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ESP: PubMed Auto Bibliography 15 Oct 2026 at 01:56 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: 2026-10-13
Cross-domain microbiome legacy of a natural Phaeocystis globosa bloom in eutrophic coastal waters: a framework for monitoring bloom onset, collapse, and post-bloom recovery.
Applied and environmental microbiology [Epub ahead of print].
When a harmful algal bloom collapses, does the coastal water quality recover? We addressed this question using the natural bloom of the haptophyte Phaeocystis globosa in coastal waters around Xiamen Island, China. Bacterial and microeukaryotic communities in the water samples (n = 105) monthly collected from five sites from September 2023 to March 2024 were analyzed using 16S and 18S rRNA amplicon sequencing, genotype-specific qPCR, iCAMP-based assembly inference, partial least squares path modeling, bloom stage-specific co-occurrence networks, and amplicon-based functional prediction. Bloom development drove coordinated physicochemical change. Both bacterial and microeukaryotic communities were displaced from their pre-bloom state but did not return to the original state within the 7-month series. However, their patterns of succession were different. Bacterial communities underwent coherent system-wide succession. They diverged spatially during the bloom. Their assembly shifted toward stochasticity, with the deterministic contribution falling from 46.3% pre-bloom to 27.8% during the bloom and recovering only to 30.3% post-bloom. Their co-occurrence network was most complex during the bloom period. In contrast, microeukaryotic communities retained stronger site-specific structure throughout succession, and their network connectivity peaked after the bloom collapsed. Water quality variables explained 45.9% of bacterial but only 13.1% of microeukaryotic community variation. Predicted functional profiles also showed stage-associated changes. The same bloom thus pushed bacterial and microeukaryotic communities toward different post-disturbance configurations on different timescales. We therefore propose a cross-domain monitoring framework that integrates stage-specific taxa, a community state index, and network complexity. This framework can diagnose bloom onset, collapse, and genuine post-bloom recovery in eutrophic coastal waters.IMPORTANCEHarmful algal blooms disturb coastal waters well beyond the period when the causative alga is abundant. This study shows that the effects of a Phaeocystis globosa bloom on the coastal microbiome lasted after the bloom itself ended and that bacteria and microeukaryotes recovered along different paths and on different timescales. Algal counts or nutrient concentrations alone therefore cannot adequately capture the recovery of coastal water quality. We suggest an alternative monitoring framework that combines stage-specific indicator taxa, a community state index, and network topology, so that coastal water quality can be assessed more reliably.
Additional Links: PMID-42867238
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@article {pmid42867238,
year = {2026},
author = {Yin, N and Ishii, S and Zhou, Y and Hu, J and Xia, X and Wang, H and Wu, Y and Jorquera, MA and Du, Z and Zhang, Q},
title = {Cross-domain microbiome legacy of a natural Phaeocystis globosa bloom in eutrophic coastal waters: a framework for monitoring bloom onset, collapse, and post-bloom recovery.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0148926},
doi = {10.1128/aem.01489-26},
pmid = {42867238},
issn = {1098-5336},
abstract = {When a harmful algal bloom collapses, does the coastal water quality recover? We addressed this question using the natural bloom of the haptophyte Phaeocystis globosa in coastal waters around Xiamen Island, China. Bacterial and microeukaryotic communities in the water samples (n = 105) monthly collected from five sites from September 2023 to March 2024 were analyzed using 16S and 18S rRNA amplicon sequencing, genotype-specific qPCR, iCAMP-based assembly inference, partial least squares path modeling, bloom stage-specific co-occurrence networks, and amplicon-based functional prediction. Bloom development drove coordinated physicochemical change. Both bacterial and microeukaryotic communities were displaced from their pre-bloom state but did not return to the original state within the 7-month series. However, their patterns of succession were different. Bacterial communities underwent coherent system-wide succession. They diverged spatially during the bloom. Their assembly shifted toward stochasticity, with the deterministic contribution falling from 46.3% pre-bloom to 27.8% during the bloom and recovering only to 30.3% post-bloom. Their co-occurrence network was most complex during the bloom period. In contrast, microeukaryotic communities retained stronger site-specific structure throughout succession, and their network connectivity peaked after the bloom collapsed. Water quality variables explained 45.9% of bacterial but only 13.1% of microeukaryotic community variation. Predicted functional profiles also showed stage-associated changes. The same bloom thus pushed bacterial and microeukaryotic communities toward different post-disturbance configurations on different timescales. We therefore propose a cross-domain monitoring framework that integrates stage-specific taxa, a community state index, and network complexity. This framework can diagnose bloom onset, collapse, and genuine post-bloom recovery in eutrophic coastal waters.IMPORTANCEHarmful algal blooms disturb coastal waters well beyond the period when the causative alga is abundant. This study shows that the effects of a Phaeocystis globosa bloom on the coastal microbiome lasted after the bloom itself ended and that bacteria and microeukaryotes recovered along different paths and on different timescales. Algal counts or nutrient concentrations alone therefore cannot adequately capture the recovery of coastal water quality. We suggest an alternative monitoring framework that combines stage-specific indicator taxa, a community state index, and network topology, so that coastal water quality can be assessed more reliably.},
}
RevDate: 2026-10-13
A high-throughput pipeline for isolation and screening of the citrus bacteriome identifies Pseudomonas chlororaphis with anti-Candidatus Liberibacter asiaticus activity.
Applied and environmental microbiology [Epub ahead of print].
Plant microbiomes are a rich source of secondary metabolites, often with pathogen- or disease-suppressive traits. Huanglongbing (HLB) is a serious disease of citrus for which there is currently no cure. Here, we tested the hypothesis that bacteria native to the citrus microbiome may possess inhibitory activity against the associated causal agent of HLB, Candidatus Liberibacter asiaticus (CLas). We coupled a robotic microfluidic isolation platform with a high-throughput antimicrobial screening assay using Liberibacter crescens, a culturable surrogate for the unculturable CLas, to identify isolates with anti-Liberibacter activity. We identified 35 bacterial isolates with activity using this pipeline. One strongly inhibitory citrus root isolate, Pseudomonas chlororaphis (SRAM11), was selected for bioassay-guided fractionation. We determined a significant driver of in vitro Liberibacter inhibition was attributed to the production of phenazine-1-carboxamide (PCN) by P. chlororaphis. We also demonstrated significant anti-CLas activity of PCN, comparable to that of oxytetracycline, using an ex vivo citrus hairy root assay. P. chlororaphis and phenazines have been implicated in successful biocontrol of other diseases and represent a new tool with possible application to HLB mitigation.IMPORTANCEHuanglongbing (HLB) is a devastating citrus disease that causes millions of dollars in crop loss each year in the United States alone. In this study, we mined the citrus microbiome for bacteria that produce antimicrobials with suppressive activity against Candidatus Liberibacter asiaticus, the causal agent of HLB. We demonstrated that the citrus microbiome is a rich source of microorganisms that inhibit Liberibacter spp. We selected a Pseudomonas chlororaphis strain for further characterization and assigned anti-Liberibacter activity to the production of phenazine-1-carboxamide. Phenazine-producing P. chlororaphis strains are known biocontrols in other pathosystems, and this study highlights their potential for mitigation of HLB.
Additional Links: PMID-42867240
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PubMed:
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@article {pmid42867240,
year = {2026},
author = {Drozd, C and Maebori, K and Ruiz Rivera, C and Callahan, K and Ramasamy, M and Mandadi, K and Maloney, KN and Roper, MC},
title = {A high-throughput pipeline for isolation and screening of the citrus bacteriome identifies Pseudomonas chlororaphis with anti-Candidatus Liberibacter asiaticus activity.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0157626},
doi = {10.1128/aem.01576-26},
pmid = {42867240},
issn = {1098-5336},
abstract = {Plant microbiomes are a rich source of secondary metabolites, often with pathogen- or disease-suppressive traits. Huanglongbing (HLB) is a serious disease of citrus for which there is currently no cure. Here, we tested the hypothesis that bacteria native to the citrus microbiome may possess inhibitory activity against the associated causal agent of HLB, Candidatus Liberibacter asiaticus (CLas). We coupled a robotic microfluidic isolation platform with a high-throughput antimicrobial screening assay using Liberibacter crescens, a culturable surrogate for the unculturable CLas, to identify isolates with anti-Liberibacter activity. We identified 35 bacterial isolates with activity using this pipeline. One strongly inhibitory citrus root isolate, Pseudomonas chlororaphis (SRAM11), was selected for bioassay-guided fractionation. We determined a significant driver of in vitro Liberibacter inhibition was attributed to the production of phenazine-1-carboxamide (PCN) by P. chlororaphis. We also demonstrated significant anti-CLas activity of PCN, comparable to that of oxytetracycline, using an ex vivo citrus hairy root assay. P. chlororaphis and phenazines have been implicated in successful biocontrol of other diseases and represent a new tool with possible application to HLB mitigation.IMPORTANCEHuanglongbing (HLB) is a devastating citrus disease that causes millions of dollars in crop loss each year in the United States alone. In this study, we mined the citrus microbiome for bacteria that produce antimicrobials with suppressive activity against Candidatus Liberibacter asiaticus, the causal agent of HLB. We demonstrated that the citrus microbiome is a rich source of microorganisms that inhibit Liberibacter spp. We selected a Pseudomonas chlororaphis strain for further characterization and assigned anti-Liberibacter activity to the production of phenazine-1-carboxamide. Phenazine-producing P. chlororaphis strains are known biocontrols in other pathosystems, and this study highlights their potential for mitigation of HLB.},
}
RevDate: 2026-10-13
Waste oil substrates reshape the black soldier fly larval gut microbiome and biomass composition during bioconversion.
Applied and environmental microbiology [Epub ahead of print].
UNLABELLED: Black soldier fly larvae (BSFL) are generalist decomposers with promise for converting agricultural and food-processing by-products into value-added bioproducts, but BSFL performance on lipid-rich waste oil streams and the role of the gut microbiome in this process remain unclear. Here, we evaluated BSFL bioconversion of a standard chicken feed diet supplemented with three chemically distinct waste oils: acidulated vegetable oil (AVO), pork grease (PG), and used cooking oil (UCO). Larval performance, bioconversion rate, gut microbiome composition, total protein and fat content, and fatty-acid profiles were measured across bioconversion. Larval age was a major driver of gut microbiome structure, but waste oil supplementation further reshaped community membership and structure, with the strongest diet-associated effects occurring during early-to-intermediate bioconversion. Most differentially abundant taxa were members of the baseline core gut community, suggesting that oil supplementation primarily altered dominance patterns among resident taxa. PG and UCO supported larval growth, and bioconversion performance did not differ significantly from the chicken feed control, whereas AVO reduced bioconversion rate and showed weaker growth outcomes. Oil supplementation also increased larval fat content, reduced protein content, and shifted fatty-acid profiles toward the corresponding oil feedstocks, although larval biomass composition remained shaped by basal diet and host or microbial metabolism. These findings suggest that selected lipid-rich waste streams can support efficient BSFL bioconversion while restructuring resident gut microbiome members that may tolerate, metabolize, or indirectly respond to oil-associated conditions, contributing to substrate-dependent changes in larval lipid accumulation and fatty-acid composition.
IMPORTANCE: Agricultural and food-processing systems generate large amounts of lipid-rich by-products that are difficult to manage using conventional waste-valorization approaches. Black soldier fly larvae (BSFL) offer a biological route for recovering nutrients from these materials, but efficient conversion depends on interactions among substrate chemistry, larval physiology, and the gut microbiome. This study suggests that some waste oil streams can support larval growth while restructuring resident gut microbial communities and altering larval fatty-acid composition. These findings are important for agricultural biotechnology because they frame BSFL production as a host-microbiome bioconversion system rather than simply an insect-based waste-reduction process. Understanding how gut microbes respond to chemically distinct lipid wastes can guide substrate selection, pretreatment, and microbiome-informed optimization strategies for converting underutilized agricultural and food-processing residues into value-added bioproducts for circular agricultural systems.
Additional Links: PMID-42867241
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@article {pmid42867241,
year = {2026},
author = {Saho, R and Trinh, D and Kojima, E and Wang, T and Owings, C and Burcham, Z},
title = {Waste oil substrates reshape the black soldier fly larval gut microbiome and biomass composition during bioconversion.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0108226},
doi = {10.1128/aem.01082-26},
pmid = {42867241},
issn = {1098-5336},
abstract = {UNLABELLED: Black soldier fly larvae (BSFL) are generalist decomposers with promise for converting agricultural and food-processing by-products into value-added bioproducts, but BSFL performance on lipid-rich waste oil streams and the role of the gut microbiome in this process remain unclear. Here, we evaluated BSFL bioconversion of a standard chicken feed diet supplemented with three chemically distinct waste oils: acidulated vegetable oil (AVO), pork grease (PG), and used cooking oil (UCO). Larval performance, bioconversion rate, gut microbiome composition, total protein and fat content, and fatty-acid profiles were measured across bioconversion. Larval age was a major driver of gut microbiome structure, but waste oil supplementation further reshaped community membership and structure, with the strongest diet-associated effects occurring during early-to-intermediate bioconversion. Most differentially abundant taxa were members of the baseline core gut community, suggesting that oil supplementation primarily altered dominance patterns among resident taxa. PG and UCO supported larval growth, and bioconversion performance did not differ significantly from the chicken feed control, whereas AVO reduced bioconversion rate and showed weaker growth outcomes. Oil supplementation also increased larval fat content, reduced protein content, and shifted fatty-acid profiles toward the corresponding oil feedstocks, although larval biomass composition remained shaped by basal diet and host or microbial metabolism. These findings suggest that selected lipid-rich waste streams can support efficient BSFL bioconversion while restructuring resident gut microbiome members that may tolerate, metabolize, or indirectly respond to oil-associated conditions, contributing to substrate-dependent changes in larval lipid accumulation and fatty-acid composition.
IMPORTANCE: Agricultural and food-processing systems generate large amounts of lipid-rich by-products that are difficult to manage using conventional waste-valorization approaches. Black soldier fly larvae (BSFL) offer a biological route for recovering nutrients from these materials, but efficient conversion depends on interactions among substrate chemistry, larval physiology, and the gut microbiome. This study suggests that some waste oil streams can support larval growth while restructuring resident gut microbial communities and altering larval fatty-acid composition. These findings are important for agricultural biotechnology because they frame BSFL production as a host-microbiome bioconversion system rather than simply an insect-based waste-reduction process. Understanding how gut microbes respond to chemically distinct lipid wastes can guide substrate selection, pretreatment, and microbiome-informed optimization strategies for converting underutilized agricultural and food-processing residues into value-added bioproducts for circular agricultural systems.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Mediterranean diet, gut microbiota, and intestinal barrier integrity: implications for digestive and systemic health.
Antonie van Leeuwenhoek, 119(11):.
The Mediterranean diet has gained increasing attention for its effects on gut microbiota, microbial metabolism, intestinal barrier function, and related clinical outcomes. This narrative review critically synthesizes evidence from 51 publications identified through structured searches of PubMed/MEDLINE and Google Scholar, including human intervention studies, observational studies, systematic and narrative reviews, and selected preclinical studies. The available evidence suggests that the MD can influence microbial composition and function, although taxonomic responses vary considerably between populations and study designs. More consistent findings involve microbial metabolic activity, particularly short-chain fatty acid production, bile acid remodeling, and polyphenol-derived metabolites. These changes may contribute to intestinal barrier regulation, mucosal homeostasis, and immune modulation. Human intervention studies provide supportive evidence in inflammatory bowel disease, functional gastrointestinal disorders, obesity, metabolic syndrome, and related conditions, while evidence for neurological, autoimmune, and cancer-related outcomes remains more limited and is often observational or mechanistic. Direct evidence for improved intestinal barrier function is still less extensive than indirect evidence based on inflammatory markers, microbial metabolites, and permeability-related measures. Differences in microbiome methodology, baseline diet, disease status, geographic background, and intervention duration contribute to variability across studies. The MD therefore represents a promising dietary framework for modulating gut microbial function and intestinal homeostasis, but further long-term and mechanistically integrated human studies are needed to define causal pathways and identify individuals most likely to benefit.
Additional Links: PMID-42867711
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Citation:
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@article {pmid42867711,
year = {2026},
author = {Perets, TT},
title = {Mediterranean diet, gut microbiota, and intestinal barrier integrity: implications for digestive and systemic health.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {11},
pages = {},
pmid = {42867711},
issn = {1572-9699},
mesh = {Humans ; Intestinal Barrier Function ; *Gastrointestinal Microbiome/physiology ; *Diet, Mediterranean ; Animals ; *Intestinal Mucosa/metabolism ; },
abstract = {The Mediterranean diet has gained increasing attention for its effects on gut microbiota, microbial metabolism, intestinal barrier function, and related clinical outcomes. This narrative review critically synthesizes evidence from 51 publications identified through structured searches of PubMed/MEDLINE and Google Scholar, including human intervention studies, observational studies, systematic and narrative reviews, and selected preclinical studies. The available evidence suggests that the MD can influence microbial composition and function, although taxonomic responses vary considerably between populations and study designs. More consistent findings involve microbial metabolic activity, particularly short-chain fatty acid production, bile acid remodeling, and polyphenol-derived metabolites. These changes may contribute to intestinal barrier regulation, mucosal homeostasis, and immune modulation. Human intervention studies provide supportive evidence in inflammatory bowel disease, functional gastrointestinal disorders, obesity, metabolic syndrome, and related conditions, while evidence for neurological, autoimmune, and cancer-related outcomes remains more limited and is often observational or mechanistic. Direct evidence for improved intestinal barrier function is still less extensive than indirect evidence based on inflammatory markers, microbial metabolites, and permeability-related measures. Differences in microbiome methodology, baseline diet, disease status, geographic background, and intervention duration contribute to variability across studies. The MD therefore represents a promising dietary framework for modulating gut microbial function and intestinal homeostasis, but further long-term and mechanistically integrated human studies are needed to define causal pathways and identify individuals most likely to benefit.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Intestinal Barrier Function
*Gastrointestinal Microbiome/physiology
*Diet, Mediterranean
Animals
*Intestinal Mucosa/metabolism
RevDate: 2026-10-13
CmpDate: 2026-10-13
BRIDGE-KO: auditable transfer learning with bridged knockoffs improves cross-cohort microbiome prediction of immunotherapy response.
Briefings in bioinformatics, 27(5):.
Transfer learning promises to reuse AI models across biomedical studies, but it often fails when differences between datasets introduce cohort-specific artifacts and 'negative transfer.' We present BRIDGE-KO, an interpretable deep-learning framework that turns transfer learning into a testable design process by asking: where to transfer from (source-target coverage and proximity), what to transfer (which representation level is most portable), and how to harmonize data to reduce technical confounding. BRIDGE-KO creates source-preserving knockoffs-synthetic 'shadow' features that capture the source dependency structure-and bridges them to a fixed target cohort, providing built-in baselines that flag non-portable signal. Applied to predicting immune checkpoint inhibitor response, transferring gut microbiome profiles from MicroBioMap (n = 168,464) to melanoma immune checkpoint inhibitor cohorts (n = 154), naive baselines performed near chance (AUC ≈ 0.52), whereas batch correction plus proximity-aware transfer improved performance (AUC = 0.67, 10 splits). BRIDGE-KO also enables an interpretable responder-specific audit of microbiome remodeling via correlation-shift spread.
Additional Links: PMID-42867969
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@article {pmid42867969,
year = {2026},
author = {Sun, J and Fan, Z and Caldino Bohn, R and Kim, S and Park, HJ},
title = {BRIDGE-KO: auditable transfer learning with bridged knockoffs improves cross-cohort microbiome prediction of immunotherapy response.},
journal = {Briefings in bioinformatics},
volume = {27},
number = {5},
pages = {},
pmid = {42867969},
issn = {1477-4054},
support = {R01GM108618//NIH/ ; },
mesh = {Humans ; *Immunotherapy ; *Microbiota ; *Gastrointestinal Microbiome ; Cohort Studies ; *Deep Learning ; },
abstract = {Transfer learning promises to reuse AI models across biomedical studies, but it often fails when differences between datasets introduce cohort-specific artifacts and 'negative transfer.' We present BRIDGE-KO, an interpretable deep-learning framework that turns transfer learning into a testable design process by asking: where to transfer from (source-target coverage and proximity), what to transfer (which representation level is most portable), and how to harmonize data to reduce technical confounding. BRIDGE-KO creates source-preserving knockoffs-synthetic 'shadow' features that capture the source dependency structure-and bridges them to a fixed target cohort, providing built-in baselines that flag non-portable signal. Applied to predicting immune checkpoint inhibitor response, transferring gut microbiome profiles from MicroBioMap (n = 168,464) to melanoma immune checkpoint inhibitor cohorts (n = 154), naive baselines performed near chance (AUC ≈ 0.52), whereas batch correction plus proximity-aware transfer improved performance (AUC = 0.67, 10 splits). BRIDGE-KO also enables an interpretable responder-specific audit of microbiome remodeling via correlation-shift spread.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Immunotherapy
*Microbiota
*Gastrointestinal Microbiome
Cohort Studies
*Deep Learning
RevDate: 2026-10-13
CmpDate: 2026-10-13
Gut Microbiome Composition and Diversity Are Associated with Heat Tolerance Plasticity in a Tropical Lizard.
Ecological and evolutionary physiology, 99(5):285-295.
AbstractClimate change is detrimentally affecting species worldwide. Against this backdrop, tropical ectotherms, which have evolved under historically stable conditions, are considered especially vulnerable to changing environmental conditions. Phenotypic plasticity may provide a rapid coping mechanism in response to warming. While plasticity is typically attributed to host mechanisms, vertebrates house diverse gut microbial communities that impact host traits and can change rapidly within the host's lifetime. Thus, it is possible that the microbiome may contribute to the capacity of ectotherms to mount plastic responses to environmental warming. We explored this possibility using the Panamanian slender anole (Anolis apletophallus), a tropical forest-dwelling lizard experiencing population declines induced by climate change. We tested for associations between the composition of the gut microbiome in slender anoles and the capacity for plasticity in their heat tolerance at three time points after exposure to an acute heat stress event. We found that the magnitude of host plasticity at two of three time points was significantly associated with gut microbiome composition before heat stress. Furthermore, up to 94% of the variation in host plasticity was explained by gut microbiome diversity at one time point. Our work suggests a potentially key role for the microbiome in modulating plastic responses to climate change in ectothermic vertebrates, although future manipulative experiments are required to confirm causality.
Additional Links: PMID-42868418
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PubMed:
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@article {pmid42868418,
year = {2026},
author = {Fontaine, SS and Wuthrich, KL and Alfonso, C and Alujević, K and Bakewell, L and Keller, J and López-Tacoaman, YF and Ponce-Chilan, NE and Vivas, A and Williams, CE and McMillan, WO and Cox, CL and Logan, ML},
title = {Gut Microbiome Composition and Diversity Are Associated with Heat Tolerance Plasticity in a Tropical Lizard.},
journal = {Ecological and evolutionary physiology},
volume = {99},
number = {5},
pages = {285-295},
doi = {10.1086/742402},
pmid = {42868418},
issn = {2993-7973},
mesh = {Animals ; *Lizards/microbiology/physiology ; *Gastrointestinal Microbiome ; *Thermotolerance ; Tropical Climate ; Climate Change ; Hot Temperature ; },
abstract = {AbstractClimate change is detrimentally affecting species worldwide. Against this backdrop, tropical ectotherms, which have evolved under historically stable conditions, are considered especially vulnerable to changing environmental conditions. Phenotypic plasticity may provide a rapid coping mechanism in response to warming. While plasticity is typically attributed to host mechanisms, vertebrates house diverse gut microbial communities that impact host traits and can change rapidly within the host's lifetime. Thus, it is possible that the microbiome may contribute to the capacity of ectotherms to mount plastic responses to environmental warming. We explored this possibility using the Panamanian slender anole (Anolis apletophallus), a tropical forest-dwelling lizard experiencing population declines induced by climate change. We tested for associations between the composition of the gut microbiome in slender anoles and the capacity for plasticity in their heat tolerance at three time points after exposure to an acute heat stress event. We found that the magnitude of host plasticity at two of three time points was significantly associated with gut microbiome composition before heat stress. Furthermore, up to 94% of the variation in host plasticity was explained by gut microbiome diversity at one time point. Our work suggests a potentially key role for the microbiome in modulating plastic responses to climate change in ectothermic vertebrates, although future manipulative experiments are required to confirm causality.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Lizards/microbiology/physiology
*Gastrointestinal Microbiome
*Thermotolerance
Tropical Climate
Climate Change
Hot Temperature
RevDate: 2026-10-13
CmpDate: 2026-10-13
Gut-Mitophagy-Ferroptosis Axis in Asthma: Microvirga-TP53-PARP11 Crosstalk as a Quantifiable Target for Childhood Asthma Prevention.
Critical reviews in eukaryotic gene expression, 36(2):65-78.
INTRODUCTION: Asthma affects over 260 million individuals globally; however, its heterogeneous subtypes pose significant challenges to precision prevention. Although gut microbiome dysbiosis and mitophagy and ferroptosis dysfunction have been implicated in asthma pathogenesis, the potential causal interactions between these pathways remain unclear.
METHODS: We performed two-sample Mendelian randomization (MR) to assess the causal effects of 473 gut microbial taxa and 49 mitophagy-related genes on four distinct asthma subtypes. Mediation and reverse MR analyses were further employed to explore potential mitophagy-mediated pathways and assess feedback effects from asthma liability on the gut microbiota. For the mitophagy-related mediator genes, we further dissected the ferroptotic pathway-mediated downstream mechanisms and performed drug candidate enrichment and molecular docking.
RESULTS: MR analysis identified 20, 19, 13, and 15 gut bacterial taxa that were causally associated with non-allergic, allergic, childhood, and eosinophilic asthma, respectively. Four mitophagy-related genes TP53, MAP1LC3A, NBR1, and CSNK2B exhibited subtype-specific associations. Mediation analysis suggested that TP53-mediated mitophagy mediates 7.7% of the total effect of Microvirga against childhood asthma. Approximately 49% of the total protective effect of TP53 was partially offset through its down-regulation of PARP11-mediated ferroptosis. DSigDB-selected baicalin and theaflavin both stably docked to TP53 at 7.8 kcal mol-1, which offers natural origin, low toxicity, and high affinity.
CONCLUSION: Our findings support the existence of a gut-mitophagy-ferroptosis-lung axis in asthma pathogenesis. Notably, the Microvirga-TP53-PARP11axis demonstrates a quantifiable protective association with childhood asthma. These insights highlight a potential opportunity for precision, subtype-specific prevention strategies targeting this pathway in early life.
Additional Links: PMID-42868581
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PubMed:
Citation:
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@article {pmid42868581,
year = {2026},
author = {Sun, T and Bi, J and Zhang, J and Ye, L},
title = {Gut-Mitophagy-Ferroptosis Axis in Asthma: Microvirga-TP53-PARP11 Crosstalk as a Quantifiable Target for Childhood Asthma Prevention.},
journal = {Critical reviews in eukaryotic gene expression},
volume = {36},
number = {2},
pages = {65-78},
doi = {10.1615/CritRevEukaryotGeneExpr.2026063605},
pmid = {42868581},
issn = {2162-6502},
mesh = {*Asthma/prevention & control/microbiology/genetics/metabolism ; Humans ; *Mitophagy/genetics ; *Tumor Suppressor Protein p53/genetics/metabolism ; *Gastrointestinal Microbiome ; *Ferroptosis/genetics ; Dysbiosis ; },
abstract = {INTRODUCTION: Asthma affects over 260 million individuals globally; however, its heterogeneous subtypes pose significant challenges to precision prevention. Although gut microbiome dysbiosis and mitophagy and ferroptosis dysfunction have been implicated in asthma pathogenesis, the potential causal interactions between these pathways remain unclear.
METHODS: We performed two-sample Mendelian randomization (MR) to assess the causal effects of 473 gut microbial taxa and 49 mitophagy-related genes on four distinct asthma subtypes. Mediation and reverse MR analyses were further employed to explore potential mitophagy-mediated pathways and assess feedback effects from asthma liability on the gut microbiota. For the mitophagy-related mediator genes, we further dissected the ferroptotic pathway-mediated downstream mechanisms and performed drug candidate enrichment and molecular docking.
RESULTS: MR analysis identified 20, 19, 13, and 15 gut bacterial taxa that were causally associated with non-allergic, allergic, childhood, and eosinophilic asthma, respectively. Four mitophagy-related genes TP53, MAP1LC3A, NBR1, and CSNK2B exhibited subtype-specific associations. Mediation analysis suggested that TP53-mediated mitophagy mediates 7.7% of the total effect of Microvirga against childhood asthma. Approximately 49% of the total protective effect of TP53 was partially offset through its down-regulation of PARP11-mediated ferroptosis. DSigDB-selected baicalin and theaflavin both stably docked to TP53 at 7.8 kcal mol-1, which offers natural origin, low toxicity, and high affinity.
CONCLUSION: Our findings support the existence of a gut-mitophagy-ferroptosis-lung axis in asthma pathogenesis. Notably, the Microvirga-TP53-PARP11axis demonstrates a quantifiable protective association with childhood asthma. These insights highlight a potential opportunity for precision, subtype-specific prevention strategies targeting this pathway in early life.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Asthma/prevention & control/microbiology/genetics/metabolism
Humans
*Mitophagy/genetics
*Tumor Suppressor Protein p53/genetics/metabolism
*Gastrointestinal Microbiome
*Ferroptosis/genetics
Dysbiosis
RevDate: 2026-10-13
Co-expression of alnA and bphC in alfalfa enhances PCB phytoremediation by coupling bioavailability modulation and intracellular detoxification.
Journal of hazardous materials, 518:143851 pii:S0304-3894(26)02832-3 [Epub ahead of print].
Phytoremediation of polychlorinated biphenyls (PCBs)-contaminated soils is hindered by low PCB bioavailability and insufficient plant detoxification. Here, we engineered transgenic alfalfa co-expressing alnA (encoding an emulsifying protein) and bphC (encoding a ring-cleavage dioxygenase) to address these barriers. Five representative congeners spanning a range of chlorination degrees were selected to evaluate the system's efficacy. The transgenic AB lines achieved sustained rhizosecretion of AlnA, enhancing PCB solubility by 2.0- to 3.2-fold relative to wild-type (WT) plants. While enhanced bioavailability typically exacerbates phytotoxicity, endogenous BphC cleaved the biphenyl ring, preventing toxic intermediate accumulation. This extracellular solubilization-intracellular detoxification synergy enabled AB alfalfa to maintain improved growth under PCB stress, increasing root accumulation by 3.7-fold and overall removal by 2-fold compared to WT alfalfa. Metagenomic and structural equation modeling revealed that while microbial genes act as "proximate executors" directly degrading PCBs, the transgenic plant functions as the "primary driver". The AB lines enriched specific degraders (Pseudomonas and certain genera within the order Burkholderiales) and assembled a functional network for aerobic PCB degradation. This integrated plant-microbiome system offers a low-maintenance strategy for in situ remediation of PCB-contaminated sites.
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@article {pmid42868780,
year = {2026},
author = {Lin, W and Ding, Y and Ren, H and Wang, Y},
title = {Co-expression of alnA and bphC in alfalfa enhances PCB phytoremediation by coupling bioavailability modulation and intracellular detoxification.},
journal = {Journal of hazardous materials},
volume = {518},
number = {},
pages = {143851},
doi = {10.1016/j.jhazmat.2026.143851},
pmid = {42868780},
issn = {1873-3336},
abstract = {Phytoremediation of polychlorinated biphenyls (PCBs)-contaminated soils is hindered by low PCB bioavailability and insufficient plant detoxification. Here, we engineered transgenic alfalfa co-expressing alnA (encoding an emulsifying protein) and bphC (encoding a ring-cleavage dioxygenase) to address these barriers. Five representative congeners spanning a range of chlorination degrees were selected to evaluate the system's efficacy. The transgenic AB lines achieved sustained rhizosecretion of AlnA, enhancing PCB solubility by 2.0- to 3.2-fold relative to wild-type (WT) plants. While enhanced bioavailability typically exacerbates phytotoxicity, endogenous BphC cleaved the biphenyl ring, preventing toxic intermediate accumulation. This extracellular solubilization-intracellular detoxification synergy enabled AB alfalfa to maintain improved growth under PCB stress, increasing root accumulation by 3.7-fold and overall removal by 2-fold compared to WT alfalfa. Metagenomic and structural equation modeling revealed that while microbial genes act as "proximate executors" directly degrading PCBs, the transgenic plant functions as the "primary driver". The AB lines enriched specific degraders (Pseudomonas and certain genera within the order Burkholderiales) and assembled a functional network for aerobic PCB degradation. This integrated plant-microbiome system offers a low-maintenance strategy for in situ remediation of PCB-contaminated sites.},
}
RevDate: 2026-10-13
Strict taxonomic cold-start benchmarking reveals when graph learning adds value beyond microbial lineage priors.
Computational biology and chemistry, 126(Pt 2):109470 pii:S1476-9271(26)00597-9 [Epub ahead of print].
Prioritising disease associations for newly observed microbial taxa is a central challenge for microbiome-driven discovery: curated links are sparse, experimental validation is costly, and deployment often begins with lineage and incomplete functional descriptors rather than known disease edges. Yet standard random or transductive benchmarks can reward taxonomic or association-derived leakage, leaving unclear whether graph learning contributes information that would remain available for an unseen taxon. We address this gap by formalising strict microbe-side taxonomic label cold start as a deployment-aligned benchmark for microbe-disease association prediction. The leakage-audited benchmark comprises 1375 MDIPID microbe-neurological disease associations across 626 taxa and 32 diseases, with Genus and Family-fixed splits, sampled-negative discrimination, and full-candidate retrieval. TaxFuse-HGCL serves as an inductive, prior-calibrated reference framework: a hypergraph neural ranker is trained inside each fold, guided by taxonomy-kNN listwise targets, and calibrated with the taxonomy-neighbour score available for the held-out taxon. Across experiments, taxonomy kNN emerged as a high-value biological prior rather than a weak baseline. In the Genus split, TaxFuse-HGCL improved the neural backbone from sampled AUC/AUPR 0.8307/0.6213 to 0.8481/0.6490, reaching the taxonomy kNN range, while taxonomy kNN retained stronger full-candidate recall. In the Family-fixed split, TaxFuse-HGCL reached sampled AUC/AUPR 0.8516/0.6591 and micro-AUPR 0.1368, the strongest discrimination and micro-averaged retrieval profile among protocol-matched baselines. Residual, oracle, and 16S probes showed that the dense neurological benchmark is dominated by lineage-carried signal, whereas on a larger, sparser Disbiome dataset fold-internal fusion produced paired gains over tuned taxonomy kNN on sampled AUC/AUPR and full-candidate AUPR endpoints. Together, these findings make strict taxonomic cold start a biological model-selection criterion: they show when graph learning adds deployable signal beyond lineage, when a simpler lineage prior is sufficient, and why prior-calibrated neural systems should be evaluated before experimental follow-up.
Additional Links: PMID-42868785
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@article {pmid42868785,
year = {2026},
author = {Zhao, R and Shen, X},
title = {Strict taxonomic cold-start benchmarking reveals when graph learning adds value beyond microbial lineage priors.},
journal = {Computational biology and chemistry},
volume = {126},
number = {Pt 2},
pages = {109470},
doi = {10.1016/j.compbiolchem.2026.109470},
pmid = {42868785},
issn = {1476-928X},
abstract = {Prioritising disease associations for newly observed microbial taxa is a central challenge for microbiome-driven discovery: curated links are sparse, experimental validation is costly, and deployment often begins with lineage and incomplete functional descriptors rather than known disease edges. Yet standard random or transductive benchmarks can reward taxonomic or association-derived leakage, leaving unclear whether graph learning contributes information that would remain available for an unseen taxon. We address this gap by formalising strict microbe-side taxonomic label cold start as a deployment-aligned benchmark for microbe-disease association prediction. The leakage-audited benchmark comprises 1375 MDIPID microbe-neurological disease associations across 626 taxa and 32 diseases, with Genus and Family-fixed splits, sampled-negative discrimination, and full-candidate retrieval. TaxFuse-HGCL serves as an inductive, prior-calibrated reference framework: a hypergraph neural ranker is trained inside each fold, guided by taxonomy-kNN listwise targets, and calibrated with the taxonomy-neighbour score available for the held-out taxon. Across experiments, taxonomy kNN emerged as a high-value biological prior rather than a weak baseline. In the Genus split, TaxFuse-HGCL improved the neural backbone from sampled AUC/AUPR 0.8307/0.6213 to 0.8481/0.6490, reaching the taxonomy kNN range, while taxonomy kNN retained stronger full-candidate recall. In the Family-fixed split, TaxFuse-HGCL reached sampled AUC/AUPR 0.8516/0.6591 and micro-AUPR 0.1368, the strongest discrimination and micro-averaged retrieval profile among protocol-matched baselines. Residual, oracle, and 16S probes showed that the dense neurological benchmark is dominated by lineage-carried signal, whereas on a larger, sparser Disbiome dataset fold-internal fusion produced paired gains over tuned taxonomy kNN on sampled AUC/AUPR and full-candidate AUPR endpoints. Together, these findings make strict taxonomic cold start a biological model-selection criterion: they show when graph learning adds deployable signal beyond lineage, when a simpler lineage prior is sufficient, and why prior-calibrated neural systems should be evaluated before experimental follow-up.},
}
RevDate: 2026-10-13
HyM[2]Surv: Hypergraph learning for cross-magnification and microbiome-attentive multimodal survival prediction.
