framework for understanding NMs-plant interactions, paving the way for the rational design of nano-agricultural tools for sustainable yield improvement.
Additional Links: PMID-42846506
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@article {pmid42846506,
year = {2026},
author = {Zhang, X and Zhang, X and Ban, Z and White, JC and Xu, Y and Yang, J and Hou, X and Wu, F and Xing, B and Zhao, Q},
title = {Understanding the regulatory mechanisms of nanomaterials on carbon metabolism in plants.},
journal = {Fundamental research},
volume = {6},
number = {5},
pages = {2974-2985},
doi = {10.1016/j.fmre.2026.04.023},
pmid = {42846506},
issn = {2667-3258},
abstract = {Agricultural nanotechnology offers innovative strategies to enhance crop productivity by modulating fundamental physiological processes in plants. Despite growing evidence that nanomaterials (NMs) can significantly promote crop growth, a standardized theoretical framework explaining the underlying mechanisms remains elusive. This review proposes a systematic framework to elucidate how NMs positively regulate plant carbon assimilation and partitioning to ultimately enhance crop yield. We categorize internal carbon flow into three interconnected modules:(1) inorganic-organic carbon inter-conversion (photosynthesis and respiration), (2) organic carbon intra-conversion (sucrose and starch metabolism, alongside amino acid and fatty acid metabolism), and (3) supporting metabolic processes (nitrogen and secondary metabolism) that supply essential substrates and energy. To enhance carbon assimilation, NMs must be strategically selected to improve photosynthetic light conversion efficiency, electron transport, and enzyme activities, promote fatty acid metabolism, and bolster the glutamine synthetase-glutamate synthase (GS-GOGAT) cycle in nitrogen metabolism. Furthermore, NMs can modulate root exudates and reshape the structure and function of the rhizosphere microbiome, which in turn establishes a feedback loop that influences plant carbon assimilation and partitioning. This review also addresses the critical trade-offs between the economic potential and environmental risks of NMs, providing essential insights for their sustainable implementation in agriculture. Collectively, it provides a mechanistic framework for understanding NMs-plant interactions, paving the way for the rational design of nano-agricultural tools for sustainable yield improvement.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Immune remodeling in HPV-associated cervical disease.
Frontiers in cellular and infection microbiology, 16:1918480.
INTRODUCTION: Persistent high-risk HPV infection is the principal cause of cervical dysplasia, but variation in disease phenotype may also be associated with differences in the local immune and microbial environment.
METHODS: We characterized the cervicovaginal immune microenvironment in relation to HPV status, vaginal community state type (CST), and cytological grade.
RESULTS: HPV-positive samples showed reduced IL-4 and IL-17E/IL-25, while IFN-α2 and IL-3 varied across community state types in a non-monotonic, CST-specific manner: IFN-α2 was relatively elevated in the Lactobacillus gasseri-dominant CST II, and IL-3 was specifically reduced in the Lactobacillus jensenii-dominant CST V. Cytological category was associated with non-monotonic, marker-specific immune variation, with LSIL showing lower IL-4, IFN-γ, IL-17F, PDGF-AB/BB, IL-17E/IL-25, and PDGF-AA levels relative to NILM, while ASC-H showed a distinct rather than uniformly progressive immune profile. CLR-based multi-kingdom analyses identified a restricted set of taxon-cytokine associations after correction of the relative-abundance scale, prespecified prevalence and abundance filtering, and multiple-testing correction. Significant bacterial associations were confined to the genus level, whereas viral associations were observed at the family, genus, and species levels and fungal associations at the family level. Phocaeicola-IL-10 and Rountreeviridae-MIP-1β were the only associations that additionally remained significant after global BH-FDR correction across all taxon-immune-marker tests. Viral and fungal findings were interpreted as exploratory because of substantially lower non-bacterial sequencing depth.
DISCUSSION: These microbial associations provide additional context for the observed immune-marker differences. These findings support further investigation of multi-kingdom host-microbiome immune relationships in HPV-associated cervical abnormalities.
Additional Links: PMID-42846579
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@article {pmid42846579,
year = {2026},
author = {Chulenbayeva, L and Rakhmankulova, A and Kamzayeva, N and Kozhakhmetov, S and Kovenskiy, A and Nurgaziyev, M and Ukybassova, T and Kushugulova, A},
title = {Immune remodeling in HPV-associated cervical disease.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1918480},
doi = {10.3389/fcimb.2026.1918480},
pmid = {42846579},
issn = {2235-2988},
mesh = {Humans ; Female ; *Papillomavirus Infections/immunology/virology/pathology ; Cytokines/metabolism ; *Human Papillomavirus Viruses/immunology ; Vagina/immunology/microbiology/virology ; Cervix Uteri/immunology/virology/pathology ; Microbiota ; *Uterine Cervical Dysplasia/immunology/virology/pathology ; *Uterine Cervical Diseases/immunology/virology/pathology ; },
abstract = {INTRODUCTION: Persistent high-risk HPV infection is the principal cause of cervical dysplasia, but variation in disease phenotype may also be associated with differences in the local immune and microbial environment.
METHODS: We characterized the cervicovaginal immune microenvironment in relation to HPV status, vaginal community state type (CST), and cytological grade.
RESULTS: HPV-positive samples showed reduced IL-4 and IL-17E/IL-25, while IFN-α2 and IL-3 varied across community state types in a non-monotonic, CST-specific manner: IFN-α2 was relatively elevated in the Lactobacillus gasseri-dominant CST II, and IL-3 was specifically reduced in the Lactobacillus jensenii-dominant CST V. Cytological category was associated with non-monotonic, marker-specific immune variation, with LSIL showing lower IL-4, IFN-γ, IL-17F, PDGF-AB/BB, IL-17E/IL-25, and PDGF-AA levels relative to NILM, while ASC-H showed a distinct rather than uniformly progressive immune profile. CLR-based multi-kingdom analyses identified a restricted set of taxon-cytokine associations after correction of the relative-abundance scale, prespecified prevalence and abundance filtering, and multiple-testing correction. Significant bacterial associations were confined to the genus level, whereas viral associations were observed at the family, genus, and species levels and fungal associations at the family level. Phocaeicola-IL-10 and Rountreeviridae-MIP-1β were the only associations that additionally remained significant after global BH-FDR correction across all taxon-immune-marker tests. Viral and fungal findings were interpreted as exploratory because of substantially lower non-bacterial sequencing depth.
DISCUSSION: These microbial associations provide additional context for the observed immune-marker differences. These findings support further investigation of multi-kingdom host-microbiome immune relationships in HPV-associated cervical abnormalities.},
}
MeSH Terms:
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Humans
Female
*Papillomavirus Infections/immunology/virology/pathology
Cytokines/metabolism
*Human Papillomavirus Viruses/immunology
Vagina/immunology/microbiology/virology
Cervix Uteri/immunology/virology/pathology
Microbiota
*Uterine Cervical Dysplasia/immunology/virology/pathology
*Uterine Cervical Diseases/immunology/virology/pathology
RevDate: 2026-10-08
CmpDate: 2026-10-08
Restoring NAD[+] pathways in brain aging and neurodegenerative diseases: roles of vitamin B3 metabolites, gut microbiota, and exercise in cognitive health.
Frontiers in nutrition, 13:1865556.
Aging and neurodegenerative disorders (NDDs) are intricately linked to a gradual deterioration in nicotinamide adenine dinucleotide (NAD[+]) metabolism, compromised mitochondrial functionality, persistent inflammation, and modified gut-brain interactions. Derivatives of vitamin B3, such as niacin, nicotinamide, nicotinamide riboside, and nicotinamide mononucleotide, have been identified as pivotal NAD[+] precursors that possess the potential to support cellular bioenergetic processes and modulate pathways associated with brain aging. Evidence from preclinical studies and emerging clinical investigations suggests that NAD[+]-enhancing interventions may improve mitochondrial function and modulate neuroinflammatory pathways, thereby supporting cellular processes involved in synaptic plasticity and cognitive function; however, their long-term efficacy and clinical relevance in NDDs remain to be fully established. Concurrently, physical exercise serves as a robust physiological stimulus that augments NAD[+] biosynthesis, modulates hypoxia-inducible factor-1α-dependent adaptive responses, fosters neurotrophic signaling, and enhances both vascular and metabolic health of the brain. Furthermore, emerging evidence suggests that the gut microbiota directly contributes to NAD[+] homeostasis by regulating vitamin B3 precursor availability, tryptophan metabolism, and host metabolic signaling, while also influencing the efficacy of NAD[+]-enhancing interventions, thereby affecting systemic inflammation, metabolic equilibrium, and the production of neuroactive metabolites. Collectively, the interaction among vitamin B3 supplementation, physical activity, and gut microbiota may represent a promising framework for investigating strategies aimed at supporting cognitive health and brain resilience during aging, although definitive therapeutic applications require further validation. This review integrates current molecular, preclinical, and clinical evidence to establish mechanistic links between NAD[+] metabolism, brain aging, cognitive dysfunction, and neurodegeneration, while emphasizing current limitations and future translational challenges associated with combining vitamin B3 metabolites, exercise, and microbiome-targeted approaches.
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@article {pmid42846758,
year = {2026},
author = {Zhang, W},
title = {Restoring NAD[+] pathways in brain aging and neurodegenerative diseases: roles of vitamin B3 metabolites, gut microbiota, and exercise in cognitive health.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1865556},
doi = {10.3389/fnut.2026.1865556},
pmid = {42846758},
issn = {2296-861X},
abstract = {Aging and neurodegenerative disorders (NDDs) are intricately linked to a gradual deterioration in nicotinamide adenine dinucleotide (NAD[+]) metabolism, compromised mitochondrial functionality, persistent inflammation, and modified gut-brain interactions. Derivatives of vitamin B3, such as niacin, nicotinamide, nicotinamide riboside, and nicotinamide mononucleotide, have been identified as pivotal NAD[+] precursors that possess the potential to support cellular bioenergetic processes and modulate pathways associated with brain aging. Evidence from preclinical studies and emerging clinical investigations suggests that NAD[+]-enhancing interventions may improve mitochondrial function and modulate neuroinflammatory pathways, thereby supporting cellular processes involved in synaptic plasticity and cognitive function; however, their long-term efficacy and clinical relevance in NDDs remain to be fully established. Concurrently, physical exercise serves as a robust physiological stimulus that augments NAD[+] biosynthesis, modulates hypoxia-inducible factor-1α-dependent adaptive responses, fosters neurotrophic signaling, and enhances both vascular and metabolic health of the brain. Furthermore, emerging evidence suggests that the gut microbiota directly contributes to NAD[+] homeostasis by regulating vitamin B3 precursor availability, tryptophan metabolism, and host metabolic signaling, while also influencing the efficacy of NAD[+]-enhancing interventions, thereby affecting systemic inflammation, metabolic equilibrium, and the production of neuroactive metabolites. Collectively, the interaction among vitamin B3 supplementation, physical activity, and gut microbiota may represent a promising framework for investigating strategies aimed at supporting cognitive health and brain resilience during aging, although definitive therapeutic applications require further validation. This review integrates current molecular, preclinical, and clinical evidence to establish mechanistic links between NAD[+] metabolism, brain aging, cognitive dysfunction, and neurodegeneration, while emphasizing current limitations and future translational challenges associated with combining vitamin B3 metabolites, exercise, and microbiome-targeted approaches.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Gut microbiome-driven mechanisms in inflammatory bowel disease-associated interstitial lung disease: from dysbiosis to therapeutic implications.
Frontiers in cellular and infection microbiology, 16:1967125.
Inflammatory bowel disease (IBD) is a chronic, relapsing immune-mediated disorder of the gastrointestinal tract. Interstitial lung disease (ILD) associated with inflammatory bowel disease has been receiving increasing attention. With advances in the gut-lung axis theory, accumulating epidemiological and mechanistic evidence indicates that the association between IBD and ILD is not coincidental or merely driven by drug toxicity, but rather reflects a systemic disease spectrum involving microbiome dysbiosis and cross-organ immune dialogue. This article presents a critical narrative review that systematically summarizes the mechanisms underlying IBD-related ILD, focusing on causal evidence from large cohort and Mendelian randomization studies. It also looks at how gut microbial metabolites remotely regulate lung immune homeostasis, the inflammatory cascades triggered by gut barrier disruption and bacterial translocation, and the therapeutic potential of microbiome-based interventions. This article examines the main limitations and controversies, including the limited accuracy of animal models, the unclear causal link between microbial changes and disease onset, and the challenges in selecting clinical trial endpoints. It also outlines future research directions, focusing on integrating multi-omics, non-invasive diagnostic models, and strategies to distinguish drug-induced lung injury from primary disease involvement. This review aims to elucidate the pathogenesis of this cross-organ disease spectrum and to provide a theoretical foundation for both basic research and clinical translation.
Additional Links: PMID-42846765
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@article {pmid42846765,
year = {2026},
author = {Yang, Y and Zhang, D and Liu, W},
title = {Gut microbiome-driven mechanisms in inflammatory bowel disease-associated interstitial lung disease: from dysbiosis to therapeutic implications.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1967125},
doi = {10.3389/fcimb.2026.1967125},
pmid = {42846765},
issn = {2235-2988},
mesh = {Humans ; *Inflammatory Bowel Diseases/complications/microbiology/therapy ; *Dysbiosis/complications ; *Lung Diseases, Interstitial/therapy/etiology/microbiology ; *Gastrointestinal Microbiome ; Animals ; Intestinal Barrier Function ; },
abstract = {Inflammatory bowel disease (IBD) is a chronic, relapsing immune-mediated disorder of the gastrointestinal tract. Interstitial lung disease (ILD) associated with inflammatory bowel disease has been receiving increasing attention. With advances in the gut-lung axis theory, accumulating epidemiological and mechanistic evidence indicates that the association between IBD and ILD is not coincidental or merely driven by drug toxicity, but rather reflects a systemic disease spectrum involving microbiome dysbiosis and cross-organ immune dialogue. This article presents a critical narrative review that systematically summarizes the mechanisms underlying IBD-related ILD, focusing on causal evidence from large cohort and Mendelian randomization studies. It also looks at how gut microbial metabolites remotely regulate lung immune homeostasis, the inflammatory cascades triggered by gut barrier disruption and bacterial translocation, and the therapeutic potential of microbiome-based interventions. This article examines the main limitations and controversies, including the limited accuracy of animal models, the unclear causal link between microbial changes and disease onset, and the challenges in selecting clinical trial endpoints. It also outlines future research directions, focusing on integrating multi-omics, non-invasive diagnostic models, and strategies to distinguish drug-induced lung injury from primary disease involvement. This review aims to elucidate the pathogenesis of this cross-organ disease spectrum and to provide a theoretical foundation for both basic research and clinical translation.},
}
MeSH Terms:
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Humans
*Inflammatory Bowel Diseases/complications/microbiology/therapy
*Dysbiosis/complications
*Lung Diseases, Interstitial/therapy/etiology/microbiology
*Gastrointestinal Microbiome
Animals
Intestinal Barrier Function
RevDate: 2026-10-08
CmpDate: 2026-10-08
Gut-brain immune dysregulation in Parkinson's disease: a hypothesis-forming narrative review of trained immunity.
Frontiers in aging neuroscience, 18:1973833.
Parkinson's disease (PD) is increasingly understood as a multisystem disorder in which gastrointestinal dysfunction, immune remodeling, protein aggregation, and central neurodegeneration interact across the disease course. Although gut microbiota alterations are repeatedly reported in PD, taxonomic differences alone do not explain how peripheral ecological signals acquire neurological relevance. This review therefore focuses on immune translation: the processes through which dysbiosis, microbial metabolites, intestinal barrier stress, and mucosal inflammation may reshape peripheral immunity and lower the threshold for central neuroinflammatory responses. Particular attention is given to trained immunity as a mechanistic framework that may connect repeated low-grade gut-derived stimulation with persistent innate immune reprogramming. Direct evidence that trained immunity drives PD remains limited; the concept is presented as a testable bridge rather than an established causal pathway. We integrate this framework with age-related immunosenescence and inflammaging, enteric nervous system vulnerability, vagal communication, alpha-synuclein pathology, blood-brain barrier signaling, and microglial priming. Human microbiome studies, Parkinsonian animal models, LPS-based innate immune-memory paradigms, and emerging intervention trials are considered according to their evidentiary level and major confounders, including constipation, diet, medication exposure, geography, and disease stage. The resulting model accommodates body-first, brain-first, and mixed trajectories rather than assigning a universal gut origin to PD. Therapeutically, the evidence supports a shift from nonspecific microbiome normalization toward mechanism-matched strategies that combine ecological, immune, metabolic, and clinical biomarkers. Longitudinal prodromal cohorts and integrated multi-omics with immune phenotyping will be essential to determine whether gut-brain immune signatures identify causal pathways, progression markers, or treatment-responsive subgroups.