Medical image analysis, 115:104343 pii:S1361-8415(26)00412-3 [Epub ahead of print].
Survival prediction is a critical task in cancer prognosis assessment. In recent years, deep learning methods based on multimodal data have been widely applied to this task. However, existing studies primarily focus on the integration of whole slide images (WSIs) and genomic data, while the utilization of intratumoral microbiome information remains limited. Meanwhile, current approaches face two limitations: (i) they fail to fully exploit the multi-magnification information of WSIs, limiting the joint representation learning across different resolutions; and (ii) high-magnification pathological features tend to dominate, leading to modality imbalance between pathology and intratumoral microbiome data. In this study, we propose HyM[2]Surv, a hypergraph-based framework for multi-magnification multimodal survival prediction. Specifically, the model first captures cross-magnification interactions in pathology by leveraging spatial proximity and phenotypic feature similarity. It then constructs dense cross-modal connections by centering on the microbiome and linking it with pathological features across all magnifications, thereby alleviating modality imbalance. Extensive experiments on four TCGA datasets demonstrate that HyM[2]Surv consistently outperforms state-of-the-art methods, achieving an average improvement of 6.10% in terms of C-index. In addition, the proposed model provides interpretable insights by identifying microbiome-pathology interaction regions that are significantly associated with patient prognosis, highlighting its potential clinical application. The code is publicly available at https://github.com/RanSuLab/HyMMSurv.
Additional Links: PMID-42868931
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@article {pmid42868931,
year = {2026},
author = {Zhang, F and Hu, K and Sun, C and Liu, X and Wei, L and Su, R},
title = {HyM[2]Surv: Hypergraph learning for cross-magnification and microbiome-attentive multimodal survival prediction.},
journal = {Medical image analysis},
volume = {115},
number = {},
pages = {104343},
doi = {10.1016/j.media.2026.104343},
pmid = {42868931},
issn = {1361-8423},
abstract = {Survival prediction is a critical task in cancer prognosis assessment. In recent years, deep learning methods based on multimodal data have been widely applied to this task. However, existing studies primarily focus on the integration of whole slide images (WSIs) and genomic data, while the utilization of intratumoral microbiome information remains limited. Meanwhile, current approaches face two limitations: (i) they fail to fully exploit the multi-magnification information of WSIs, limiting the joint representation learning across different resolutions; and (ii) high-magnification pathological features tend to dominate, leading to modality imbalance between pathology and intratumoral microbiome data. In this study, we propose HyM[2]Surv, a hypergraph-based framework for multi-magnification multimodal survival prediction. Specifically, the model first captures cross-magnification interactions in pathology by leveraging spatial proximity and phenotypic feature similarity. It then constructs dense cross-modal connections by centering on the microbiome and linking it with pathological features across all magnifications, thereby alleviating modality imbalance. Extensive experiments on four TCGA datasets demonstrate that HyM[2]Surv consistently outperforms state-of-the-art methods, achieving an average improvement of 6.10% in terms of C-index. In addition, the proposed model provides interpretable insights by identifying microbiome-pathology interaction regions that are significantly associated with patient prognosis, highlighting its potential clinical application. The code is publicly available at https://github.com/RanSuLab/HyMMSurv.},
}
RevDate: 2026-10-13
Rhizosphere functional microbiome remodeling by Streptomyces and jasmonic acid mitigates cadmium accumulation in rice.
Microbiological research, 315:128761 pii:S0944-5013(26)00325-3 [Epub ahead of print].
Cadmium (Cd) contamination poses a serious threat to rice production and food safety because of its high mobility in soil and its accumulation in edible rice tissues. Although beneficial microorganisms and plant signaling regulators have individually shown potential for alleviating Cd stress, whether their combined application can reduce Cd accumulation by restructuring rhizosphere microbial functions remains poorly understood. This study investigated the effects of two Cd-tolerant, plant growth-promoting Streptomyces strains, alone or in combination with jasmonic acid (JA), on Cd stress, Cd accumulation, and rhizosphere microbial communities and functions in rice. The results indicated that Streptomyces co-inoculation improved rice growth, photosynthetic performance, antioxidant defense, and osmotic regulation. It also reduced soil Cd bioavailability and altered Cd partitioning within rice plants. JA alone exerted relatively limited effects on the rhizosphere microbiome but strengthened Streptomyces-mediated physiological and microbial responses when applied in combination. Metagenomic analysis showed that the treatments altered microbial community composition and enriched COG functions associated with inorganic ion transport, signal transduction, and cell envelope biogenesis. KEGG analysis further revealed changes in pathways associated with environmental sensing and Cd detoxification, particularly the two-component system and glutathione metabolism. BacMet analysis identified 37 Cd-related resistance genes. Streptomyces co-inoculation broadly enriched resistance modules involved in metal sensing, transport, efflux, and detoxification, whereas the combined treatment selectively enriched core resistance genes, including czcA, czcP, zntA, and nccB. These changes were consistent with the reduced bioavailable Cd in rhizosphere soil and lower Cd accumulation in rice. Rather than increasing the number of responsive genes, the addition of JA to Streptomyces co-inoculation was associated with a more focused Cd resistance gene response, particularly involving metal transport and efflux. Overall, the reduction in Cd accumulation was associated with coordinated changes in rhizosphere microbial communities, metabolic pathways, and Cd resistance genes. These findings highlight the potential of combining Streptomyces co-inoculation with JA as a microbiome based strategy for rice cultivation in Cd contaminated soils.
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@article {pmid42868958,
year = {2026},
author = {Yan, C and Liu, J and Ma, S and Cheng, Z and Xu, H and Shangguan, YX and Liu, H},
title = {Rhizosphere functional microbiome remodeling by Streptomyces and jasmonic acid mitigates cadmium accumulation in rice.},
journal = {Microbiological research},
volume = {315},
number = {},
pages = {128761},
doi = {10.1016/j.micres.2026.128761},
pmid = {42868958},
issn = {1618-0623},
abstract = {Cadmium (Cd) contamination poses a serious threat to rice production and food safety because of its high mobility in soil and its accumulation in edible rice tissues. Although beneficial microorganisms and plant signaling regulators have individually shown potential for alleviating Cd stress, whether their combined application can reduce Cd accumulation by restructuring rhizosphere microbial functions remains poorly understood. This study investigated the effects of two Cd-tolerant, plant growth-promoting Streptomyces strains, alone or in combination with jasmonic acid (JA), on Cd stress, Cd accumulation, and rhizosphere microbial communities and functions in rice. The results indicated that Streptomyces co-inoculation improved rice growth, photosynthetic performance, antioxidant defense, and osmotic regulation. It also reduced soil Cd bioavailability and altered Cd partitioning within rice plants. JA alone exerted relatively limited effects on the rhizosphere microbiome but strengthened Streptomyces-mediated physiological and microbial responses when applied in combination. Metagenomic analysis showed that the treatments altered microbial community composition and enriched COG functions associated with inorganic ion transport, signal transduction, and cell envelope biogenesis. KEGG analysis further revealed changes in pathways associated with environmental sensing and Cd detoxification, particularly the two-component system and glutathione metabolism. BacMet analysis identified 37 Cd-related resistance genes. Streptomyces co-inoculation broadly enriched resistance modules involved in metal sensing, transport, efflux, and detoxification, whereas the combined treatment selectively enriched core resistance genes, including czcA, czcP, zntA, and nccB. These changes were consistent with the reduced bioavailable Cd in rhizosphere soil and lower Cd accumulation in rice. Rather than increasing the number of responsive genes, the addition of JA to Streptomyces co-inoculation was associated with a more focused Cd resistance gene response, particularly involving metal transport and efflux. Overall, the reduction in Cd accumulation was associated with coordinated changes in rhizosphere microbial communities, metabolic pathways, and Cd resistance genes. These findings highlight the potential of combining Streptomyces co-inoculation with JA as a microbiome based strategy for rice cultivation in Cd contaminated soils.},
}
RevDate: 2026-10-13
SPP1[+] TAMs drive colorectal tumorigenesis through an ARG2-orchestrated metabolic-immune crosstalk.
Cancer letters pii:S0304-3835(26)00654-3 [Epub ahead of print].
Rising incidence of colorectal cancer (CRC) and limited therapeutic options highlight the urgent need to define the drivers of its progression. The SPP1[+] tumor-associated macrophage (TAM) subset identified by single-cell transcriptomics is a functionally dominant population that extends beyond the classical M1/M2 paradigm. Here, we dissected the molecular mechanisms by which SPP1[+] TAMs reprogram tumor progression and determined whether the gut microbiota regulates this process in colorectal cancer. Using a multi-platform strategy integrating clinical specimens, murine models and CRC cell lines, we found that SPP1[+] TAMs increase progressively during CRC evolution and exhibit crosstalk with malignant epithelial cells, and their abundance is associated with adverse clinical outcome. Integrative analysis reveals a significant positive correlation between SPP1 and ARG2 expression. Further, TAM-derived SPP1 engages CD44 on CRC cells to induce ARG2 expression. Mechanistically, ARG2 facilitates the interaction between USP10 and c-Myc to deubiquitinate and stabilize c-Myc, which transactivates the glycolytic enzyme HK2, driving Warburg metabolism that fuels CRC cell proliferation. Moreover, ARG2 secreted by CRC cells is internalized by TAMs, which reciprocally upregulates SPP1, creating a feed-forward loop that drives a pro-tumorigenic microenvironment. Notably, Bifidobacterium longum downregulates CD44 expression on tumor cells, thereby disrupting the SPP1-ARG2 axis and attenuating CRC progression. These findings identify the SPP1-ARG2 circuit as a therapeutic target and propose B. longum as a microbiome-derived precision adjuvant therapy for CRC suppression.
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@article {pmid42869126,
year = {2026},
author = {Song, L and Yan, T and Lu, SY and Tong, T and Wang, Z and Zhou, CB and Zhuang, ZY and Xie, Y and Leng, X and Zhang, C and Chen, Y and Gu, WQ and Cui, Y and Zhang, ZZ and Chen, J and Chen, H and Hong, J and Chen, H and Chen, YX and Fang, JY},
title = {SPP1[+] TAMs drive colorectal tumorigenesis through an ARG2-orchestrated metabolic-immune crosstalk.},
journal = {Cancer letters},
volume = {},
number = {},
pages = {218890},
doi = {10.1016/j.canlet.2026.218890},
pmid = {42869126},
issn = {1872-7980},
abstract = {Rising incidence of colorectal cancer (CRC) and limited therapeutic options highlight the urgent need to define the drivers of its progression. The SPP1[+] tumor-associated macrophage (TAM) subset identified by single-cell transcriptomics is a functionally dominant population that extends beyond the classical M1/M2 paradigm. Here, we dissected the molecular mechanisms by which SPP1[+] TAMs reprogram tumor progression and determined whether the gut microbiota regulates this process in colorectal cancer. Using a multi-platform strategy integrating clinical specimens, murine models and CRC cell lines, we found that SPP1[+] TAMs increase progressively during CRC evolution and exhibit crosstalk with malignant epithelial cells, and their abundance is associated with adverse clinical outcome. Integrative analysis reveals a significant positive correlation between SPP1 and ARG2 expression. Further, TAM-derived SPP1 engages CD44 on CRC cells to induce ARG2 expression. Mechanistically, ARG2 facilitates the interaction between USP10 and c-Myc to deubiquitinate and stabilize c-Myc, which transactivates the glycolytic enzyme HK2, driving Warburg metabolism that fuels CRC cell proliferation. Moreover, ARG2 secreted by CRC cells is internalized by TAMs, which reciprocally upregulates SPP1, creating a feed-forward loop that drives a pro-tumorigenic microenvironment. Notably, Bifidobacterium longum downregulates CD44 expression on tumor cells, thereby disrupting the SPP1-ARG2 axis and attenuating CRC progression. These findings identify the SPP1-ARG2 circuit as a therapeutic target and propose B. longum as a microbiome-derived precision adjuvant therapy for CRC suppression.},
}
RevDate: 2026-10-13
β-Hydroxybutyrate alleviates intestinal aGVHD via remodeling gut microbiota-bile acid axis and inhibiting TLR4-NF-κB-driven Th1/Th17 differentiation.
Life sciences pii:S0024-3205(26)00546-1 [Epub ahead of print].
The intestine is a major target organ in acute graft-versus-host disease (aGVHD), and its microbial homeostasis critically influences disease pathogenesis and progression. Emerging evidence indicates that beta-hydroxybutyrate (BHB) can remodel the gut microbiota and dampen pro-inflammatory immune activity. To investigate the therapeutic potential of BHB in aGVHD, we first reanalyzed publicly available transcriptomic and single-cell RNA sequencing data from patients with aGVHD, which revealed that genes involved in ketone body metabolism and transport were significantly decreased in intestinal tissues. We then used a murine model of aGVHD to evaluate the therapeutic effects of BHB by clinical scoring and intestinal histopathological examination. To define the immunological and microbial mechanisms, we integrated flow cytometry and ELISA for Th1/Th17, intestinal tissue-resident T and circulating T cells assessment, and with multi-omics analyses, including fecal 16S rRNA sequencing, fecal metabolomics, and intestinal transcriptomics. We further explored whether BHB directly regulates T-cell migration and differentiation and therefore assessed its effects on Th1 and Th17 differentiation in vitro. BHB treatment reduced the clinical score of aGVHD, alleviated intestinal injury in mice, and showed effects similar to those of methotrexate (MTX). BHB also corrected gut microbial dysbiosis, enriched Akkermansia muciniphila, and ameliorated bile acid metabolism dysregulation. Moreover, BHB inhibited intestinal T cell migration and Th1/Th17 differentiation both in vivo and in vitro. Mechanistically, transcriptome sequencing suggested that suppression of the TLR4-NF-κB pathway may underlie these anti-inflammatory effects. In summary, BHB effectively alleviates intestinal damage in aGVHD mice, likely through coordinated microbial, metabolic, and immunological regulation, and may represent a promising therapeutic strategy for aGVHD.
Additional Links: PMID-42869131
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@article {pmid42869131,
year = {2026},
author = {Tian, R and Deng, C and Liu, K and Lai, H and Liao, C and Tu, H and Li, J},
title = {β-Hydroxybutyrate alleviates intestinal aGVHD via remodeling gut microbiota-bile acid axis and inhibiting TLR4-NF-κB-driven Th1/Th17 differentiation.},
journal = {Life sciences},
volume = {},
number = {},
pages = {124737},
doi = {10.1016/j.lfs.2026.124737},
pmid = {42869131},
issn = {1879-0631},
abstract = {The intestine is a major target organ in acute graft-versus-host disease (aGVHD), and its microbial homeostasis critically influences disease pathogenesis and progression. Emerging evidence indicates that beta-hydroxybutyrate (BHB) can remodel the gut microbiota and dampen pro-inflammatory immune activity. To investigate the therapeutic potential of BHB in aGVHD, we first reanalyzed publicly available transcriptomic and single-cell RNA sequencing data from patients with aGVHD, which revealed that genes involved in ketone body metabolism and transport were significantly decreased in intestinal tissues. We then used a murine model of aGVHD to evaluate the therapeutic effects of BHB by clinical scoring and intestinal histopathological examination. To define the immunological and microbial mechanisms, we integrated flow cytometry and ELISA for Th1/Th17, intestinal tissue-resident T and circulating T cells assessment, and with multi-omics analyses, including fecal 16S rRNA sequencing, fecal metabolomics, and intestinal transcriptomics. We further explored whether BHB directly regulates T-cell migration and differentiation and therefore assessed its effects on Th1 and Th17 differentiation in vitro. BHB treatment reduced the clinical score of aGVHD, alleviated intestinal injury in mice, and showed effects similar to those of methotrexate (MTX). BHB also corrected gut microbial dysbiosis, enriched Akkermansia muciniphila, and ameliorated bile acid metabolism dysregulation. Moreover, BHB inhibited intestinal T cell migration and Th1/Th17 differentiation both in vivo and in vitro. Mechanistically, transcriptome sequencing suggested that suppression of the TLR4-NF-κB pathway may underlie these anti-inflammatory effects. In summary, BHB effectively alleviates intestinal damage in aGVHD mice, likely through coordinated microbial, metabolic, and immunological regulation, and may represent a promising therapeutic strategy for aGVHD.},
}
RevDate: 2026-10-13
From animal behavior to human perioperative neurocognitive disorders: translational boundaries of the gut-brain axis.
Behavioural brain research pii:S0166-4328(26)00509-7 [Epub ahead of print].
Perioperative neurocognitive disorders (PND), including postoperative delirium (POD), delayed neurocognitive recovery (DNR), and postoperative neurocognitive disorder, are common after surgery in older adults, and the gut-brain axis has been proposed as a contributing pathway. Most mechanistic support rests on rodent behavioral assays, yet these endpoints and human clinical diagnoses are routinely treated as interchangeable. This critical narrative review examines that translational boundary. PND is used here as a clinically consequential test case for a broader behavioral-neuroscience problem: how animal behavioral phenotypes, microbiome-associated signals, and intervention effects should be translated into human diagnostic constructs. A structured search identified and appraised the principal evidence rather than an exhaustive synthesis; no formal risk-of-bias or certainty-of-evidence assessment was performed. Evidence was separated into human perioperative studies reporting a neurocognitive outcome with either a measured gut-brain exposure or a gut-directed intervention; those reporting gut-brain change without a cognitive outcome; perioperative preclinical evidence; and indirect non-perioperative evidence. The retrieved human perioperative evidence spans observational cohorts across gastric, orthopedic, spinal and cardiac surgery, multi-omic and metabolomic cohorts, and randomized perioperative probiotic trials reporting lower rates of study-defined cognitive outcomes. It nonetheless remains heterogeneous and largely single-center, with modest event numbers, inconsistent sampling and assessment, and limited external validation. Mechanistic support still comes mainly from perioperative rodent models using water maze, fear-conditioning, recognition-memory, and delirium-like readouts, which measure narrow, species-specific capacities and are not diagnostic equivalents of POD, DNR, or postoperative neurocognitive disorder. Microbiome-mediated causation is unproven, and cross-species endpoint alignment remains a central route to improved translation.
Additional Links: PMID-42869281
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@article {pmid42869281,
year = {2026},
author = {Zhu, C and Wei, J},
title = {From animal behavior to human perioperative neurocognitive disorders: translational boundaries of the gut-brain axis.},
journal = {Behavioural brain research},
volume = {},
number = {},
pages = {116533},
doi = {10.1016/j.bbr.2026.116533},
pmid = {42869281},
issn = {1872-7549},
abstract = {Perioperative neurocognitive disorders (PND), including postoperative delirium (POD), delayed neurocognitive recovery (DNR), and postoperative neurocognitive disorder, are common after surgery in older adults, and the gut-brain axis has been proposed as a contributing pathway. Most mechanistic support rests on rodent behavioral assays, yet these endpoints and human clinical diagnoses are routinely treated as interchangeable. This critical narrative review examines that translational boundary. PND is used here as a clinically consequential test case for a broader behavioral-neuroscience problem: how animal behavioral phenotypes, microbiome-associated signals, and intervention effects should be translated into human diagnostic constructs. A structured search identified and appraised the principal evidence rather than an exhaustive synthesis; no formal risk-of-bias or certainty-of-evidence assessment was performed. Evidence was separated into human perioperative studies reporting a neurocognitive outcome with either a measured gut-brain exposure or a gut-directed intervention; those reporting gut-brain change without a cognitive outcome; perioperative preclinical evidence; and indirect non-perioperative evidence. The retrieved human perioperative evidence spans observational cohorts across gastric, orthopedic, spinal and cardiac surgery, multi-omic and metabolomic cohorts, and randomized perioperative probiotic trials reporting lower rates of study-defined cognitive outcomes. It nonetheless remains heterogeneous and largely single-center, with modest event numbers, inconsistent sampling and assessment, and limited external validation. Mechanistic support still comes mainly from perioperative rodent models using water maze, fear-conditioning, recognition-memory, and delirium-like readouts, which measure narrow, species-specific capacities and are not diagnostic equivalents of POD, DNR, or postoperative neurocognitive disorder. Microbiome-mediated causation is unproven, and cross-species endpoint alignment remains a central route to improved translation.},
}
RevDate: 2026-10-13
Parsing the relationships among gut microbiome, neurotransmitter metabolome, glymphatic function, and cognition across healthy elderly, mild cognitive impairment, and probable Alzheimer's disease.
Brain, behavior, and immunity pii:S0889-1591(26)00815-9 [Epub ahead of print].
BACKGROUND: Evidence has suggested brain glymphatic dysfunction and gut microbial metabolic disturbance in Alzheimer's disease (AD), yet the relationships among gut microbiota, neurotransmitter metabolites, glymphatic function, and cognition across clinically defined groups of healthy elderly, mild cognitive impairment (MCI), and probable AD remain unclear.
METHODS: Using metagenomic sequencing, targeted metabolomics, and multi-modal magnetic resonance imaging, we measured the gut microbiome, neurotransmitter metabolome, and a variety of glymphatic markers in 30 patients with clinically diagnosed probable AD, 75 individuals with MCI, and 59 healthy controls (HC).
RESULTS: Although global microbial diversity showed no group difference, MCI and AD showed shared and unique species-level microbial alterations relative to HC. Despite the absence of overall metabolomic divergence, AD exhibited reduced levels of multiple neurotransmitter metabolites compared with MCI and HC. Prominent alterations in multiple glymphatic markers were present in AD rather than in MCI. Further integrated analyses revealed a wide range of associations among these multi-omics changes and established potential serial mediation pathways, manifesting as a pattern of gut microbiota → neurotransmitter metabolites → glymphatic function → cognition.
CONCLUSIONS: These findings could enrich our understanding of the biological mechanisms involved in cognitive impairment and clinically diagnosed probable AD, but also may inform future preventive and therapeutic interventions by targeting the established pathways.
Additional Links: PMID-42869338
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@article {pmid42869338,
year = {2026},
author = {Tao, C and Wan, K and Song, Y and Xu, X and She, M and Sun, Z and Zhu, J and Yu, Y},
title = {Parsing the relationships among gut microbiome, neurotransmitter metabolome, glymphatic function, and cognition across healthy elderly, mild cognitive impairment, and probable Alzheimer's disease.},
journal = {Brain, behavior, and immunity},
volume = {},
number = {},
pages = {107067},
doi = {10.1016/j.bbi.2026.107067},
pmid = {42869338},
issn = {1090-2139},
abstract = {BACKGROUND: Evidence has suggested brain glymphatic dysfunction and gut microbial metabolic disturbance in Alzheimer's disease (AD), yet the relationships among gut microbiota, neurotransmitter metabolites, glymphatic function, and cognition across clinically defined groups of healthy elderly, mild cognitive impairment (MCI), and probable AD remain unclear.
METHODS: Using metagenomic sequencing, targeted metabolomics, and multi-modal magnetic resonance imaging, we measured the gut microbiome, neurotransmitter metabolome, and a variety of glymphatic markers in 30 patients with clinically diagnosed probable AD, 75 individuals with MCI, and 59 healthy controls (HC).
RESULTS: Although global microbial diversity showed no group difference, MCI and AD showed shared and unique species-level microbial alterations relative to HC. Despite the absence of overall metabolomic divergence, AD exhibited reduced levels of multiple neurotransmitter metabolites compared with MCI and HC. Prominent alterations in multiple glymphatic markers were present in AD rather than in MCI. Further integrated analyses revealed a wide range of associations among these multi-omics changes and established potential serial mediation pathways, manifesting as a pattern of gut microbiota → neurotransmitter metabolites → glymphatic function → cognition.
CONCLUSIONS: These findings could enrich our understanding of the biological mechanisms involved in cognitive impairment and clinically diagnosed probable AD, but also may inform future preventive and therapeutic interventions by targeting the established pathways.},
}
RevDate: 2026-10-13
Early-Life exposure to environmental pollutants and endocrine disruptors: emerging risks and mechanistic insights in maternal, fetal, and child health.
Environmental research pii:S0013-9351(26)02210-3 [Epub ahead of print].
Exposure to environmental pollutants and endocrine-disrupting chemicals (EDCs) in early life is a critical public health issue because it can alter developmental programming that impacts susceptibility to disease throughout life. The prenatal and early postnatal periods are times of vulnerability when exposure to environmental stressors may impact endocrine signalling, placental function, epigenetic regulation, and metabolic homeostasis. There is increasing evidence that exposure to bisphenols, phthalates, per- and polyfluoroalkyl substances (PFAS), pesticides, heavy metals, and air pollutants has been associated with pregnancy outcomes, neurodevelopmental disorders, metabolic dysfunction, endocrine abnormalities and reproductive impairments. Exposomics, high-resolution mass spectrometry, biomonitoring, and passive sampling technologies have made crucial advances in characterising complex environmental exposures. At the same time, novel methods such as multi-omics, single-cell sequencing, spatial biology and microbiome studies have yielded more detailed mechanistic understanding of how environmental factors can impact developmental processes via epigenetic, inflammatory, oxidative stress, and endocrine pathways. The placenta has emerged as a valuable biomarker matrix for assessing fetal exposure and developmental programming. Exposure routes, biomonitoring methods, placental processes, molecular and epigenetic modifications, and the impacts of early-life environmental exposures on neurodevelopment, metabolism, endocrine function, and reproduction are all summarised in this review. It also emphasises current advancements in exposure assessment, preventive measures, and policy frameworks, highlighting the importance of life-course perspectives and environmental justice. To identify important windows of susceptibility, improve risk assessment, and develop strategies to safeguard maternal and child health, exposomics in conjunction with systems biology and longitudinal epidemiological approaches will be essential.
Additional Links: PMID-42869363
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@article {pmid42869363,
year = {2026},
author = {Nishanthini, B and Yazhini, A and Kumar, P and Saravanan, P and Rajeshkannan, R and Rajasimman, M and Kumar, SV},
title = {Early-Life exposure to environmental pollutants and endocrine disruptors: emerging risks and mechanistic insights in maternal, fetal, and child health.},
journal = {Environmental research},
volume = {},
number = {},
pages = {125878},
doi = {10.1016/j.envres.2026.125878},
pmid = {42869363},
issn = {1096-0953},
abstract = {Exposure to environmental pollutants and endocrine-disrupting chemicals (EDCs) in early life is a critical public health issue because it can alter developmental programming that impacts susceptibility to disease throughout life. The prenatal and early postnatal periods are times of vulnerability when exposure to environmental stressors may impact endocrine signalling, placental function, epigenetic regulation, and metabolic homeostasis. There is increasing evidence that exposure to bisphenols, phthalates, per- and polyfluoroalkyl substances (PFAS), pesticides, heavy metals, and air pollutants has been associated with pregnancy outcomes, neurodevelopmental disorders, metabolic dysfunction, endocrine abnormalities and reproductive impairments. Exposomics, high-resolution mass spectrometry, biomonitoring, and passive sampling technologies have made crucial advances in characterising complex environmental exposures. At the same time, novel methods such as multi-omics, single-cell sequencing, spatial biology and microbiome studies have yielded more detailed mechanistic understanding of how environmental factors can impact developmental processes via epigenetic, inflammatory, oxidative stress, and endocrine pathways. The placenta has emerged as a valuable biomarker matrix for assessing fetal exposure and developmental programming. Exposure routes, biomonitoring methods, placental processes, molecular and epigenetic modifications, and the impacts of early-life environmental exposures on neurodevelopment, metabolism, endocrine function, and reproduction are all summarised in this review. It also emphasises current advancements in exposure assessment, preventive measures, and policy frameworks, highlighting the importance of life-course perspectives and environmental justice. To identify important windows of susceptibility, improve risk assessment, and develop strategies to safeguard maternal and child health, exposomics in conjunction with systems biology and longitudinal epidemiological approaches will be essential.},
}
RevDate: 2026-10-13
Divergent bacterial signatures in dental clinic bioaerosols: a real-field investigation.
The Journal of hospital infection pii:S0195-6701(26)00397-X [Epub ahead of print].
BACKGROUND: Dental procedures generate bioaerosols containing oral microorganisms, posing a potential cross-infection risk. Effective infection control requires real-world data on aerosol behaviour in clinical settings.
OBJECTIVE: To characterize particulate matter and bacterial profiles during active ultrasonic periodontal scaling under routine clinical conditions.
METHODS: Sampling occurred under background and ultrasonic scaling conditions. Airborne particles were monitored in real-time using an optical particle sizer. Bioaerosols were collected using an Andersen six-stage sampler (culturable) and a filter-based high-flow pump (non-culturable). Surface samples were obtained from personal protective equipment (PPE) and environmental surfaces. Bacterial communities were analyzed via 16S rRNA sequencing.
FINDINGS: A notable decoupling was observed between physical and biological aerosol profiles: although ultrasonic instrumentation produced a substantial surge in sub-micron particles, culturable microbial recovery was predominantly concentrated within the respirable 1.1-3.3 μm fractions. High-throughput sequencing revealed clear spatial differentiation in bacterial communities. Microbial contamination was heavily confined to the clinician's PPE within the immediate splash zone. Airborne bacteria differed significantly from those on PPE (ANOSIM R = 0.633, p = 0.001), whereas clinical air and peripheral non-touch surfaces shared an indistinguishable ambient microbiome (R = 0.095, p = 0.249), with oral pathogens rarely detected in either compartment.
CONCLUSION: Under the specific conditions evaluated, total particle counts do not reflect culturable bacterial load, which is concentrated in the 1.1-3.3 μm respirable fraction. Bacterial contamination remains predominantly localized to the operative field and PPE, with minimal dispersion to ambient air. Accordingly, physical particle metrics should not be used as direct indicators of bacterial hazard, and clinician protection relies primarily on strict PPE compliance.
Additional Links: PMID-42869382
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PubMed:
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@article {pmid42869382,
year = {2026},
author = {Liu, Y and Chen, C and Zhang, D and Huang, J and Zhao, B and An, N},
title = {Divergent bacterial signatures in dental clinic bioaerosols: a real-field investigation.},
journal = {The Journal of hospital infection},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jhin.2026.10.003},
pmid = {42869382},
issn = {1532-2939},
abstract = {BACKGROUND: Dental procedures generate bioaerosols containing oral microorganisms, posing a potential cross-infection risk. Effective infection control requires real-world data on aerosol behaviour in clinical settings.
OBJECTIVE: To characterize particulate matter and bacterial profiles during active ultrasonic periodontal scaling under routine clinical conditions.
METHODS: Sampling occurred under background and ultrasonic scaling conditions. Airborne particles were monitored in real-time using an optical particle sizer. Bioaerosols were collected using an Andersen six-stage sampler (culturable) and a filter-based high-flow pump (non-culturable). Surface samples were obtained from personal protective equipment (PPE) and environmental surfaces. Bacterial communities were analyzed via 16S rRNA sequencing.
FINDINGS: A notable decoupling was observed between physical and biological aerosol profiles: although ultrasonic instrumentation produced a substantial surge in sub-micron particles, culturable microbial recovery was predominantly concentrated within the respirable 1.1-3.3 μm fractions. High-throughput sequencing revealed clear spatial differentiation in bacterial communities. Microbial contamination was heavily confined to the clinician's PPE within the immediate splash zone. Airborne bacteria differed significantly from those on PPE (ANOSIM R = 0.633, p = 0.001), whereas clinical air and peripheral non-touch surfaces shared an indistinguishable ambient microbiome (R = 0.095, p = 0.249), with oral pathogens rarely detected in either compartment.
CONCLUSION: Under the specific conditions evaluated, total particle counts do not reflect culturable bacterial load, which is concentrated in the 1.1-3.3 μm respirable fraction. Bacterial contamination remains predominantly localized to the operative field and PPE, with minimal dispersion to ambient air. Accordingly, physical particle metrics should not be used as direct indicators of bacterial hazard, and clinician protection relies primarily on strict PPE compliance.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Discovery and characterization of outer membrane vesicles produced by the bee gut microbiota.
Biology letters, 22(10):.
Bacteria use diverse mechanisms to interact with each other and with eukaryotic hosts, thereby shaping microbiome composition and influencing host health. One of these mechanisms is the production of outer membrane vesicles (OMVs), nanoscale structures that bud off from bacterial cells into the extracellular space. OMVs can deliver bioactive cargoes, including enzymes, RNA and DNA, enabling functions such as cell-to-cell communication, nutrient acquisition and immunomodulation. However, the role of OMVs in beneficial host-associated microbiomes remains unclear. Here, we investigated OMV production in the gut bacteria of the western honeybee (Apis mellifera), which forms a highly conserved and stable microbial community. Using electron microscopy, fluorescence labelling and nanoparticle tracking analysis, we detected OMV production in every Gram-negative species of the bee gut microbiota that we investigated. Vesicles were observed in gut contents of wild and laboratory-inoculated bees, but absent in bees lacking a microbiota. OMVs contained nucleic acids, with more RNA than DNA. Bacterial strains varied in OMV properties, including abundance, size and zeta potential. These findings indicate that OMVs are likely significant mediators of interbacterial and host-microbe interactions in the bee gut.
Additional Links: PMID-42869450
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@article {pmid42869450,
year = {2026},
author = {Eyles, RP and Kwong, WK},
title = {Discovery and characterization of outer membrane vesicles produced by the bee gut microbiota.},
journal = {Biology letters},
volume = {22},
number = {10},
pages = {},
doi = {10.1098/rsbl.2026.0327},
pmid = {42869450},
issn = {1744-957X},
support = {//GIMM-CARE/ ; 101060102//European Union/ ; //ARICA-Investimentos/ ; //Participações e Gestão/ ; //Jerónimo Martins/ ; //Gulbenkian Institute for Molecular Medicine/ ; //CAML-Lisbon Academic Medical Centre/ ; LA/P/0082/2020//national funds through FCT/ ; UID/06357/2025//R&D Unit funding programme/ ; 101042912-BEE_GEMS/ERC_/European Research Council/International ; 5045-2022//European Molecular Biology Organization Installation/ ; CEECIND/01358/2021//FCT/ ; },
mesh = {Animals ; Bees/microbiology ; *Gastrointestinal Microbiome/physiology ; *Bacterial Outer Membrane ; Bacteria ; },
abstract = {Bacteria use diverse mechanisms to interact with each other and with eukaryotic hosts, thereby shaping microbiome composition and influencing host health. One of these mechanisms is the production of outer membrane vesicles (OMVs), nanoscale structures that bud off from bacterial cells into the extracellular space. OMVs can deliver bioactive cargoes, including enzymes, RNA and DNA, enabling functions such as cell-to-cell communication, nutrient acquisition and immunomodulation. However, the role of OMVs in beneficial host-associated microbiomes remains unclear. Here, we investigated OMV production in the gut bacteria of the western honeybee (Apis mellifera), which forms a highly conserved and stable microbial community. Using electron microscopy, fluorescence labelling and nanoparticle tracking analysis, we detected OMV production in every Gram-negative species of the bee gut microbiota that we investigated. Vesicles were observed in gut contents of wild and laboratory-inoculated bees, but absent in bees lacking a microbiota. OMVs contained nucleic acids, with more RNA than DNA. Bacterial strains varied in OMV properties, including abundance, size and zeta potential. These findings indicate that OMVs are likely significant mediators of interbacterial and host-microbe interactions in the bee gut.},
}
MeSH Terms:
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Animals
Bees/microbiology
*Gastrointestinal Microbiome/physiology
*Bacterial Outer Membrane
Bacteria
RevDate: 2026-10-13
CmpDate: 2026-10-13
Uncovering the role of biogeography, resources, food web composition and time during microbial primary succession.
Proceedings. Biological sciences, 293(2080):.
Ecological succession is shaped by multiple processes that operate simultaneously across spatial and temporal scales. While classical succession theory generally focuses on a single trophic level within a single location, often in plants or other macroscopic organisms, recent efforts have extended this framework to microorganisms across multiple ecological dimensions. The aquatic micro-ecosystem within the pitcher plant, Sarracenia purpurea, provides a natural model of primary succession replicated across a continental latitudinal gradient. Using this model system, we investigated how biogeography, food web structure and resource availability influenced bacterial succession. Over 12 weeks, we repeatedly sampled bacterial communities from seven sites spanning the latitudinal range of S. purpurea and characterized communities using 16S rRNA gene sequencing. Both taxonomic and phylogenetic diversity increased over succession. These diversity patterns were not explained by temporal changes in food web composition, resources or environmental conditions, although pH, water volume, latitude and midge abundance, each influenced diversity independently of time. Latent Dirichlet allocation models identified six compositional groups with distinct temporal and biogeographic signatures. Early-successional groups were enriched in putative diazotrophs, while late-successional groups contained metabolically diverse taxa adapted to low-oxygen conditions. Our findings show that microbial primary succession in S. purpurea is shaped by time, biogeography and pitcher-scale environmental filters.