Additional Links: PMID-42846826
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@article {pmid42846826,
year = {2026},
author = {Tang, M and Li, J and Zhang, C and Tu, R and Wang, S},
title = {Gut-brain immune dysregulation in Parkinson's disease: a hypothesis-forming narrative review of trained immunity.},
journal = {Frontiers in aging neuroscience},
volume = {18},
number = {},
pages = {1973833},
doi = {10.3389/fnagi.2026.1973833},
pmid = {42846826},
issn = {1663-4365},
abstract = {Parkinson's disease (PD) is increasingly understood as a multisystem disorder in which gastrointestinal dysfunction, immune remodeling, protein aggregation, and central neurodegeneration interact across the disease course. Although gut microbiota alterations are repeatedly reported in PD, taxonomic differences alone do not explain how peripheral ecological signals acquire neurological relevance. This review therefore focuses on immune translation: the processes through which dysbiosis, microbial metabolites, intestinal barrier stress, and mucosal inflammation may reshape peripheral immunity and lower the threshold for central neuroinflammatory responses. Particular attention is given to trained immunity as a mechanistic framework that may connect repeated low-grade gut-derived stimulation with persistent innate immune reprogramming. Direct evidence that trained immunity drives PD remains limited; the concept is presented as a testable bridge rather than an established causal pathway. We integrate this framework with age-related immunosenescence and inflammaging, enteric nervous system vulnerability, vagal communication, alpha-synuclein pathology, blood-brain barrier signaling, and microglial priming. Human microbiome studies, Parkinsonian animal models, LPS-based innate immune-memory paradigms, and emerging intervention trials are considered according to their evidentiary level and major confounders, including constipation, diet, medication exposure, geography, and disease stage. The resulting model accommodates body-first, brain-first, and mixed trajectories rather than assigning a universal gut origin to PD. Therapeutically, the evidence supports a shift from nonspecific microbiome normalization toward mechanism-matched strategies that combine ecological, immune, metabolic, and clinical biomarkers. Longitudinal prodromal cohorts and integrated multi-omics with immune phenotyping will be essential to determine whether gut-brain immune signatures identify causal pathways, progression markers, or treatment-responsive subgroups.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Translational approaches in microbiome research: from functional mechanisms to next-generation therapeutics.
Frontiers in microbiology, 17:1943873.
Microbiome research has made substantial progress toward clinical translation over the past 2 decades, moving from associative observations toward mechanistic investigation, validation, and therapeutic intervention. This narrative review examines recent advances in the clinical application of microbiome research over the past 5 years, focusing on non-invasive microbiome-derived biomarkers and therapeutic strategies, including personalized probiotics and prebiotics, fecal microbiota transplantation (FMT), and engineered microbial therapeutics, while evaluating the strength of the supporting evidence. Microbiota-based treatments for recurrent Clostridium difficile infection are currently at the forefront of clinical translation, whereas applications in inflammatory, metabolic, neurological, and oncological disorders remain largely investigational. We further examine these translational barriers while highlighting opportunities to integrate microbiome data with systems biology and advanced analytics to improve clinical outcomes and advance precision medicine. By linking mechanistic discoveries with their current level of clinical development, this narrative review critically evaluates the available translational microbiome evidence, identifies key bottlenecks and unresolved knowledge gaps, and outlines priorities for the responsible integration of microbiome-based diagnostics and therapeutics into clinical practice.
Additional Links: PMID-42846861
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@article {pmid42846861,
year = {2026},
author = {Kumar, M and Singh, P and Almohannadi, N and Al Khodor, S},
title = {Translational approaches in microbiome research: from functional mechanisms to next-generation therapeutics.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1943873},
doi = {10.3389/fmicb.2026.1943873},
pmid = {42846861},
issn = {1664-302X},
abstract = {Microbiome research has made substantial progress toward clinical translation over the past 2 decades, moving from associative observations toward mechanistic investigation, validation, and therapeutic intervention. This narrative review examines recent advances in the clinical application of microbiome research over the past 5 years, focusing on non-invasive microbiome-derived biomarkers and therapeutic strategies, including personalized probiotics and prebiotics, fecal microbiota transplantation (FMT), and engineered microbial therapeutics, while evaluating the strength of the supporting evidence. Microbiota-based treatments for recurrent Clostridium difficile infection are currently at the forefront of clinical translation, whereas applications in inflammatory, metabolic, neurological, and oncological disorders remain largely investigational. We further examine these translational barriers while highlighting opportunities to integrate microbiome data with systems biology and advanced analytics to improve clinical outcomes and advance precision medicine. By linking mechanistic discoveries with their current level of clinical development, this narrative review critically evaluates the available translational microbiome evidence, identifies key bottlenecks and unresolved knowledge gaps, and outlines priorities for the responsible integration of microbiome-based diagnostics and therapeutics into clinical practice.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Longitudinal dynamics of the gut microbiome during methamphetamine addiction and abstinence.
Frontiers in microbiology, 17:1911776.
INTRODUCTION: Methamphetamine (METH) addiction is a chronic neuropsychiatric disorder characterized by severe abstinence symptoms and high relapse rates, yet the temporal dynamics of gut microbiota alterations across addiction and abstinence phases remain poorly understood.
METHODS: In this study, we performed a longitudinal microbiome analysis to characterize differences between phases and time-dependent remodeling of the gut microbiota in a mouse model. Fecal samples were collected at defined time points across a 60-day addiction phase followed by a 60-day abstinence phase and analyzed using 16S rRNA gene sequencing.
RESULTS: Distinct microbial compositions, diversity and community structure differences were observed between addiction and abstinence phases. Microbial communities during the addiction phase exhibited greater dispersion, whereas progressive stabilization was observed during abstinence. Time-series analyses revealed characteristic alterations in Verrucomicrobia and Actinobacteria during prolonged addiction and early abstinence. At the genus level, Butyricimonas, Candidatus Arthromitus, Enterococcus, and Turicibacter exhibited reproducible phase- and temporal-dependent dynamic patterns. Based on these microbial signatures, random forest models were constructed for phase classification and temporal prediction. The classification model achieved higher model performance during the addiction phase, whereas performance declined during abstinence, reflected by reduced variance explained and increased heterogeneity in gut microbiota composition. Temporal prediction models further demonstrated differential predictive performance between phases.
DISCUSSION: These findings identify reproducible temporal changes in gut microbiota across addiction and abstinence and highlight candidate microbial signatures for understanding addiction progression and distinguishing different phases.
Additional Links: PMID-42846992
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@article {pmid42846992,
year = {2026},
author = {Wang, L and Wang, J and Zhang, Y and Wang, B and Sun, X and Li, Y and Yan, J and Yun, K and Su, H},
title = {Longitudinal dynamics of the gut microbiome during methamphetamine addiction and abstinence.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1911776},
doi = {10.3389/fmicb.2026.1911776},
pmid = {42846992},
issn = {1664-302X},
abstract = {INTRODUCTION: Methamphetamine (METH) addiction is a chronic neuropsychiatric disorder characterized by severe abstinence symptoms and high relapse rates, yet the temporal dynamics of gut microbiota alterations across addiction and abstinence phases remain poorly understood.
METHODS: In this study, we performed a longitudinal microbiome analysis to characterize differences between phases and time-dependent remodeling of the gut microbiota in a mouse model. Fecal samples were collected at defined time points across a 60-day addiction phase followed by a 60-day abstinence phase and analyzed using 16S rRNA gene sequencing.
RESULTS: Distinct microbial compositions, diversity and community structure differences were observed between addiction and abstinence phases. Microbial communities during the addiction phase exhibited greater dispersion, whereas progressive stabilization was observed during abstinence. Time-series analyses revealed characteristic alterations in Verrucomicrobia and Actinobacteria during prolonged addiction and early abstinence. At the genus level, Butyricimonas, Candidatus Arthromitus, Enterococcus, and Turicibacter exhibited reproducible phase- and temporal-dependent dynamic patterns. Based on these microbial signatures, random forest models were constructed for phase classification and temporal prediction. The classification model achieved higher model performance during the addiction phase, whereas performance declined during abstinence, reflected by reduced variance explained and increased heterogeneity in gut microbiota composition. Temporal prediction models further demonstrated differential predictive performance between phases.
DISCUSSION: These findings identify reproducible temporal changes in gut microbiota across addiction and abstinence and highlight candidate microbial signatures for understanding addiction progression and distinguishing different phases.},
}
RevDate: 2026-10-08
Lung microbiome community state types are associated with ventilator-associated pneumonia risk: a secondary analysis of the MicroNAV cohort.
Microbiology spectrum [Epub ahead of print].
UNLABELLED: In the publicly available MicroNAV cohort, baseline diversity analyses did not distinguish patients who developed ventilator-associated pneumonia (VAP) from non-VAP patients, leaving it unresolved whether community-state structure contains risk information. In an independent secondary analysis, we reprocessed raw 16S rRNA gene sequencing data from bronchoalveolar lavage samples using DADA2 exact amplicon sequence variant inference and decontam quality control, and analyzed 75 at-risk mechanically ventilated patients with paired longitudinal sampling (40 VAP and 35 non-VAP). No baseline genus distinguished future VAP from non-VAP by DESeq2 or MaAsLin3 after adjustment for sex and Glasgow Coma Scale (all adjusted P > 0.05). Dirichlet multinomial mixture modeling identified three community state types (CSTs) with distinct ecological profiles. In cause-specific Cox regression, CST1, a high-burden, oral-associated state, was associated with higher VAP hazard than CST2, a low-burden, diverse state (hazard ratio, 2.85; 95% CI, 1.15-7.02, P = 0.023; Gray's test, P = 0.042). Adding CST to a burden-only model improved fit (likelihood-ratio test, P = 0.041), whereas pathogen species cultured at VAP onset did not differ by baseline CST (simulated Fisher's exact test, P = 0.98). During ventilation, 12 oral-associated genera declined while total bacterial burden remained stable (linear mixed model, P = 0.66), but the association between commensal loss and subsequent VAP was not consistent across abundance scales. Baseline IL-1β and TNF-α concentrations were explained primarily by bacterial burden rather than community composition. These findings suggest that baseline lower-airway ecological states capture VAP susceptibility information not resolved by single-taxon, diversity, or burden-only analyses.
IMPORTANCE: In mechanically ventilated ICU patients without pulmonary infection at baseline, the early lower-airway ecosystem may contain information about subsequent ventilator-associated pneumonia (VAP) susceptibility. In this independent reanalysis of the public MicroNAV cohort, baseline lower-airway communities classified by Dirichlet multinomial mixture modeling resolved into ecological states with different subsequent VAP risk, while individual genera, bacterial burden alone, and the eventual cultured pathogen did not explain the signal. Mechanical ventilation produced shared community restructuring: oral-associated genera declined and other taxa expanded, yet total bacterial burden remained stable, indicating ecological replacement rather than bacterial clearance. This restructuring was not consistently VAP-specific, and apparent community state type-dependent differences in declining-genus loss partly reflected different starting proportions. Together, these findings extend the original cohort by separating starting state heterogeneity from ventilation-associated restructuring. They suggest that initially noninfected ventilated airways represent distinct host-microbial terrains that may differ in vulnerability to pneumonia.
Additional Links: PMID-42847684
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@article {pmid42847684,
year = {2026},
author = {Xiao, S and Zhuang, Q and Cui, G and Li, Y},
title = {Lung microbiome community state types are associated with ventilator-associated pneumonia risk: a secondary analysis of the MicroNAV cohort.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0126326},
doi = {10.1128/spectrum.01263-26},
pmid = {42847684},
issn = {2165-0497},
abstract = {UNLABELLED: In the publicly available MicroNAV cohort, baseline diversity analyses did not distinguish patients who developed ventilator-associated pneumonia (VAP) from non-VAP patients, leaving it unresolved whether community-state structure contains risk information. In an independent secondary analysis, we reprocessed raw 16S rRNA gene sequencing data from bronchoalveolar lavage samples using DADA2 exact amplicon sequence variant inference and decontam quality control, and analyzed 75 at-risk mechanically ventilated patients with paired longitudinal sampling (40 VAP and 35 non-VAP). No baseline genus distinguished future VAP from non-VAP by DESeq2 or MaAsLin3 after adjustment for sex and Glasgow Coma Scale (all adjusted P > 0.05). Dirichlet multinomial mixture modeling identified three community state types (CSTs) with distinct ecological profiles. In cause-specific Cox regression, CST1, a high-burden, oral-associated state, was associated with higher VAP hazard than CST2, a low-burden, diverse state (hazard ratio, 2.85; 95% CI, 1.15-7.02, P = 0.023; Gray's test, P = 0.042). Adding CST to a burden-only model improved fit (likelihood-ratio test, P = 0.041), whereas pathogen species cultured at VAP onset did not differ by baseline CST (simulated Fisher's exact test, P = 0.98). During ventilation, 12 oral-associated genera declined while total bacterial burden remained stable (linear mixed model, P = 0.66), but the association between commensal loss and subsequent VAP was not consistent across abundance scales. Baseline IL-1β and TNF-α concentrations were explained primarily by bacterial burden rather than community composition. These findings suggest that baseline lower-airway ecological states capture VAP susceptibility information not resolved by single-taxon, diversity, or burden-only analyses.
IMPORTANCE: In mechanically ventilated ICU patients without pulmonary infection at baseline, the early lower-airway ecosystem may contain information about subsequent ventilator-associated pneumonia (VAP) susceptibility. In this independent reanalysis of the public MicroNAV cohort, baseline lower-airway communities classified by Dirichlet multinomial mixture modeling resolved into ecological states with different subsequent VAP risk, while individual genera, bacterial burden alone, and the eventual cultured pathogen did not explain the signal. Mechanical ventilation produced shared community restructuring: oral-associated genera declined and other taxa expanded, yet total bacterial burden remained stable, indicating ecological replacement rather than bacterial clearance. This restructuring was not consistently VAP-specific, and apparent community state type-dependent differences in declining-genus loss partly reflected different starting proportions. Together, these findings extend the original cohort by separating starting state heterogeneity from ventilation-associated restructuring. They suggest that initially noninfected ventilated airways represent distinct host-microbial terrains that may differ in vulnerability to pneumonia.},
}
RevDate: 2026-10-08
Deep-sea siliceous sponges harbor distinct and functionally diverse microbiomes.
Applied and environmental microbiology [Epub ahead of print].