Additional Links: PMID-42869474
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@article {pmid42869474,
year = {2026},
author = {Baiser, B and Bernardin, J and Young, EB and Cagle, GA and Freedman, ZB and Gray, SM and Divinagracia, E and Fluck, IE and Gravel, D and LeClare, S and Long, ZT and Record, S and Rhyner, KM and Bittleston, LS},
title = {Uncovering the role of biogeography, resources, food web composition and time during microbial primary succession.},
journal = {Proceedings. Biological sciences},
volume = {293},
number = {2080},
pages = {},
doi = {10.1098/rspb.2026.0396},
pmid = {42869474},
issn = {1471-2954},
support = {//National Science Foundation (NSF)/ ; 2025250//Understanding the Rules of Life-Microbiome Theory and Mechanisms 2 Collaborative/ ; 2025262//Understanding the Rules of Life-Microbiome Theory and Mechanisms 2 Collaborative/ ; 2025337//Understanding the Rules of Life-Microbiome Theory and Mechanisms 2 Collaborative/ ; 2025110//Understanding the Rules of Life-Microbiome Theory and Mechanisms 2 Collaborative/ ; ECIAMEE-00001638//Simons Foundation/ ; 2236782//NSF CAREER/ ; MEO-022425//Hatch/ ; //U.S. Department of Agriculture's National Institute of Food and Agriculture/ ; IZSEZ0_186214/SNSF_/Swiss National Science Foundation/Switzerland ; },
mesh = {RNA, Ribosomal, 16S/genetics/analysis ; *Food Chain ; *Bacteria/classification/genetics ; *Sarraceniaceae/microbiology ; Phylogeny ; Biodiversity ; *Microbiota ; },
abstract = {Ecological succession is shaped by multiple processes that operate simultaneously across spatial and temporal scales. While classical succession theory generally focuses on a single trophic level within a single location, often in plants or other macroscopic organisms, recent efforts have extended this framework to microorganisms across multiple ecological dimensions. The aquatic micro-ecosystem within the pitcher plant, Sarracenia purpurea, provides a natural model of primary succession replicated across a continental latitudinal gradient. Using this model system, we investigated how biogeography, food web structure and resource availability influenced bacterial succession. Over 12 weeks, we repeatedly sampled bacterial communities from seven sites spanning the latitudinal range of S. purpurea and characterized communities using 16S rRNA gene sequencing. Both taxonomic and phylogenetic diversity increased over succession. These diversity patterns were not explained by temporal changes in food web composition, resources or environmental conditions, although pH, water volume, latitude and midge abundance, each influenced diversity independently of time. Latent Dirichlet allocation models identified six compositional groups with distinct temporal and biogeographic signatures. Early-successional groups were enriched in putative diazotrophs, while late-successional groups contained metabolically diverse taxa adapted to low-oxygen conditions. Our findings show that microbial primary succession in S. purpurea is shaped by time, biogeography and pitcher-scale environmental filters.},
}
MeSH Terms:
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RNA, Ribosomal, 16S/genetics/analysis
*Food Chain
*Bacteria/classification/genetics
*Sarraceniaceae/microbiology
Phylogeny
Biodiversity
*Microbiota
RevDate: 2026-10-13
CmpDate: 2026-10-13
Microbiome-mediated resilience and cross-generational consequences in male Drosophila exposed to combined environmental stressors.
Proceedings. Biological sciences, 293(2080):.
Climate change exposes organisms to multiple, interacting stressors, yet their joint effects on reproduction and inheritance remain poorly understood. This study investigated the interactive effects of acute heat stress and sublethal imidacloprid exposure on the reproductive success of male Drosophila melanogaster and the subsequent fitness of their offspring. We manipulated the gut microbiome of male flies (germ-free or colonized with one or five bacterial species) and subjected them to individual or combined stress. We show that combined stressors act synergistically to reduce male fitness traits, an effect that is partially buffered by higher microbiome diversity. Paternal stress exposure further reduced offspring fertility, demonstrating cross-generational fitness costs largely independent of microbial transmission. Our results underscore the gut microbiome as an important, but stress-sensitive, contributor to host resilience, and demonstrate how multi-stressor interactions can amplify reproductive failure, with broad implications for population persistence and biodiversity loss in a warming, chemically altered world.
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PubMed:
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@article {pmid42869476,
year = {2026},
author = {Maggu, K and Meena, A and De Nardo, AN and Eggs, B and Sbilordo, SH and Al Toma Sho, R and Lüpold, S},
title = {Microbiome-mediated resilience and cross-generational consequences in male Drosophila exposed to combined environmental stressors.},
journal = {Proceedings. Biological sciences},
volume = {293},
number = {2080},
pages = {},
doi = {10.1098/rspb.2026.1300},
pmid = {42869476},
issn = {1471-2954},
support = {PP00P3_202662/SNSF_/Swiss National Science Foundation/Switzerland ; FK-23-127//University of Zurich Postdoctoral Fellowship/ ; },
mesh = {Animals ; Male ; *Drosophila melanogaster/microbiology/physiology ; *Neonicotinoids/adverse effects ; *Nitro Compounds/adverse effects/toxicity ; Stress, Physiological ; Reproduction/drug effects ; Hot Temperature/adverse effects ; *Gastrointestinal Microbiome ; *Insecticides/adverse effects/toxicity ; Fertility ; Climate Change ; },
abstract = {Climate change exposes organisms to multiple, interacting stressors, yet their joint effects on reproduction and inheritance remain poorly understood. This study investigated the interactive effects of acute heat stress and sublethal imidacloprid exposure on the reproductive success of male Drosophila melanogaster and the subsequent fitness of their offspring. We manipulated the gut microbiome of male flies (germ-free or colonized with one or five bacterial species) and subjected them to individual or combined stress. We show that combined stressors act synergistically to reduce male fitness traits, an effect that is partially buffered by higher microbiome diversity. Paternal stress exposure further reduced offspring fertility, demonstrating cross-generational fitness costs largely independent of microbial transmission. Our results underscore the gut microbiome as an important, but stress-sensitive, contributor to host resilience, and demonstrate how multi-stressor interactions can amplify reproductive failure, with broad implications for population persistence and biodiversity loss in a warming, chemically altered world.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Male
*Drosophila melanogaster/microbiology/physiology
*Neonicotinoids/adverse effects
*Nitro Compounds/adverse effects/toxicity
Stress, Physiological
Reproduction/drug effects
Hot Temperature/adverse effects
*Gastrointestinal Microbiome
*Insecticides/adverse effects/toxicity
Fertility
Climate Change
RevDate: 2026-10-13
Siderophores: chemical threads of rhizosphere health.
Trends in microbiology pii:S0966-842X(26)00272-6 [Epub ahead of print].
Rhizosphere microbiomes are central to plant nutrition, pathogen suppression, and rhizosphere health, yet their functions remain difficult to predict from taxonomic composition alone. We argue that microbial siderophores offer a chemically explicit route from taxonomic associations to trait-based rhizosphere ecology. These structurally diverse iron-chelating metabolites link iron mobilization to ecological interactions across microbial, plant, and soil-fauna interfaces. In microbe-microbe systems, siderophore structure-receptor compatibility provides a well-established mechanism underlying resource sharing, competitive exclusion, and pathogen suppression. At plant and nematode interfaces, siderophore functions are increasingly evident, although recognition mechanisms remain less resolved. A siderophore-centered perspective can help move rhizosphere microbiome research from descriptive associations toward predictive, testable, and context-specific ecological engineering.
Additional Links: PMID-42869754
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@article {pmid42869754,
year = {2026},
author = {Gu, S and Cui, D and Shao, J and Wang, K and Wei, Z and Zuo, Y},
title = {Siderophores: chemical threads of rhizosphere health.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2026.09.006},
pmid = {42869754},
issn = {1878-4380},
abstract = {Rhizosphere microbiomes are central to plant nutrition, pathogen suppression, and rhizosphere health, yet their functions remain difficult to predict from taxonomic composition alone. We argue that microbial siderophores offer a chemically explicit route from taxonomic associations to trait-based rhizosphere ecology. These structurally diverse iron-chelating metabolites link iron mobilization to ecological interactions across microbial, plant, and soil-fauna interfaces. In microbe-microbe systems, siderophore structure-receptor compatibility provides a well-established mechanism underlying resource sharing, competitive exclusion, and pathogen suppression. At plant and nematode interfaces, siderophore functions are increasingly evident, although recognition mechanisms remain less resolved. A siderophore-centered perspective can help move rhizosphere microbiome research from descriptive associations toward predictive, testable, and context-specific ecological engineering.},
}
RevDate: 2026-10-13
Inadequate waste management drives the spread of antimicrobial resistance across the watershed of a large African city.
Environment international, 216:110554 pii:S0160-4120(26)00512-X [Epub ahead of print].
Rapid urbanization in the Global South consistently outpaces sanitation infrastructure, transforming urban rivers into AMR reservoirs. Yet watershed-scale quantification of resistomes in such settings remains scarce, limiting exposure risk assessment and intervention planning. Here we present the most detailed spatial baseline for waterborne AMR in sub-Saharan Africa, using the Akaki River (Addis Ababa, Ethiopia) as a model system for rapidly urbanizing megacity watersheds with inadequate sanitation. We sampled 38 sites across an extreme pollution gradient during the dry season, when low flow produces maximum pollutant concentrations and the highest resident exposure risk. Water quality, microbiome marker data, 309 antibiotic resistance genes (ARGs), and 57 mobile genetic elements (MGEs) were quantified by high-throughput quantitative PCR. ARG and MGE abundances in central urban reaches exceeded 10[10] gene copies L[-1], indistinguishable from untreated sewage. Critically, clinically important ARGs co-occurred widely with broad-host-range MGEs, including the IncP-1α plasmid backbone, IS26, ISEcp1, IS6100, and class 1 integron integrase genes, indicating that ARGs are primed for potential horizontal gene transfer in waters where hundreds of thousands of Addis residents bathe, wash, and irrigate food crops. Dissolved oxygen depletion and elevated NH4-N correlated significantly with resistome expansion (p < 0.01), serving as robust chemical proxies for diffuse, system-wide raw sewage inputs that carry the actual mechanistic AMR drivers (e.g., heavy metals, antibiotic residues, and resistant hosts). The 38-site spatial design and dry-season worst-case conditions together provide a replicable model for AMR exposure assessment in comparable Global South cities.
Additional Links: PMID-42869870
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PubMed:
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@article {pmid42869870,
year = {2026},
author = {Zhou, Y and Haile, AT and Kibret, M and Li, H and Haileselassie, MM and Bekele, TW and Kassa, JM and Demissie, K and Wyrsch, ER and Djordjevic, SP and Jobling, K and Quintela-Baluja, M and Su, JQ and Mateo-Sagasta, J and Graham, DW},
title = {Inadequate waste management drives the spread of antimicrobial resistance across the watershed of a large African city.},
journal = {Environment international},
volume = {216},
number = {},
pages = {110554},
doi = {10.1016/j.envint.2026.110554},
pmid = {42869870},
issn = {1873-6750},
abstract = {Rapid urbanization in the Global South consistently outpaces sanitation infrastructure, transforming urban rivers into AMR reservoirs. Yet watershed-scale quantification of resistomes in such settings remains scarce, limiting exposure risk assessment and intervention planning. Here we present the most detailed spatial baseline for waterborne AMR in sub-Saharan Africa, using the Akaki River (Addis Ababa, Ethiopia) as a model system for rapidly urbanizing megacity watersheds with inadequate sanitation. We sampled 38 sites across an extreme pollution gradient during the dry season, when low flow produces maximum pollutant concentrations and the highest resident exposure risk. Water quality, microbiome marker data, 309 antibiotic resistance genes (ARGs), and 57 mobile genetic elements (MGEs) were quantified by high-throughput quantitative PCR. ARG and MGE abundances in central urban reaches exceeded 10[10] gene copies L[-1], indistinguishable from untreated sewage. Critically, clinically important ARGs co-occurred widely with broad-host-range MGEs, including the IncP-1α plasmid backbone, IS26, ISEcp1, IS6100, and class 1 integron integrase genes, indicating that ARGs are primed for potential horizontal gene transfer in waters where hundreds of thousands of Addis residents bathe, wash, and irrigate food crops. Dissolved oxygen depletion and elevated NH4-N correlated significantly with resistome expansion (p < 0.01), serving as robust chemical proxies for diffuse, system-wide raw sewage inputs that carry the actual mechanistic AMR drivers (e.g., heavy metals, antibiotic residues, and resistant hosts). The 38-site spatial design and dry-season worst-case conditions together provide a replicable model for AMR exposure assessment in comparable Global South cities.},
}
RevDate: 2026-10-13
Interspecies regulation of virulence through gingipain inhibition by a Tannerella forsythia serpin.
EMBO reports [Epub ahead of print].
Periodontitis is driven by dysbiotic microbial communities in which Porphyromonas gingivalis (Pg) acts as a keystone pathogen through its caspase-like fold (Clan CD) proteases, gingipains. Tannerella forsythia (Tf), another member of the periodontal pathogenic community, uniquely produces the broad-spectrum serpin termed miropin, yet its biological significance as an inhibitor in periodontal inflammation remains unclear. Here, we demonstrate that miropin directly inhibits the lysine-specific gingipain Kgp and the calpain-like protease Tpr produced by Pg, forming irreversible covalent inhibitory complexes. While recombinant native miropin impairs Pg growth, an engineered variant targeting both lysine- and arginine-specific gingipains entirely abolishes bacterial growth in a defined medium. In vivo, recombinant miropin reduces Pg virulence and, when co-infected with wild-type Tf, prevents lethal infection and significantly reduces alveolar bone loss, but not when co-infected with a miropin-deficient mutant. Protection is associated with inhibition of gingipain activity and normalization of the RANKL/OPG ratio in periodontal tissues. These findings identify miropin as a potent interspecies virulence modulator and challenge the prevailing view of Tf as an exclusively pathogenic member of the oral microbiome.
Additional Links: PMID-42870048
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Citation:
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@article {pmid42870048,
year = {2026},
author = {Książek, M and Benedyk-Machaczka, M and Mizgalska, D and Sochaj-Gregorczyk, A and Waligórska, I and Drzazga, K and Nowak, M and Kaczor, A and Potempa, B and Fuchs, A and Thøgersen, IB and Enghild, JJ and Scavenius, C and Mydel, P and Moris, SC and Bagaitkar, J and Potempa, J},
title = {Interspecies regulation of virulence through gingipain inhibition by a Tannerella forsythia serpin.},
journal = {EMBO reports},
volume = {},
number = {},
pages = {},
pmid = {42870048},
issn = {1469-3178},
support = {DE030939//HHS | NIH | National Institute of Dental and Craniofacial Research (NIDR)/ ; DE030939//HHS | NIH | National Institute of Dental and Craniofacial Research (NIDR)/ ; 2015/17/B/NZ1/00666//National Science Center Poland/ ; },
abstract = {Periodontitis is driven by dysbiotic microbial communities in which Porphyromonas gingivalis (Pg) acts as a keystone pathogen through its caspase-like fold (Clan CD) proteases, gingipains. Tannerella forsythia (Tf), another member of the periodontal pathogenic community, uniquely produces the broad-spectrum serpin termed miropin, yet its biological significance as an inhibitor in periodontal inflammation remains unclear. Here, we demonstrate that miropin directly inhibits the lysine-specific gingipain Kgp and the calpain-like protease Tpr produced by Pg, forming irreversible covalent inhibitory complexes. While recombinant native miropin impairs Pg growth, an engineered variant targeting both lysine- and arginine-specific gingipains entirely abolishes bacterial growth in a defined medium. In vivo, recombinant miropin reduces Pg virulence and, when co-infected with wild-type Tf, prevents lethal infection and significantly reduces alveolar bone loss, but not when co-infected with a miropin-deficient mutant. Protection is associated with inhibition of gingipain activity and normalization of the RANKL/OPG ratio in periodontal tissues. These findings identify miropin as a potent interspecies virulence modulator and challenge the prevailing view of Tf as an exclusively pathogenic member of the oral microbiome.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Levothyroxine dose requirements, oral bioavailability and gut microbiome enterotype dynamics during the early post-bariatric period: a single-centre, prospective, cohort study.
BMC endocrine disorders, 26(1):.
BACKGROUND: Bariatric surgery induces profound metabolic changes; however, its impact on levothyroxine (LT4) requirements, hormone pharmacokinetics, and gut microbiome composition remains incompletely understood. The current study is aimed to evaluate longitudinal changes in metabolic parameters, LT4 dose requirements, free thyroxin (FT4) absorption (AUC0-6h), and gut microbiome features following Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG).
METHODS: In this prospective cohort study, 79 patients with hypothyroidism undergoing bariatric surgery (RYGB n = 40; SG n = 39) were followed at baseline, 3 month, and 6 months postoperatively. Metabolic parameters, thyroid function, LT4 dose, FT4 AUC₀-₆h, and gut microbiome diversity were assessed using linear mixed-effects models.
RESULTS: Both groups showed significant metabolic improvement at 6 months, including reductions in body mass index (RYGB: 44.5 → 32.1 kg/m²; SG: 42.9 → 33.0 kg/m², p < 0.001) and fasting blood sugar (RYGB: 114.8 → 92.4 mg/dL; SG: 109.9 → 96.1 mg/dL, p < 0.001). LT4 requirements increased significantly, particularly in RYGB (137.5 → 158.2 µg/day; p = 0.018) and SG (133.3 → 144.8 µg/day; p = 0.067), with a stronger effect in weight-adjusted dose (both p < 0.05). FT4 AUC₀-₆h increased significantly after surgery (RYGB: +330 ± 210, p = 0.003; SG: +185 ± 190, p = 0.041), indicating altered LT4 pharmacokinetics. Gut microbiome analysis revealed increased Shannon diversity (RYGB p-trend = 0.048) and significant enrichment of Akkermansia muciniphila (1.20% → 2.40%, p < 0.001), particularly in RYGB. After false discovery rate (FDR) adjustment, the major longitudinal changes remained significant, particularly for metabolic parameters, LT4 dose (µg/kg/day), and Akkermansia muciniphila in the RYGB group. Patient-level analyses showed a modest positive association between changes in A. muciniphila abundance and FT4 AUC₀-₆h after multivariable adjustment, whereas other microbiome-LT4 associations were not significant.
CONCLUSION: Bariatric surgery was associated with substantial metabolic improvement, increased LT4 requirements, increased systemic FT4 exposure, and changes in gut microbiome composition. The observed microbiome-LT4 association was modest and should be considered exploratory and hypothesis-generating rather than causal. These findings highlight the need for individualized thyroid function monitoring and LT4 dose adjustment during the postoperative period.
CLINICAL TRIAL NUMBER: Not applicable.
Additional Links: PMID-42870254
PubMed:
Citation:
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@article {pmid42870254,
year = {2026},
author = {El-Sehrawy, AAMA and Gameil, MA and Nakib, AME and Aseeri, AA and Alanazi, MA and Alharbi, SS and Taki-Eldin, A and Maashi, MS and ELmazny, GM and Almansour, H and Abdalla, R and Kandil, I},
title = {Levothyroxine dose requirements, oral bioavailability and gut microbiome enterotype dynamics during the early post-bariatric period: a single-centre, prospective, cohort study.},
journal = {BMC endocrine disorders},
volume = {26},
number = {1},
pages = {},
pmid = {42870254},
issn = {1472-6823},
mesh = {Humans ; Female ; Male ; Prospective Studies ; *Thyroxine/administration & dosage/pharmacokinetics ; *Gastrointestinal Microbiome/physiology/drug effects ; Adult ; Middle Aged ; *Hypothyroidism/drug therapy/metabolism ; *Gastric Bypass ; *Bariatric Surgery ; *Obesity, Morbid/surgery ; Biological Availability ; Follow-Up Studies ; Gastrectomy ; Body Mass Index ; Administration, Oral ; },
abstract = {BACKGROUND: Bariatric surgery induces profound metabolic changes; however, its impact on levothyroxine (LT4) requirements, hormone pharmacokinetics, and gut microbiome composition remains incompletely understood. The current study is aimed to evaluate longitudinal changes in metabolic parameters, LT4 dose requirements, free thyroxin (FT4) absorption (AUC0-6h), and gut microbiome features following Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG).
METHODS: In this prospective cohort study, 79 patients with hypothyroidism undergoing bariatric surgery (RYGB n = 40; SG n = 39) were followed at baseline, 3 month, and 6 months postoperatively. Metabolic parameters, thyroid function, LT4 dose, FT4 AUC₀-₆h, and gut microbiome diversity were assessed using linear mixed-effects models.
RESULTS: Both groups showed significant metabolic improvement at 6 months, including reductions in body mass index (RYGB: 44.5 → 32.1 kg/m²; SG: 42.9 → 33.0 kg/m², p < 0.001) and fasting blood sugar (RYGB: 114.8 → 92.4 mg/dL; SG: 109.9 → 96.1 mg/dL, p < 0.001). LT4 requirements increased significantly, particularly in RYGB (137.5 → 158.2 µg/day; p = 0.018) and SG (133.3 → 144.8 µg/day; p = 0.067), with a stronger effect in weight-adjusted dose (both p < 0.05). FT4 AUC₀-₆h increased significantly after surgery (RYGB: +330 ± 210, p = 0.003; SG: +185 ± 190, p = 0.041), indicating altered LT4 pharmacokinetics. Gut microbiome analysis revealed increased Shannon diversity (RYGB p-trend = 0.048) and significant enrichment of Akkermansia muciniphila (1.20% → 2.40%, p < 0.001), particularly in RYGB. After false discovery rate (FDR) adjustment, the major longitudinal changes remained significant, particularly for metabolic parameters, LT4 dose (µg/kg/day), and Akkermansia muciniphila in the RYGB group. Patient-level analyses showed a modest positive association between changes in A. muciniphila abundance and FT4 AUC₀-₆h after multivariable adjustment, whereas other microbiome-LT4 associations were not significant.
CONCLUSION: Bariatric surgery was associated with substantial metabolic improvement, increased LT4 requirements, increased systemic FT4 exposure, and changes in gut microbiome composition. The observed microbiome-LT4 association was modest and should be considered exploratory and hypothesis-generating rather than causal. These findings highlight the need for individualized thyroid function monitoring and LT4 dose adjustment during the postoperative period.
CLINICAL TRIAL NUMBER: Not applicable.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
Male
Prospective Studies
*Thyroxine/administration & dosage/pharmacokinetics
*Gastrointestinal Microbiome/physiology/drug effects
Adult
Middle Aged
*Hypothyroidism/drug therapy/metabolism
*Gastric Bypass
*Bariatric Surgery
*Obesity, Morbid/surgery
Biological Availability
Follow-Up Studies
Gastrectomy
Body Mass Index
Administration, Oral
RevDate: 2026-10-14
CmpDate: 2026-10-14
Synergistic effect of gastric microbiome and host genetic factor predispose to gastric cancer.
Journal of translational medicine, 24(1):.
OBJECTIVE: Complex interaction between host genetic and environmental factors has a role in Helicobacter pylori (H. pylori)-related gastric tumorigenesis, while involvement of non-Helicobacter pylori gastric microbiome may be also relevant to this process. We aimed to evaluate whether combining the non-Helicobacter pylori gastric microbiome signatures and the gastric cancer (GC) predisposing genetic factors (PSCA rs2294008 and MUC1 rs4072037 polymorphisms) stratify a high GC risk subpopulation in a Japanese cohort.
METHODS: In 620 subjects including 219 GC patients and 410 non-cancers, microbiome-based GC risk was defined as the gastric microbiome signatures of 47 GC-predisposing bacteria. Genetic risk of GC was also defined as the presence of PSCA rs2294008 and MUC1 rs4072037 risk alleles. Adding effect of gastric microbiome and genetic factor was evaluated in relation to GC susceptibility, histological degree of gastritis and somatic changes in the gastric mucosa including DNA methylation and telomere shortening.
RESULTS: Individuals possessing the risk of both microbiome and genotype showed significant risk for developing GC with highest OR (odds ratio, e.g., OR = 23.55 in comparison with non-cancer) compared to individuals having risk microbiome or genotype alone (microbiome, OR = 11.16; genotype, OR = 2.76). The individuals having both risks also showed highest degrees of intestinal metaplasia and DNA methylation, and shortest telomere.
CONCLUSIONS: Our findings suggested an existence of combined effect of host genetic factor and gastric microbiome predispose to gastric tumorigenesis, that can be used as the diagnostic tool to further stratify a high GC risk subpopulation.
Additional Links: PMID-42870271
PubMed:
Citation:
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@article {pmid42870271,
year = {2026},
author = {Shimogama, T and Tahara, T and Shijimaya, T and Yamazaki, J and Yano, N and Ohtsu, T and Yasuoka, R and Kobayashi, S and Nakamura, N and Takahashi, Y and Tomiyama, T and Honzawa, Y and Fukui, T and Naganuma, M},
title = {Synergistic effect of gastric microbiome and host genetic factor predispose to gastric cancer.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
pmid = {42870271},
issn = {1479-5876},
support = {26K18751//Japan Society for the Promotion of Science/ ; },
mesh = {Humans ; *Stomach Neoplasms/genetics/microbiology/pathology ; *Genetic Predisposition to Disease ; Polymorphism, Single Nucleotide/genetics ; Female ; Male ; *Microbiota ; GPI-Linked Proteins/genetics ; Mucin-1/genetics ; Middle Aged ; Neoplasm Proteins/genetics ; DNA Methylation/genetics ; Risk Factors ; *Stomach/microbiology/pathology ; Antigens, Neoplasm ; },
abstract = {OBJECTIVE: Complex interaction between host genetic and environmental factors has a role in Helicobacter pylori (H. pylori)-related gastric tumorigenesis, while involvement of non-Helicobacter pylori gastric microbiome may be also relevant to this process. We aimed to evaluate whether combining the non-Helicobacter pylori gastric microbiome signatures and the gastric cancer (GC) predisposing genetic factors (PSCA rs2294008 and MUC1 rs4072037 polymorphisms) stratify a high GC risk subpopulation in a Japanese cohort.
METHODS: In 620 subjects including 219 GC patients and 410 non-cancers, microbiome-based GC risk was defined as the gastric microbiome signatures of 47 GC-predisposing bacteria. Genetic risk of GC was also defined as the presence of PSCA rs2294008 and MUC1 rs4072037 risk alleles. Adding effect of gastric microbiome and genetic factor was evaluated in relation to GC susceptibility, histological degree of gastritis and somatic changes in the gastric mucosa including DNA methylation and telomere shortening.
RESULTS: Individuals possessing the risk of both microbiome and genotype showed significant risk for developing GC with highest OR (odds ratio, e.g., OR = 23.55 in comparison with non-cancer) compared to individuals having risk microbiome or genotype alone (microbiome, OR = 11.16; genotype, OR = 2.76). The individuals having both risks also showed highest degrees of intestinal metaplasia and DNA methylation, and shortest telomere.
CONCLUSIONS: Our findings suggested an existence of combined effect of host genetic factor and gastric microbiome predispose to gastric tumorigenesis, that can be used as the diagnostic tool to further stratify a high GC risk subpopulation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Stomach Neoplasms/genetics/microbiology/pathology
*Genetic Predisposition to Disease
Polymorphism, Single Nucleotide/genetics
Female
Male
*Microbiota
GPI-Linked Proteins/genetics
Mucin-1/genetics
Middle Aged
Neoplasm Proteins/genetics
DNA Methylation/genetics
Risk Factors
*Stomach/microbiology/pathology
Antigens, Neoplasm
RevDate: 2026-10-14
CmpDate: 2026-10-14
Synthetic horizontal gene transfer for ecosystem restoration.
Biology direct, 21(1):.
Restoring endangered ecosystems has become a pressing issue as the effects of global warming continue to harm existing communities. During the last decade, several studies have suggested the use of synthetic biology as a tool to protect these biodiverse communities by increasing their functionality. A critical example concerns soil microbiome communities in drylands, where increasing water retention by some of the constituent species could effectively protect the ecosystem from abrupt degradation. However, how to effectively deploy a functional synthetic construct that can scale its impact to the community level remains an open question. Recent experimental research has designed recombinant gene plasmids with the capacity to horizontally transfer across soil microbial communities. Here, we explore the impacts of synthetic horizontal gene transfer in models of ecological consortia. We define a consumer-resource model in which species can share an engineered plasmid that reduces resource loss, effectively coupling multispecies dynamics and gene spreading. By doing so, we identify a wide range of parameters and the optimal gene transfer conditions for which the intervention promotes biodiversity and biomass gains, while regulating gene propagation and the spread of engineered organisms. Our work provides a first step toward understanding the mechanisms and opportunities of engineered plasmid transfer in multispecies ecological communities.
Additional Links: PMID-42870292
PubMed:
Citation:
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@article {pmid42870292,
year = {2026},
author = {Maull, V and Aguadé-Gorgorió, G and de Lorenzo, V and Solé, R},
title = {Synthetic horizontal gene transfer for ecosystem restoration.},
journal = {Biology direct},
volume = {21},
number = {1},
pages = {},
pmid = {42870292},
issn = {1745-6150},
mesh = {*Gene Transfer, Horizontal ; *Ecosystem ; *Soil Microbiology ; Plasmids/genetics ; *Genes, Synthetic ; *Synthetic Biology ; },
abstract = {Restoring endangered ecosystems has become a pressing issue as the effects of global warming continue to harm existing communities. During the last decade, several studies have suggested the use of synthetic biology as a tool to protect these biodiverse communities by increasing their functionality. A critical example concerns soil microbiome communities in drylands, where increasing water retention by some of the constituent species could effectively protect the ecosystem from abrupt degradation. However, how to effectively deploy a functional synthetic construct that can scale its impact to the community level remains an open question. Recent experimental research has designed recombinant gene plasmids with the capacity to horizontally transfer across soil microbial communities. Here, we explore the impacts of synthetic horizontal gene transfer in models of ecological consortia. We define a consumer-resource model in which species can share an engineered plasmid that reduces resource loss, effectively coupling multispecies dynamics and gene spreading. By doing so, we identify a wide range of parameters and the optimal gene transfer conditions for which the intervention promotes biodiversity and biomass gains, while regulating gene propagation and the spread of engineered organisms. Our work provides a first step toward understanding the mechanisms and opportunities of engineered plasmid transfer in multispecies ecological communities.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Gene Transfer, Horizontal
*Ecosystem
*Soil Microbiology
Plasmids/genetics
*Genes, Synthetic
*Synthetic Biology
RevDate: 2026-10-14
Food, Dietary Supplement, and Gut Microbiome Interactions in Oral Anticancer Therapy: Mechanisms, Clinical Consequences, and Management.
American journal of therapeutics pii:00045391-990000000-00558 [Epub ahead of print].
BACKGROUND: The shift toward oral targeted therapies and immune checkpoint inhibitors (ICIs) in oncology has introduced pharmacokinetic variability driven by food-drug interactions (FDIs), which can cause therapeutic failure or increased toxicity.
AREAS OF UNCERTAINTY: FDI effects depend on drug composition and food-intake timing. Evidence for traditional antineoplastic drugs is well documented, but data on newer targeted therapies and on diet-mediated or microbiome-mediated modulation of ICI efficacy remain inconsistent-dietary fiber and probiotic supplementation, for example, appear associated with divergent clinical outcomes. The role of high-dose antioxidant supplementation during cytotoxic therapy also requires further study.
DATA SOURCES: A structured search of Web of Science, PubMed, and Embase (through July 2026) informed this narrative review of pharmacokinetic mechanisms, clinical outcomes, and management strategies for the concomitant use of food, dietary supplements, and antineoplastic drugs.
RESULTS: Food can alter oral antineoplastic drug bioavailability through changes in gastric pH, cytochrome P450 (CYP) modulation, and efflux-transporter inhibition (eg, P-glycoprotein). High-fat meals increase exposure to tyrosine kinase inhibitors (TKIs) such as lapatinib and abiraterone, while newer agents (sotorasib and lorlatinib) show different food-interaction profiles. ICI efficacy correlates with gut microbiome composition, modulated by dietary fiber and short-chain fatty acid production. High-dose antioxidant supplementation during cytotoxic therapy may compromise treatment outcomes.
CONCLUSION: Food-drug interactions are an increasingly important clinical concern in modern oncology. Pharmacokinetic interactions mediated by gastric pH, CYP3A4, and P-glycoprotein transport are well supported by clinical data and already inform drug labeling, whereas diet-microbiome-immunotherapy associations remain less mature and should be regarded as hypothesis generating. Structured, multidisciplinary management-periodic regimen review, patient education, decision algorithms, and therapeutic drug monitoring-can mitigate established risks, while prospective studies are still needed before diet-based and microbiome-based interventions can be considered clinically actionable.
Additional Links: PMID-42870343
Publisher:
PubMed:
Citation:
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@article {pmid42870343,
year = {2026},
author = {Mîrza, O and Leah, OM and Codruța Hegheş, S and Filip, L and Rogozea, LM},
title = {Food, Dietary Supplement, and Gut Microbiome Interactions in Oral Anticancer Therapy: Mechanisms, Clinical Consequences, and Management.},
journal = {American journal of therapeutics},
volume = {},
number = {},
pages = {},
doi = {10.1097/MJT.0000000000002240},
pmid = {42870343},
issn = {1536-3686},
abstract = {BACKGROUND: The shift toward oral targeted therapies and immune checkpoint inhibitors (ICIs) in oncology has introduced pharmacokinetic variability driven by food-drug interactions (FDIs), which can cause therapeutic failure or increased toxicity.
AREAS OF UNCERTAINTY: FDI effects depend on drug composition and food-intake timing. Evidence for traditional antineoplastic drugs is well documented, but data on newer targeted therapies and on diet-mediated or microbiome-mediated modulation of ICI efficacy remain inconsistent-dietary fiber and probiotic supplementation, for example, appear associated with divergent clinical outcomes. The role of high-dose antioxidant supplementation during cytotoxic therapy also requires further study.
DATA SOURCES: A structured search of Web of Science, PubMed, and Embase (through July 2026) informed this narrative review of pharmacokinetic mechanisms, clinical outcomes, and management strategies for the concomitant use of food, dietary supplements, and antineoplastic drugs.
RESULTS: Food can alter oral antineoplastic drug bioavailability through changes in gastric pH, cytochrome P450 (CYP) modulation, and efflux-transporter inhibition (eg, P-glycoprotein). High-fat meals increase exposure to tyrosine kinase inhibitors (TKIs) such as lapatinib and abiraterone, while newer agents (sotorasib and lorlatinib) show different food-interaction profiles. ICI efficacy correlates with gut microbiome composition, modulated by dietary fiber and short-chain fatty acid production. High-dose antioxidant supplementation during cytotoxic therapy may compromise treatment outcomes.
CONCLUSION: Food-drug interactions are an increasingly important clinical concern in modern oncology. Pharmacokinetic interactions mediated by gastric pH, CYP3A4, and P-glycoprotein transport are well supported by clinical data and already inform drug labeling, whereas diet-microbiome-immunotherapy associations remain less mature and should be regarded as hypothesis generating. Structured, multidisciplinary management-periodic regimen review, patient education, decision algorithms, and therapeutic drug monitoring-can mitigate established risks, while prospective studies are still needed before diet-based and microbiome-based interventions can be considered clinically actionable.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Site, Fertilization and Season Structure the Soil Microbiome and Its Interactions With Bdellovibrio and Like Organisms Predators.
Environmental microbiology, 28(10):e70447.
The contribution of predation between bacteria to microbial community dynamics in agricultural soil has hardly been investigated. Here, dynamics of general prokaryotes (GEP) and the predatory Bdellovibrionales (Bd) and Bacteriovoracales (Bac) (Bdellovibrio-and-Like Organisms, BALOs) were studied in two agricultural fields differing in organic and mineral inputs for 1 year. Season, but not fertilization, affected absolute sizes of GEP and of BALO communities. 16S rRNA gene analysis identified numerous previously undetected Bd and Bac lineages, with none of the BALOs related to characterized isolates. A few dominant BALO amplicon sequence variants (ASVs) persisted year-round, whereas others showed seasonal or treatment specific responses. Alpha diversity of the GEP, Bd and Bac communities was influenced by season, with some changes due to fertilization observed for Bd and Bac. Seasonal variation, site and fertilization regime also significantly influenced beta diversity and the structure of BALO-gram-negative bacterial association networks, revealing distinct community associations under different environmental conditions. Accordingly, we suggest that environmental variation and agricultural practice influence bacterial community structure and are associated with corresponding changes in BALO communities and their potential associations with gram-negative bacteria. These dynamics may be harnessed to manipulate the soil microbiome to benefit sustainable environmental and agricultural outcomes.