Sponges, phylum Porifera, are long-lived and basal-branching metazoans that play important roles in ocean biogeochemistry and host diverse microbial communities. Siliceous sponges form a major clade of the Porifera; however, their microbiome is not well characterized, particularly in the deep ocean. Here, we used shotgun metagenomics to investigate the composition of the microbial communities of 13 siliceous sponges collected from four sites near Puerto Rico from depths ranging from 400 to 1,900 meters. Nine of the sponges in this study are from five sponge families that have not previously been sequenced using shotgun metagenomics. We assembled a total of 176 metagenome-assembled genomes from 20 bacterial phyla and 1 archaeal phylum. Ammonia-oxidizing archaea (AOA) Nitrosopumilaceae dominated most siliceous sponge microbial communities and was strikingly the sole symbiont associated with one sponge (Farrea). Overall, microbiome diversity was relatively low across siliceous sponges, except for a Phloeodictyidae, which is likely a high microbial abundance (HMA) sponge. Our results suggest that host sponge phylogeny may shape microbial community structure, with limited evidence for an environmental role. The sponge-associated microbial communities contained genetic capabilities for diverse metabolic functions, particularly contributing to the carbon, nitrogen, and sulfur cycles. In addition to the AOA, evidence of potential for microbial autotrophy was found through the presence of genes for RuBisCO, methanotrophy, and ATP citrate lyase. These results reveal both conserved relationships and metabolic flexibility across siliceous sponge lineages, suggesting unique evolutionary dynamics and demonstrating the importance of microbial metabolism to sponge host health and nutrient cycling in the oligotrophic deep ocean.IMPORTANCEMarine sponges, emerging ~600 million years ago, have close relationships with microorganisms, but the microbiome of deep-sea siliceous sponges is not well understood. Siliceous sponges play essential roles in deep-sea ecosystems by providing habitats for other metazoans and mediating carbon, nitrogen, and sulfur cycling; however, they remain some of the least-studied sponges. By shotgun sequencing DNA from 13 siliceous sponges collected near Puerto Rico, this study found that host sponge phylogeny is linked to microbial community composition and structure. Ammonia-oxidizing archaea dominated the microbial communities associated with marine sponges, likely playing key roles in utilizing metabolic byproducts and supporting host health. Other microbes also contributed to nutrient cycling and contained the potential to fix carbon, suggesting metabolic flexibility, which may benefit sponge hosts in low-resource environments. These findings emphasize the ecological importance of siliceous sponge-microbe symbioses and contribute to our understanding of the drivers shaping their structure and function.
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@article {pmid42847686,
year = {2026},
author = {Lane, KR and Meyer-Kaiser, KS and Collens, AB and Leal, CV and Collins, AG and Herrera, S and Hansel, CM},
title = {Deep-sea siliceous sponges harbor distinct and functionally diverse microbiomes.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0174726},
doi = {10.1128/aem.01747-26},
pmid = {42847686},
issn = {1098-5336},
abstract = {Sponges, phylum Porifera, are long-lived and basal-branching metazoans that play important roles in ocean biogeochemistry and host diverse microbial communities. Siliceous sponges form a major clade of the Porifera; however, their microbiome is not well characterized, particularly in the deep ocean. Here, we used shotgun metagenomics to investigate the composition of the microbial communities of 13 siliceous sponges collected from four sites near Puerto Rico from depths ranging from 400 to 1,900 meters. Nine of the sponges in this study are from five sponge families that have not previously been sequenced using shotgun metagenomics. We assembled a total of 176 metagenome-assembled genomes from 20 bacterial phyla and 1 archaeal phylum. Ammonia-oxidizing archaea (AOA) Nitrosopumilaceae dominated most siliceous sponge microbial communities and was strikingly the sole symbiont associated with one sponge (Farrea). Overall, microbiome diversity was relatively low across siliceous sponges, except for a Phloeodictyidae, which is likely a high microbial abundance (HMA) sponge. Our results suggest that host sponge phylogeny may shape microbial community structure, with limited evidence for an environmental role. The sponge-associated microbial communities contained genetic capabilities for diverse metabolic functions, particularly contributing to the carbon, nitrogen, and sulfur cycles. In addition to the AOA, evidence of potential for microbial autotrophy was found through the presence of genes for RuBisCO, methanotrophy, and ATP citrate lyase. These results reveal both conserved relationships and metabolic flexibility across siliceous sponge lineages, suggesting unique evolutionary dynamics and demonstrating the importance of microbial metabolism to sponge host health and nutrient cycling in the oligotrophic deep ocean.IMPORTANCEMarine sponges, emerging ~600 million years ago, have close relationships with microorganisms, but the microbiome of deep-sea siliceous sponges is not well understood. Siliceous sponges play essential roles in deep-sea ecosystems by providing habitats for other metazoans and mediating carbon, nitrogen, and sulfur cycling; however, they remain some of the least-studied sponges. By shotgun sequencing DNA from 13 siliceous sponges collected near Puerto Rico, this study found that host sponge phylogeny is linked to microbial community composition and structure. Ammonia-oxidizing archaea dominated the microbial communities associated with marine sponges, likely playing key roles in utilizing metabolic byproducts and supporting host health. Other microbes also contributed to nutrient cycling and contained the potential to fix carbon, suggesting metabolic flexibility, which may benefit sponge hosts in low-resource environments. These findings emphasize the ecological importance of siliceous sponge-microbe symbioses and contribute to our understanding of the drivers shaping their structure and function.},
}
RevDate: 2026-10-08
Microbial communities on station and train surfaces in Chennai Metro: insights into urban transit microbiome.
mSphere [Epub ahead of print].
UNLABELLED: Urban public transport systems, particularly metro networks, serve as key hubs for microbial transmission, yet the urban microbiome in densely populated regions like India remains poorly characterized. Understanding these environments is crucial for public health, especially in light of the COVID-19 pandemic and growing concerns about antimicrobial resistance (AMR). This study is the first of its kind to investigate the microbial communities and the presence of AMR genes in the Chennai Metro system. We collected 96 surface swabs from 12 metro stations across two lines, focusing on surfaces that people frequently touch, such as handrails, kiosks, banisters, and ticket counters. Of the collected samples, 47 met quality control standards and were subjected to shotgun metagenomic sequencing, and 41 samples with more than 1 million reads were included in our analysis. Our findings indicate that surface type significantly influences microbial community structure, with kiosks exhibiting the highest microbial diversity. Comparative analysis with global urban data sets revealed unique microbial patterns specific to Chennai, including nine species that were notably more prevalent in our samples than in other urban transit systems worldwide. Furthermore, through pangenome analysis, we generated high-quality metagenome-assembled genomes that elucidated the adaptive strategies of dominant microbial species in this urban environment. Despite their relatively low abundance, several AMR families were widely distributed across the data set, with over 80% of samples containing at least one associated AMR gene, including families linked to rifamycins, multidrug resistance, and sulfonamides. This study lays a foundation for understanding the urban microbiome in India, emphasizing distinct regional characteristics and underscoring the need for sustained monitoring to mitigate disease transmission risks in high-density transit settings.
IMPORTANCE: Densely populated urban transit systems are critical hubs for microbial exchange, yet the mass transit microbiomes of Indian cities remain largely uncharacterized, representing a significant gap in global surveillance. Our study provides the first comprehensive metagenomic analysis of the Chennai Metro, a high-traffic transit network serving millions. Our findings highlight the unique environmental drivers shaping urban microbiota in India. Chennai, with over 12 million residents and a metro system serving over 105 million passengers annually, is an ideal yet uncharacterized environment for studying microbial dynamics, surface-microbe interactions, and environmental antimicrobial resistance reservoirs.
Additional Links: PMID-42847700
Publisher:
PubMed:
Citation:
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hide bibtex listing
@article {pmid42847700,
year = {2026},
author = {Singh, VY and Gadekar, VP and Sasikumar, S and Lokshanan, RMR and Senthamizhan, V and Prithiviraj, B and Sinha, H and Raman, K},
title = {Microbial communities on station and train surfaces in Chennai Metro: insights into urban transit microbiome.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0043326},
doi = {10.1128/msphere.00433-26},
pmid = {42847700},
issn = {2379-5042},
abstract = {UNLABELLED: Urban public transport systems, particularly metro networks, serve as key hubs for microbial transmission, yet the urban microbiome in densely populated regions like India remains poorly characterized. Understanding these environments is crucial for public health, especially in light of the COVID-19 pandemic and growing concerns about antimicrobial resistance (AMR). This study is the first of its kind to investigate the microbial communities and the presence of AMR genes in the Chennai Metro system. We collected 96 surface swabs from 12 metro stations across two lines, focusing on surfaces that people frequently touch, such as handrails, kiosks, banisters, and ticket counters. Of the collected samples, 47 met quality control standards and were subjected to shotgun metagenomic sequencing, and 41 samples with more than 1 million reads were included in our analysis. Our findings indicate that surface type significantly influences microbial community structure, with kiosks exhibiting the highest microbial diversity. Comparative analysis with global urban data sets revealed unique microbial patterns specific to Chennai, including nine species that were notably more prevalent in our samples than in other urban transit systems worldwide. Furthermore, through pangenome analysis, we generated high-quality metagenome-assembled genomes that elucidated the adaptive strategies of dominant microbial species in this urban environment. Despite their relatively low abundance, several AMR families were widely distributed across the data set, with over 80% of samples containing at least one associated AMR gene, including families linked to rifamycins, multidrug resistance, and sulfonamides. This study lays a foundation for understanding the urban microbiome in India, emphasizing distinct regional characteristics and underscoring the need for sustained monitoring to mitigate disease transmission risks in high-density transit settings.
IMPORTANCE: Densely populated urban transit systems are critical hubs for microbial exchange, yet the mass transit microbiomes of Indian cities remain largely uncharacterized, representing a significant gap in global surveillance. Our study provides the first comprehensive metagenomic analysis of the Chennai Metro, a high-traffic transit network serving millions. Our findings highlight the unique environmental drivers shaping urban microbiota in India. Chennai, with over 12 million residents and a metro system serving over 105 million passengers annually, is an ideal yet uncharacterized environment for studying microbial dynamics, surface-microbe interactions, and environmental antimicrobial resistance reservoirs.},
}
RevDate: 2026-10-08
Making a case for dental clinical practice guidelines for elective antibiotic use: an institutional retrospective study.
Quintessence international (Berlin, Germany : 1985), 0(0):0 pii:7121933 [Epub ahead of print].
BACKGROUND: Antibiotic overuse disrupts host-microbiome equilibrium, and increases risks of diarrhea, drug allergies, and multi-drug resistance. Dentists are the third largest prescribers of oral antibiotics in the US. Investigating antibiotic prescribing patterns alongside dental procedures may identify opportunities to reduce antibiotic overuse.
METHOD: Institutional antibiotic prescriptions (Abx-Rx) dispensed with dental procedures were retrospectively reviewed from 2017-2022. Augmentin® (USAntibiotics, TN) and clindamycin prescriptions were investigated for nonindicated vs. well-reasoned use, comparing implant-related and extraction-related procedures.
RESULTS: Over 7,158 Abx-Rx, dispensed with 3,320 (56% of) implant-related, 4,084 (14% of) extraction-related, and 256 overlapping visits, included amoxicillin (79.75%), clindamycin (7.23%), Augmentin® (6.3%), azithromycin (4.2%), and penicillin VK (1.53%). Implant-related procedures were 7.8-fold more likely than extraction-related to involve Abx-Rx [95% CI: 7.392-8.373, p<0.05]. Use of Augmentin® and clindamycin (the two most dispensed broad-spectrum antibiotics) in dental procedures was evaluated further. Over 60% of Augmentin® prescriptions (n=352) were implant-related, of which 88% were nonindicated, versus 48% of dental extractions-related. Implant-related Augmentin® prescriptions were 8-fold more likely to be pre-emptive [95% CI 4.676, 14.47, p<0.05)]. Of 460 clindamycin prescriptions, implant-related prescriptions (30%) were 1.5-fold more likely nonindicated than were extraction-related [95%CI 1.019, 2.443, p<0.05]; 76% occurred in patients reporting penicillin allergy.
CONCLUSION: Implant-related procedures more frequently involved nonindicated, broad-spectrum antibiotic use, highlighting the need for evidence-based guidelines to reduce antibiotic overuse. Clindamycin use can further be reduced with the justified use of alternative safer antibiotics and minimizing mislabeling of penicillin allergy. Clinical Practice Guidelines for antibiotic use following dental procedures can promote judicious antibiotic use.
Additional Links: PMID-42847788
Publisher:
PubMed:
Citation:
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@article {pmid42847788,
year = {2026},
author = {Mikhail, A and Bhullar, H and Dalal, R and Goyal, P and Shah, N and Pan, B and Fredericks-Younger, J and Feldman, CA and Subramanian, G},
title = {Making a case for dental clinical practice guidelines for elective antibiotic use: an institutional retrospective study.},
journal = {Quintessence international (Berlin, Germany : 1985)},
volume = {0},
number = {0},
pages = {0},
doi = {10.3290/j.qi.b7121933},
pmid = {42847788},
issn = {1936-7163},
abstract = {BACKGROUND: Antibiotic overuse disrupts host-microbiome equilibrium, and increases risks of diarrhea, drug allergies, and multi-drug resistance. Dentists are the third largest prescribers of oral antibiotics in the US. Investigating antibiotic prescribing patterns alongside dental procedures may identify opportunities to reduce antibiotic overuse.
METHOD: Institutional antibiotic prescriptions (Abx-Rx) dispensed with dental procedures were retrospectively reviewed from 2017-2022. Augmentin® (USAntibiotics, TN) and clindamycin prescriptions were investigated for nonindicated vs. well-reasoned use, comparing implant-related and extraction-related procedures.
RESULTS: Over 7,158 Abx-Rx, dispensed with 3,320 (56% of) implant-related, 4,084 (14% of) extraction-related, and 256 overlapping visits, included amoxicillin (79.75%), clindamycin (7.23%), Augmentin® (6.3%), azithromycin (4.2%), and penicillin VK (1.53%). Implant-related procedures were 7.8-fold more likely than extraction-related to involve Abx-Rx [95% CI: 7.392-8.373, p<0.05]. Use of Augmentin® and clindamycin (the two most dispensed broad-spectrum antibiotics) in dental procedures was evaluated further. Over 60% of Augmentin® prescriptions (n=352) were implant-related, of which 88% were nonindicated, versus 48% of dental extractions-related. Implant-related Augmentin® prescriptions were 8-fold more likely to be pre-emptive [95% CI 4.676, 14.47, p<0.05)]. Of 460 clindamycin prescriptions, implant-related prescriptions (30%) were 1.5-fold more likely nonindicated than were extraction-related [95%CI 1.019, 2.443, p<0.05]; 76% occurred in patients reporting penicillin allergy.
CONCLUSION: Implant-related procedures more frequently involved nonindicated, broad-spectrum antibiotic use, highlighting the need for evidence-based guidelines to reduce antibiotic overuse. Clindamycin use can further be reduced with the justified use of alternative safer antibiotics and minimizing mislabeling of penicillin allergy. Clinical Practice Guidelines for antibiotic use following dental procedures can promote judicious antibiotic use.},
}
RevDate: 2026-10-08
Nitrogen fertilization outweighs plant species loss in shaping bacterial belowground diversity in an alpine meadow on the central Tibetan Plateau.
FEMS microbiology ecology pii:8885591 [Epub ahead of print].
Plant species loss and nitrogen fertilization affect grassland biodiversity. However, their interactive effects on plant communities, soil properties, and the soil microbiome remain insufficiently understood. We analyzed how the removal of plant species, with and without urea addition, influenced plant diversity, soil properties, and soil bacterial communities in a Tibetan Plateau grassland. Continuous plant species removal and urea addition over seven years modified plant beta-diversity equally strong, while urea exerted a stronger negative effect on plant alpha-diversity. Both, plant species removal and urea addition caused soil acidification and an increase in NO2[-]/NO3[-], while dynamics in TOC and TON were mainly driven by the growing season. Structural equation modeling identified soil acidification via urea addition as the most important indirect driver that negatively affected bacterial alpha-diversity and shifted bacterial beta-diversity. Urea addition also exerted direct negative effects on bacterial alpha- and beta-diversity, causing repression of oligotrophic (Acidobacteriota, Chloroflexota, Planctomycetota, Gemmatimonadota) and stimulation of copiotrophic (Bacillota, Bacteroidota, Pseudomonadota) bacterial taxa. Plant species removal caused slight increases in bacterial alpha-diversity, paralleled by less diverse but more even plant communities. We show that soil acidification by urea fertilization outweighs plant species loss in its negative effect on bacterial soil biodiversity in Tibetan grasslands.