Additional Links: PMID-42870370
Publisher:
PubMed:
Citation:
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@article {pmid42870370,
year = {2026},
author = {Kumari, A and Lood, R and Matan, O and Cytryn, E and Laor, Y and Eshel, G and Jurkevitch, E},
title = {Site, Fertilization and Season Structure the Soil Microbiome and Its Interactions With Bdellovibrio and Like Organisms Predators.},
journal = {Environmental microbiology},
volume = {28},
number = {10},
pages = {e70447},
doi = {10.1111/1462-2920.70447},
pmid = {42870370},
issn = {1462-2920},
support = {2021-52//Ekhagastiftelsen/ ; },
mesh = {*Soil Microbiology ; Seasons ; *Microbiota ; RNA, Ribosomal, 16S/genetics ; *Bdellovibrio/genetics/physiology/isolation & purification/classification ; Bacteria/classification/genetics/isolation & purification ; Agriculture ; Animals ; Fertilizers/analysis ; *Deltaproteobacteria/genetics/isolation & purification/classification/physiology ; Phylogeny ; },
abstract = {The contribution of predation between bacteria to microbial community dynamics in agricultural soil has hardly been investigated. Here, dynamics of general prokaryotes (GEP) and the predatory Bdellovibrionales (Bd) and Bacteriovoracales (Bac) (Bdellovibrio-and-Like Organisms, BALOs) were studied in two agricultural fields differing in organic and mineral inputs for 1 year. Season, but not fertilization, affected absolute sizes of GEP and of BALO communities. 16S rRNA gene analysis identified numerous previously undetected Bd and Bac lineages, with none of the BALOs related to characterized isolates. A few dominant BALO amplicon sequence variants (ASVs) persisted year-round, whereas others showed seasonal or treatment specific responses. Alpha diversity of the GEP, Bd and Bac communities was influenced by season, with some changes due to fertilization observed for Bd and Bac. Seasonal variation, site and fertilization regime also significantly influenced beta diversity and the structure of BALO-gram-negative bacterial association networks, revealing distinct community associations under different environmental conditions. Accordingly, we suggest that environmental variation and agricultural practice influence bacterial community structure and are associated with corresponding changes in BALO communities and their potential associations with gram-negative bacteria. These dynamics may be harnessed to manipulate the soil microbiome to benefit sustainable environmental and agricultural outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Soil Microbiology
Seasons
*Microbiota
RNA, Ribosomal, 16S/genetics
*Bdellovibrio/genetics/physiology/isolation & purification/classification
Bacteria/classification/genetics/isolation & purification
Agriculture
Animals
Fertilizers/analysis
*Deltaproteobacteria/genetics/isolation & purification/classification/physiology
Phylogeny
RevDate: 2026-10-14
Gut microbiome and metabolite signatures in critical limb threatening ischemia.
VASA. Zeitschrift fur Gefasskrankheiten [Epub ahead of print].
Background: Atherosclerotic disease entails with distinct clinical phenotypes, of which chronic coronary syndrome (CCS) and critical limb-threatening ischemia (CLTI) are key manifestations. While plaque morphology and clinical course differ in vascular territory, the underlying pathophysiology leading to distinct diseases remain unexplored. The gut-microbiome axis with derived mediators trimethylamine-N-oxide (TMAO) and short-chain fatty acids (SCFAs) has emerged as proatherogenic or protective in vascular diseases, however the differential abundance, composition and metabolites have not been investigated in CCS or CLTI. Patients and methods: In this cross-sectional clinical trial, we included patients with CCS and CLTI within 24 h of clinical presentation. Analyses of the gut microbiome and downstream metabolites were assessed. Microbiome-derived metabolites were analyzed from peripheral blood samples. Gut microbiome samples were characterized by 16S rRNA gene analysis. Results: We enrolled 40 patients with 20 patients each presenting with CCS and CLTI, respectively. While alpha and beta diversity were similar, CCS patients exhibited distinct microbial signatures, including higher abundance of Dialister, Monoglobus, Lachnospira, Barnesiella, Fusicatenibacter, Collinsella, and Roseburia. Subsequent analysis of microbiome-derived metabolites revealed significantly lower serum concentrations of isovaleric acid and a non-significant trend toward TMAO elevation in the CLTI group compared to the CCS group. Conclusions: In this pilot trial we demonstrate that distinct differences in gut bacteria and microbiome-derived metabolites exist between patients with CCS and CLTI. These findings may highlight microbiome-metabolite interactions in chronic atherosclerotic disease and support larger studies to elucidate causal mechanisms.
Additional Links: PMID-42870417
Publisher:
PubMed:
Citation:
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@article {pmid42870417,
year = {2026},
author = {Messiha, D and Lange, E and Tratnik, A and Westendorf, AM and Rinke, M and Lenz, S and Hendgen-Cotta, UB and Buer, J and Rassaf, T and Rammos, C},
title = {Gut microbiome and metabolite signatures in critical limb threatening ischemia.},
journal = {VASA. Zeitschrift fur Gefasskrankheiten},
volume = {},
number = {},
pages = {},
doi = {10.1024/0301-1526/a001312},
pmid = {42870417},
issn = {0301-1526},
abstract = {Background: Atherosclerotic disease entails with distinct clinical phenotypes, of which chronic coronary syndrome (CCS) and critical limb-threatening ischemia (CLTI) are key manifestations. While plaque morphology and clinical course differ in vascular territory, the underlying pathophysiology leading to distinct diseases remain unexplored. The gut-microbiome axis with derived mediators trimethylamine-N-oxide (TMAO) and short-chain fatty acids (SCFAs) has emerged as proatherogenic or protective in vascular diseases, however the differential abundance, composition and metabolites have not been investigated in CCS or CLTI. Patients and methods: In this cross-sectional clinical trial, we included patients with CCS and CLTI within 24 h of clinical presentation. Analyses of the gut microbiome and downstream metabolites were assessed. Microbiome-derived metabolites were analyzed from peripheral blood samples. Gut microbiome samples were characterized by 16S rRNA gene analysis. Results: We enrolled 40 patients with 20 patients each presenting with CCS and CLTI, respectively. While alpha and beta diversity were similar, CCS patients exhibited distinct microbial signatures, including higher abundance of Dialister, Monoglobus, Lachnospira, Barnesiella, Fusicatenibacter, Collinsella, and Roseburia. Subsequent analysis of microbiome-derived metabolites revealed significantly lower serum concentrations of isovaleric acid and a non-significant trend toward TMAO elevation in the CLTI group compared to the CCS group. Conclusions: In this pilot trial we demonstrate that distinct differences in gut bacteria and microbiome-derived metabolites exist between patients with CCS and CLTI. These findings may highlight microbiome-metabolite interactions in chronic atherosclerotic disease and support larger studies to elucidate causal mechanisms.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
DecBin: Bayesian-optimized deep clustering for long-read metagenomic binning.
Briefings in bioinformatics, 27(5):.
Accurate metagenomic binning is essential for reconstructing microbial genomes, thereby facilitating the discovery of novel taxa, the identification of pathogens, and the characterization of antimicrobial resistance genes. Most existing methods are designed for assembled contigs and cannot be directly applied to raw long reads. Although a few dedicated long-read binning methods have emerged, challenges remain in bin-number estimation and representation learning. Here, we propose Deep Embedded Clustering for Long-read Binning (DecBin), an adaptive method for directly binning raw long reads through integrating a variational autoencoder (VAE), Bayesian optimization, and deep embedded clustering within a unified framework. Computational experiments on large-scale simulated and mock-community datasets demonstrate that DecBin outperforms state-of-the-art methods in both long-read binning and metagenome-assembled genome recovery, while also achieving strain-level resolution in a low-complexity natural microbiome. Further analysis shows that the advantage of DecBin is partly attributable to its Davies-Bouldin index-guided Bayesian optimization, which explicitly evaluates candidate cluster numbers using a global cluster-validity criterion, thereby improving bin-number estimation across communities of varying complexity. Meanwhile, joint fine-tuning of the VAE encoder and clustering layer enables clustering feedback to refine the latent space, yielding representations better aligned with genome partitions. These findings highlight the potential of adaptive deep clustering for metagenomic binning directly from raw long reads without prior assembly. The source code of DecBin is freely available at https://github.com/LorMeBioAI/DecBin.
Additional Links: PMID-42870579
Publisher:
PubMed:
Citation:
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@article {pmid42870579,
year = {2026},
author = {Zhu, YH and Li, X and Liu, Z and Liu, J and Ye, R and Xue, W and Jiang, G},
title = {DecBin: Bayesian-optimized deep clustering for long-read metagenomic binning.},
journal = {Briefings in bioinformatics},
volume = {27},
number = {5},
pages = {},
doi = {10.1093/bib/bbag571},
pmid = {42870579},
issn = {1477-4054},
support = {2025AIYJSZX-YB006//Fundamental Research Funds for the Central Universities/ ; BK20230102//Natural Science Foundation of Jiangsu Province/ ; 62402227//National Natural Science Foundation of China/ ; 42677660//National Natural Science Foundation of China/ ; 42477122//National Natural Science Foundation of China/ ; },
mesh = {*Metagenomics/methods ; Bayes Theorem ; Clustering Algorithms ; *Metagenome ; Microbiota ; Cluster Analysis ; Algorithms ; Autoencoder ; },
abstract = {Accurate metagenomic binning is essential for reconstructing microbial genomes, thereby facilitating the discovery of novel taxa, the identification of pathogens, and the characterization of antimicrobial resistance genes. Most existing methods are designed for assembled contigs and cannot be directly applied to raw long reads. Although a few dedicated long-read binning methods have emerged, challenges remain in bin-number estimation and representation learning. Here, we propose Deep Embedded Clustering for Long-read Binning (DecBin), an adaptive method for directly binning raw long reads through integrating a variational autoencoder (VAE), Bayesian optimization, and deep embedded clustering within a unified framework. Computational experiments on large-scale simulated and mock-community datasets demonstrate that DecBin outperforms state-of-the-art methods in both long-read binning and metagenome-assembled genome recovery, while also achieving strain-level resolution in a low-complexity natural microbiome. Further analysis shows that the advantage of DecBin is partly attributable to its Davies-Bouldin index-guided Bayesian optimization, which explicitly evaluates candidate cluster numbers using a global cluster-validity criterion, thereby improving bin-number estimation across communities of varying complexity. Meanwhile, joint fine-tuning of the VAE encoder and clustering layer enables clustering feedback to refine the latent space, yielding representations better aligned with genome partitions. These findings highlight the potential of adaptive deep clustering for metagenomic binning directly from raw long reads without prior assembly. The source code of DecBin is freely available at https://github.com/LorMeBioAI/DecBin.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Metagenomics/methods
Bayes Theorem
Clustering Algorithms
*Metagenome
Microbiota
Cluster Analysis
Algorithms
Autoencoder
RevDate: 2026-10-14
CmpDate: 2026-10-14
Reframing the gut-lung axis: Microbiota dysbiosis, immune-redox regulation, and the potential role of vitamin C.
International journal of immunopathology and pharmacology, 40:3946320261497604.
The respiratory system is continuously exposed to environmental antigens, pathogens, and pollutants, requiring tightly regulated immunity to balance inflammation and host defense. Increasing evidence indicates that the microbiome-within the airways and through the gut-lung axis-plays a critical role in shaping pulmonary immune responses. Microbial metabolites such as short-chain fatty acids (SCFAs), tryptophan-derived indoles, and bile acid intermediates, influence the maturation and functional programming of alveolar macrophages, dendritic cells, and T lymphocytes. Using the emerging framework of microbiota dysbiosis-related disorders, this review distinguishes descriptive microbial alterations from functionally and clinically relevant dysbiosis involving microbial metabolites, barrier integrity, immune regulation, and respiratory outcomes. Nutritional and microbiome-targeted interventions-such as dietary fiber, probiotics, and antioxidant micronutrients including vitamin C-may help restore immune homeostasis and reduce inflammatory burden through microbiota-mediated and redox-regulatory pathways. By supporting epithelial barrier integrity, modulating oxidative stress, and promoting regulatory immune signaling, vitamin C may complement microbiome-directed strategies aimed at maintaining respiratory immune resilience. The review critically synthesizes mechanistic, observational, and clinical evidence linking microbiota dysbiosis to respiratory immune homeostasis and evaluates microbiome-targeted and vitamin C-related strategies according to their current level of evidentiary support.
Additional Links: PMID-42870637
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@article {pmid42870637,
year = {2026},
author = {Bennett, LL},
title = {Reframing the gut-lung axis: Microbiota dysbiosis, immune-redox regulation, and the potential role of vitamin C.},
journal = {International journal of immunopathology and pharmacology},
volume = {40},
number = {},
pages = {3946320261497604},
doi = {10.1177/03946320261497604},
pmid = {42870637},
issn = {2058-7384},
mesh = {Humans ; *Dysbiosis/immunology/microbiology/metabolism ; *Ascorbic Acid/therapeutic use/pharmacology ; *Lung/immunology/microbiology/metabolism ; Animals ; Oxidation-Reduction ; *Gastrointestinal Microbiome/drug effects/immunology ; Microbiota ; },
abstract = {The respiratory system is continuously exposed to environmental antigens, pathogens, and pollutants, requiring tightly regulated immunity to balance inflammation and host defense. Increasing evidence indicates that the microbiome-within the airways and through the gut-lung axis-plays a critical role in shaping pulmonary immune responses. Microbial metabolites such as short-chain fatty acids (SCFAs), tryptophan-derived indoles, and bile acid intermediates, influence the maturation and functional programming of alveolar macrophages, dendritic cells, and T lymphocytes. Using the emerging framework of microbiota dysbiosis-related disorders, this review distinguishes descriptive microbial alterations from functionally and clinically relevant dysbiosis involving microbial metabolites, barrier integrity, immune regulation, and respiratory outcomes. Nutritional and microbiome-targeted interventions-such as dietary fiber, probiotics, and antioxidant micronutrients including vitamin C-may help restore immune homeostasis and reduce inflammatory burden through microbiota-mediated and redox-regulatory pathways. By supporting epithelial barrier integrity, modulating oxidative stress, and promoting regulatory immune signaling, vitamin C may complement microbiome-directed strategies aimed at maintaining respiratory immune resilience. The review critically synthesizes mechanistic, observational, and clinical evidence linking microbiota dysbiosis to respiratory immune homeostasis and evaluates microbiome-targeted and vitamin C-related strategies according to their current level of evidentiary support.},
}
MeSH Terms:
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Humans
*Dysbiosis/immunology/microbiology/metabolism
*Ascorbic Acid/therapeutic use/pharmacology
*Lung/immunology/microbiology/metabolism
Animals
Oxidation-Reduction
*Gastrointestinal Microbiome/drug effects/immunology
Microbiota
RevDate: 2026-10-14
Phytochemicals in colorectal cancer therapy: emerging mechanisms, translational opportunities, and global research evolution.
Journal of materials chemistry. B [Epub ahead of print].
Colorectal cancer is still a leading cause of cancer morbidity and mortality in the world. This is a reflection of the limitations of current chemotherapy and the need for additional therapeutic strategies. Phytochemicals from plants have been of great interest recently because they can affect several pathways involved in cancer. In this review, we combine bibliometric mapping with a narrative synthesis to discuss the changing nature of phytochemical research in colorectal cancer. A total of 1029 records from Web of Science, covering January 2000 to December 2025, were analyzed using VOSviewer, Bibliometrix, and CiteSpace. The trend of publications is steadily increasing, particularly since 2020. Keyword mapping revealed some common themes, particularly apoptosis, flavonoids, curcumin, quercetin, network pharmacology, nanoparticles, and ferroptosis. The literature shows a transition from early screening studies to more in-depth mechanistic and translational studies. From the bibliometric findings, five areas are identified that might influence the future development of the field. These areas include modulation of multiple signaling pathways, regulated cell death, interactions between the gut microbiome and immune system, overcoming chemoresistance, and innovative delivery systems to enhance bioavailability. Taken together, these findings suggest that phytochemicals act as multi-target compounds rather than single cytotoxic agents with promising potential in combination therapies for colorectal cancer. Materials and delivery research accounts for a rising share of this corpus, increasing from 0.0% of records published between 2000 and 2011 to 16.0% of those published between 2020 and 2025, and nanoparticles emerge as a major keyword cluster although no materials term appears in the search string. The review therefore treats biomaterial design as a component of the field rather than as an adjunct to it, covering polymeric, lipid, inorganic, biomimetic and stimuli-responsive platforms against a common set of performance criteria.
Additional Links: PMID-42870741
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@article {pmid42870741,
year = {2026},
author = {Adil, M and Dawe, GS and Subramaniyan, V},
title = {Phytochemicals in colorectal cancer therapy: emerging mechanisms, translational opportunities, and global research evolution.},
journal = {Journal of materials chemistry. B},
volume = {},
number = {},
pages = {},
doi = {10.1039/d6tb01393g},
pmid = {42870741},
issn = {2050-7518},
abstract = {Colorectal cancer is still a leading cause of cancer morbidity and mortality in the world. This is a reflection of the limitations of current chemotherapy and the need for additional therapeutic strategies. Phytochemicals from plants have been of great interest recently because they can affect several pathways involved in cancer. In this review, we combine bibliometric mapping with a narrative synthesis to discuss the changing nature of phytochemical research in colorectal cancer. A total of 1029 records from Web of Science, covering January 2000 to December 2025, were analyzed using VOSviewer, Bibliometrix, and CiteSpace. The trend of publications is steadily increasing, particularly since 2020. Keyword mapping revealed some common themes, particularly apoptosis, flavonoids, curcumin, quercetin, network pharmacology, nanoparticles, and ferroptosis. The literature shows a transition from early screening studies to more in-depth mechanistic and translational studies. From the bibliometric findings, five areas are identified that might influence the future development of the field. These areas include modulation of multiple signaling pathways, regulated cell death, interactions between the gut microbiome and immune system, overcoming chemoresistance, and innovative delivery systems to enhance bioavailability. Taken together, these findings suggest that phytochemicals act as multi-target compounds rather than single cytotoxic agents with promising potential in combination therapies for colorectal cancer. Materials and delivery research accounts for a rising share of this corpus, increasing from 0.0% of records published between 2000 and 2011 to 16.0% of those published between 2020 and 2025, and nanoparticles emerge as a major keyword cluster although no materials term appears in the search string. The review therefore treats biomaterial design as a component of the field rather than as an adjunct to it, covering polymeric, lipid, inorganic, biomimetic and stimuli-responsive platforms against a common set of performance criteria.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Does Mother Provide? Re-Examination of Maternal and Embryonic Microbiomes of Diploptera punctata.
Ecology and evolution, 16(10):e74504.
The cockroach endosymbiont Blattabacterium cuenotii plays a central role in host nutrition throughout development, particularly during embryogenesis in the viviparous cockroach Diploptera punctata. However, the presence and potential functional relevance of non-blattabacterial taxa in developing embryos of this species remain unclear. Previous studies of maternal and embryonic microbiomes in D. punctata, based on Illumina 16S rRNA sequencing, have yielded inconsistent findings, partly due to differences in how endosymbiotic sequences were treated. Here, we reanalyzed microbiome data from two studies, with and without Blattabacterial reads, to reevaluate the presence and composition of non-blattabacterial taxa in embryonic microbiomes. Embryonic microbial communities (1) differed significantly from each other between datasets and (2) from associated maternal gut communities, suggesting that environmental (maternal, dietary, and laboratory) and sequencing factors may influence their acquisition and composition rather than reflecting a stable, consistently transmitted microbiome. Nevertheless, the detection of non-blattabacterial taxa in embryonic microbiomes suggests the possible acquisition of non-endosymbiotic bacteria by developing embryos. The functions of these microbes are speculated, but were not explicitly tested in this study and remain to be verified. Overall, our findings suggest that although non-endosymbiotic embryonic bacteria may be environmentally acquired and variable, their biological relevance remains unresolved and cannot be determined from 16S amplicon data alone. This highlights the importance of investigating acquired non-endosymbiotic bacteria and their potential functional roles in the development of viviparous cockroaches.
Additional Links: PMID-42870792
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@article {pmid42870792,
year = {2026},
author = {Jonas, B and Arrowsmith, V and Ayayee, P},
title = {Does Mother Provide? Re-Examination of Maternal and Embryonic Microbiomes of Diploptera punctata.},
journal = {Ecology and evolution},
volume = {16},
number = {10},
pages = {e74504},
pmid = {42870792},
issn = {2045-7758},
abstract = {The cockroach endosymbiont Blattabacterium cuenotii plays a central role in host nutrition throughout development, particularly during embryogenesis in the viviparous cockroach Diploptera punctata. However, the presence and potential functional relevance of non-blattabacterial taxa in developing embryos of this species remain unclear. Previous studies of maternal and embryonic microbiomes in D. punctata, based on Illumina 16S rRNA sequencing, have yielded inconsistent findings, partly due to differences in how endosymbiotic sequences were treated. Here, we reanalyzed microbiome data from two studies, with and without Blattabacterial reads, to reevaluate the presence and composition of non-blattabacterial taxa in embryonic microbiomes. Embryonic microbial communities (1) differed significantly from each other between datasets and (2) from associated maternal gut communities, suggesting that environmental (maternal, dietary, and laboratory) and sequencing factors may influence their acquisition and composition rather than reflecting a stable, consistently transmitted microbiome. Nevertheless, the detection of non-blattabacterial taxa in embryonic microbiomes suggests the possible acquisition of non-endosymbiotic bacteria by developing embryos. The functions of these microbes are speculated, but were not explicitly tested in this study and remain to be verified. Overall, our findings suggest that although non-endosymbiotic embryonic bacteria may be environmentally acquired and variable, their biological relevance remains unresolved and cannot be determined from 16S amplicon data alone. This highlights the importance of investigating acquired non-endosymbiotic bacteria and their potential functional roles in the development of viviparous cockroaches.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Saccharomyces boulardii reduces food intake and attenuates weight gain in diet-induced obese mice: links to gut microbial, metabolic, and immune remodeling.
Frontiers in immunology, 17:1925200.
INTRODUCTION: The gut microbiome is a key regulator of metabolic homeostasis and contributes to obesity progression through effects on immune signaling, gut barrier integrity, and systemic inflammation. Microbiome-targeted strategies are therefore being explored as complementary approaches to conventional weight-loss therapies. Here, we investigated whether the probiotic yeast Saccharomyces boulardii modulates the gut-immune-metabolic axis in diet-induced obesity (DIO).
METHODS: Male C57BL/6JRj mice maintained on a 60% kcal high-fat diet (HFD) for eight weeks were randomized by body weight (n = 9 per group) and received daily oral gavage of S. boulardii or vehicle for seven weeks, with HFD continued throughout. Body weight and food intake were recorded by a caretaker blinded to treatment assignment. Endpoint analyses combined metabolic phenotyping, gut microbiome profiling, untargeted cecal metabolomics, colonic transcriptomics, and portal vein cytokine profiling.
RESULTS: S. boulardii reduced food intake and attenuated weight gain without major changes in circulating metabolic hormone levels. Microbial diversity remained largely preserved, but Bacteroidales lineages, including Muribaculaceae, were selectively enriched alongside functional remodeling of microbial pathways. Cecal metabolomics revealed increased B vitamins, betaine, and GABA, with reduced stress-associated metabolites. Colonic transcriptomics showed attenuation of TNF-α/NF-κB signaling and enrichment of interferon and epithelial programs, while portal cytokine profiling revealed a significant treatment-associated shift in the overall cytokine profile, with trends toward lower inflammatory chemokines and increased IL-17A and IL-22. Integrated multi-omics analysis identified coordinated host-microbe interactions across metabolic, transcriptional, and immune layers.
DISCUSSION: These exploratory findings show that S. boulardii modulates the gut-immune-metabolic axis in obesity, coupling reduced energy intake with microbial, metabolic, and mucosal immune remodeling. The design does not establish causal ordering between the omics layers, and mechanistic follow-up is required. Collectively, the results support microbiome-based interventions as potential adjunct strategies targeting metabolic inflammation.
Additional Links: PMID-42870945
PubMed:
Citation:
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@article {pmid42870945,
year = {2026},
author = {Hedin, KA and Vaaben, TH and Lützhøft, DO and Jensen, BAH and Sommer, MOA},
title = {Saccharomyces boulardii reduces food intake and attenuates weight gain in diet-induced obese mice: links to gut microbial, metabolic, and immune remodeling.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1925200},
pmid = {42870945},
issn = {1664-3224},
mesh = {Animals ; *Saccharomyces boulardii/physiology ; *Obesity/metabolism/immunology/etiology/microbiology ; Male ; Mice ; *Probiotics/pharmacology ; Mice, Inbred C57BL ; *Gastrointestinal Microbiome/immunology ; *Weight Gain ; *Eating ; Diet, High-Fat/adverse effects ; Cytokines/metabolism ; Mice, Obese ; },
abstract = {INTRODUCTION: The gut microbiome is a key regulator of metabolic homeostasis and contributes to obesity progression through effects on immune signaling, gut barrier integrity, and systemic inflammation. Microbiome-targeted strategies are therefore being explored as complementary approaches to conventional weight-loss therapies. Here, we investigated whether the probiotic yeast Saccharomyces boulardii modulates the gut-immune-metabolic axis in diet-induced obesity (DIO).
METHODS: Male C57BL/6JRj mice maintained on a 60% kcal high-fat diet (HFD) for eight weeks were randomized by body weight (n = 9 per group) and received daily oral gavage of S. boulardii or vehicle for seven weeks, with HFD continued throughout. Body weight and food intake were recorded by a caretaker blinded to treatment assignment. Endpoint analyses combined metabolic phenotyping, gut microbiome profiling, untargeted cecal metabolomics, colonic transcriptomics, and portal vein cytokine profiling.
RESULTS: S. boulardii reduced food intake and attenuated weight gain without major changes in circulating metabolic hormone levels. Microbial diversity remained largely preserved, but Bacteroidales lineages, including Muribaculaceae, were selectively enriched alongside functional remodeling of microbial pathways. Cecal metabolomics revealed increased B vitamins, betaine, and GABA, with reduced stress-associated metabolites. Colonic transcriptomics showed attenuation of TNF-α/NF-κB signaling and enrichment of interferon and epithelial programs, while portal cytokine profiling revealed a significant treatment-associated shift in the overall cytokine profile, with trends toward lower inflammatory chemokines and increased IL-17A and IL-22. Integrated multi-omics analysis identified coordinated host-microbe interactions across metabolic, transcriptional, and immune layers.
DISCUSSION: These exploratory findings show that S. boulardii modulates the gut-immune-metabolic axis in obesity, coupling reduced energy intake with microbial, metabolic, and mucosal immune remodeling. The design does not establish causal ordering between the omics layers, and mechanistic follow-up is required. Collectively, the results support microbiome-based interventions as potential adjunct strategies targeting metabolic inflammation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Saccharomyces boulardii/physiology
*Obesity/metabolism/immunology/etiology/microbiology
Male
Mice
*Probiotics/pharmacology
Mice, Inbred C57BL
*Gastrointestinal Microbiome/immunology
*Weight Gain
*Eating
Diet, High-Fat/adverse effects
Cytokines/metabolism
Mice, Obese
RevDate: 2026-10-14
CmpDate: 2026-10-14
Not all stress is equal: Examination stress and cortisol reactivity are associated with exploratory species-level variation but not broad restructuring of the gut microbiome.
Neurobiology of stress, 45:100855.
BACKGROUND: Psychological stress has been implicated in gut microbiome variation, but human evidence remains inconsistent and often does not distinguish exposure to stressful contexts from individual differences in physiological stress reactivity. This repeated-measures study examined whether naturalistic examination stress and post-awakening cortisol reactivity were associated with gut microbiome diversity, community composition, and species-level differential abundance.
METHODS: Thirty-nine healthy university students were assessed during examination and non-examination periods. At each assessment, participants completed validated measures of perceived stress, anxiety, affect, self-esteem, sleep, diet, and physical activity; provided salivary cortisol samples at awakening, 30 min, and 45 min post-awakening; and collected a stool sample for whole-metagenome shotgun sequencing. Post-awakening cortisol reactivity was indexed using area under the curve with respect to increase.
RESULTS: Examination stress was associated with increased perceived stress, state and trait anxiety, negative affect, poorer subjective sleep, and amplified post-awakening cortisol reactivity. Alpha and beta diversity of the gut microbiome did not differ between examination and non-examination periods, and within-subject changes in community composition were not associated with changes in cortisol reactivity. However, exploratory species-level analyses identified nominal selective microbial differences. Examination stress was associated with higher relative abundance of Dialister massiliensis and Lawsonibacter asaccharolyticus, alongside lower Duodenibacillus massiliensis and Sutterella wadsworthensis. Cortisol reactivity showed distinct associations with higher Roseburia hominis and Ruminococcus bicirculans, and lower Methanobrevibacter smithii. Within-subject increases in cortisol reactivity also covaried with higher Dabirmavirus hominis, Phascolarctobacterium succinatutens and lower Coprococcus catus.
CONCLUSIONS: Short-term examination stress was associated with marked psychological and endocrine responses but was not accompanied by broad restructuring of the adult gut microbiome. Instead, exploratory findings suggest that examination stress and cortisol reactivity may be reflected in selective species-level microbial variation, supporting further longitudinal and functional investigation of stress-related microbiome dynamics.
Additional Links: PMID-42871005
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Citation:
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@article {pmid42871005,
year = {2026},
author = {O'Reilly, CB and Giesbrecht, T and Tyson-Carr, J and Murphy, B and Cagney, K and Lenzi, L and Fallon, N and Roberts, CA},
title = {Not all stress is equal: Examination stress and cortisol reactivity are associated with exploratory species-level variation but not broad restructuring of the gut microbiome.},
journal = {Neurobiology of stress},
volume = {45},
number = {},
pages = {100855},
pmid = {42871005},
issn = {2352-2895},
abstract = {BACKGROUND: Psychological stress has been implicated in gut microbiome variation, but human evidence remains inconsistent and often does not distinguish exposure to stressful contexts from individual differences in physiological stress reactivity. This repeated-measures study examined whether naturalistic examination stress and post-awakening cortisol reactivity were associated with gut microbiome diversity, community composition, and species-level differential abundance.
METHODS: Thirty-nine healthy university students were assessed during examination and non-examination periods. At each assessment, participants completed validated measures of perceived stress, anxiety, affect, self-esteem, sleep, diet, and physical activity; provided salivary cortisol samples at awakening, 30 min, and 45 min post-awakening; and collected a stool sample for whole-metagenome shotgun sequencing. Post-awakening cortisol reactivity was indexed using area under the curve with respect to increase.
RESULTS: Examination stress was associated with increased perceived stress, state and trait anxiety, negative affect, poorer subjective sleep, and amplified post-awakening cortisol reactivity. Alpha and beta diversity of the gut microbiome did not differ between examination and non-examination periods, and within-subject changes in community composition were not associated with changes in cortisol reactivity. However, exploratory species-level analyses identified nominal selective microbial differences. Examination stress was associated with higher relative abundance of Dialister massiliensis and Lawsonibacter asaccharolyticus, alongside lower Duodenibacillus massiliensis and Sutterella wadsworthensis. Cortisol reactivity showed distinct associations with higher Roseburia hominis and Ruminococcus bicirculans, and lower Methanobrevibacter smithii. Within-subject increases in cortisol reactivity also covaried with higher Dabirmavirus hominis, Phascolarctobacterium succinatutens and lower Coprococcus catus.
CONCLUSIONS: Short-term examination stress was associated with marked psychological and endocrine responses but was not accompanied by broad restructuring of the adult gut microbiome. Instead, exploratory findings suggest that examination stress and cortisol reactivity may be reflected in selective species-level microbial variation, supporting further longitudinal and functional investigation of stress-related microbiome dynamics.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Beyond community state types: vaginal microbial diversity and CST-IV signatures are associated with pregnancy in euploid embryo transfer cycles.
Frontiers in endocrinology, 17:1881146.
BACKGROUND: Despite significant progress in assisted reproductive technology, in vitro fertilization (IVF) pregnancy rates remain suboptimal. Although the vaginal microbiome has been implicated in IVF outcomes, prior studies often overlooked embryonic aneuploidy, a major confounder. This study aimed to investigate the association between the vaginal microbiome and pregnancy outcomes in euploid embryo transfer cycles.
METHODS: This prospective study included 109 single euploid blastocyst transfer cycles. Upper vaginal swabs were collected on the transfer day and subjected to 16S rRNA gene sequencing. Microbial α- and β-diversity, community state types (CSTs), and differentially abundant taxa were compared between the clinical pregnancy (CP, n = 55) and non-clinical pregnancy (NCP, n = 54) groups.
RESULTS: The NCP group exhibited significantly higher vaginal microbial richness (Chao1, p = 0.029; ACE, p = 0.029) and distinct β-diversity compared with the CP group (R² = 0.049, p = 0.002), whereas CST distribution did not differ between groups. Within the non-Lactobacillus-dominant CST-IV subgroup, the CP group was relatively enriched in Bifidobacteriaceae (LDA = 5.0) with predicted fermentative pathways, whereas the NCP group showed higher relative abundances of Prevotella (LDA = -4.1), Dialister (LDA = -3.6), and Peptoniphilus (LDA = -2.3), accompanied by predicted tryptophan degradation and oxidative stress pathways.
DISCUSSION: These findings, derived mainly from computational prediction, suggest that fine-scale taxonomic and functional composition, rather than broad CST classification, may influence pregnancy outcomes following euploid embryo transfer, offering preliminary insights for microbiome-informed strategies to optimize reproductive outcomes. Future longitudinal studies incorporating shotgun metagenomics and metabolomics in independent cohorts are warranted to validate these preliminary observations and to clarify the dynamic association between vaginal microbiota and IVF pregnancy outcomes.
Additional Links: PMID-42871043
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Citation:
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@article {pmid42871043,
year = {2026},
author = {Zou, Y and Zhang, W and Gao, A and Fu, J and Sui, Y},
title = {Beyond community state types: vaginal microbial diversity and CST-IV signatures are associated with pregnancy in euploid embryo transfer cycles.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1881146},
pmid = {42871043},
issn = {1664-2392},
mesh = {Female ; Humans ; *Embryo Transfer/methods ; *Vagina/microbiology ; Pregnancy ; *Microbiota ; Pregnancy Outcome ; Adult ; Fertilization in Vitro ; Prospective Studies ; RNA, Ribosomal, 16S/genetics ; Pregnancy Rate ; },
abstract = {BACKGROUND: Despite significant progress in assisted reproductive technology, in vitro fertilization (IVF) pregnancy rates remain suboptimal. Although the vaginal microbiome has been implicated in IVF outcomes, prior studies often overlooked embryonic aneuploidy, a major confounder. This study aimed to investigate the association between the vaginal microbiome and pregnancy outcomes in euploid embryo transfer cycles.
METHODS: This prospective study included 109 single euploid blastocyst transfer cycles. Upper vaginal swabs were collected on the transfer day and subjected to 16S rRNA gene sequencing. Microbial α- and β-diversity, community state types (CSTs), and differentially abundant taxa were compared between the clinical pregnancy (CP, n = 55) and non-clinical pregnancy (NCP, n = 54) groups.
RESULTS: The NCP group exhibited significantly higher vaginal microbial richness (Chao1, p = 0.029; ACE, p = 0.029) and distinct β-diversity compared with the CP group (R² = 0.049, p = 0.002), whereas CST distribution did not differ between groups. Within the non-Lactobacillus-dominant CST-IV subgroup, the CP group was relatively enriched in Bifidobacteriaceae (LDA = 5.0) with predicted fermentative pathways, whereas the NCP group showed higher relative abundances of Prevotella (LDA = -4.1), Dialister (LDA = -3.6), and Peptoniphilus (LDA = -2.3), accompanied by predicted tryptophan degradation and oxidative stress pathways.
DISCUSSION: These findings, derived mainly from computational prediction, suggest that fine-scale taxonomic and functional composition, rather than broad CST classification, may influence pregnancy outcomes following euploid embryo transfer, offering preliminary insights for microbiome-informed strategies to optimize reproductive outcomes. Future longitudinal studies incorporating shotgun metagenomics and metabolomics in independent cohorts are warranted to validate these preliminary observations and to clarify the dynamic association between vaginal microbiota and IVF pregnancy outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Female
Humans
*Embryo Transfer/methods
*Vagina/microbiology
Pregnancy
*Microbiota
Pregnancy Outcome
Adult
Fertilization in Vitro
Prospective Studies
RNA, Ribosomal, 16S/genetics
Pregnancy Rate
RevDate: 2026-10-14
CmpDate: 2026-10-14
Microbiome-based probiotic intervention to reduce chemotherapy-induced gastrointestinal toxicity.
Frontiers in cellular and infection microbiology, 16:1887323.
INTRODUCTION: Chemotherapy is one of the primary treatment options for cancer; however, its gastrointestinal toxicity and disruption of gut microbial homeostasis can adversely affect patient health and treatment outcomes. This study investigated chemotherapy-induced alterations in the gut microbiome and evaluated the effects of probiotic supplementation on microbial diversity, gastrointestinal toxicity, and treatment response in cancer patients.