Additional Links: PMID-42847914
Publisher:
PubMed:
Citation:
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@article {pmid42847914,
year = {2026},
author = {Wu, D and Quzong, C and Jia, Z and Schwalb, A and Guggenberger, G and Wang, S and Dorji, T and Pester, M},
title = {Nitrogen fertilization outweighs plant species loss in shaping bacterial belowground diversity in an alpine meadow on the central Tibetan Plateau.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag110},
pmid = {42847914},
issn = {1574-6941},
abstract = {Plant species loss and nitrogen fertilization affect grassland biodiversity. However, their interactive effects on plant communities, soil properties, and the soil microbiome remain insufficiently understood. We analyzed how the removal of plant species, with and without urea addition, influenced plant diversity, soil properties, and soil bacterial communities in a Tibetan Plateau grassland. Continuous plant species removal and urea addition over seven years modified plant beta-diversity equally strong, while urea exerted a stronger negative effect on plant alpha-diversity. Both, plant species removal and urea addition caused soil acidification and an increase in NO2[-]/NO3[-], while dynamics in TOC and TON were mainly driven by the growing season. Structural equation modeling identified soil acidification via urea addition as the most important indirect driver that negatively affected bacterial alpha-diversity and shifted bacterial beta-diversity. Urea addition also exerted direct negative effects on bacterial alpha- and beta-diversity, causing repression of oligotrophic (Acidobacteriota, Chloroflexota, Planctomycetota, Gemmatimonadota) and stimulation of copiotrophic (Bacillota, Bacteroidota, Pseudomonadota) bacterial taxa. Plant species removal caused slight increases in bacterial alpha-diversity, paralleled by less diverse but more even plant communities. We show that soil acidification by urea fertilization outweighs plant species loss in its negative effect on bacterial soil biodiversity in Tibetan grasslands.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
The gut-pancreas axis: microbial dysbiosis as a pathogenic driver of diabetes and pancreatic cancer.
Medical oncology (Northwood, London, England), 43(11):.
The gut microbiome dysbiosis is a potential contributing mediator for the gut and pancreas link. The gut microbiome contributes to the development of both diabetes and pancreatic cancer. There are approximately two distinct ways through which the gut microbiome leads to cell damage and then systemic inflammatory responses. The gut microbiome generates a unique set of metabolic products, activating diverse pathways and cytokines. The bottom line for this process leads to the generation of systemic inflammation. In type 2 diabetes, inflammatory signaling predominantly disrupts IRS-1/PI3K/AKT signaling, impairing insulin receptor pathways and glucose absorption, triggering β-cell malfunction and insulin resistance. Dysbiosis-associated inflammatory signaling in pancreatic cancer stimulates the growth of the tumour via activating oncogenic pathways, immune evasion, and epithelial-mesenchymal transition (EMT). The bacterial metabolites can cause. DNA mutations and affect the signaling pathways of cancer cells. In addition, this review offers an integrated microbiome-driven inflammatory-metabolic paradigm utilizing the gut-pancreas axis to associate pancreatic cancer and diabetes. A realistic and in-depth understanding of the above-described processes could result in the development of new techniques for the targeted modification of the gut microbiome for the prevention and management of such diseases.
Additional Links: PMID-42848148
PubMed:
Citation:
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@article {pmid42848148,
year = {2026},
author = {Li, Y},
title = {The gut-pancreas axis: microbial dysbiosis as a pathogenic driver of diabetes and pancreatic cancer.},
journal = {Medical oncology (Northwood, London, England)},
volume = {43},
number = {11},
pages = {},
pmid = {42848148},
issn = {1559-131X},
mesh = {Humans ; *Pancreatic Neoplasms/microbiology/metabolism/pathology ; *Dysbiosis/complications/microbiology ; *Gastrointestinal Microbiome/physiology ; *Diabetes Mellitus, Type 2/microbiology ; Animals ; *Pancreas/metabolism/microbiology/pathology ; Signal Transduction ; },
abstract = {The gut microbiome dysbiosis is a potential contributing mediator for the gut and pancreas link. The gut microbiome contributes to the development of both diabetes and pancreatic cancer. There are approximately two distinct ways through which the gut microbiome leads to cell damage and then systemic inflammatory responses. The gut microbiome generates a unique set of metabolic products, activating diverse pathways and cytokines. The bottom line for this process leads to the generation of systemic inflammation. In type 2 diabetes, inflammatory signaling predominantly disrupts IRS-1/PI3K/AKT signaling, impairing insulin receptor pathways and glucose absorption, triggering β-cell malfunction and insulin resistance. Dysbiosis-associated inflammatory signaling in pancreatic cancer stimulates the growth of the tumour via activating oncogenic pathways, immune evasion, and epithelial-mesenchymal transition (EMT). The bacterial metabolites can cause. DNA mutations and affect the signaling pathways of cancer cells. In addition, this review offers an integrated microbiome-driven inflammatory-metabolic paradigm utilizing the gut-pancreas axis to associate pancreatic cancer and diabetes. A realistic and in-depth understanding of the above-described processes could result in the development of new techniques for the targeted modification of the gut microbiome for the prevention and management of such diseases.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Pancreatic Neoplasms/microbiology/metabolism/pathology
*Dysbiosis/complications/microbiology
*Gastrointestinal Microbiome/physiology
*Diabetes Mellitus, Type 2/microbiology
Animals
*Pancreas/metabolism/microbiology/pathology
Signal Transduction
RevDate: 2026-10-08
Converging etiopathogenetic pathways and early prevention opportunities for autism and neurodevelopmental disorders in the first 1000 days of life: a brief narrative review.
Neuropsychiatrie : Klinik, Diagnostik, Therapie und Rehabilitation : Organ der Gesellschaft Osterreichischer Nervenarzte und Psychiater [Epub ahead of print].
Neurodevelopmental disorders, including autism spectrum disorder, result from complex interactions between genetic susceptibility and early-life environmental exposures that shape brain development. Their increasing prevalence represents a major public health challenge, highlighting the need for effective preventive strategies. This brief narrative review synthesizes current evidence on the converging etiopathogenetic pathways-including genetic vulnerability, environmental risk factors, epigenetic regulation, neuroinflammation, and gut microbiome alterations-that operate during the first 1000 days of life and collectively influence neurodevelopmental trajectories. We also discuss early prevention opportunities targeting modifiable risk factors during this critical developmental window, when heightened neuroplasticity may maximize the effectiveness of preventive interventions. Viewing autism spectrum disorder and related neurodevelopmental disorders through the lens of shared biological mechanisms, provides a framework for precision prevention, facilitates earlier identification of at-risk individuals, and supports the development of multidisciplinary strategies aimed at improving lifelong neurodevelopmental health and reducing the long-term burden on affected individuals, families, and healthcare systems.
Additional Links: PMID-42848192
PubMed:
Citation:
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@article {pmid42848192,
year = {2026},
author = {Giardino, M and Pasquini, V},
title = {Converging etiopathogenetic pathways and early prevention opportunities for autism and neurodevelopmental disorders in the first 1000 days of life: a brief narrative review.},
journal = {Neuropsychiatrie : Klinik, Diagnostik, Therapie und Rehabilitation : Organ der Gesellschaft Osterreichischer Nervenarzte und Psychiater},
volume = {},
number = {},
pages = {},
pmid = {42848192},
issn = {2194-1327},
abstract = {Neurodevelopmental disorders, including autism spectrum disorder, result from complex interactions between genetic susceptibility and early-life environmental exposures that shape brain development. Their increasing prevalence represents a major public health challenge, highlighting the need for effective preventive strategies. This brief narrative review synthesizes current evidence on the converging etiopathogenetic pathways-including genetic vulnerability, environmental risk factors, epigenetic regulation, neuroinflammation, and gut microbiome alterations-that operate during the first 1000 days of life and collectively influence neurodevelopmental trajectories. We also discuss early prevention opportunities targeting modifiable risk factors during this critical developmental window, when heightened neuroplasticity may maximize the effectiveness of preventive interventions. Viewing autism spectrum disorder and related neurodevelopmental disorders through the lens of shared biological mechanisms, provides a framework for precision prevention, facilitates earlier identification of at-risk individuals, and supports the development of multidisciplinary strategies aimed at improving lifelong neurodevelopmental health and reducing the long-term burden on affected individuals, families, and healthcare systems.},
}
RevDate: 2026-10-08
CmpDate: 2026-10-08
Tumor microenvironment and gut microbiome in immunotherapy resistance in gastric cancer: clinical questions, biological mechanisms, and evidence-based therapeutic perspectives.
Medical oncology (Northwood, London, England), 43(11):.
Immune checkpoint inhibitors (ICIs) have improved systemic therapy for advanced gastric and gastroesophageal junction cancer, yet primary and acquired resistance remain common and are incompletely explained by established tumor biomarkers. This narrative review evaluates the connected roles of the tumor microenvironment (TME), host immunity, and the gut microbiome in shaping ICI resistance in gastric cancer. We performed a structured PubMed search through 28 August 2026 and prioritized gastric cancer-specific clinical and translational evidence, supplemented by systematic reviews, meta-analyses, and mechanistically relevant studies from other tumor types when necessary. Within the gastric cancer TME, cancer-associated fibroblasts, myeloid cells, regulatory T cells, extracellular matrix remodeling, hypoxia, angiogenesis, and T-cell exhaustion can promote immune exclusion or dysfunction. Microbial diversity, microbial metabolites, antibiotics, proton pump inhibitors, defined live biotherapeutics, fecal microbiota transplantation, and diet may influence systemic antitumor immunity, but most human evidence is retrospective, cross-sectional, or derived from non-gastric cancers. Clinically, antibiotic stewardship, reassessment of unnecessary acid suppression, and nutritional optimization are reasonable supportive measures, whereas routine probiotic supplementation, Clostridium butyricum MIYAIRI 588 for ICI sensitization, and fecal microbiota transplantation remain investigational in gastric cancer. Future studies should integrate longitudinal exposures, serial TME profiling, stool metagenomics, medication use, nutritional status, and clinical outcomes. The TME-gut microbiome axis is therefore a biologically plausible framework for biomarker-guided research, but current evidence does not justify empiric microbiome-directed anticancer therapy in gastric cancer.
Additional Links: PMID-42848247
PubMed:
Citation:
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@article {pmid42848247,
year = {2026},
author = {Sagawa, T and Hirakawa, M and Nagashima, H and Fujikawa, K},
title = {Tumor microenvironment and gut microbiome in immunotherapy resistance in gastric cancer: clinical questions, biological mechanisms, and evidence-based therapeutic perspectives.},
journal = {Medical oncology (Northwood, London, England)},
volume = {43},
number = {11},
pages = {},
pmid = {42848247},
issn = {1559-131X},
mesh = {Humans ; *Stomach Neoplasms/immunology/microbiology/drug therapy/therapy/pathology ; *Tumor Microenvironment/immunology ; *Drug Resistance, Neoplasm/immunology ; *Gastrointestinal Microbiome/immunology/drug effects ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; *Immunotherapy/methods ; },
abstract = {Immune checkpoint inhibitors (ICIs) have improved systemic therapy for advanced gastric and gastroesophageal junction cancer, yet primary and acquired resistance remain common and are incompletely explained by established tumor biomarkers. This narrative review evaluates the connected roles of the tumor microenvironment (TME), host immunity, and the gut microbiome in shaping ICI resistance in gastric cancer. We performed a structured PubMed search through 28 August 2026 and prioritized gastric cancer-specific clinical and translational evidence, supplemented by systematic reviews, meta-analyses, and mechanistically relevant studies from other tumor types when necessary. Within the gastric cancer TME, cancer-associated fibroblasts, myeloid cells, regulatory T cells, extracellular matrix remodeling, hypoxia, angiogenesis, and T-cell exhaustion can promote immune exclusion or dysfunction. Microbial diversity, microbial metabolites, antibiotics, proton pump inhibitors, defined live biotherapeutics, fecal microbiota transplantation, and diet may influence systemic antitumor immunity, but most human evidence is retrospective, cross-sectional, or derived from non-gastric cancers. Clinically, antibiotic stewardship, reassessment of unnecessary acid suppression, and nutritional optimization are reasonable supportive measures, whereas routine probiotic supplementation, Clostridium butyricum MIYAIRI 588 for ICI sensitization, and fecal microbiota transplantation remain investigational in gastric cancer. Future studies should integrate longitudinal exposures, serial TME profiling, stool metagenomics, medication use, nutritional status, and clinical outcomes. The TME-gut microbiome axis is therefore a biologically plausible framework for biomarker-guided research, but current evidence does not justify empiric microbiome-directed anticancer therapy in gastric cancer.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Stomach Neoplasms/immunology/microbiology/drug therapy/therapy/pathology
*Tumor Microenvironment/immunology
*Drug Resistance, Neoplasm/immunology
*Gastrointestinal Microbiome/immunology/drug effects
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
*Immunotherapy/methods
RevDate: 2026-10-08
The Wheat Seed Microbiome as a Model for Understanding the Transmission of Beneficial Plant-Associated Bacteria.
Journal of experimental botany pii:8885637 [Epub ahead of print].
Beneficial plant-microbe interactions are fundamental to plant nutrition, growth, stress tolerance and disease resistance. However, because microorganisms are not encoded by the plant genome, the mechanisms by which microbial associations persist across generations remain unresolved. In this review, we examine the emerging evidence that seeds function not only as reproductive structures but also as reservoirs of microorganisms that may facilitate the maintenance and transmission of selected microbial partners. We synthesize current knowledge of seed microbiome diversity, ecological functions and assembly processes, highlighting the roles of maternal, floral, pollen-mediated and environmental transmission, together with host selection and microbial interactions. We then evaluate evidence that seed-borne microorganisms contribute to plant microbiome assembly and may support the multigenerational persistence of beneficial taxa. Using wheat as a model system, we explore how domestication and host genetic control have shaped microbial communities, assess evidence for recurrent the seed-borne presence of specific bacterial taxa, propose a candidate wheat seed bacterial meta-core based on taxa repeatedly detected across independent studies, and highlight Pantoea as a candidate lineage showing evidence of within-generation persistence and multigenerational transmission across generations. Finally, we discuss the conceptual and methodological challenges that currently limit our understanding of microbiome inheritance as a general biological principle and explore how this knowledge may guide future microbiome-assisted crop improvement. Together, these findings position seeds as key ecological and evolutionary hubs through which beneficial plant-microbe interactions may persist and potentially be inherited across generations.
Additional Links: PMID-42848321
Publisher:
PubMed:
Citation:
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@article {pmid42848321,
year = {2026},
author = {Sanz-Puente, I and Abdelfattah, A and Robledo, M},
title = {The Wheat Seed Microbiome as a Model for Understanding the Transmission of Beneficial Plant-Associated Bacteria.},
journal = {Journal of experimental botany},
volume = {},
number = {},
pages = {},
doi = {10.1093/jxb/erag499},
pmid = {42848321},
issn = {1460-2431},
abstract = {Beneficial plant-microbe interactions are fundamental to plant nutrition, growth, stress tolerance and disease resistance. However, because microorganisms are not encoded by the plant genome, the mechanisms by which microbial associations persist across generations remain unresolved. In this review, we examine the emerging evidence that seeds function not only as reproductive structures but also as reservoirs of microorganisms that may facilitate the maintenance and transmission of selected microbial partners. We synthesize current knowledge of seed microbiome diversity, ecological functions and assembly processes, highlighting the roles of maternal, floral, pollen-mediated and environmental transmission, together with host selection and microbial interactions. We then evaluate evidence that seed-borne microorganisms contribute to plant microbiome assembly and may support the multigenerational persistence of beneficial taxa. Using wheat as a model system, we explore how domestication and host genetic control have shaped microbial communities, assess evidence for recurrent the seed-borne presence of specific bacterial taxa, propose a candidate wheat seed bacterial meta-core based on taxa repeatedly detected across independent studies, and highlight Pantoea as a candidate lineage showing evidence of within-generation persistence and multigenerational transmission across generations. Finally, we discuss the conceptual and methodological challenges that currently limit our understanding of microbiome inheritance as a general biological principle and explore how this knowledge may guide future microbiome-assisted crop improvement. Together, these findings position seeds as key ecological and evolutionary hubs through which beneficial plant-microbe interactions may persist and potentially be inherited across generations.},
}
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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.
ESP Help
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.
ESP Picks from Around the Web (updated 28 JUL 2024 )
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Fossils of miniature humans (hobbits) discovered in Indonesia
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Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.