METHODS: The probiotic strain was isolated from a commercial formulation and identified as Lactobacillus casei using biochemical characterization and 16S rRNA gene sequencing. Its secreted metabolites were characterized using Fourier-transform infrared spectroscopy (FTIR), gas chromatography-mass spectrometry (GC-MS), high-performance liquid chromatography (HPLC), and nuclear magnetic resonance (NMR) spectroscopy. A total of 150 patients receiving platinum-based chemotherapy were enrolled and divided into control and probiotic intervention groups. Fecal samples were collected before and after chemotherapy and subjected to 16S rRNA sequencing to assess microbial diversity and taxonomic composition.
RESULTS: Chemotherapy induced significant gut microbial dysbiosis, characterized by reduced alpha diversity, decreased abundance of beneficial bacteria, including Lactobacillus, Bifidobacterium, and Faecalibacterium, and increased abundance of opportunistic pathogens such as Escherichia-Shigella and Klebsiella. In contrast, probiotic-treated patients maintained a relatively balanced gut microbiota and exhibited less pronounced dysbiosis after chemotherapy. Gastrointestinal complications were also reduced following probiotic supplementation. Overall gastrointestinal toxicity was observed in 85% of control patients compared with 65% of probiotic-treated patients, while diarrhea occurred in 60% and 35%, respectively. Grade 3-4 gastrointestinal toxicity was reported in 40% of control patients compared with 20% of probiotic-treated patients. Probiotic supplementation was additionally associated with lower incidence and severity of mucositis, nausea, and vomiting. Chemotherapy responders exhibited a more favorable microbial profile with greater abundance of beneficial commensal bacteria than non-responders. Receiver operating characteristic analysis identified microbial taxa as potential predictors of chemotherapy outcomes, with AUC values of 0.81 for Bacteroides ovatus, 0.78 for Faecalibacterium prausnitzii, and 0.86 for the combined response model. The combined microbial model achieved an AUC of 0.88 for predicting severe gastrointestinal toxicity.
DISCUSSION: Overall, probiotic supplementation may help preserve intestinal microbial homeostasis, reduce chemotherapy-associated gastrointestinal toxicity, and support improved treatment outcomes in cancer patients.
Additional Links: PMID-42871065
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Citation:
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@article {pmid42871065,
year = {2026},
author = {Li, H and Hou, C and Pan, Y},
title = {Microbiome-based probiotic intervention to reduce chemotherapy-induced gastrointestinal toxicity.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1887323},
pmid = {42871065},
issn = {2235-2988},
mesh = {Humans ; *Probiotics/administration & dosage/therapeutic use ; RNA, Ribosomal, 16S/genetics ; *Antineoplastic Agents/adverse effects/therapeutic use ; *Gastrointestinal Microbiome/drug effects ; Feces/microbiology ; Female ; Male ; Middle Aged ; Lacticaseibacillus casei/isolation & purification ; Neoplasms/drug therapy ; Dysbiosis/chemically induced/therapy ; *Gastrointestinal Diseases/chemically induced/prevention & control ; Bacteria/classification/genetics ; Aged ; DNA, Ribosomal/genetics/chemistry ; Adult ; *Gastrointestinal Tract/drug effects/microbiology ; DNA, Bacterial/genetics/chemistry ; },
abstract = {INTRODUCTION: Chemotherapy is one of the primary treatment options for cancer; however, its gastrointestinal toxicity and disruption of gut microbial homeostasis can adversely affect patient health and treatment outcomes. This study investigated chemotherapy-induced alterations in the gut microbiome and evaluated the effects of probiotic supplementation on microbial diversity, gastrointestinal toxicity, and treatment response in cancer patients.
METHODS: The probiotic strain was isolated from a commercial formulation and identified as Lactobacillus casei using biochemical characterization and 16S rRNA gene sequencing. Its secreted metabolites were characterized using Fourier-transform infrared spectroscopy (FTIR), gas chromatography-mass spectrometry (GC-MS), high-performance liquid chromatography (HPLC), and nuclear magnetic resonance (NMR) spectroscopy. A total of 150 patients receiving platinum-based chemotherapy were enrolled and divided into control and probiotic intervention groups. Fecal samples were collected before and after chemotherapy and subjected to 16S rRNA sequencing to assess microbial diversity and taxonomic composition.
RESULTS: Chemotherapy induced significant gut microbial dysbiosis, characterized by reduced alpha diversity, decreased abundance of beneficial bacteria, including Lactobacillus, Bifidobacterium, and Faecalibacterium, and increased abundance of opportunistic pathogens such as Escherichia-Shigella and Klebsiella. In contrast, probiotic-treated patients maintained a relatively balanced gut microbiota and exhibited less pronounced dysbiosis after chemotherapy. Gastrointestinal complications were also reduced following probiotic supplementation. Overall gastrointestinal toxicity was observed in 85% of control patients compared with 65% of probiotic-treated patients, while diarrhea occurred in 60% and 35%, respectively. Grade 3-4 gastrointestinal toxicity was reported in 40% of control patients compared with 20% of probiotic-treated patients. Probiotic supplementation was additionally associated with lower incidence and severity of mucositis, nausea, and vomiting. Chemotherapy responders exhibited a more favorable microbial profile with greater abundance of beneficial commensal bacteria than non-responders. Receiver operating characteristic analysis identified microbial taxa as potential predictors of chemotherapy outcomes, with AUC values of 0.81 for Bacteroides ovatus, 0.78 for Faecalibacterium prausnitzii, and 0.86 for the combined response model. The combined microbial model achieved an AUC of 0.88 for predicting severe gastrointestinal toxicity.
DISCUSSION: Overall, probiotic supplementation may help preserve intestinal microbial homeostasis, reduce chemotherapy-associated gastrointestinal toxicity, and support improved treatment outcomes in cancer patients.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Probiotics/administration & dosage/therapeutic use
RNA, Ribosomal, 16S/genetics
*Antineoplastic Agents/adverse effects/therapeutic use
*Gastrointestinal Microbiome/drug effects
Feces/microbiology
Female
Male
Middle Aged
Lacticaseibacillus casei/isolation & purification
Neoplasms/drug therapy
Dysbiosis/chemically induced/therapy
*Gastrointestinal Diseases/chemically induced/prevention & control
Bacteria/classification/genetics
Aged
DNA, Ribosomal/genetics/chemistry
Adult
*Gastrointestinal Tract/drug effects/microbiology
DNA, Bacterial/genetics/chemistry
RevDate: 2026-10-14
CmpDate: 2026-10-14
Tryptophan metabolism and plant health: mechanisms of action and application prospects.
Frontiers in plant science, 17:1872762.
UNLABELLED: Pathogen infection poses a severe threat to the global crop yield and quality. Recent studies have highlighted the pivotal role of tryptophan and its metabolites in regulating plant disease resistance. However, owing to the highly branched nature of the tryptophan metabolic network and the functional pleiotropy of its products, the mechanisms by which these metabolites influence plant health have yet to be systematically elucidated. To address this gap, this review first summarizes the biosynthesis and metabolic routing of tryptophan in both plants and microorganisms, along with the key regulatory factors governing these processes. Building on this foundation, we elaborate on the multifaceted mechanisms through which tryptophan and its derivatives regulate plant health, including direct pathogen inhibition, reshaping of the soil microbiome, strengthening of cell wall physical barriers, crosstalk with reactive oxygen/nitrogen species (ROS/RNS), interactions with plant hormones, as well as induction of defense gene expression. Eventually, there is an in-depth discussion about the application prospects and major challenges of leveraging tryptophan metabolites in agricultural development. Altogether, our overarching goal is to establish a theoretical framework and chart new investigative avenues for fostering sustainable plant protection strategies and improving crop resilience.
https://orcid.org/0009-0008-8550-2347.
Additional Links: PMID-42871074
PubMed:
Citation:
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@article {pmid42871074,
year = {2026},
author = {Li, X and Bao, H and Chen, X and Zhou, F and Tang, L},
title = {Tryptophan metabolism and plant health: mechanisms of action and application prospects.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1872762},
pmid = {42871074},
issn = {1664-462X},
abstract = {UNLABELLED: Pathogen infection poses a severe threat to the global crop yield and quality. Recent studies have highlighted the pivotal role of tryptophan and its metabolites in regulating plant disease resistance. However, owing to the highly branched nature of the tryptophan metabolic network and the functional pleiotropy of its products, the mechanisms by which these metabolites influence plant health have yet to be systematically elucidated. To address this gap, this review first summarizes the biosynthesis and metabolic routing of tryptophan in both plants and microorganisms, along with the key regulatory factors governing these processes. Building on this foundation, we elaborate on the multifaceted mechanisms through which tryptophan and its derivatives regulate plant health, including direct pathogen inhibition, reshaping of the soil microbiome, strengthening of cell wall physical barriers, crosstalk with reactive oxygen/nitrogen species (ROS/RNS), interactions with plant hormones, as well as induction of defense gene expression. Eventually, there is an in-depth discussion about the application prospects and major challenges of leveraging tryptophan metabolites in agricultural development. Altogether, our overarching goal is to establish a theoretical framework and chart new investigative avenues for fostering sustainable plant protection strategies and improving crop resilience.
https://orcid.org/0009-0008-8550-2347.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Anatomy of urethro-vesical segment and vaginal microbiota: is there any connection at stress urinary incontinence?.
Frontiers in medicine, 13:1915642.
BACKGROUND: Stress urinary incontinence (SUI) is one of the most prevalent pelvic floor disorders in women. While previous studies have demonstrated associations between urinary incontinence and changes in vaginal microbial composition, the relationship between vaginal microbiota and anatomical characteristics of the lower urinary tract remains insufficiently investigated.
OBJECTIVE: To evaluate the association between vaginal microbiota composition and sonographic parameters of the urethrovesical segment in women with SUI before and after surgery.
METHODS: This study included 100 women with SUI. Ultrasound assessment included measurements of urethral length and diameter, bladder neck mobility, α and β angles, and the internal bladder angle at rest and during the Valsalva maneuver. Vaginal samples were cultured and analyzed using MALDI-TOF mass spectrometry for species identification. All patients underwent transobturator midurethral sling surgery. Follow-up examinations were performed one month postoperatively.
RESULTS: Prior to surgery, 238 microbial strains representing 49 species were isolated. Gram-positive microorganisms predominated, with Staphylococcus spp. (32.8%), Enterococcus spp. (19.8%), and Lactobacillus spp. (13.0%) being the most common taxa. Following surgery, the proportion of Lactobacillus spp. increased significantly from 13.0% to 33.5% (p=0.0001), while Staphylococcus spp. and Enterococcus spp. decreased significantly (p=0.007 and p=0.030, respectively). Overall bacterial load was also reduced (p=0.037). Significant clinical improvement was observed, reflected by marked reductions in ICIQ-SF, UDI-6, and OABSS scores. Correlation analysis demonstrated significant associations between vaginal microbiota and urethrovesical anatomy. Longer urethral length was associated with gram-positive flora and staphylococcal colonization, whereas gram-negative microorganisms, particularly Enterobacterales, were associated with shorter urethral length and smaller urethral diameter. Enterobacterial colonization was linked to a 12.1% narrower urethra (p=0.003). Additional associations were identified between specific bacterial groups and dynamic changes in β-angle and internal bladder angle measurements.
CONCLUSIONS: Surgical treatment of SUI is associated with significant symptom improvement and early changes in the structure of the cultivable vaginal microbiota, including an increased representation of Lactobacillus spp. The observed associations between characteristics of the vaginal microbiota and sonographic parameters of the urethrovesical segment suggest a possible relationship between the anatomical and functional characteristics of the lower urinary tract and the local microbial environment. However, the nature of these associations and their causal direction remain undetermined. The findings should therefore be considered hypothesis-generating and require confirmation in prospective studies with a control group, longer follow-up, and the use of modern microbiome profiling methods.
Additional Links: PMID-42871127
PubMed:
Citation:
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@article {pmid42871127,
year = {2026},
author = {Turgunov, YM and Sevastyanov, LV and Lavrinenko, AV and Avilova, YV},
title = {Anatomy of urethro-vesical segment and vaginal microbiota: is there any connection at stress urinary incontinence?.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1915642},
pmid = {42871127},
issn = {2296-858X},
abstract = {BACKGROUND: Stress urinary incontinence (SUI) is one of the most prevalent pelvic floor disorders in women. While previous studies have demonstrated associations between urinary incontinence and changes in vaginal microbial composition, the relationship between vaginal microbiota and anatomical characteristics of the lower urinary tract remains insufficiently investigated.
OBJECTIVE: To evaluate the association between vaginal microbiota composition and sonographic parameters of the urethrovesical segment in women with SUI before and after surgery.
METHODS: This study included 100 women with SUI. Ultrasound assessment included measurements of urethral length and diameter, bladder neck mobility, α and β angles, and the internal bladder angle at rest and during the Valsalva maneuver. Vaginal samples were cultured and analyzed using MALDI-TOF mass spectrometry for species identification. All patients underwent transobturator midurethral sling surgery. Follow-up examinations were performed one month postoperatively.
RESULTS: Prior to surgery, 238 microbial strains representing 49 species were isolated. Gram-positive microorganisms predominated, with Staphylococcus spp. (32.8%), Enterococcus spp. (19.8%), and Lactobacillus spp. (13.0%) being the most common taxa. Following surgery, the proportion of Lactobacillus spp. increased significantly from 13.0% to 33.5% (p=0.0001), while Staphylococcus spp. and Enterococcus spp. decreased significantly (p=0.007 and p=0.030, respectively). Overall bacterial load was also reduced (p=0.037). Significant clinical improvement was observed, reflected by marked reductions in ICIQ-SF, UDI-6, and OABSS scores. Correlation analysis demonstrated significant associations between vaginal microbiota and urethrovesical anatomy. Longer urethral length was associated with gram-positive flora and staphylococcal colonization, whereas gram-negative microorganisms, particularly Enterobacterales, were associated with shorter urethral length and smaller urethral diameter. Enterobacterial colonization was linked to a 12.1% narrower urethra (p=0.003). Additional associations were identified between specific bacterial groups and dynamic changes in β-angle and internal bladder angle measurements.
CONCLUSIONS: Surgical treatment of SUI is associated with significant symptom improvement and early changes in the structure of the cultivable vaginal microbiota, including an increased representation of Lactobacillus spp. The observed associations between characteristics of the vaginal microbiota and sonographic parameters of the urethrovesical segment suggest a possible relationship between the anatomical and functional characteristics of the lower urinary tract and the local microbial environment. However, the nature of these associations and their causal direction remain undetermined. The findings should therefore be considered hypothesis-generating and require confirmation in prospective studies with a control group, longer follow-up, and the use of modern microbiome profiling methods.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Gut microbial dynamics and antibiotic resistance during rifaximin therapy in severe cirrhosis: a ProPILA-Rifax ancillary study.
Frontiers in cellular and infection microbiology, 16:1930709.
INTRODUCTION: Increasing evidence implicates gut dysbiosis in the pathophysiology of advanced cirrhosis. This is an ancillary study of the ProPILA-Rifax trial (NCT03069131), which evaluated rifaximin (RFX) as primary prophylaxis of spontaneous bacterial peritonitis (SBP) in patients with severe cirrhosis. Although the combined use of RFX and lactulose is effective in preventing recurrent hepatic encephalopathy (HE), its longitudinal impact on microbial communities and antibiotic resistance remains poorly characterized.
METHODS: We characterized longitudinal changes in the gut microbiome of 42 patients (21 RFX, 21 placebo) over 12 months using 16S rRNA gene sequencing and culture-based phenotypic susceptibility testing. Exploratory analyses between patient bacterial profiles and clinical outcomes (disease severity, overall survival, and incidence of SBP) were conducted.
RESULTS: RFX treatment reduced microbial richness and decreased the abundance of taxa typically enriched in advanced cirrhosis (e.g., Escherichia, Streptococcus, Veillonella). RFX increased the proportion of Escherichia coli isolates exhibiting phenotypic resistance to rifampicin, without observed cross-resistance to ciprofloxacin or cefotaxime. In exploratory analyses, a decrease in Child-Pugh scores was correlated with enrichment of commensal taxa. Moreover, higher abundances of Ruminococcus bromii and Blautia obeum at inclusion were respectively associated with improved 12-month survival and a lower incidence of SBP.
DISCUSSION: In severe cirrhosis, RFX profoundly alters gut microbial composition by reducing pathobiont abundance while promoting rifampicin resistance in E. coli. Furthermore, microbiota-derived signatures were associated with Child-Pugh scores, highlighting their potential to improve patient stratification.
Additional Links: PMID-42871147
PubMed:
Citation:
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@article {pmid42871147,
year = {2026},
author = {Ladeira, R and Biguenet, A and Meunier, A and Gonthier, M and Di Martino, V and Pitta, A and Bardou-Jacquet, E and Jolivet-Gougeon, A and Desmarets, M and Thévenot, T and Hocquet, D and Valot, B},
title = {Gut microbial dynamics and antibiotic resistance during rifaximin therapy in severe cirrhosis: a ProPILA-Rifax ancillary study.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1930709},
pmid = {42871147},
issn = {2235-2988},
mesh = {Humans ; *Rifaximin/therapeutic use ; *Liver Cirrhosis/complications/drug therapy/microbiology ; *Gastrointestinal Microbiome/drug effects ; Peritonitis/prevention & control/microbiology ; *Anti-Bacterial Agents/therapeutic use ; Female ; RNA, Ribosomal, 16S/genetics ; Male ; *Bacteria/drug effects/classification/genetics/isolation & purification ; Middle Aged ; *Drug Resistance, Bacterial ; Hepatic Encephalopathy/prevention & control ; Dysbiosis ; Rifamycins ; Bacterial Infections/prevention & control ; Aged ; Microbial Sensitivity Tests ; Treatment Outcome ; },
abstract = {INTRODUCTION: Increasing evidence implicates gut dysbiosis in the pathophysiology of advanced cirrhosis. This is an ancillary study of the ProPILA-Rifax trial (NCT03069131), which evaluated rifaximin (RFX) as primary prophylaxis of spontaneous bacterial peritonitis (SBP) in patients with severe cirrhosis. Although the combined use of RFX and lactulose is effective in preventing recurrent hepatic encephalopathy (HE), its longitudinal impact on microbial communities and antibiotic resistance remains poorly characterized.
METHODS: We characterized longitudinal changes in the gut microbiome of 42 patients (21 RFX, 21 placebo) over 12 months using 16S rRNA gene sequencing and culture-based phenotypic susceptibility testing. Exploratory analyses between patient bacterial profiles and clinical outcomes (disease severity, overall survival, and incidence of SBP) were conducted.
RESULTS: RFX treatment reduced microbial richness and decreased the abundance of taxa typically enriched in advanced cirrhosis (e.g., Escherichia, Streptococcus, Veillonella). RFX increased the proportion of Escherichia coli isolates exhibiting phenotypic resistance to rifampicin, without observed cross-resistance to ciprofloxacin or cefotaxime. In exploratory analyses, a decrease in Child-Pugh scores was correlated with enrichment of commensal taxa. Moreover, higher abundances of Ruminococcus bromii and Blautia obeum at inclusion were respectively associated with improved 12-month survival and a lower incidence of SBP.
DISCUSSION: In severe cirrhosis, RFX profoundly alters gut microbial composition by reducing pathobiont abundance while promoting rifampicin resistance in E. coli. Furthermore, microbiota-derived signatures were associated with Child-Pugh scores, highlighting their potential to improve patient stratification.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Rifaximin/therapeutic use
*Liver Cirrhosis/complications/drug therapy/microbiology
*Gastrointestinal Microbiome/drug effects
Peritonitis/prevention & control/microbiology
*Anti-Bacterial Agents/therapeutic use
Female
RNA, Ribosomal, 16S/genetics
Male
*Bacteria/drug effects/classification/genetics/isolation & purification
Middle Aged
*Drug Resistance, Bacterial
Hepatic Encephalopathy/prevention & control
Dysbiosis
Rifamycins
Bacterial Infections/prevention & control
Aged
Microbial Sensitivity Tests
Treatment Outcome
RevDate: 2026-10-14
CmpDate: 2026-10-14
The gut microbiome and metabolome of people living with HIV altered during treatment.
Frontiers in microbiology, 17:1920281.
BACKGROUND: Despite effective viral suppression with antiretroviral therapy (ART), people living with HIV (PLWH) often experience persistent immune activation and incomplete immune reconstitution. Gut barrier disruption and gut microbial dysbiosis contribute to chronic inflammation in PLWH. Shen Ling Ai Cao pill (SLAC) may have immunomodulatory effects, however, changes in the gut microbiota and fecal metabolome during SLAC administration remain unclear. This study aimed to characterize changes in the gut microbiota and fecal metabolome during SLAC administration in PLWH.
METHODS: In this single-arm study, 46 PLWH on long-term ART received adjunctive SLAC for 6 months. Fecal samples were collected, and peripheral CD4+ and CD8+ T-cell counts and the CD4/CD8 ratio were measured at baseline and month 6. Gut microbiota were profiled by 16S rRNA gene sequencing, and untargeted metabolomics was performed to characterize fecal metabolic changes. Microbial diversity, differential taxa, functional pathways, differential metabolites, and KEGG enrichment were analyzed. Correlation analyses were conducted to explore associations among gut microbiota, metabolites, and T-cell subsets.
RESULTS: Among the 46 PLWH enrolled, 42 completed the 6-month follow-up and were included in the final analysis. From M0 to M6, median CD8+ T-cell counts increased from 448.5 to 565.0 cells/mm[3] (P = 0.047), whereas median CD4+ T-cell counts increased non-significantly from 308.0 to 330.0 cells/mm[3] (P = 0.118), with no change in the CD4/CD8 ratio (P = 0.89). Differences were also observed in gut microbial composition and fecal metabolomic profiles. Correlation analyses identified associations between gut microbial taxa and CD4+ and CD8+ T-cell counts. A total of 59 differential metabolites were identified, and enrichment analysis implicated lipid metabolism, bile acid metabolism, cholesterol metabolism, and mTOR signaling.
CONCLUSIONS: In this single-arm longitudinal study of ART-treated PLWH, 6 months of adjunctive SLAC administration was associated with changes in fecal microbial composition, fecal metabolomic profiles, and CD8+ T cell counts, whereas CD4+ T cell counts showed a nonsignificant increasing trend. Controlled studies are needed to determine whether these changes are attributable to SLAC.
Additional Links: PMID-42871189
PubMed:
Citation:
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@article {pmid42871189,
year = {2026},
author = {Ding, X and Li, J and Qian, P and Yue, J and Ma, X and Xu, L},
title = {The gut microbiome and metabolome of people living with HIV altered during treatment.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1920281},
pmid = {42871189},
issn = {1664-302X},
abstract = {BACKGROUND: Despite effective viral suppression with antiretroviral therapy (ART), people living with HIV (PLWH) often experience persistent immune activation and incomplete immune reconstitution. Gut barrier disruption and gut microbial dysbiosis contribute to chronic inflammation in PLWH. Shen Ling Ai Cao pill (SLAC) may have immunomodulatory effects, however, changes in the gut microbiota and fecal metabolome during SLAC administration remain unclear. This study aimed to characterize changes in the gut microbiota and fecal metabolome during SLAC administration in PLWH.
METHODS: In this single-arm study, 46 PLWH on long-term ART received adjunctive SLAC for 6 months. Fecal samples were collected, and peripheral CD4+ and CD8+ T-cell counts and the CD4/CD8 ratio were measured at baseline and month 6. Gut microbiota were profiled by 16S rRNA gene sequencing, and untargeted metabolomics was performed to characterize fecal metabolic changes. Microbial diversity, differential taxa, functional pathways, differential metabolites, and KEGG enrichment were analyzed. Correlation analyses were conducted to explore associations among gut microbiota, metabolites, and T-cell subsets.
RESULTS: Among the 46 PLWH enrolled, 42 completed the 6-month follow-up and were included in the final analysis. From M0 to M6, median CD8+ T-cell counts increased from 448.5 to 565.0 cells/mm[3] (P = 0.047), whereas median CD4+ T-cell counts increased non-significantly from 308.0 to 330.0 cells/mm[3] (P = 0.118), with no change in the CD4/CD8 ratio (P = 0.89). Differences were also observed in gut microbial composition and fecal metabolomic profiles. Correlation analyses identified associations between gut microbial taxa and CD4+ and CD8+ T-cell counts. A total of 59 differential metabolites were identified, and enrichment analysis implicated lipid metabolism, bile acid metabolism, cholesterol metabolism, and mTOR signaling.
CONCLUSIONS: In this single-arm longitudinal study of ART-treated PLWH, 6 months of adjunctive SLAC administration was associated with changes in fecal microbial composition, fecal metabolomic profiles, and CD8+ T cell counts, whereas CD4+ T cell counts showed a nonsignificant increasing trend. Controlled studies are needed to determine whether these changes are attributable to SLAC.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Artificial intelligence-based tongue image analysis for non-invasive screening of gastric cancer, precancerous lesions, and related gastrointestinal disorders: a systematic review.
Frontiers in medicine, 13:1931256.
BACKGROUND: Gastric cancer remains a major cause of cancer-related mortality, largely because many cases are diagnosed at an advanced stage. Upper gastrointestinal endoscopy with histopathological confirmation is the diagnostic gold standard, but its invasiveness, cost, and limited accessibility restrict population-level use. Artificial intelligence (AI)-based tongue-image analysis may provide an objective, low-cost, and non-invasive adjunct for pre-endoscopic risk stratification.
METHODS: This systematic review was conducted according to PRISMA 2020 principles and was informed by diagnostic test accuracy and prediction-model reporting frameworks. PubMed/MEDLINE, Scopus, Web of Science, and IEEE Xplore were searched from inception to 10 June 2026. Eligible studies were original investigations applying machine-learning or deep-learning methods to digital tongue images for gastric cancer, precancerous gastric lesions, or related gastrointestinal disorders and reporting at least one quantitative performance metric. Data were extracted on study design, sample size, target condition, reference standard, image-acquisition protocol, model architecture, validation strategy, diagnostic performance, calibration, interpretability, and risk of bias. A narrative synthesis was performed because of substantial heterogeneity.
RESULTS: The search identified 139 records, of which 78 remained after duplicate removal. After title, abstract, and full-text screening, 9 studies published between 2018 and 2025 were included. The evidence covered gastric cancer, precancerous gastric lesions or high-risk gastric screening, and related gastrointestinal disorders. Models included logistic regression and XGBoost classifiers based on handcrafted features, convolutional neural networks, transformer-based architectures, segmentation-assisted pipelines, and multimodal models combining tongue images with clinical, questionnaire, biomarker, or microbiome data. Internally validated AUCs ranged from 0.61 to 0.99 across target conditions. External validation was reported in only three studies and generally showed performance degradation, particularly for precancerous gastric lesions. Calibration assessment was uncommon, and most studies did not report calibration curves, Brier scores, expected calibration error, or recalibration procedures.
CONCLUSION: AI-based tongue-image analysis is a promising but early-stage approach for non-invasive gastric disease screening. Current evidence supports its potential role as an adjunctive pre-endoscopic triage tool rather than a replacement for gastroscopy. Prospective external validation, standardized image acquisition, transparent model reporting, calibration assessment, and evaluation in diverse populations are required before clinical deployment.
https://www.crd.york.ac.uk/PROSPERO/view/CRD420261444857, PROSPERO CRD420261444857.
Additional Links: PMID-42871270
PubMed:
Citation:
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@article {pmid42871270,
year = {2026},
author = {Wang, R and Li, C and Zhang, H and Shao, P and Gao, Z and Zhang, C},
title = {Artificial intelligence-based tongue image analysis for non-invasive screening of gastric cancer, precancerous lesions, and related gastrointestinal disorders: a systematic review.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1931256},
pmid = {42871270},
issn = {2296-858X},
abstract = {BACKGROUND: Gastric cancer remains a major cause of cancer-related mortality, largely because many cases are diagnosed at an advanced stage. Upper gastrointestinal endoscopy with histopathological confirmation is the diagnostic gold standard, but its invasiveness, cost, and limited accessibility restrict population-level use. Artificial intelligence (AI)-based tongue-image analysis may provide an objective, low-cost, and non-invasive adjunct for pre-endoscopic risk stratification.
METHODS: This systematic review was conducted according to PRISMA 2020 principles and was informed by diagnostic test accuracy and prediction-model reporting frameworks. PubMed/MEDLINE, Scopus, Web of Science, and IEEE Xplore were searched from inception to 10 June 2026. Eligible studies were original investigations applying machine-learning or deep-learning methods to digital tongue images for gastric cancer, precancerous gastric lesions, or related gastrointestinal disorders and reporting at least one quantitative performance metric. Data were extracted on study design, sample size, target condition, reference standard, image-acquisition protocol, model architecture, validation strategy, diagnostic performance, calibration, interpretability, and risk of bias. A narrative synthesis was performed because of substantial heterogeneity.
RESULTS: The search identified 139 records, of which 78 remained after duplicate removal. After title, abstract, and full-text screening, 9 studies published between 2018 and 2025 were included. The evidence covered gastric cancer, precancerous gastric lesions or high-risk gastric screening, and related gastrointestinal disorders. Models included logistic regression and XGBoost classifiers based on handcrafted features, convolutional neural networks, transformer-based architectures, segmentation-assisted pipelines, and multimodal models combining tongue images with clinical, questionnaire, biomarker, or microbiome data. Internally validated AUCs ranged from 0.61 to 0.99 across target conditions. External validation was reported in only three studies and generally showed performance degradation, particularly for precancerous gastric lesions. Calibration assessment was uncommon, and most studies did not report calibration curves, Brier scores, expected calibration error, or recalibration procedures.
CONCLUSION: AI-based tongue-image analysis is a promising but early-stage approach for non-invasive gastric disease screening. Current evidence supports its potential role as an adjunctive pre-endoscopic triage tool rather than a replacement for gastroscopy. Prospective external validation, standardized image acquisition, transparent model reporting, calibration assessment, and evaluation in diverse populations are required before clinical deployment.
https://www.crd.york.ac.uk/PROSPERO/view/CRD420261444857, PROSPERO CRD420261444857.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
The active immune role of keratinocytes: from passive targets to key hubs in psoriatic inflammation.
Frontiers in immunology, 17:1970701.
Psoriasis is a chronic immune-mediated inflammatory skin disease historically viewed as a disorder of keratinocyte hyperplasia, with subsequent recognition of central immune cell involvement. However, accumulating multi-omics and functional genomic evidence has reshaped this paradigm, positioning keratinocytes not merely as passive targets of immune attack but as active participants within a bidirectional epithelial-immune network that drives inflammatory initiation, maintenance, and amplification. This critical narrative review synthesizes the molecular mechanisms by which keratinocytes integrate genetic susceptibility, environmental triggers, metabolic reprogramming, and cell death programs to modulate psoriatic inflammation. We examine interleukin (IL)-1/IL-36 cytokines, the dual function of the antimicrobial peptide LL-37, danger signal release and dendritic cell recruitment, chemokine networks and exosome-mediated communication, the neuropeptide-keratinocyte axis, carbohydrate and lipid metabolic abnormalities, mitochondrial dysfunction and reactive oxygen species (ROS)-mediated feedback, epidermal barrier defects and microbiome dysregulation, diagnostic biomarkers, and therapeutic innovations. We further critically evaluate controversies, conceptual challenges, research gaps, and future directions. A keratinocyte-centric framework-situated within the broader context of epithelial-immune reciprocity-advances understanding of psoriasis pathogenesis and informs precision therapies targeting the barrier-immune axis.
Additional Links: PMID-42871309
PubMed:
Citation:
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@article {pmid42871309,
year = {2026},
author = {Pei, Y},
title = {The active immune role of keratinocytes: from passive targets to key hubs in psoriatic inflammation.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1970701},
pmid = {42871309},
issn = {1664-3224},
mesh = {Humans ; *Keratinocytes/immunology/metabolism ; *Psoriasis/immunology/metabolism/pathology/etiology ; Animals ; Inflammation/immunology ; Skin Microbiome ; },
abstract = {Psoriasis is a chronic immune-mediated inflammatory skin disease historically viewed as a disorder of keratinocyte hyperplasia, with subsequent recognition of central immune cell involvement. However, accumulating multi-omics and functional genomic evidence has reshaped this paradigm, positioning keratinocytes not merely as passive targets of immune attack but as active participants within a bidirectional epithelial-immune network that drives inflammatory initiation, maintenance, and amplification. This critical narrative review synthesizes the molecular mechanisms by which keratinocytes integrate genetic susceptibility, environmental triggers, metabolic reprogramming, and cell death programs to modulate psoriatic inflammation. We examine interleukin (IL)-1/IL-36 cytokines, the dual function of the antimicrobial peptide LL-37, danger signal release and dendritic cell recruitment, chemokine networks and exosome-mediated communication, the neuropeptide-keratinocyte axis, carbohydrate and lipid metabolic abnormalities, mitochondrial dysfunction and reactive oxygen species (ROS)-mediated feedback, epidermal barrier defects and microbiome dysregulation, diagnostic biomarkers, and therapeutic innovations. We further critically evaluate controversies, conceptual challenges, research gaps, and future directions. A keratinocyte-centric framework-situated within the broader context of epithelial-immune reciprocity-advances understanding of psoriasis pathogenesis and informs precision therapies targeting the barrier-immune axis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Keratinocytes/immunology/metabolism
*Psoriasis/immunology/metabolism/pathology/etiology
Animals
Inflammation/immunology
Skin Microbiome
RevDate: 2026-10-14
CmpDate: 2026-10-14
Cross-organ microbes modulate host upper gastrointestinal health and disease via the oral-gastric microbiome axis.
Frontiers in cellular and infection microbiology, 16:1941478.
The human body harbors highly diverse and complex microbial communities across various regions. Among these, the oral cavity and stomach are directly connected and engage in dynamic microbial interactions. Microorganisms capable of migrating between these two distinct niches are referred to as trans-organ microbes, which constitute a core component of the oral-gastric microbiome axis. In this review, we elucidate the mechanisms underlying microbial translocation along the oral-gastric axis. We further discuss how these cross-organ microbes exert bidirectional influences on health and disease in upper gastrointestinal environments. They contribute to mucosal homeostasis and modulate immune responses, yet under certain conditions, they can also promote pathologies such as gastritis, gastric cancer, and oral disorders. The migration and colonization patterns of microbes across organs also hold potential for developing diagnostic biomarkers, as well as for designing innovative microbiome-based interventions targeting the upper gastrointestinal tract. In summary, this review highlights the oral-gastric microbiome axis as a critical frontier for understanding and manipulating microbiome dynamics in human health and disease.
Additional Links: PMID-42871354
PubMed:
Citation:
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@article {pmid42871354,
year = {2026},
author = {Peng, X and Peng, W and Zou, Y and Li, Z},
title = {Cross-organ microbes modulate host upper gastrointestinal health and disease via the oral-gastric microbiome axis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1941478},
pmid = {42871354},
issn = {2235-2988},
mesh = {Humans ; *Mouth/microbiology ; *Gastrointestinal Microbiome/physiology ; *Upper Gastrointestinal Tract/microbiology ; Animals ; *Microbiota ; *Stomach/microbiology ; *Host Microbial Interactions ; Bacterial Translocation ; },
abstract = {The human body harbors highly diverse and complex microbial communities across various regions. Among these, the oral cavity and stomach are directly connected and engage in dynamic microbial interactions. Microorganisms capable of migrating between these two distinct niches are referred to as trans-organ microbes, which constitute a core component of the oral-gastric microbiome axis. In this review, we elucidate the mechanisms underlying microbial translocation along the oral-gastric axis. We further discuss how these cross-organ microbes exert bidirectional influences on health and disease in upper gastrointestinal environments. They contribute to mucosal homeostasis and modulate immune responses, yet under certain conditions, they can also promote pathologies such as gastritis, gastric cancer, and oral disorders. The migration and colonization patterns of microbes across organs also hold potential for developing diagnostic biomarkers, as well as for designing innovative microbiome-based interventions targeting the upper gastrointestinal tract. In summary, this review highlights the oral-gastric microbiome axis as a critical frontier for understanding and manipulating microbiome dynamics in human health and disease.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Mouth/microbiology
*Gastrointestinal Microbiome/physiology
*Upper Gastrointestinal Tract/microbiology
Animals
*Microbiota
*Stomach/microbiology
*Host Microbial Interactions
Bacterial Translocation
RevDate: 2026-10-14
Correction: The intratumoral microbiome in colorectal cancer: origins, microenvironmental interactions, and new horizons in precision medicine.
Frontiers in immunology, 17:1991410.
[This corrects the article DOI: 10.3389/fimmu.2026.1795736.].
Additional Links: PMID-42871395
Full Text:
Publisher:
PubMed:
Citation:
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@article {pmid42871395,
year = {2026},
author = {Li, X and Wang, Q and Yuan, Q and Wang, L},
title = {Correction: The intratumoral microbiome in colorectal cancer: origins, microenvironmental interactions, and new horizons in precision medicine.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1991410},
doi = {10.3389/fimmu.2026.1991410},
pmid = {42871395},
issn = {1664-3224},
abstract = {[This corrects the article DOI: 10.3389/fimmu.2026.1795736.].},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Deciphering the gut-liver axis in MASLD: from dysbiosis-driven pathogenesis to precision microbiome therapeutics.
Frontiers in microbiology, 17:1971785.
Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most prevalent chronic liver disorder worldwide, characterized by a multifactorial pathogenesis involving genetic predisposition, metabolic disturbances, environmental influences, and gut microbiota interactions. In recent years, the gut microbiota has garnered significant attention for its pivotal role in MASLD development and progression through the gut-liver axis. This review comprehensively summarizes current understanding of the molecular mechanisms by which gut microbiota and their metabolites contribute to MASLD pathogenesis, including intestinal barrier dysfunction, bile acid metabolism dysregulation, abnormalities in short-chain fatty acid and tryptophan metabolism, oxidative stress, and mitochondrial impairment. Furthermore, we comprehensively discuss advances in therapeutic strategies targeting gut microbiota modulation, such as probiotics/prebiotics, fecal microbiota transplantation, dietary interventions, bioactive compounds from traditional Chinese medicine, and surgical approaches. By integrating these insights, this review aims to provide novel perspectives for precise prevention and treatment of MASLD, highlighting the gut microbiota as a promising target for future clinical management.
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@article {pmid42871658,
year = {2026},
author = {Liu, W and Lan, Y and Chen, X and Wei, H and Zhang, T and Wang, Y},
title = {Deciphering the gut-liver axis in MASLD: from dysbiosis-driven pathogenesis to precision microbiome therapeutics.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1971785},
pmid = {42871658},
issn = {1664-302X},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most prevalent chronic liver disorder worldwide, characterized by a multifactorial pathogenesis involving genetic predisposition, metabolic disturbances, environmental influences, and gut microbiota interactions. In recent years, the gut microbiota has garnered significant attention for its pivotal role in MASLD development and progression through the gut-liver axis. This review comprehensively summarizes current understanding of the molecular mechanisms by which gut microbiota and their metabolites contribute to MASLD pathogenesis, including intestinal barrier dysfunction, bile acid metabolism dysregulation, abnormalities in short-chain fatty acid and tryptophan metabolism, oxidative stress, and mitochondrial impairment. Furthermore, we comprehensively discuss advances in therapeutic strategies targeting gut microbiota modulation, such as probiotics/prebiotics, fecal microbiota transplantation, dietary interventions, bioactive compounds from traditional Chinese medicine, and surgical approaches. By integrating these insights, this review aims to provide novel perspectives for precise prevention and treatment of MASLD, highlighting the gut microbiota as a promising target for future clinical management.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Maternal microbiota and fetal brain development: a multidisciplinary review of cognitive, neurological, and metabolic outcomes.
Frontiers in neurology, 17:1778399.
OBJECTIVE: The prenatal period represents a critical window for the programming of the central nervous system. This multidisciplinary narrative review aims to synthesize current evidence regarding the maternal microbiota-gut-fetal brain axis, examining how maternal gut composition may influence fetal neurogenesis, synaptogenesis, and long-term neurobehavioural outcomes.
MECHANISM: We analyse three primary pathways of influence: the systemic translocation of neuroactive bacterial metabolites (specifically short-chain fatty acids), the modulation of the maternal immune system leading to maternal immune activation (MIA), and the endocrine regulation of the hypothalamic-pituitary-adrenal axis. These pathways are interconnected and their synergistic effects are considered throughout.
RESULTS: Neurological data, predominantly from animal models, suggest that maternal dysbiosis may disrupt microglial maturation and cortical lamination through epigenetic modifications mediated by butyrate and serotonin precursors. Endocrinological evidence highlights the role of the estrobolome and the bacterial conversion of glucocorticoids into neuroactive progestins. Obstetric and pediatric findings indicate associations between maternal microbiome composition, preterm birth risks, and the incidence of autism spectrum disorders and ADHD in offspring, though causal inference from human data remains limited. Nutritional analysis suggests that dietary fibers and Omega-3 fatty acids may act as modulators of this axis.
CONCLUSION: The maternal microbiota is a potentially modifiable determinant of fetal neurological health. Microbiome-based interventions carry potential risks and require careful clinical evaluation. A comprehensive, individualized approach integrating neurology, endocrinology, obstetrics, and nutrition is required to develop evidence-based preventive strategies.
Additional Links: PMID-42871661
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@article {pmid42871661,
year = {2026},
author = {Satanovsky, D and Beloyartseva, M and Kuznetsov, P and Savin, N and Nesterenko, A and Vekilova, K},
title = {Maternal microbiota and fetal brain development: a multidisciplinary review of cognitive, neurological, and metabolic outcomes.},
journal = {Frontiers in neurology},
volume = {17},
number = {},
pages = {1778399},
pmid = {42871661},
issn = {1664-2295},
mesh = {Humans ; Female ; Pregnancy ; *Brain/metabolism/growth & development/embryology ; *Fetal Development/physiology ; Animals ; Neurodevelopment ; *Gastrointestinal Microbiome/physiology ; Developmental Origins of Health and Disease ; *Microbiota ; Cognition/physiology ; },
abstract = {OBJECTIVE: The prenatal period represents a critical window for the programming of the central nervous system. This multidisciplinary narrative review aims to synthesize current evidence regarding the maternal microbiota-gut-fetal brain axis, examining how maternal gut composition may influence fetal neurogenesis, synaptogenesis, and long-term neurobehavioural outcomes.
MECHANISM: We analyse three primary pathways of influence: the systemic translocation of neuroactive bacterial metabolites (specifically short-chain fatty acids), the modulation of the maternal immune system leading to maternal immune activation (MIA), and the endocrine regulation of the hypothalamic-pituitary-adrenal axis. These pathways are interconnected and their synergistic effects are considered throughout.
RESULTS: Neurological data, predominantly from animal models, suggest that maternal dysbiosis may disrupt microglial maturation and cortical lamination through epigenetic modifications mediated by butyrate and serotonin precursors. Endocrinological evidence highlights the role of the estrobolome and the bacterial conversion of glucocorticoids into neuroactive progestins. Obstetric and pediatric findings indicate associations between maternal microbiome composition, preterm birth risks, and the incidence of autism spectrum disorders and ADHD in offspring, though causal inference from human data remains limited. Nutritional analysis suggests that dietary fibers and Omega-3 fatty acids may act as modulators of this axis.
CONCLUSION: The maternal microbiota is a potentially modifiable determinant of fetal neurological health. Microbiome-based interventions carry potential risks and require careful clinical evaluation. A comprehensive, individualized approach integrating neurology, endocrinology, obstetrics, and nutrition is required to develop evidence-based preventive strategies.},
}
MeSH Terms:
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Humans
Female
Pregnancy
*Brain/metabolism/growth & development/embryology
*Fetal Development/physiology
Animals
Neurodevelopment
*Gastrointestinal Microbiome/physiology
Developmental Origins of Health and Disease
*Microbiota
Cognition/physiology
RevDate: 2026-10-14
CmpDate: 2026-10-14
Host diets drive microbiome evolution and functional divergence.
Genes & diseases, 14(2):102068.
Substantial variation in gut microbiome function across individuals underscores the pivotal role of the host in shaping microbial diversity. Increasing evidence indicates that diet is a major selective force driving the evolutionary trajectory of the gut microbiome. In response to dietary inputs, the microbiome adapts by shifting the relative abundance of taxa, species, and sub-strains. The gut microbiome also acquires novel genetic features through selecting advantageous mutations and genes, as well as colonizing exogenous bacterial species that enhance nutrient utilization. These adaptive processes occur not only across human evolutionary history but also within an individual's lifetime, consequently generating functionally divergent microbiomes with important consequences for health. Diets of poor nutritional quality, such as the Western-style diet, foster disease-permissive microbial functions. Understanding how dietary patterns and components influence microbiome evolution, and thereby affect health, is essential for developing diet-based strategies to modulate microbial functions. This review presents compelling evidence to demonstrate how host diet shapes gut microbiome evolution and leads to a functionally divergent gut microbiome that impacts human health.
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@article {pmid42871726,
year = {2027},
author = {Nguyen, KL and Xia, JS and Mei, W},
title = {Host diets drive microbiome evolution and functional divergence.},
journal = {Genes & diseases},
volume = {14},
number = {2},
pages = {102068},
pmid = {42871726},
issn = {2352-3042},
abstract = {Substantial variation in gut microbiome function across individuals underscores the pivotal role of the host in shaping microbial diversity. Increasing evidence indicates that diet is a major selective force driving the evolutionary trajectory of the gut microbiome. In response to dietary inputs, the microbiome adapts by shifting the relative abundance of taxa, species, and sub-strains. The gut microbiome also acquires novel genetic features through selecting advantageous mutations and genes, as well as colonizing exogenous bacterial species that enhance nutrient utilization. These adaptive processes occur not only across human evolutionary history but also within an individual's lifetime, consequently generating functionally divergent microbiomes with important consequences for health. Diets of poor nutritional quality, such as the Western-style diet, foster disease-permissive microbial functions. Understanding how dietary patterns and components influence microbiome evolution, and thereby affect health, is essential for developing diet-based strategies to modulate microbial functions. This review presents compelling evidence to demonstrate how host diet shapes gut microbiome evolution and leads to a functionally divergent gut microbiome that impacts human health.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Bifidobacterium adolescentis protects the intestinal barrier from obesity-related inflammatory stimuli in association with the nuclear translocation of nuclear factor kappa B.
Bioscience of microbiota, food and health, 45(4):264-271.
The intestinal barrier plays a crucial role in host metabolic and immune homeostasis; however, its integrity can be disrupted by factors such as lipopolysaccharides, inflammatory cytokines, and oxidative stress. Although Bifidobacterium species are considered beneficial members of the gut microbiota, their strain-specific effects on epithelial barrier integrity and the underlying mechanisms remain incompletely understood. We investigated the protective effects of four heat-killed strains of bifidobacteria, B. pseudocatenulatum YIT 11057, B. adolescentis YIT 13021, B. bifidum YIT 10347, and B. breve YIT 4014, on intestinal barrier function using T84 monolayers, a widely used in vitro model of the intestinal epithelium that retains many colon-like properties. Among the tested strains, only B. adolescentis YIT 13021 (YIT 13021) consistently protected against barrier disruption induced by lipopolysaccharide (LPS), oxidative stress, and inflammatory cytokines, highlighting species-enriched but strain-dependent functional properties within B. adolescentis. YIT 13021 preserved tight junction integrity in association with preserved localization of zonula occludens-1 and attenuated stimulus-induced nuclear localization of nuclear factor-kappa B. Furthermore, live YIT 13021 exerted superior barrier-protective effects than its heat-killed counterpart, and its protective efficacy was further increased when cultured in the presence of starch, suggesting that metabolic activity and substrate availability influence functional outcomes. These findings demonstrate functional heterogeneity among Bifidobacterium strains, provide insights into potential mechanisms underlying microbiota-mediated modulation of epithelial integrity, and identify B. adolescentis YIT 13021 as a promising candidate for supporting intestinal barrier homeostasis.
Additional Links: PMID-42871880
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@article {pmid42871880,
year = {2026},
author = {Ibuki, T and Shigeyama, T and Tsukimoto, M and Nagara, Y and Kawai, M and Yamazaki, R},
title = {Bifidobacterium adolescentis protects the intestinal barrier from obesity-related inflammatory stimuli in association with the nuclear translocation of nuclear factor kappa B.},
journal = {Bioscience of microbiota, food and health},
volume = {45},
number = {4},
pages = {264-271},
pmid = {42871880},
issn = {2186-6953},
abstract = {The intestinal barrier plays a crucial role in host metabolic and immune homeostasis; however, its integrity can be disrupted by factors such as lipopolysaccharides, inflammatory cytokines, and oxidative stress. Although Bifidobacterium species are considered beneficial members of the gut microbiota, their strain-specific effects on epithelial barrier integrity and the underlying mechanisms remain incompletely understood. We investigated the protective effects of four heat-killed strains of bifidobacteria, B. pseudocatenulatum YIT 11057, B. adolescentis YIT 13021, B. bifidum YIT 10347, and B. breve YIT 4014, on intestinal barrier function using T84 monolayers, a widely used in vitro model of the intestinal epithelium that retains many colon-like properties. Among the tested strains, only B. adolescentis YIT 13021 (YIT 13021) consistently protected against barrier disruption induced by lipopolysaccharide (LPS), oxidative stress, and inflammatory cytokines, highlighting species-enriched but strain-dependent functional properties within B. adolescentis. YIT 13021 preserved tight junction integrity in association with preserved localization of zonula occludens-1 and attenuated stimulus-induced nuclear localization of nuclear factor-kappa B. Furthermore, live YIT 13021 exerted superior barrier-protective effects than its heat-killed counterpart, and its protective efficacy was further increased when cultured in the presence of starch, suggesting that metabolic activity and substrate availability influence functional outcomes. These findings demonstrate functional heterogeneity among Bifidobacterium strains, provide insights into potential mechanisms underlying microbiota-mediated modulation of epithelial integrity, and identify B. adolescentis YIT 13021 as a promising candidate for supporting intestinal barrier homeostasis.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Microbiome research in liver transplantation.
Hepatobiliary surgery and nutrition, 15(5):138.
Additional Links: PMID-42871940
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@article {pmid42871940,
year = {2026},
author = {Wirth, U and Schardey, J and Schulz, C and Andrassy, J},
title = {Microbiome research in liver transplantation.},
journal = {Hepatobiliary surgery and nutrition},
volume = {15},
number = {5},
pages = {138},
pmid = {42871940},
issn = {2304-3881},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Gut Microbial Metabolism Inactivates Trifluridine and Drives Loss of Anticancer Efficacy.
ACS pharmacology & translational science, 9(10):2842-2852.
Human-associated gut bacteria harbor diverse genetic and metabolic potential. Orally administered therapeutic drugs can interact with these bacteria in the gastrointestinal tract. Recent evidence shows modifications of multiple drugs via gut bacteria, influencing therapeutic outcomes. Trifluridine, a fluoropyrimidine drug used in colorectal cancer treatment, is susceptible to microbial metabolism and premature inactivation, yet the breadth and functional consequences of this metabolism remain incompletely defined. In this work, we further explore the potential of additional gut bacterial strains that can metabolize trifluridine and characterize how this microbial metabolism impacts cancer cell responses. Sequence-based similarity search revealed trifluridine metabolizing homologues in multiple Enterobacteriaceae species including Klebsiella oxytoca. LCMS analysis confirms that gut isolates, Escherichia coli NS-12 and K. oxytoca S-22, efficiently degraded TF within 2 h. Tipiracil, the clinical inhibitor of host thymidine phosphorylase, only partially blocked microbial TF metabolism dependent on oxygen availability and the bacterial strain. Functionally, the treatment efficacy of TF was reduced, and it lost its cytotoxic potential in cancer when pre-exposed to E. coli and K. oxytoca. Also, microbially degraded TF could not induce the oncogenic p53-dependent pathways in cancer cells compared to the intact TF drug. These findings demonstrate that microbial TF metabolism is widespread across the gut bacteria and can directly undermine its anticancer efficacy and highlight the need to consider gut microbial composition when optimizing TF-based cancer therapies.
Additional Links: PMID-42872031
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@article {pmid42872031,
year = {2026},
author = {Ahmad, S and Igbalaye, JO and Perez, V and Wenning, E and Gauthier, S and Ridlon, J and Irudayaraj, J},
title = {Gut Microbial Metabolism Inactivates Trifluridine and Drives Loss of Anticancer Efficacy.},
journal = {ACS pharmacology & translational science},
volume = {9},
number = {10},
pages = {2842-2852},
pmid = {42872031},
issn = {2575-9108},
abstract = {Human-associated gut bacteria harbor diverse genetic and metabolic potential. Orally administered therapeutic drugs can interact with these bacteria in the gastrointestinal tract. Recent evidence shows modifications of multiple drugs via gut bacteria, influencing therapeutic outcomes. Trifluridine, a fluoropyrimidine drug used in colorectal cancer treatment, is susceptible to microbial metabolism and premature inactivation, yet the breadth and functional consequences of this metabolism remain incompletely defined. In this work, we further explore the potential of additional gut bacterial strains that can metabolize trifluridine and characterize how this microbial metabolism impacts cancer cell responses. Sequence-based similarity search revealed trifluridine metabolizing homologues in multiple Enterobacteriaceae species including Klebsiella oxytoca. LCMS analysis confirms that gut isolates, Escherichia coli NS-12 and K. oxytoca S-22, efficiently degraded TF within 2 h. Tipiracil, the clinical inhibitor of host thymidine phosphorylase, only partially blocked microbial TF metabolism dependent on oxygen availability and the bacterial strain. Functionally, the treatment efficacy of TF was reduced, and it lost its cytotoxic potential in cancer when pre-exposed to E. coli and K. oxytoca. Also, microbially degraded TF could not induce the oncogenic p53-dependent pathways in cancer cells compared to the intact TF drug. These findings demonstrate that microbial TF metabolism is widespread across the gut bacteria and can directly undermine its anticancer efficacy and highlight the need to consider gut microbial composition when optimizing TF-based cancer therapies.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Graphene oxide remodels the rhizosphere microbiome and induces metabolic reprogramming of flavor-related compounds in tea leaves.
Food chemistry. Molecular sciences, 13:100461.
The flavor quality of Camellia sinensis is strongly influenced by their secondary metabolites and associated microbial communities. Graphene oxide (GO) is a carbon-based nanomaterial with unique physicochemical properties. While its potential to modulate plant physiology has been recognized, its specific effects on tea plant metabolism and associated rhizosphere microbiomes remain largely unexplored. To address this gap, a pot experiment was established to evaluate the impact of varying GO concentrations (0, 25, 50, 100 mg/L) on both the foliar metabolic profiles of tea plants and the structural composition of their rhizosphere microbial communities. Untargeted metabolomics and 16S rRNA sequencing were integrated to systematically analyze changes in metabolite accumulation and microbial composition under GO treatments. The results revealed that GO treatments significantly altered the metabolite composition in tea leaves, with key flavor-related compounds such as flavonoids, phenolic acids, amino acids, and their derivatives showing concentration-dependent accumulation. Furthermore, GO application notably increased the richness and diversity of the rhizosphere microbial community and shifted its structure. LEfSe analysis identified distinct microbial biomarkers across GO concentrations, including beneficial taxa (Micrococcaceae, Rhizobiales) in the low-dose group and stress-tolerant taxa (Rhodanobacter, γ-proteobacteria) in the high-dose group. GO treatments also enhanced microbial metabolic pathways associated with secondary metabolite biosynthesis, antibiotic production, and nutrient transport. Co-occurrence network analysis further revealed a reorganization of microbial interactions in the rhizosphere under GO treatment. This study uncovers novel mechanistic insights into the regulatory effects of graphene oxide on the metabolic pathways of tea plants and the compositional dynamics of their rhizosphere microbiomes.
Additional Links: PMID-42872044
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@article {pmid42872044,
year = {2026},
author = {Yang, J and An, Q and Du, S and Wu, F and Niu, J and Zhou, G},
title = {Graphene oxide remodels the rhizosphere microbiome and induces metabolic reprogramming of flavor-related compounds in tea leaves.},
journal = {Food chemistry. Molecular sciences},
volume = {13},
number = {},
pages = {100461},
pmid = {42872044},
issn = {2666-5662},
abstract = {The flavor quality of Camellia sinensis is strongly influenced by their secondary metabolites and associated microbial communities. Graphene oxide (GO) is a carbon-based nanomaterial with unique physicochemical properties. While its potential to modulate plant physiology has been recognized, its specific effects on tea plant metabolism and associated rhizosphere microbiomes remain largely unexplored. To address this gap, a pot experiment was established to evaluate the impact of varying GO concentrations (0, 25, 50, 100 mg/L) on both the foliar metabolic profiles of tea plants and the structural composition of their rhizosphere microbial communities. Untargeted metabolomics and 16S rRNA sequencing were integrated to systematically analyze changes in metabolite accumulation and microbial composition under GO treatments. The results revealed that GO treatments significantly altered the metabolite composition in tea leaves, with key flavor-related compounds such as flavonoids, phenolic acids, amino acids, and their derivatives showing concentration-dependent accumulation. Furthermore, GO application notably increased the richness and diversity of the rhizosphere microbial community and shifted its structure. LEfSe analysis identified distinct microbial biomarkers across GO concentrations, including beneficial taxa (Micrococcaceae, Rhizobiales) in the low-dose group and stress-tolerant taxa (Rhodanobacter, γ-proteobacteria) in the high-dose group. GO treatments also enhanced microbial metabolic pathways associated with secondary metabolite biosynthesis, antibiotic production, and nutrient transport. Co-occurrence network analysis further revealed a reorganization of microbial interactions in the rhizosphere under GO treatment. This study uncovers novel mechanistic insights into the regulatory effects of graphene oxide on the metabolic pathways of tea plants and the compositional dynamics of their rhizosphere microbiomes.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
From humans to the wild: revisiting assumptions in gut microbiome analysis.
ISME communications, 6(1):ycag168.
Additional Links: PMID-42872065
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@article {pmid42872065,
year = {2026},
author = {Alberdi, A and Aizpurua, O},
title = {From humans to the wild: revisiting assumptions in gut microbiome analysis.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag168},
pmid = {42872065},
issn = {2730-6151},
}
RevDate: 2026-10-14
The relationship between gut microbiota-friendly diet and the prevalence and severity of asthma in children.
Journal of pediatric gastroenterology and nutrition [Epub ahead of print].
OBJECTIVES: Dietary factors may impact asthma indirectly by modulating the composition and activity of the gut microbiota. This study aimed to explore the potential relationship between gut microbiota-friendly diet and both the prevalence and severity of asthma in children.
METHODS: We selected a total of 2256 children from the 2021-2023 National Health and Nutrition Examination Survey. The gut microbiota-friendly diet was assessed using the Diet-Gut Microbiome Index (DI-GM), which incorporates 14 specific food constituents. To calculate the DI-GM, two non-consecutive 24-h dietary recalls data were used, from which the relevant food constituents were derived. A higher DI-GM score indicates greater alignment with a gut microbiota-friendly diet.
RESULTS: Among the 2256 U.S. children, the weighted prevalence of asthma is 13.36%. In fully adjusted models, DI-GM was not significantly associated with asthma prevalence overall or within any subgroups. However, higher DI-GM (T2) was significantly associated with a lower risk of the mild asthma phenotype in the 5-16 age group. In contrast, no significant associations were observed between DI-GM and asthma severity in the other age groups. Subgroup analysis showed a higher DI-GM score was significantly correlated with a lower risk for asthma in subgroups stratified by obesity status.
CONCLUSIONS: Higher DI-GM scores were significantly inversely associated with asthma severity risk in children aged 5-16 years and in obese individuals. These cross-sectional findings support the need for longitudinal studies to determine whether dietary modulation may affect asthma severity via microbiota-dependent mechanisms.
Additional Links: PMID-42872540
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@article {pmid42872540,
year = {2026},
author = {Tan, LJ and Tang, X and Shan, Y and Ren, Y and Sun, T and Zhou, Y and Fu, J and Zhang, Y and Cui, Y},
title = {The relationship between gut microbiota-friendly diet and the prevalence and severity of asthma in children.},
journal = {Journal of pediatric gastroenterology and nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1002/jpn3.70605},
pmid = {42872540},
issn = {1536-4801},
support = {25PJA120//Shanghai Municipal Talent Work Bureau/ ; },
abstract = {OBJECTIVES: Dietary factors may impact asthma indirectly by modulating the composition and activity of the gut microbiota. This study aimed to explore the potential relationship between gut microbiota-friendly diet and both the prevalence and severity of asthma in children.
METHODS: We selected a total of 2256 children from the 2021-2023 National Health and Nutrition Examination Survey. The gut microbiota-friendly diet was assessed using the Diet-Gut Microbiome Index (DI-GM), which incorporates 14 specific food constituents. To calculate the DI-GM, two non-consecutive 24-h dietary recalls data were used, from which the relevant food constituents were derived. A higher DI-GM score indicates greater alignment with a gut microbiota-friendly diet.
RESULTS: Among the 2256 U.S. children, the weighted prevalence of asthma is 13.36%. In fully adjusted models, DI-GM was not significantly associated with asthma prevalence overall or within any subgroups. However, higher DI-GM (T2) was significantly associated with a lower risk of the mild asthma phenotype in the 5-16 age group. In contrast, no significant associations were observed between DI-GM and asthma severity in the other age groups. Subgroup analysis showed a higher DI-GM score was significantly correlated with a lower risk for asthma in subgroups stratified by obesity status.
CONCLUSIONS: Higher DI-GM scores were significantly inversely associated with asthma severity risk in children aged 5-16 years and in obese individuals. These cross-sectional findings support the need for longitudinal studies to determine whether dietary modulation may affect asthma severity via microbiota-dependent mechanisms.},
}
RevDate: 2026-10-14
Interindividual variability in food-derived peptide bioavailability and function: peptide metabotypes and responder phenotypes.
Food & function [Epub ahead of print].
Food-derived bioactive peptides are commonly evaluated as though a standardised protein, hydrolysate, or peptide-containing food produces comparable biological exposure across consumers. Emerging human evidence challenges this assumption because food structure, gastrointestinal physiology, intestinal peptidases, epithelial transport, microbial metabolism, age, metabolic status, medication use, and habitual diet can alter the peptides and metabolites generated after ingestion. This critical review examines interindividual variability as a determinant of food-peptide efficacy and develops a precision-nutrition framework linking product composition to digestive peptide profiles and physiological response. We synthesise evidence from human digestion studies, jejunal peptidomics, transport and metabolism models, microbiome research, peptide pharmacokinetics, and clinical interventions involving antihypertensive lactotripeptides, dipeptidyl peptidase-IV (DPP-IV)-inhibitory hydrolysates, and collagen peptides. We propose two testable concepts: the peptide metabotype, defined as an individual's reproducible time-resolved profile of food-derived peptides and metabolites after a standardised challenge, and the peptide responder phenotype, defined as the corresponding exposure-response pattern. We outline a core design comprising a characterised product, an appropriate comparator, repeated measurements, a targeted exposure panel and a prespecified physiological endpoint, with additional host profiling guided by the mechanism. This perspective shifts peptide research from universal bioactivity claims toward identifying when, where, and in whom peptide-containing foods are most likely to produce meaningful physiological effects and offers a testable approach to improving reproducibility and evaluating translational relevance.
Additional Links: PMID-42872573
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@article {pmid42872573,
year = {2026},
author = {Suttikhana, I and Ashaolu, TJ},
title = {Interindividual variability in food-derived peptide bioavailability and function: peptide metabotypes and responder phenotypes.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d6fo03963d},
pmid = {42872573},
issn = {2042-650X},
abstract = {Food-derived bioactive peptides are commonly evaluated as though a standardised protein, hydrolysate, or peptide-containing food produces comparable biological exposure across consumers. Emerging human evidence challenges this assumption because food structure, gastrointestinal physiology, intestinal peptidases, epithelial transport, microbial metabolism, age, metabolic status, medication use, and habitual diet can alter the peptides and metabolites generated after ingestion. This critical review examines interindividual variability as a determinant of food-peptide efficacy and develops a precision-nutrition framework linking product composition to digestive peptide profiles and physiological response. We synthesise evidence from human digestion studies, jejunal peptidomics, transport and metabolism models, microbiome research, peptide pharmacokinetics, and clinical interventions involving antihypertensive lactotripeptides, dipeptidyl peptidase-IV (DPP-IV)-inhibitory hydrolysates, and collagen peptides. We propose two testable concepts: the peptide metabotype, defined as an individual's reproducible time-resolved profile of food-derived peptides and metabolites after a standardised challenge, and the peptide responder phenotype, defined as the corresponding exposure-response pattern. We outline a core design comprising a characterised product, an appropriate comparator, repeated measurements, a targeted exposure panel and a prespecified physiological endpoint, with additional host profiling guided by the mechanism. This perspective shifts peptide research from universal bioactivity claims toward identifying when, where, and in whom peptide-containing foods are most likely to produce meaningful physiological effects and offers a testable approach to improving reproducibility and evaluating translational relevance.},
}
RevDate: 2026-10-14
CmpDate: 2026-10-14
Alginate and Glycine Betaine Enhance Biofilm Formation in Psychrophilic Activated Sludge Systems.
Environmental microbiology, 28(10):e70428.
Activated sludge systems at sub-optimal temperatures (8°C-16°C) suffer from inhibited biofilm development, diminished extracellular polymeric substances (EPS) secretion and reduced carbon/nitrogen removal. To counteract this, we investigated the synergistic effect of alginic acid (AA, a structural polysaccharide) and betaine (BET, a compatible solute) in sequencing-batch reactors (SBRs) at 8°C-16°C The combined AA + BET amendment elicited a rapid, pronounced response, doubling attached biofilm biomass compared to the control, a significantly greater enhancement than with single amendments. This suggests a synergistic effect in which BET mitigates osmotic stress, thereby improving microbial capacity to utilise AA for structural development. Microbial community analysis revealed that the combined addition of AA and BET reshaped the microbial community, enabling the consortium to acquire a high capacity for EPS production, which conferred cold tolerance, while simultaneously suppressing the growth of filamentous Acidovorax. Principal component analysis (PCA) segregated the AA + BET community, and increased diversity indices indicated greater functional richness. The control group contained 11.43% of microbial taxa that were distinct from those in the experimental group; these taxa, likely lacking targeted regulation, exhibited a lower contribution to the activated sludge process (ASP) system. This dual-stress-alleviation strategy effectively orchestrates a resilient, EPS-rich biofilm with a psychrotolerant core microbiome, offering a practical approach to maintaining robust activated-sludge performance during cold weather However, further pilot-scale validation and techno-economic assessment are needed before practical implementation in full-scale wastewater treatment systems.
Additional Links: PMID-42872712
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@article {pmid42872712,
year = {2026},
author = {Ullah, N and Shao, S and Zhou, C and Li, W and Wang, C},
title = {Alginate and Glycine Betaine Enhance Biofilm Formation in Psychrophilic Activated Sludge Systems.},
journal = {Environmental microbiology},
volume = {28},
number = {10},
pages = {e70428},
doi = {10.1111/1462-2920.70428},
pmid = {42872712},
issn = {1462-2920},
support = {2025ZD1202400//National Science and Technology Major Project for Jing-Jin-Ji Regional Integrated Environmental Improvement/ ; 2025ZD1202401//National Science and Technology Major Project for Jing-Jin-Ji Regional Integrated Environmental Improvement/ ; 2025ZD1202404//National Science and Technology Major Project for Jing-Jin-Ji Regional Integrated Environmental Improvement/ ; 20252BCF320025//Key R&D Program of Jiangxi Province, China/ ; 52170114//National Natural Science Foundation of China/ ; 52670144//National Natural Science Foundation of China/ ; 21JCJQJC00080//Science and Technology Project of Tianjin, China/ ; B2021208033//Key Project of Natural Science Foundation of Hebei Province, China/ ; 20224BAB213053//Natural Science Foundation of Jiangxi Province, China/ ; },
mesh = {*Betaine/pharmacology/metabolism ; *Biofilms/growth & development/drug effects ; *Sewage/microbiology ; *Alginates/pharmacology/metabolism ; Bioreactors/microbiology ; Glucuronic Acid/pharmacology ; Hexuronic Acids/pharmacology ; Cold Temperature ; Bacteria/classification/genetics/drug effects/metabolism/growth & development ; Extracellular Polymeric Substance Matrix/metabolism ; Microbiota/drug effects ; },
abstract = {Activated sludge systems at sub-optimal temperatures (8°C-16°C) suffer from inhibited biofilm development, diminished extracellular polymeric substances (EPS) secretion and reduced carbon/nitrogen removal. To counteract this, we investigated the synergistic effect of alginic acid (AA, a structural polysaccharide) and betaine (BET, a compatible solute) in sequencing-batch reactors (SBRs) at 8°C-16°C The combined AA + BET amendment elicited a rapid, pronounced response, doubling attached biofilm biomass compared to the control, a significantly greater enhancement than with single amendments. This suggests a synergistic effect in which BET mitigates osmotic stress, thereby improving microbial capacity to utilise AA for structural development. Microbial community analysis revealed that the combined addition of AA and BET reshaped the microbial community, enabling the consortium to acquire a high capacity for EPS production, which conferred cold tolerance, while simultaneously suppressing the growth of filamentous Acidovorax. Principal component analysis (PCA) segregated the AA + BET community, and increased diversity indices indicated greater functional richness. The control group contained 11.43% of microbial taxa that were distinct from those in the experimental group; these taxa, likely lacking targeted regulation, exhibited a lower contribution to the activated sludge process (ASP) system. This dual-stress-alleviation strategy effectively orchestrates a resilient, EPS-rich biofilm with a psychrotolerant core microbiome, offering a practical approach to maintaining robust activated-sludge performance during cold weather However, further pilot-scale validation and techno-economic assessment are needed before practical implementation in full-scale wastewater treatment systems.},
}
MeSH Terms:
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*Betaine/pharmacology/metabolism
*Biofilms/growth & development/drug effects
*Sewage/microbiology
*Alginates/pharmacology/metabolism
Bioreactors/microbiology
Glucuronic Acid/pharmacology
Hexuronic Acids/pharmacology
Cold Temperature
Bacteria/classification/genetics/drug effects/metabolism/growth & development
Extracellular Polymeric Substance Matrix/metabolism
Microbiota/drug effects
RevDate: 2026-10-14
mums2: an R package for database-dependent and -independent analysis of untargeted metabolomics data.
Microbiology resource announcements [Epub ahead of print].
mums2 is an open-source R package that enables users to analyze data from untargeted metabolomics analyses. mums2 provides features that parallel existing tools for analyzing 16S rRNA gene sequence data, including data curation, annotation, clustering of features into operational metabolomic units (OMUs), and analyses based on ecological metrics.
Additional Links: PMID-42872836
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@article {pmid42872836,
year = {2026},
author = {Johnson, G and Mason, AR and Krampen, JM and Nguyen, JNT and Balunas, MJ and Schloss, PD},
title = {mums2: an R package for database-dependent and -independent analysis of untargeted metabolomics data.},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0078026},
doi = {10.1128/mra.00780-26},
pmid = {42872836},
issn = {2576-098X},
abstract = {mums2 is an open-source R package that enables users to analyze data from untargeted metabolomics analyses. mums2 provides features that parallel existing tools for analyzing 16S rRNA gene sequence data, including data curation, annotation, clustering of features into operational metabolomic units (OMUs), and analyses based on ecological metrics.},
}
RevDate: 2026-10-14
Environmental gradients shape the hydrocarbon-degrading microbiome in two mid-Atlantic bays.
mSystems [Epub ahead of print].
UNLABELLED: Hydrocarbons are recalcitrant organic matter that is released into the environment via natural and anthropogenic activities. We hypothesized that abiotic and biotic factors, including salinity, temperature, seasonality, microbial interactions, and functional redundancy, influence the abundance and activity of potential hydrocarbon degraders in the Delaware and Chesapeake Bays. We identified key genes in hydrocarbon degradation pathways in metagenomes, metatranscriptomes, and metagenome-assembled genomes (MAGs) from these estuaries. In the surface waters of both estuaries, aerobic aromatic and alkane degradation pathways predominated, with higher gene abundances observed in low-salinity spring and summer samples. Salinity significantly structured both hydrocarbon-degrading MAG abundances, alongside temperature, nitrate, and silicate concentrations, and hydrocarbon degradation gene expression, which additionally varied seasonally, with the highest relative expression of aromatic degradation genes in low-salinity samples. Catechol degradation pathways exhibited high functional redundancy, whereas the naphthalene degradation pathway showed restricted distribution. Co-expression analysis revealed that Burkholderiales displayed condition-dependent metabolic coupling, while Pseudomonadales integrated hydrocarbon degradation with fermentation and central metabolism, demonstrating complementary strategies that support multi-scale ecosystem resilience. Together, these results support our hypothesis that environmental gradients and taxon-specific metabolic strategies jointly structure the abundance and in situ activity of hydrocarbon degraders, with implications for predicting ecosystem responses to hydrocarbon inputs under changing conditions.
IMPORTANCE: Coastal estuaries are among the most contaminated aquatic environments on Earth, receiving continuous hydrocarbon inputs from industrial activity, urban runoff, and natural sources. Microorganisms are the primary agents of hydrocarbon breakdown in these systems, yet predicting when and where this capacity is active and how resilient it is to environmental change remains a major challenge. Using paired genomic and transcriptomic data from microbial genomes across two major mid-Atlantic estuaries, we show that hydrocarbon degradation capacity is not uniformly distributed but is instead shaped by salinity, nutrients, and seasonality in pathway-specific ways. Critically, dominant degrader taxa employ fundamentally different metabolic strategies to sustain this function across fluctuating conditions, providing a form of community-level insurance against environmental disturbance. These findings advance our ability to predict microbial hydrocarbon degradation in coastal systems and inform nature-based approaches to bioremediation under increasing climate and anthropogenic pressures.
Additional Links: PMID-42872861
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@article {pmid42872861,
year = {2026},
author = {Patabandige, DLJ and John, J and Ortiz, M and Campbell, BJ},
title = {Environmental gradients shape the hydrocarbon-degrading microbiome in two mid-Atlantic bays.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0086626},
doi = {10.1128/msystems.00866-26},
pmid = {42872861},
issn = {2379-5077},
abstract = {UNLABELLED: Hydrocarbons are recalcitrant organic matter that is released into the environment via natural and anthropogenic activities. We hypothesized that abiotic and biotic factors, including salinity, temperature, seasonality, microbial interactions, and functional redundancy, influence the abundance and activity of potential hydrocarbon degraders in the Delaware and Chesapeake Bays. We identified key genes in hydrocarbon degradation pathways in metagenomes, metatranscriptomes, and metagenome-assembled genomes (MAGs) from these estuaries. In the surface waters of both estuaries, aerobic aromatic and alkane degradation pathways predominated, with higher gene abundances observed in low-salinity spring and summer samples. Salinity significantly structured both hydrocarbon-degrading MAG abundances, alongside temperature, nitrate, and silicate concentrations, and hydrocarbon degradation gene expression, which additionally varied seasonally, with the highest relative expression of aromatic degradation genes in low-salinity samples. Catechol degradation pathways exhibited high functional redundancy, whereas the naphthalene degradation pathway showed restricted distribution. Co-expression analysis revealed that Burkholderiales displayed condition-dependent metabolic coupling, while Pseudomonadales integrated hydrocarbon degradation with fermentation and central metabolism, demonstrating complementary strategies that support multi-scale ecosystem resilience. Together, these results support our hypothesis that environmental gradients and taxon-specific metabolic strategies jointly structure the abundance and in situ activity of hydrocarbon degraders, with implications for predicting ecosystem responses to hydrocarbon inputs under changing conditions.
IMPORTANCE: Coastal estuaries are among the most contaminated aquatic environments on Earth, receiving continuous hydrocarbon inputs from industrial activity, urban runoff, and natural sources. Microorganisms are the primary agents of hydrocarbon breakdown in these systems, yet predicting when and where this capacity is active and how resilient it is to environmental change remains a major challenge. Using paired genomic and transcriptomic data from microbial genomes across two major mid-Atlantic estuaries, we show that hydrocarbon degradation capacity is not uniformly distributed but is instead shaped by salinity, nutrients, and seasonality in pathway-specific ways. Critically, dominant degrader taxa employ fundamentally different metabolic strategies to sustain this function across fluctuating conditions, providing a form of community-level insurance against environmental disturbance. These findings advance our ability to predict microbial hydrocarbon degradation in coastal systems and inform nature-based approaches to bioremediation under increasing climate and anthropogenic pressures.},
}
RevDate: 2026-10-12
A global atlas of the gut virome reveals subtype-specific and functional alterations in irritable bowel syndrome.
mSystems [Epub ahead of print].
The gut virome is a critical component of the microbiome-gut-brain axis; however, its role in irritable bowel syndrome (IBS) remains poorly understood due to limited sample sizes and geographic bias. We aimed to construct a comprehensive global atlas of the IBS gut virome to elucidate its composition, functional potential, and clinical relevance across diverse populations and IBS subtypes. We integrated multi-cohort data comprising 1,104 samples (790 IBS patients and 314 healthy controls) from 11 cohorts across 10 geographic regions. A standardized bioinformatic pipeline was employed to perform viral mining from metagenomic and virus-like particle-enriched metaviromic data. The IBS virome exhibited significant taxonomic alterations, with specific viral signatures distinguishing IBS-D, IBS-C, and IBS-M subtypes. Geographic region was identified as a significant factor influencing the viral community structure. Functionally, the IBS virome was enriched in auxiliary metabolic genes involved in carbon metabolism and neurotransmitter precursor synthesis (histidine and tryptophan metabolism), as well as a distinct profile of virulence factors and antibiotic resistance genes. Furthermore, in a specific cohort, certain viral taxa were significantly correlated with the severity of anxiety and depression. Machine learning models based on viral signatures achieved robust performance for IBS subtyping (area under the curve = 0.92). This study establishes a global baseline for the IBS gut virome, demonstrating that viral communities are dynamically shaped by geography and disease subtypes while encoding gene repertoires with the potential to influence host physiology, thereby providing a foundational resource for precision medicine.IMPORTANCEResearch on the human gut microbiome in IBS has focused primarily on bacteria, leaving the viral component as a vast and poorly understood reservoir. By profiling over 1,000 human samples globally, this study characterizes the taxonomic and functional features of the IBS gut virome. We demonstrate that these viral communities vary across geographic populations and IBS subtypes and are enriched in specific auxiliary metabolic genes, virulence factors, and antibiotic resistance genes. In addition, certain viral profiles show significant correlations with patient psychological symptoms such as anxiety and depression. This study also evaluates the potential of virome-based diagnostic biomarkers. Consequently, our findings provide a valuable reference for future in-depth research into the specific roles and mechanistic contributions of the gut virome in the pathogenesis of IBS.
Additional Links: PMID-42861963
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PubMed:
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@article {pmid42861963,
year = {2026},
author = {Xie, P and Luo, M and Fan, J and Xiong, L},
title = {A global atlas of the gut virome reveals subtype-specific and functional alterations in irritable bowel syndrome.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0090126},
doi = {10.1128/msystems.00901-26},
pmid = {42861963},
issn = {2379-5077},
abstract = {The gut virome is a critical component of the microbiome-gut-brain axis; however, its role in irritable bowel syndrome (IBS) remains poorly understood due to limited sample sizes and geographic bias. We aimed to construct a comprehensive global atlas of the IBS gut virome to elucidate its composition, functional potential, and clinical relevance across diverse populations and IBS subtypes. We integrated multi-cohort data comprising 1,104 samples (790 IBS patients and 314 healthy controls) from 11 cohorts across 10 geographic regions. A standardized bioinformatic pipeline was employed to perform viral mining from metagenomic and virus-like particle-enriched metaviromic data. The IBS virome exhibited significant taxonomic alterations, with specific viral signatures distinguishing IBS-D, IBS-C, and IBS-M subtypes. Geographic region was identified as a significant factor influencing the viral community structure. Functionally, the IBS virome was enriched in auxiliary metabolic genes involved in carbon metabolism and neurotransmitter precursor synthesis (histidine and tryptophan metabolism), as well as a distinct profile of virulence factors and antibiotic resistance genes. Furthermore, in a specific cohort, certain viral taxa were significantly correlated with the severity of anxiety and depression. Machine learning models based on viral signatures achieved robust performance for IBS subtyping (area under the curve = 0.92). This study establishes a global baseline for the IBS gut virome, demonstrating that viral communities are dynamically shaped by geography and disease subtypes while encoding gene repertoires with the potential to influence host physiology, thereby providing a foundational resource for precision medicine.IMPORTANCEResearch on the human gut microbiome in IBS has focused primarily on bacteria, leaving the viral component as a vast and poorly understood reservoir. By profiling over 1,000 human samples globally, this study characterizes the taxonomic and functional features of the IBS gut virome. We demonstrate that these viral communities vary across geographic populations and IBS subtypes and are enriched in specific auxiliary metabolic genes, virulence factors, and antibiotic resistance genes. In addition, certain viral profiles show significant correlations with patient psychological symptoms such as anxiety and depression. This study also evaluates the potential of virome-based diagnostic biomarkers. Consequently, our findings provide a valuable reference for future in-depth research into the specific roles and mechanistic contributions of the gut virome in the pathogenesis of IBS.},
}
RevDate: 2026-10-12
Association of quantitative sputum Candida load with respiratory dysbiosis and airway inflammation in suspected invasive pulmonary candidiasis.
mSystems [Epub ahead of print].
UNLABELLED: The clinical significance of Candida species isolation from sputum remains ambiguous due to the colonization-infection dilemma. Integrating quantitative culture with microbiome profiling may clarify its role, yet systematic evidence is scarce. In this exploratory study (June 2023-June 2026), we enrolled 140 hospitalized patients suspected of invasive pulmonary candidiasis (IPC) and stratified them into possible IPC (n = 36), probable IPC (n = 71), and negative control (n = 33) groups based on clinical criteria. All underwent quantitative fungal culture of sputum and metagenomic next-generation sequencing (mNGS). Patients were stratified by sputum Candida species load into low (<10[5] CFU/mL), high (≥10[5] CFU/mL), and negative control (0 CFU/mL) groups. We investigated associations between Candida species burden, respiratory microbiota, local inflammation (IL-8), and clinical outcomes. Higher Candida species load was significantly associated with prolonged hospitalization, elevated sputum IL-8, an increased microbial dysbiosis index, and depletion of key commensals (e.g., Neisseria, Prevotella, Rothia, Streptococcus, and Veillonella). Counterintuitively, it correlated negatively with several classic bacterial pathogens (such as Acinetobacter baumannii, Escherichia coli, Klebsiella pneumoniae, Mycobacterium tuberculosis, and Pseudomonas aeruginosa). A random forest model identified a nine-species microbiome signature that effectively discriminated probable from possible IPC (AUC, 0.877; 95% CI, 0.662-0.944). In patients with suspected IPC, higher sputum Candida species load is associated with exacerbated respiratory dysbiosis and airway inflammation. Quantitative Candida species assessment combined with microbiome signatures may serve as a complementary tool for stratifying disease severity and ecological disruption, meriting further validation in larger, multicenter cohorts.
IMPORTANCE: Respiratory specimens dominate clinical fungal cultures, yet interpreting the role of Candida spp. in sputum remains a diagnostic dilemma. Here, by integrating quantitative culture with metagenomic sequencing, we show that a high sputum Candida species load is a marker of profound ecological disruption. High Candida species burden was associated with significant depletion of key commensals, an elevated dysbiosis index, and heightened local inflammation. Counterintuitively, it correlated negatively with several classic bacterial pathogens, revealing a distinct dysbiotic signature. Moreover, a microbiome-based model accurately discriminated patients with probable invasive pulmonary candidiasis. Our findings suggest that quantitative sputum Candida species load, interpreted within the context of the microbial community, may be a practical biomarker for identifying patients with significant respiratory dysbiosis and inflammation, offering a path toward more refined, ecology-informed therapeutic strategies.
Additional Links: PMID-42861989
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PubMed:
Citation:
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@article {pmid42861989,
year = {2026},
author = {Wang, G and Zhang, N and Peng, Y and Wen, X and Chen, X and Zou, M and Gao, S and Min, C and Min, X and Huang, J},
title = {Association of quantitative sputum Candida load with respiratory dysbiosis and airway inflammation in suspected invasive pulmonary candidiasis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0083726},
doi = {10.1128/msystems.00837-26},
pmid = {42861989},
issn = {2379-5077},
abstract = {UNLABELLED: The clinical significance of Candida species isolation from sputum remains ambiguous due to the colonization-infection dilemma. Integrating quantitative culture with microbiome profiling may clarify its role, yet systematic evidence is scarce. In this exploratory study (June 2023-June 2026), we enrolled 140 hospitalized patients suspected of invasive pulmonary candidiasis (IPC) and stratified them into possible IPC (n = 36), probable IPC (n = 71), and negative control (n = 33) groups based on clinical criteria. All underwent quantitative fungal culture of sputum and metagenomic next-generation sequencing (mNGS). Patients were stratified by sputum Candida species load into low (<10[5] CFU/mL), high (≥10[5] CFU/mL), and negative control (0 CFU/mL) groups. We investigated associations between Candida species burden, respiratory microbiota, local inflammation (IL-8), and clinical outcomes. Higher Candida species load was significantly associated with prolonged hospitalization, elevated sputum IL-8, an increased microbial dysbiosis index, and depletion of key commensals (e.g., Neisseria, Prevotella, Rothia, Streptococcus, and Veillonella). Counterintuitively, it correlated negatively with several classic bacterial pathogens (such as Acinetobacter baumannii, Escherichia coli, Klebsiella pneumoniae, Mycobacterium tuberculosis, and Pseudomonas aeruginosa). A random forest model identified a nine-species microbiome signature that effectively discriminated probable from possible IPC (AUC, 0.877; 95% CI, 0.662-0.944). In patients with suspected IPC, higher sputum Candida species load is associated with exacerbated respiratory dysbiosis and airway inflammation. Quantitative Candida species assessment combined with microbiome signatures may serve as a complementary tool for stratifying disease severity and ecological disruption, meriting further validation in larger, multicenter cohorts.
IMPORTANCE: Respiratory specimens dominate clinical fungal cultures, yet interpreting the role of Candida spp. in sputum remains a diagnostic dilemma. Here, by integrating quantitative culture with metagenomic sequencing, we show that a high sputum Candida species load is a marker of profound ecological disruption. High Candida species burden was associated with significant depletion of key commensals, an elevated dysbiosis index, and heightened local inflammation. Counterintuitively, it correlated negatively with several classic bacterial pathogens, revealing a distinct dysbiotic signature. Moreover, a microbiome-based model accurately discriminated patients with probable invasive pulmonary candidiasis. Our findings suggest that quantitative sputum Candida species load, interpreted within the context of the microbial community, may be a practical biomarker for identifying patients with significant respiratory dysbiosis and inflammation, offering a path toward more refined, ecology-informed therapeutic strategies.},
}
RevDate: 2026-10-12
Comparative transcriptional network analysis reveals ecological specialization in infant-associated species of Bifidobacterium.
mSystems [Epub ahead of print].
UNLABELLED: Bifidobacterium species are important microorganisms in the infant gut microbiota displaying substantial genomic diversity, yet how this variability is reflected in transcriptional regulatory architecture remains an open question. Here, we integrated pangenome analysis with transcription factor binding site inference and network-based approaches to compare regulatory architectures across Bifidobacterium longum subsp. infantis, Bifidobacterium breve, and B. longum subsp. longum using over 300 high-quality genomes. All three species exhibited open pangenomes, with regulatory interactions frequently involving accessory genes. Inferred network metrics were compared with score-randomized controls across motif-score thresholds. Increasing score stringency reduced network size while increasing the number of detected communities, indicating greater fragmentation of the retained networks rather than a measured increase in modularity. NrdR showed an intermediate overlap in the Clusters of Orthologous Groups (COG) category sets represented among its predicted targets and species-dependent target prevalence. HMO-related regulators (FucR, NanR, and NagR) differed descriptively between Bifidobacterium infantis and B. breve, the two species included in the complete three-regulator comparison, in predicted target counts, represented COG category sets, and genomic-prevalence patterns; only FucR showed a significant difference in accessory-target fraction. These findings identify species-dependent differences in predicted regulon composition and genomic prevalence and provide testable hypotheses about how regulatory architecture may relate to ecological specialization in the infant gut.
IMPORTANCE: Bifidobacterium species are among the most abundant microorganisms in the breast-fed infant gut microbiota, where they display distinct patterns of genomic diversification and host association. However, the transcriptional regulatory mechanisms underlying these species-specific differences remain incompletely characterized. Here, we reconstructed and compared genome-scale transcriptional regulatory networks across three infant-associated Bifidobacterium species, integrating pangenome structure with transcription factor binding site inference across more than 300 genomes. Our analyses identified predicted regulatory interactions involving accessory genes and species-specific differences in network structure, regulon composition, and target prevalence. These associations provide hypotheses for experimental studies of how gene content and regulatory architecture may contribute to niche adaptation. This pangenome-scale framework can support the prioritization of regulatory hypotheses for future functional studies of infant-associated Bifidobacterium.
Additional Links: PMID-42861994
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PubMed:
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@article {pmid42861994,
year = {2026},
author = {Melis-Arcos, F and Arita, M and Garrido, D},
title = {Comparative transcriptional network analysis reveals ecological specialization in infant-associated species of Bifidobacterium.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0108226},
doi = {10.1128/msystems.01082-26},
pmid = {42861994},
issn = {2379-5077},
abstract = {UNLABELLED: Bifidobacterium species are important microorganisms in the infant gut microbiota displaying substantial genomic diversity, yet how this variability is reflected in transcriptional regulatory architecture remains an open question. Here, we integrated pangenome analysis with transcription factor binding site inference and network-based approaches to compare regulatory architectures across Bifidobacterium longum subsp. infantis, Bifidobacterium breve, and B. longum subsp. longum using over 300 high-quality genomes. All three species exhibited open pangenomes, with regulatory interactions frequently involving accessory genes. Inferred network metrics were compared with score-randomized controls across motif-score thresholds. Increasing score stringency reduced network size while increasing the number of detected communities, indicating greater fragmentation of the retained networks rather than a measured increase in modularity. NrdR showed an intermediate overlap in the Clusters of Orthologous Groups (COG) category sets represented among its predicted targets and species-dependent target prevalence. HMO-related regulators (FucR, NanR, and NagR) differed descriptively between Bifidobacterium infantis and B. breve, the two species included in the complete three-regulator comparison, in predicted target counts, represented COG category sets, and genomic-prevalence patterns; only FucR showed a significant difference in accessory-target fraction. These findings identify species-dependent differences in predicted regulon composition and genomic prevalence and provide testable hypotheses about how regulatory architecture may relate to ecological specialization in the infant gut.
IMPORTANCE: Bifidobacterium species are among the most abundant microorganisms in the breast-fed infant gut microbiota, where they display distinct patterns of genomic diversification and host association. However, the transcriptional regulatory mechanisms underlying these species-specific differences remain incompletely characterized. Here, we reconstructed and compared genome-scale transcriptional regulatory networks across three infant-associated Bifidobacterium species, integrating pangenome structure with transcription factor binding site inference across more than 300 genomes. Our analyses identified predicted regulatory interactions involving accessory genes and species-specific differences in network structure, regulon composition, and target prevalence. These associations provide hypotheses for experimental studies of how gene content and regulatory architecture may contribute to niche adaptation. This pangenome-scale framework can support the prioritization of regulatory hypotheses for future functional studies of infant-associated Bifidobacterium.},
}
RevDate: 2026-10-13
Sex- and Time-Resolved Physiological and Gut Ecosystem Responses to a Food-Grade Microbiome-Targeted Intervention in Collegiate Endurance Athletes.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Endurance athletes experience sustained physiological demands during high-volume training, yet evidence for microbiome-targeted interventions in real-world settings remains limited. We conducted a two-stage, randomized, double-blind, placebo-controlled trial in 150 athletes allocated 2:1 to combined probiotics-yeast extract (CPYE) or placebo for 6 weeks; 44 completers confirmed for the 12th Inner Mongolia Autonomous Region University Games entered an exploratory 6-week extension with intensified training. Integrating wearable-derived phenotyping, field-based cardiorespiratory indices, clinical assessments, fecal metagenomics, and metabolomics, we found that during the randomized short-term phase, CPYE was associated with changes in device-estimated maximal oxygen uptake, exercise heart-rate indices, lactate, and redox biomarkers versus placebo. Exploratory sex-stratified analyses suggested heterogeneous response patterns, while the selected long-term extension indicated time-dependent changes requiring confirmation. Multi-omics identified sex- and phase-associated differences in microbial taxa, functions, metabolites, and network topology. Indirect-effect models nominated candidate features (rmlD, PISD-linked phosphatidylethanolamine pathways, Bacteroides ovatus, and folate-related functions) as potential indirect correlates of host outcomes. These findings support further evaluation of CPYE-associated responses in collegiate endurance athletes; subgroup, long-term, network, and indirect-effect results are hypothesis-generating.
Additional Links: PMID-42862002
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Citation:
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@article {pmid42862002,
year = {2026},
author = {Zhang, M and Ge, L and Liu, K and Liu, Y and Zhao, G and Kwok, LY and Sun, Z and Sun, Z and Zhang, W},
title = {Sex- and Time-Resolved Physiological and Gut Ecosystem Responses to a Food-Grade Microbiome-Targeted Intervention in Collegiate Endurance Athletes.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e77664},
pmid = {42862002},
issn = {2198-3844},
support = {NMGLLY2025-02//Inner Mongolia Autonomous Region Special Project for Scientific and Technological Innovation Research in Key Fields of the "Two Barriers," "Two Bases," and "One Bridgehead" Initiative/ ; 32325040//National Natural Science Foundation of China/ ; 32502149//National Natural Science Foundation of China/ ; U25A20733//National Natural Science Foundation of China/ ; CARS36//Earmarked Fund for China Agriculture Research System/ ; },
abstract = {Endurance athletes experience sustained physiological demands during high-volume training, yet evidence for microbiome-targeted interventions in real-world settings remains limited. We conducted a two-stage, randomized, double-blind, placebo-controlled trial in 150 athletes allocated 2:1 to combined probiotics-yeast extract (CPYE) or placebo for 6 weeks; 44 completers confirmed for the 12th Inner Mongolia Autonomous Region University Games entered an exploratory 6-week extension with intensified training. Integrating wearable-derived phenotyping, field-based cardiorespiratory indices, clinical assessments, fecal metagenomics, and metabolomics, we found that during the randomized short-term phase, CPYE was associated with changes in device-estimated maximal oxygen uptake, exercise heart-rate indices, lactate, and redox biomarkers versus placebo. Exploratory sex-stratified analyses suggested heterogeneous response patterns, while the selected long-term extension indicated time-dependent changes requiring confirmation. Multi-omics identified sex- and phase-associated differences in microbial taxa, functions, metabolites, and network topology. Indirect-effect models nominated candidate features (rmlD, PISD-linked phosphatidylethanolamine pathways, Bacteroides ovatus, and folate-related functions) as potential indirect correlates of host outcomes. These findings support further evaluation of CPYE-associated responses in collegiate endurance athletes; subgroup, long-term, network, and indirect-effect results are hypothesis-generating.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-12
Subclinical Mastitis and Antibiotic Exposure Reshape the Milk Bacteriome, Resistome, and Metabolic Functional Profiles in Dairy Cows.
MicrobiologyOpen, 15(5):e70440.
Subclinical mastitis (SCM) reduces milk yield and promotes antibiotic use, contributing to antimicrobial resistance. However, information on milk microbiome dysbiosis and resistome alterations in dairy cows remains limited. We performed shotgun metagenomic sequencing of 30 milk samples from 20 cows classified as SCM (n = 10), antibiotic-treated (ANT; n = 10), and healthy milk (HM; n = 10). Bacteriome, resistome, and metabolic functions were analyzed using bioinformatic tools. Microbial alpha diversity was significantly higher in HM than SCM and ANT samples (p < 0.05), with the greatest richness observed in Local Zebu and Middle-aged (5-8 years) cows. However, beta diversity did not differ significantly among groups (PERMANOVA, p > 0.05). A total of 665 bacterial species belonging to 15 phyla were identified, with Pseudomonadota, Actinomycetota, and Bacillota comprising 90%-99% of total abundance. SCM milk was dominated by Actinoalloteichus sp. (40.55%) and Vibrio furnissii (37.01%), while Staphylococcus aureus was enriched (1.74%) compared with HM and ANT (< 0.01%). ANT milk showed increased abundance of Acinetobacter johnsonii (10.52%), whereas HM samples contained beneficial commensals, including Pseudomonas lundensis, Bacteroides thetaiotaomicron, and Lactococcus lactis. Similar taxonomic shifts were observed across breeds and age groups. In total, 194 antimicrobial resistance genes (ARGs) were detected, with SCM harboring the largest repertoire (n = 161). Nevertheless, macrolide-, aminoglycoside-, and β-lactam-resistance genes were significantly enriched in ANT samples (p < 0.01). Correlation analyses linked Escherichia coli and A. johnsonii with multiple ARGs, while Acinetobacter and Pseudomonas were associated with lipid metabolism, membrane transport, and xenobiotic biodegradation pathways. These findings reveal bacteriome disruption, ARG enrichment, and functional alterations in SCM and antibiotic-exposed milk.
Additional Links: PMID-42862088
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@article {pmid42862088,
year = {2026},
author = {Hoque, MN and Rahman, MS and Hossain, MG and Rahman, MT and Islam, T and Hossain, MA},
title = {Subclinical Mastitis and Antibiotic Exposure Reshape the Milk Bacteriome, Resistome, and Metabolic Functional Profiles in Dairy Cows.},
journal = {MicrobiologyOpen},
volume = {15},
number = {5},
pages = {e70440},
pmid = {42862088},
issn = {2045-8827},
support = {LS20221764//Bangladesh Bureau of Educational Information & Statistics (BANBEIS), Ministry of Education/ ; },
mesh = {Animals ; *Milk/microbiology ; Female ; *Anti-Bacterial Agents/pharmacology/therapeutic use ; Cattle ; *Bacteria/drug effects/classification/genetics/isolation & purification ; *Mastitis, Bovine/microbiology/drug therapy ; Metagenomics ; *Microbiota/drug effects ; Drug Resistance, Bacterial ; },
abstract = {Subclinical mastitis (SCM) reduces milk yield and promotes antibiotic use, contributing to antimicrobial resistance. However, information on milk microbiome dysbiosis and resistome alterations in dairy cows remains limited. We performed shotgun metagenomic sequencing of 30 milk samples from 20 cows classified as SCM (n = 10), antibiotic-treated (ANT; n = 10), and healthy milk (HM; n = 10). Bacteriome, resistome, and metabolic functions were analyzed using bioinformatic tools. Microbial alpha diversity was significantly higher in HM than SCM and ANT samples (p < 0.05), with the greatest richness observed in Local Zebu and Middle-aged (5-8 years) cows. However, beta diversity did not differ significantly among groups (PERMANOVA, p > 0.05). A total of 665 bacterial species belonging to 15 phyla were identified, with Pseudomonadota, Actinomycetota, and Bacillota comprising 90%-99% of total abundance. SCM milk was dominated by Actinoalloteichus sp. (40.55%) and Vibrio furnissii (37.01%), while Staphylococcus aureus was enriched (1.74%) compared with HM and ANT (< 0.01%). ANT milk showed increased abundance of Acinetobacter johnsonii (10.52%), whereas HM samples contained beneficial commensals, including Pseudomonas lundensis, Bacteroides thetaiotaomicron, and Lactococcus lactis. Similar taxonomic shifts were observed across breeds and age groups. In total, 194 antimicrobial resistance genes (ARGs) were detected, with SCM harboring the largest repertoire (n = 161). Nevertheless, macrolide-, aminoglycoside-, and β-lactam-resistance genes were significantly enriched in ANT samples (p < 0.01). Correlation analyses linked Escherichia coli and A. johnsonii with multiple ARGs, while Acinetobacter and Pseudomonas were associated with lipid metabolism, membrane transport, and xenobiotic biodegradation pathways. These findings reveal bacteriome disruption, ARG enrichment, and functional alterations in SCM and antibiotic-exposed milk.},
}
MeSH Terms:
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Animals
*Milk/microbiology
Female
*Anti-Bacterial Agents/pharmacology/therapeutic use
Cattle
*Bacteria/drug effects/classification/genetics/isolation & purification
*Mastitis, Bovine/microbiology/drug therapy
Metagenomics
*Microbiota/drug effects
Drug Resistance, Bacterial
RevDate: 2026-10-12
Dietary modulation of the gut microbiota in type 2 diabetes and obesity: mechanisms, interventions, and clinical perspectives.
Acta diabetologica [Epub ahead of print].
Obesity and type 2 diabetes mellitus (T2DM) are associated with heterogeneous changes in gut microbial composition and function, while mechanistic studies support plausible links among diet, microbial metabolism, intestinal barrier function, immune signaling, and host metabolism. This narrative review integrates diet-microbiome mechanisms, dietary-assessment and multi-omics methodology, major dietary patterns, quantitative clinical intervention evidence, treatment-related microbiome modulation, and implications for precision nutrition. High-fiber, Mediterranean, plant-based, and Western-style dietary patterns can modify microbial functions and metabolites, but responses vary across populations, substrates, baseline microbiota, medications, and study methods. Randomized trials and meta-analyses show selected metabolic effects of dietary and microbiome-targeted interventions; effects are generally modest and heterogeneous, and prebiotics, probiotics, synbiotics, and postbiotics are not interchangeable across products or populations. Medication and procedural exposures can also alter microbiome and metabolome readouts and confound interpretation. Current evidence does not provide a validated basis for routine microbiome-guided pharmacological or surgical treatment selection. Integration of dietary, microbiome, metabolome, and clinical data may identify metabotypes and candidate response patterns, but individualized microbiome-based nutrition remains an emerging, validation-dependent research domain rather than routine clinical practice.
Additional Links: PMID-42862338
PubMed:
Citation:
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@article {pmid42862338,
year = {2026},
author = {Kubica, A and Maszczyk, W},
title = {Dietary modulation of the gut microbiota in type 2 diabetes and obesity: mechanisms, interventions, and clinical perspectives.},
journal = {Acta diabetologica},
volume = {},
number = {},
pages = {},
pmid = {42862338},
issn = {1432-5233},
abstract = {Obesity and type 2 diabetes mellitus (T2DM) are associated with heterogeneous changes in gut microbial composition and function, while mechanistic studies support plausible links among diet, microbial metabolism, intestinal barrier function, immune signaling, and host metabolism. This narrative review integrates diet-microbiome mechanisms, dietary-assessment and multi-omics methodology, major dietary patterns, quantitative clinical intervention evidence, treatment-related microbiome modulation, and implications for precision nutrition. High-fiber, Mediterranean, plant-based, and Western-style dietary patterns can modify microbial functions and metabolites, but responses vary across populations, substrates, baseline microbiota, medications, and study methods. Randomized trials and meta-analyses show selected metabolic effects of dietary and microbiome-targeted interventions; effects are generally modest and heterogeneous, and prebiotics, probiotics, synbiotics, and postbiotics are not interchangeable across products or populations. Medication and procedural exposures can also alter microbiome and metabolome readouts and confound interpretation. Current evidence does not provide a validated basis for routine microbiome-guided pharmacological or surgical treatment selection. Integration of dietary, microbiome, metabolome, and clinical data may identify metabotypes and candidate response patterns, but individualized microbiome-based nutrition remains an emerging, validation-dependent research domain rather than routine clinical practice.},
}
RevDate: 2026-10-12
CmpDate: 2026-10-12
Inflammatory bowel disease and breast cancer: epidemiological evidence, shared biology, and clinical management.
Inflammation research : official journal of the European Histamine Research Society ... [et al.], 75(1):.
OBJECTIVE AND DESIGN: This narrative review examines epidemiological, genetic, mechanistic, microbial, and therapeutic evidence concerning inflammatory bowel disease (IBD) and breast cancer.
METHODS: Relevant literature was identified through targeted PubMed searches completed through May 2026 and reference-list screening. Evidence was selected for its relevance to epidemiology, candidate mechanisms, microbiome-related pathways, and treatment interactions.
RESULTS: Pooled cohort evidence does not show a significant overall increase in breast cancer risk among patients with IBD. Several inflammatory, stromal, microbial, and endocrine pathways are relevant to both diseases, although most evidence comes from separate study populations and experimental models. Studies of patients with prior malignancy have not shown a clear increase in new or recurrent cancer during commonly used IBD therapies, but few analyses have focused specifically on breast cancer. Microbiome-directed treatments have been studied in IBD and, more recently, in oncology; their value for patients with both diseases is unknown.
CONCLUSIONS: Current evidence does not support classifying IBD as a breast cancer risk state. The main clinical concern is the interaction between treatments for the two diseases, which requires individualized assessment and coordinated gastroenterology and oncology care.
Additional Links: PMID-42862350
PubMed:
Citation:
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@article {pmid42862350,
year = {2026},
author = {Han, Q and Zhang, X and Li, S},
title = {Inflammatory bowel disease and breast cancer: epidemiological evidence, shared biology, and clinical management.},
journal = {Inflammation research : official journal of the European Histamine Research Society ... [et al.]},
volume = {75},
number = {1},
pages = {},
pmid = {42862350},
issn = {1420-908X},
mesh = {Humans ; *Inflammatory Bowel Diseases/epidemiology/therapy/microbiology/genetics/complications/immunology ; *Breast Neoplasms/epidemiology/therapy/genetics/immunology ; Female ; Animals ; Gastrointestinal Microbiome ; },
abstract = {OBJECTIVE AND DESIGN: This narrative review examines epidemiological, genetic, mechanistic, microbial, and therapeutic evidence concerning inflammatory bowel disease (IBD) and breast cancer.
METHODS: Relevant literature was identified through targeted PubMed searches completed through May 2026 and reference-list screening. Evidence was selected for its relevance to epidemiology, candidate mechanisms, microbiome-related pathways, and treatment interactions.
RESULTS: Pooled cohort evidence does not show a significant overall increase in breast cancer risk among patients with IBD. Several inflammatory, stromal, microbial, and endocrine pathways are relevant to both diseases, although most evidence comes from separate study populations and experimental models. Studies of patients with prior malignancy have not shown a clear increase in new or recurrent cancer during commonly used IBD therapies, but few analyses have focused specifically on breast cancer. Microbiome-directed treatments have been studied in IBD and, more recently, in oncology; their value for patients with both diseases is unknown.
CONCLUSIONS: Current evidence does not support classifying IBD as a breast cancer risk state. The main clinical concern is the interaction between treatments for the two diseases, which requires individualized assessment and coordinated gastroenterology and oncology care.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Inflammatory Bowel Diseases/epidemiology/therapy/microbiology/genetics/complications/immunology
*Breast Neoplasms/epidemiology/therapy/genetics/immunology
Female
Animals
Gastrointestinal Microbiome
RevDate: 2026-10-12
CmpDate: 2026-10-12
Innate and adaptive immunity pathways linking Mycoplasma pneumoniae to pediatric asthma phenotypes.
European journal of pediatrics, 185(11):.
UNLABELLED: Mycoplasma pneumoniae (Mp) is repeatedly detected during pediatric wheeze and asthma exacerbations, but its clinical significance depends on the host-response context. This review evaluates the clinical and mechanistic evidence linking Mp to pediatric asthma phenotypes and examines approaches for distinguishing biologically meaningful infection from incidental detection. We narratively synthesized clinical, experimental, immunological, toxin, and proteomic literature addressing Mp-associated wheeze, asthma exacerbation, epithelial injury, allergic amplification, and inflammatory endotyping. Evidence was distinguished by population and experimental system. Experimental studies show that Mp adheres to airway epithelium; disrupts mucociliary function; activates TLR2/TLR4, NF-κB, autophagy, and inflammasome pathways; and promotes cytokine networks that overlap with allergic asthma. In experimental allergic-airway models, epithelial alarmins, IgE responses, mast cells, and type 2 inflammation may amplify Mp-driven signals, whereas IL-23/IL-17 pathways recruit neutrophils and suggest mixed endotypes; altered corticosteroid responsiveness has not been established in pediatric Mp-associated asthma. CARDS toxin induces eosinophilic inflammation, mucus metaplasia, airway hyperresponsiveness, functional IgE responses, and worsening allergen-driven disease in experimental models. Upper-airway PCR positivity, however, may reflect carriage or prolonged detection rather than active lower-airway infection.
CONCLUSION: Quantitative pathogen testing, paired serology, viral co-detection, age, atopy, microbiome context, and host-response biomarkers merit integrated evaluation in research. Proteomic and multi-omics signatures may support precision endotyping, improve causal attribution, and strengthen pediatric asthma trial design. Their diagnostic and treatment-predictive value remains unvalidated.
WHAT IS KNOWN: • M. pneumoniae is linked to pediatric wheeze and asthma exacerbations, but upper-airway PCR may reflect carriage rather than active lower-airway infection. • Epithelial injury, type 2/Th17 responses, and CARDS toxin can promote asthma-like inflammation in experimental systems.
WHAT IS NEW: • This review integrates diagnostic attribution, toxin biology, immune crosstalk, and proteomic endotyping in one pediatric framework. • It proposes an unvalidated combined pathogen-load and host-response assessment to investigate clinically meaningful M. pneumoniae-driven endotypes and guide trials.
Additional Links: PMID-42862369
PubMed:
Citation:
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@article {pmid42862369,
year = {2026},
author = {Filippatos, F and Michos, A and Kakleas, K},
title = {Innate and adaptive immunity pathways linking Mycoplasma pneumoniae to pediatric asthma phenotypes.},
journal = {European journal of pediatrics},
volume = {185},
number = {11},
pages = {},
pmid = {42862369},
issn = {1432-1076},
mesh = {Humans ; *Asthma/immunology/microbiology ; Child ; *Mycoplasma pneumoniae/immunology ; *Pneumonia, Mycoplasma/immunology/complications ; *Immunity, Innate/immunology ; Phenotype ; *Adaptive Immunity ; },
abstract = {UNLABELLED: Mycoplasma pneumoniae (Mp) is repeatedly detected during pediatric wheeze and asthma exacerbations, but its clinical significance depends on the host-response context. This review evaluates the clinical and mechanistic evidence linking Mp to pediatric asthma phenotypes and examines approaches for distinguishing biologically meaningful infection from incidental detection. We narratively synthesized clinical, experimental, immunological, toxin, and proteomic literature addressing Mp-associated wheeze, asthma exacerbation, epithelial injury, allergic amplification, and inflammatory endotyping. Evidence was distinguished by population and experimental system. Experimental studies show that Mp adheres to airway epithelium; disrupts mucociliary function; activates TLR2/TLR4, NF-κB, autophagy, and inflammasome pathways; and promotes cytokine networks that overlap with allergic asthma. In experimental allergic-airway models, epithelial alarmins, IgE responses, mast cells, and type 2 inflammation may amplify Mp-driven signals, whereas IL-23/IL-17 pathways recruit neutrophils and suggest mixed endotypes; altered corticosteroid responsiveness has not been established in pediatric Mp-associated asthma. CARDS toxin induces eosinophilic inflammation, mucus metaplasia, airway hyperresponsiveness, functional IgE responses, and worsening allergen-driven disease in experimental models. Upper-airway PCR positivity, however, may reflect carriage or prolonged detection rather than active lower-airway infection.
CONCLUSION: Quantitative pathogen testing, paired serology, viral co-detection, age, atopy, microbiome context, and host-response biomarkers merit integrated evaluation in research. Proteomic and multi-omics signatures may support precision endotyping, improve causal attribution, and strengthen pediatric asthma trial design. Their diagnostic and treatment-predictive value remains unvalidated.
WHAT IS KNOWN: • M. pneumoniae is linked to pediatric wheeze and asthma exacerbations, but upper-airway PCR may reflect carriage rather than active lower-airway infection. • Epithelial injury, type 2/Th17 responses, and CARDS toxin can promote asthma-like inflammation in experimental systems.
WHAT IS NEW: • This review integrates diagnostic attribution, toxin biology, immune crosstalk, and proteomic endotyping in one pediatric framework. • It proposes an unvalidated combined pathogen-load and host-response assessment to investigate clinically meaningful M. pneumoniae-driven endotypes and guide trials.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Asthma/immunology/microbiology
Child
*Mycoplasma pneumoniae/immunology
*Pneumonia, Mycoplasma/immunology/complications
*Immunity, Innate/immunology
Phenotype
*Adaptive Immunity
RevDate: 2026-10-12
CmpDate: 2026-10-12
Race, Diet, and Cardiometabolic Risk in US Young Adults: A Biosocial Framework Integrating Biological Mechanisms and Structural Inequities Toward Precision Nutrition.
Current nutrition reports, 15(1):.
Cardiometabolic disease disproportionately affects Black populations in the US, yet dietary interventions have not reduced these disparities. This review examines race as a biosocial construct integrating ancestry-related biology and structural exposures to understand cardiometabolic risk and dietary response in precision nutrition RECENT FINDINGS: Evidence suggests racial differences in glucoregulatory physiology, metabolically relevant allele frequencies, stress-related epigenetic regulation, gut microbiome composition, and metabolomic profiles. Functional foods, including fruits, vegetables, and nuts, target pathways linked to these phenotypes. However, most intervention studies involve older, predominantly White populations, limiting understanding of race-specific responses. The review proposes the "cumulative racial biological phenotype" framework, where ancestry-related biology and structural exposures jointly influence cardiometabolic risk. It advances the greater plasticity hypothesis, suggesting greater baseline biological perturbation may predict larger dietary responses. Testing these concepts requires race-stratified, multi-omics dietary intervention trials in young adults using culturally and structurally responsive designs to improve the effectiveness and equity of precision nutrition.
Additional Links: PMID-42862416
PubMed:
Citation:
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@article {pmid42862416,
year = {2026},
author = {Ani, OG},
title = {Race, Diet, and Cardiometabolic Risk in US Young Adults: A Biosocial Framework Integrating Biological Mechanisms and Structural Inequities Toward Precision Nutrition.},
journal = {Current nutrition reports},
volume = {15},
number = {1},
pages = {},
pmid = {42862416},
issn = {2161-3311},
mesh = {Humans ; *Diet ; United States/epidemiology ; *Cardiovascular Diseases/ethnology/epidemiology ; *Cardiometabolic Risk Factors ; Precision Medicine ; *Health Status Disparities ; Gastrointestinal Microbiome ; *Racial Groups ; Black or African American ; },
abstract = {Cardiometabolic disease disproportionately affects Black populations in the US, yet dietary interventions have not reduced these disparities. This review examines race as a biosocial construct integrating ancestry-related biology and structural exposures to understand cardiometabolic risk and dietary response in precision nutrition RECENT FINDINGS: Evidence suggests racial differences in glucoregulatory physiology, metabolically relevant allele frequencies, stress-related epigenetic regulation, gut microbiome composition, and metabolomic profiles. Functional foods, including fruits, vegetables, and nuts, target pathways linked to these phenotypes. However, most intervention studies involve older, predominantly White populations, limiting understanding of race-specific responses. The review proposes the "cumulative racial biological phenotype" framework, where ancestry-related biology and structural exposures jointly influence cardiometabolic risk. It advances the greater plasticity hypothesis, suggesting greater baseline biological perturbation may predict larger dietary responses. Testing these concepts requires race-stratified, multi-omics dietary intervention trials in young adults using culturally and structurally responsive designs to improve the effectiveness and equity of precision nutrition.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Diet
United States/epidemiology
*Cardiovascular Diseases/ethnology/epidemiology
*Cardiometabolic Risk Factors
Precision Medicine
*Health Status Disparities
Gastrointestinal Microbiome
*Racial Groups
Black or African American
RevDate: 2026-10-12
CmpDate: 2026-10-12
Toxic Metals and Metalloids Exposure and the Gut-Cardiometabolic Axis: A Narrative Review of Microbiome Dysbiosis, Gut Barrier Dysfunction, and Metabolic Inflammation.
Cardiovascular toxicology, 26(11):.
Toxic elements and metalloids exposure is an important environmental contributor to cardiometabolic disease, yet the gut-mediated mechanisms linking toxic elements to systemic metabolic and vascular injury remain incompletely understood. Lead, cadmium, arsenic, and mercury can enter the gastrointestinal tract through contaminated food, water, dust, smoking, seafood, and occupational sources, allowing direct interaction with the intestinal lumen, epithelial barrier, immune system, and gut microbiome. This narrative review examines the gut-cardiometabolic axis as a mechanistic framework connecting toxic metal exposure to microbiome dysbiosis, barrier dysfunction, endotoxemia, microbial metabolite imbalance, and chronic metabolic inflammation. Available evidence, derived from human, animal, and in-vitro studies of varying quality, suggests that toxic elements may alter microbial diversity and function, affect tight-junction integrity, and increase intestinal permeability; however, a consistent metal-specific signature and a complete causal chain have not been established. These changes may promote lipopolysaccharide passage through the intestinal barrier, activate innate immune pathways, and maintain systemic inflammatory signaling. At the same time, disruption of microbial metabolite profiles, including lower short-chain fatty acid production and altered trimethylamine N-oxide, bile acid and uremic toxin pathways, may promote insulin resistance, dyslipidemia, endothelial dysfunction, hypertension, atherosclerosis and overall cardiometabolic vulnerability. Viewing toxic-metal exposure through the gut-cardiometabolic axis provides a hypothesis-generating framework for integrating exposure reduction with conventional cardiometabolic risk management; the clinical value of microbiome-targeted strategies remains to be established. Longitudinal and multi-omics studies are still needed to define causal relationships and identify populations at greatest susceptibility.
Additional Links: PMID-42862482
PubMed:
Citation:
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@article {pmid42862482,
year = {2026},
author = {Gadelmawla, AF and El-Farargy, SH and Alsubaiei, AA and AlSejari, NY and Sharara, MR and Abdul-Hafez, HA and Mohamed, AE and Hageen, AW and Alharran, AM and Andò, G and Aronow, WS},
title = {Toxic Metals and Metalloids Exposure and the Gut-Cardiometabolic Axis: A Narrative Review of Microbiome Dysbiosis, Gut Barrier Dysfunction, and Metabolic Inflammation.},
journal = {Cardiovascular toxicology},
volume = {26},
number = {11},
pages = {},
pmid = {42862482},
issn = {1559-0259},
mesh = {Humans ; *Intestinal Barrier Function/drug effects ; Animals ; Dysbiosis ; *Gastrointestinal Microbiome/drug effects ; *Inflammation Mediators/metabolism ; *Metalloids/adverse effects ; *Bacteria/metabolism/drug effects ; *Inflammation/metabolism/chemically induced/microbiology ; *Intestines/microbiology/drug effects/physiopathology ; Host-Pathogen Interactions ; *Metals ; *Environmental Exposure/adverse effects ; Risk Assessment ; *Environmental Pollutants/adverse effects ; Cardiotoxicity ; },
abstract = {Toxic elements and metalloids exposure is an important environmental contributor to cardiometabolic disease, yet the gut-mediated mechanisms linking toxic elements to systemic metabolic and vascular injury remain incompletely understood. Lead, cadmium, arsenic, and mercury can enter the gastrointestinal tract through contaminated food, water, dust, smoking, seafood, and occupational sources, allowing direct interaction with the intestinal lumen, epithelial barrier, immune system, and gut microbiome. This narrative review examines the gut-cardiometabolic axis as a mechanistic framework connecting toxic metal exposure to microbiome dysbiosis, barrier dysfunction, endotoxemia, microbial metabolite imbalance, and chronic metabolic inflammation. Available evidence, derived from human, animal, and in-vitro studies of varying quality, suggests that toxic elements may alter microbial diversity and function, affect tight-junction integrity, and increase intestinal permeability; however, a consistent metal-specific signature and a complete causal chain have not been established. These changes may promote lipopolysaccharide passage through the intestinal barrier, activate innate immune pathways, and maintain systemic inflammatory signaling. At the same time, disruption of microbial metabolite profiles, including lower short-chain fatty acid production and altered trimethylamine N-oxide, bile acid and uremic toxin pathways, may promote insulin resistance, dyslipidemia, endothelial dysfunction, hypertension, atherosclerosis and overall cardiometabolic vulnerability. Viewing toxic-metal exposure through the gut-cardiometabolic axis provides a hypothesis-generating framework for integrating exposure reduction with conventional cardiometabolic risk management; the clinical value of microbiome-targeted strategies remains to be established. Longitudinal and multi-omics studies are still needed to define causal relationships and identify populations at greatest susceptibility.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Intestinal Barrier Function/drug effects
Animals
Dysbiosis
*Gastrointestinal Microbiome/drug effects
*Inflammation Mediators/metabolism
*Metalloids/adverse effects
*Bacteria/metabolism/drug effects
*Inflammation/metabolism/chemically induced/microbiology
*Intestines/microbiology/drug effects/physiopathology
Host-Pathogen Interactions
*Metals
*Environmental Exposure/adverse effects
Risk Assessment
*Environmental Pollutants/adverse effects
Cardiotoxicity
RevDate: 2026-10-12
The Bidirectional Relationship Between Diabetes and Cancer: Mechanistic Insights, Epigenetic Intermediaries, and Therapeutic Approaches.
Diabetes therapy : research, treatment and education of diabetes and related disorders [Epub ahead of print].
OBJECTIVES: The global rise in diabetes mellitus parallels an increasing cancer burden, highlighting an incompletely understood relationship between these two complex diseases. Accumulating epidemiological evidence indicates that diabetes is associated with an increased incidence and mortality of several site-specific cancers, whereas cancer and its treatment may contribute to dysglycemia and diabetes through diverse mechanisms. In addition, shared metabolic and environmental risk factors further contribute to the observed association between these conditions.
METHODOLOGY: This narrative review comprehensively examined peer-reviewed literature retrieved from PubMed, Scopus, Web of Science, and Google Scholar, focusing on the epidemiological, mechanistic, and epigenetic links between diabetes and cancer.
RESULTS: Beyond shared lifestyle risk factors, converging molecular mechanisms-including chronic hyperglycemia, insulin resistance, low-grade inflammation, oxidative stress, and metabolic reprogramming-provide a biological framework linking diabetes and cancer. Emerging evidence suggests that epigenetic dysregulation acts as a central intermediary in this relationship by integrating metabolic stress with sustained alterations in gene expression through DNA methylation, histone modifications, non-coding RNAs, chromatin remodeling, and epigenetic aging. Diabetes-related epigenetic memory, microbiome-driven epigenetic modulation, and sex-specific epigenetic signatures may further contribute to cancer susceptibility and disease heterogeneity, although the strength of evidence varies across experimental and clinical studies.
CONCLUSIONS: This review synthesizes current epidemiological, mechanistic, and epigenetic evidence linking diabetes and cancer, with particular emphasis on metabolic-epigenetic crosstalk and clinically relevant signaling pathways. It also critically evaluates the dual metabolic and oncologic effects of antidiabetic and anticancer therapies while highlighting current evidence gaps and the need for precision medicine approaches in the prevention and management of both diseases.
Additional Links: PMID-42862527
PubMed:
Citation:
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@article {pmid42862527,
year = {2026},
author = {Mishra, P and PramodKumar, TA and Pradhan, B and Ghosh, U and Mishra, PK and Dash, P and Anjana, RM and Patra, SK and Mohan, V},
title = {The Bidirectional Relationship Between Diabetes and Cancer: Mechanistic Insights, Epigenetic Intermediaries, and Therapeutic Approaches.},
journal = {Diabetes therapy : research, treatment and education of diabetes and related disorders},
volume = {},
number = {},
pages = {},
pmid = {42862527},
issn = {1869-6953},
abstract = {OBJECTIVES: The global rise in diabetes mellitus parallels an increasing cancer burden, highlighting an incompletely understood relationship between these two complex diseases. Accumulating epidemiological evidence indicates that diabetes is associated with an increased incidence and mortality of several site-specific cancers, whereas cancer and its treatment may contribute to dysglycemia and diabetes through diverse mechanisms. In addition, shared metabolic and environmental risk factors further contribute to the observed association between these conditions.
METHODOLOGY: This narrative review comprehensively examined peer-reviewed literature retrieved from PubMed, Scopus, Web of Science, and Google Scholar, focusing on the epidemiological, mechanistic, and epigenetic links between diabetes and cancer.
RESULTS: Beyond shared lifestyle risk factors, converging molecular mechanisms-including chronic hyperglycemia, insulin resistance, low-grade inflammation, oxidative stress, and metabolic reprogramming-provide a biological framework linking diabetes and cancer. Emerging evidence suggests that epigenetic dysregulation acts as a central intermediary in this relationship by integrating metabolic stress with sustained alterations in gene expression through DNA methylation, histone modifications, non-coding RNAs, chromatin remodeling, and epigenetic aging. Diabetes-related epigenetic memory, microbiome-driven epigenetic modulation, and sex-specific epigenetic signatures may further contribute to cancer susceptibility and disease heterogeneity, although the strength of evidence varies across experimental and clinical studies.
CONCLUSIONS: This review synthesizes current epidemiological, mechanistic, and epigenetic evidence linking diabetes and cancer, with particular emphasis on metabolic-epigenetic crosstalk and clinically relevant signaling pathways. It also critically evaluates the dual metabolic and oncologic effects of antidiabetic and anticancer therapies while highlighting current evidence gaps and the need for precision medicine approaches in the prevention and management of both diseases.},
}
RevDate: 2026-10-12
CmpDate: 2026-10-12
Discovery and characterization of miranthins, "Trojan horse" antibiotic modulators of bacterial composition in the oral microbiome.
Proceedings of the National Academy of Sciences of the United States of America, 123(42):e2621138123.
Bacteria of the human microbiota encode an abundance of natural products that likely mediate bacterial competition, local colonization patterns, and human health and disease. However, very few of these compounds have been identified and characterized to date. During our investigation of Streptococcus mitis, an important early colonizer of the oral cavity, we identified and structurally characterized a family of peptide natural products, termed miranthins herein, that contain an unusual macrocycle formed by an Asp-Cys β-carbon thioether crosslink. We determined that the most abundantly secreted miranthin is a "Trojan horse" antibiotic that enters sensitive cells via the Ami oligopeptide transporter, is hydrolyzed and activated by aminopeptidase N, and subsequently inhibits ribosomal translation to curb the growth of streptococcal competitors. The miranthins are narrow-spectrum antibiotics that could enable S. mitis to modulate community dynamics in the oral cavity, highlighting the importance of peptide natural products in interspecies competition in the microbiome.
Additional Links: PMID-42863060
Publisher:
PubMed:
Citation:
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@article {pmid42863060,
year = {2026},
author = {Dalvano, BE and Covington, BC and Seyedsayamdost, MR},
title = {Discovery and characterization of miranthins, "Trojan horse" antibiotic modulators of bacterial composition in the oral microbiome.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {42},
pages = {e2621138123},
doi = {10.1073/pnas.2621138123},
pmid = {42863060},
issn = {1091-6490},
support = {R35 GM152049//HHS | NIH | National Institute of General Medical Sciences (NIGMS)/ ; 2023A004123//Leona M. and Harry B. Helmsley Charitable Trust (Helmsley)/ ; Fellowship//John D. and Catherine T. MacArthur Foundation (JDCTMF)/ ; },
mesh = {*Microbiota/drug effects ; Humans ; *Anti-Bacterial Agents/pharmacology/chemistry ; *Mouth/microbiology ; *Streptococcus mitis/drug effects/metabolism ; *Peptides/pharmacology/chemistry ; Biological Products/pharmacology/chemistry ; },
abstract = {Bacteria of the human microbiota encode an abundance of natural products that likely mediate bacterial competition, local colonization patterns, and human health and disease. However, very few of these compounds have been identified and characterized to date. During our investigation of Streptococcus mitis, an important early colonizer of the oral cavity, we identified and structurally characterized a family of peptide natural products, termed miranthins herein, that contain an unusual macrocycle formed by an Asp-Cys β-carbon thioether crosslink. We determined that the most abundantly secreted miranthin is a "Trojan horse" antibiotic that enters sensitive cells via the Ami oligopeptide transporter, is hydrolyzed and activated by aminopeptidase N, and subsequently inhibits ribosomal translation to curb the growth of streptococcal competitors. The miranthins are narrow-spectrum antibiotics that could enable S. mitis to modulate community dynamics in the oral cavity, highlighting the importance of peptide natural products in interspecies competition in the microbiome.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Microbiota/drug effects
Humans
*Anti-Bacterial Agents/pharmacology/chemistry
*Mouth/microbiology
*Streptococcus mitis/drug effects/metabolism
*Peptides/pharmacology/chemistry
Biological Products/pharmacology/chemistry
RevDate: 2026-10-12
Integrating free-living amoebae into climate-microbiome and One Health frameworks.
Protist, 183:126188 pii:S1434-4610(26)00044-1 [Epub ahead of print].
Climate change is altering microbial ecosystems at a global scale, yet the role of free-living amoebae within these shifting microbiomes remains incompletely understood. Free-living amoebae occupy soil, water, air, and built environments, where they contribute to microbial diversity, regulate nutrient cycling, and host diverse bacterial, fungal, and viral microorganisms. As temperature, moisture, and land-use patterns change, amoebal behaviour and their associated microbiomes may shift in ways that may affect soil fertility, water quality, microbial network stability, and the persistence of opportunistic pathogens. Through grazing, amoebae regulate bacterial turnover and mineral nutrient release from microbial biomass, providing a mechanistic link between nutrient cycling and plant accessible nutrient pools that underpin soil fertility. Understanding these dynamics is essential for planetary microbiome research and for strengthening One Health approaches that link environmental, animal, and human health. Herein, we discuss free-living amoebae in the context of climate change, the planetary microbiome, and One Health, and consider how their ecological roles may relate to broader shifts in microbial systems. We synthesise current evidence linking free-living amoebae to climate-responsive microbiome dynamics and propose their inclusion within planetary microbiome and One Health frameworks as responsive ecological indicators. Integrating amoebae into surveillance, ecological modelling, and climate-adaptation strategies may improve predictive capacity for tracking climate-driven microbial change.
Additional Links: PMID-42863159
Publisher:
PubMed:
Citation:
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@article {pmid42863159,
year = {2026},
author = {Siddiqui, R and Maciver, SK and Lloyd, D and Khan, NA},
title = {Integrating free-living amoebae into climate-microbiome and One Health frameworks.},
journal = {Protist},
volume = {183},
number = {},
pages = {126188},
doi = {10.1016/j.protis.2026.126188},
pmid = {42863159},
issn = {1618-0941},
abstract = {Climate change is altering microbial ecosystems at a global scale, yet the role of free-living amoebae within these shifting microbiomes remains incompletely understood. Free-living amoebae occupy soil, water, air, and built environments, where they contribute to microbial diversity, regulate nutrient cycling, and host diverse bacterial, fungal, and viral microorganisms. As temperature, moisture, and land-use patterns change, amoebal behaviour and their associated microbiomes may shift in ways that may affect soil fertility, water quality, microbial network stability, and the persistence of opportunistic pathogens. Through grazing, amoebae regulate bacterial turnover and mineral nutrient release from microbial biomass, providing a mechanistic link between nutrient cycling and plant accessible nutrient pools that underpin soil fertility. Understanding these dynamics is essential for planetary microbiome research and for strengthening One Health approaches that link environmental, animal, and human health. Herein, we discuss free-living amoebae in the context of climate change, the planetary microbiome, and One Health, and consider how their ecological roles may relate to broader shifts in microbial systems. We synthesise current evidence linking free-living amoebae to climate-responsive microbiome dynamics and propose their inclusion within planetary microbiome and One Health frameworks as responsive ecological indicators. Integrating amoebae into surveillance, ecological modelling, and climate-adaptation strategies may improve predictive capacity for tracking climate-driven microbial change.},
}
RevDate: 2026-10-12
Temporal dynamics of cecal microbiota composition and diversity in broiler chickens challenged with different doses of Eimeria spp.
Veterinary parasitology, 348:110932 pii:S0304-4017(26)00251-7 [Epub ahead of print].
Coccidiosis, caused by Eimeria spp., is one of the major enteric diseases affecting broiler chickens, compromising gut integrity and altering gut microbiota composition. This study aimed to evaluate the effects of different Fortegra® Eimeria spp. challenge doses on the composition and diversity of the cecal microbiota over time postinfection. Broiler chickens were allocated into three groups: a control group receiving PBS, G1 challenged with a 10 × vaccine dose, and G2 challenged with a 20 × vaccine dose. Cecal content samples were collected at 7, 14, and 21 days post-inoculation and analyzed using 16S rRNA next-generation sequencing (NGS). Across all groups, the dominant bacterial phyla were Firmicutes and Bacteroidota. A transient increase in Proteobacteria was observed at 7 days postinfection, suggesting an early phase of microbial instability. Taxonomic shifts indicated an initial disruption of the cecal microbiota, followed by progressive microbial reorganization over time. Alpha diversity analysis revealed marked temporal changes in both G1 and G2, with increased richness and diversity at later time points, consistent with a process of microbial succession. In terms of beta diversity, Jaccard distance analysis demonstrated temporal shifts in taxa presence and absence. G1 exhibited a pronounced temporal pattern characterized by continuous species turnover, whereas G2 showed a constrained temporal shift with indications of progressive stabilization. Overall, the findings suggest that temporal dynamics exert a greater influence than challenge intensity in shaping the gut microbiota, reflecting a succession process associated with the partial restoration of gut homeostasis.
Additional Links: PMID-42863256
Publisher:
PubMed:
Citation:
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@article {pmid42863256,
year = {2026},
author = {Lima, PPABM and Paulino, PG and Reis, TL and Valentim, JK and Santos, LM and Cavalheiro, MF and Dilelis, F and Maitre, A and Kratou, M and Cabezas-Cruz, A and Santos, HA},
title = {Temporal dynamics of cecal microbiota composition and diversity in broiler chickens challenged with different doses of Eimeria spp.},
journal = {Veterinary parasitology},
volume = {348},
number = {},
pages = {110932},
doi = {10.1016/j.vetpar.2026.110932},
pmid = {42863256},
issn = {1873-2550},
abstract = {Coccidiosis, caused by Eimeria spp., is one of the major enteric diseases affecting broiler chickens, compromising gut integrity and altering gut microbiota composition. This study aimed to evaluate the effects of different Fortegra® Eimeria spp. challenge doses on the composition and diversity of the cecal microbiota over time postinfection. Broiler chickens were allocated into three groups: a control group receiving PBS, G1 challenged with a 10 × vaccine dose, and G2 challenged with a 20 × vaccine dose. Cecal content samples were collected at 7, 14, and 21 days post-inoculation and analyzed using 16S rRNA next-generation sequencing (NGS). Across all groups, the dominant bacterial phyla were Firmicutes and Bacteroidota. A transient increase in Proteobacteria was observed at 7 days postinfection, suggesting an early phase of microbial instability. Taxonomic shifts indicated an initial disruption of the cecal microbiota, followed by progressive microbial reorganization over time. Alpha diversity analysis revealed marked temporal changes in both G1 and G2, with increased richness and diversity at later time points, consistent with a process of microbial succession. In terms of beta diversity, Jaccard distance analysis demonstrated temporal shifts in taxa presence and absence. G1 exhibited a pronounced temporal pattern characterized by continuous species turnover, whereas G2 showed a constrained temporal shift with indications of progressive stabilization. Overall, the findings suggest that temporal dynamics exert a greater influence than challenge intensity in shaping the gut microbiota, reflecting a succession process associated with the partial restoration of gut homeostasis.},
}
RevDate: 2026-10-12
Digital health technologies for the prevention and management of urinary tract infections in menopausal women: A systematic review.
Maturitas, 214:109151 pii:S0378-5122(26)00328-2 [Epub ahead of print].
BACKGROUND: Urinary tract infections are among the most common infectious diseases in women, with incidence increasing after menopause. The genitourinary syndrome of menopause increases susceptibility to recurrent urinary tract infections through urogenital atrophy and microbiome disruption, compounding the risk of antimicrobial resistance.
OBJECTIVE: To synthesise evidence on digital health technologies for the prevention and management of urinary tract infections in menopausal women.
METHODS: Four databases (PubMed/MEDLINE, Scopus, Web of Science, Cochrane) were systematically searched from January 2000 to March 2026 following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Study quality was assessed using risk-of-bias and critical appraisal tools. Menopausal status was classified as explicitly, proxy or not reported.
RESULTS: Of 9935 records identified, 14 studies met the inclusion criteria. Certainty of evidence ranged from very low to moderate. Four technology clusters emerged: patient-facing digital interventions (n = 4), predictive machine-learning models (n = 7), clinician-facing electronic health record-integrated decision support systems (n = 2), and point-of-care biosensors (n = 1). Digital tools reduced inappropriate antibiotic prescribing by up to 60% and ciprofloxacin use by 80.5%. Predictive models achieved discrimination values of 0.57-0.96 but lacked prospective validation. No study applied formal staging criteria for reproductive aging or integrated hormonal variables. Time to diagnosis and treatment were not assessed.
CONCLUSIONS: Digital health technologies show potential for antimicrobial stewardship in menopausal women with urinary tract infections but remain largely insensitive to menopause-specific biological factors. One randomised controlled trial demonstrated increased uptake of vaginal oestrogen therapy with the use of these technologies, providing evidence of digitally supported non-antibiotic prevention. Future research should integrate menopausal staging, hormonal variables, and user-centred design.
PROSPERO REGISTRATION: CRD420251052764.
Additional Links: PMID-42863282
Publisher:
PubMed:
Citation:
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@article {pmid42863282,
year = {2026},
author = {Cappelli, E and Cappelli, MA and Cappelli, F and Addis, E and Nazeri, A and Pesce, M and De Vita, D},
title = {Digital health technologies for the prevention and management of urinary tract infections in menopausal women: A systematic review.},
journal = {Maturitas},
volume = {214},
number = {},
pages = {109151},
doi = {10.1016/j.maturitas.2026.109151},
pmid = {42863282},
issn = {1873-4111},
abstract = {BACKGROUND: Urinary tract infections are among the most common infectious diseases in women, with incidence increasing after menopause. The genitourinary syndrome of menopause increases susceptibility to recurrent urinary tract infections through urogenital atrophy and microbiome disruption, compounding the risk of antimicrobial resistance.
OBJECTIVE: To synthesise evidence on digital health technologies for the prevention and management of urinary tract infections in menopausal women.
METHODS: Four databases (PubMed/MEDLINE, Scopus, Web of Science, Cochrane) were systematically searched from January 2000 to March 2026 following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Study quality was assessed using risk-of-bias and critical appraisal tools. Menopausal status was classified as explicitly, proxy or not reported.
RESULTS: Of 9935 records identified, 14 studies met the inclusion criteria. Certainty of evidence ranged from very low to moderate. Four technology clusters emerged: patient-facing digital interventions (n = 4), predictive machine-learning models (n = 7), clinician-facing electronic health record-integrated decision support systems (n = 2), and point-of-care biosensors (n = 1). Digital tools reduced inappropriate antibiotic prescribing by up to 60% and ciprofloxacin use by 80.5%. Predictive models achieved discrimination values of 0.57-0.96 but lacked prospective validation. No study applied formal staging criteria for reproductive aging or integrated hormonal variables. Time to diagnosis and treatment were not assessed.
CONCLUSIONS: Digital health technologies show potential for antimicrobial stewardship in menopausal women with urinary tract infections but remain largely insensitive to menopause-specific biological factors. One randomised controlled trial demonstrated increased uptake of vaginal oestrogen therapy with the use of these technologies, providing evidence of digitally supported non-antibiotic prevention. Future research should integrate menopausal staging, hormonal variables, and user-centred design.
PROSPERO REGISTRATION: CRD420251052764.},
}
RevDate: 2026-10-12
Understanding genetic determinants of bacterial adaptation to plant niches: Toward more robust bioinoculant design.
Microbiological research, 314:128760 pii:S0944-5013(26)00324-1 [Epub ahead of print].
Plant-associated bacteria offer a sustainable alternative to chemical inputs in agriculture, yet the field performance of microbial inoculants remains inconsistent. A central but frequently overlooked cause is that bioprospecting pipelines still select strains on the basis of plant-growth-promoting activities, while the bacterial genetic traits that determine whether a strain can reach, colonise and persist in a given root compartment are rarely assessed. Previous reviews have largely catalogued growth-promoting functions or described root microbiome assembly from the plant's perspective, here we take the bacterium's. We trace the journey of a bacterium from bulk soil to its final niche and, at each stage, identify the genes and pathways (genetic determinants) that encode key bacterial traits involved, such as chemotaxis and motility, nutrient acquisition and metabolic independence, competitive and defensive arsenals, attachment and biofilm formation, evasion of plant immunity, and endophytic entry and persistence. Throughout, we use evidence from comparative genomics and metagenomics, (meta)transcriptomics, targeted mutagenesis and genome-wide screens such as Tn-seq, obtained in systems ranging from binary interactions to synthetic communities and natural soils. For each stage we examine the current state of knowledge, identify critical gaps, and propose avenues to deepen our mechanistic understanding of the bacterial traits involved in plant colonisation. We argue that this mechanistic understanding is the missing foundation for developing inoculants with more consistent and robust performance across diverse agroecosystems.
Additional Links: PMID-42863410
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PubMed:
Citation:
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@article {pmid42863410,
year = {2026},
author = {Villa-RodrÃguez, E and Ferguson, S and Stougaard, J and Radutoiu, S},
title = {Understanding genetic determinants of bacterial adaptation to plant niches: Toward more robust bioinoculant design.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128760},
doi = {10.1016/j.micres.2026.128760},
pmid = {42863410},
issn = {1618-0623},
abstract = {Plant-associated bacteria offer a sustainable alternative to chemical inputs in agriculture, yet the field performance of microbial inoculants remains inconsistent. A central but frequently overlooked cause is that bioprospecting pipelines still select strains on the basis of plant-growth-promoting activities, while the bacterial genetic traits that determine whether a strain can reach, colonise and persist in a given root compartment are rarely assessed. Previous reviews have largely catalogued growth-promoting functions or described root microbiome assembly from the plant's perspective, here we take the bacterium's. We trace the journey of a bacterium from bulk soil to its final niche and, at each stage, identify the genes and pathways (genetic determinants) that encode key bacterial traits involved, such as chemotaxis and motility, nutrient acquisition and metabolic independence, competitive and defensive arsenals, attachment and biofilm formation, evasion of plant immunity, and endophytic entry and persistence. Throughout, we use evidence from comparative genomics and metagenomics, (meta)transcriptomics, targeted mutagenesis and genome-wide screens such as Tn-seq, obtained in systems ranging from binary interactions to synthetic communities and natural soils. For each stage we examine the current state of knowledge, identify critical gaps, and propose avenues to deepen our mechanistic understanding of the bacterial traits involved in plant colonisation. We argue that this mechanistic understanding is the missing foundation for developing inoculants with more consistent and robust performance across diverse agroecosystems.},
}
RevDate: 2026-10-12
Associations between fermented dairy food intake during pregnancy and gestational weight gain, macrosomia, and gut microbiota.
Clinical nutrition ESPEN pii:S2405-4577(26)02291-6 [Epub ahead of print].
BACKGROUND AND AIMS: Fermented dairy food (FDF) operationalized in this study as cheese and yogurt, contains beneficial microbes and bioactive metabolites that may support maternal and offspring health, yet FDF intake and its association with maternal-offspring health outcomes is understudied in the US population. We evaluated the associations between FDF intake during pregnancy from the participants of The Growing Life, Optimizing Wellness Study (GLOWING, ClinicalTrials.gov ID: NCT01131117) and gestational weight gain (GWG), macrosomia (body weight ≥4000g at birth), and mother and infant microbiota composition.
METHODS: Dietary data were collected using 3-day food records at six pregnancy visits and FDF intake (cheese, yogurt) were extracted based on food descriptions and codes. Maternal microbiota composition was evaluated at each trimester of pregnancy, while the infant microbiota composition was assessed at one month, 6 months and 12 months of age using 16S rRNA gene sequencing.
RESULTS: In this cohort, the mean FDF intake during pregnancy was 63 g/day. Higher FDF intake was positively associated with healthier body weight at enrollment and overall Healthy Eating Index score during pregnancy. No significant associations between FDF intake and GWG or macrosomia were observed. FDF intake during pregnancy was negatively associated with only one taxon, Bacteroidetes (now Bacteroidota) in infants aged 6 months.
CONCLUSION: While FDF intake during pregnancy was positively associated with healthier pre- or early pregnancy weight and diet quality during pregnancy, it was not associated with GWG, macrosomia, or maternal microbiome. These results need to be interpreted in the context of the limited variety and amount of fermented food consumed during pregnancy in this cohort. Future studies that include participants from larger geographical locations with broader FDF intakes could provide more insight into the associations between FDF and maternal and infant health outcomes.
Additional Links: PMID-42863670
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PubMed:
Citation:
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@article {pmid42863670,
year = {2026},
author = {Gurung, M and Chandrashekar, R and Thomson, JL and Landry, AS and Read, QD and Martinez, AE and Andres, A and Yeruva, L},
title = {Associations between fermented dairy food intake during pregnancy and gestational weight gain, macrosomia, and gut microbiota.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105194},
doi = {10.1016/j.clnesp.2026.105194},
pmid = {42863670},
issn = {2405-4577},
abstract = {BACKGROUND AND AIMS: Fermented dairy food (FDF) operationalized in this study as cheese and yogurt, contains beneficial microbes and bioactive metabolites that may support maternal and offspring health, yet FDF intake and its association with maternal-offspring health outcomes is understudied in the US population. We evaluated the associations between FDF intake during pregnancy from the participants of The Growing Life, Optimizing Wellness Study (GLOWING, ClinicalTrials.gov ID: NCT01131117) and gestational weight gain (GWG), macrosomia (body weight ≥4000g at birth), and mother and infant microbiota composition.
METHODS: Dietary data were collected using 3-day food records at six pregnancy visits and FDF intake (cheese, yogurt) were extracted based on food descriptions and codes. Maternal microbiota composition was evaluated at each trimester of pregnancy, while the infant microbiota composition was assessed at one month, 6 months and 12 months of age using 16S rRNA gene sequencing.
RESULTS: In this cohort, the mean FDF intake during pregnancy was 63 g/day. Higher FDF intake was positively associated with healthier body weight at enrollment and overall Healthy Eating Index score during pregnancy. No significant associations between FDF intake and GWG or macrosomia were observed. FDF intake during pregnancy was negatively associated with only one taxon, Bacteroidetes (now Bacteroidota) in infants aged 6 months.
CONCLUSION: While FDF intake during pregnancy was positively associated with healthier pre- or early pregnancy weight and diet quality during pregnancy, it was not associated with GWG, macrosomia, or maternal microbiome. These results need to be interpreted in the context of the limited variety and amount of fermented food consumed during pregnancy in this cohort. Future studies that include participants from larger geographical locations with broader FDF intakes could provide more insight into the associations between FDF and maternal and infant health outcomes.},
}
RevDate: 2026-10-12
LC-MS/MS quantification of trimethylamine N-oxide in plasma and volumetric absorptive microsamples: analytical validation and feasibility in pediatric kidney transplant recipients.
Clinica chimica acta; international journal of clinical chemistry pii:S0009-8981(26)02076-0 [Epub ahead of print].
Trimethylamine N-oxide (TMAO) is a gut microbiome-related metabolite that may be associated with kidney injury and cardiovascular risk. Measuring TMAO in children after kidney transplantation may support investigation of the gut-kidney-cardiovascular axis; however, repeated venous sampling is often impractical in pediatric longitudinal studies. This study aimed to validate a rapid LC-MS/MS method for measuring TMAO in plasma and 10 μL dried capillary blood samples collected using volumetric absorptive microsampling (VAMS). TMAO was quantified using its stable-isotope-labelled internal standard, TMAO-d9, by hydrophilic interaction chromatography (HILIC) with positive electrospray ionization. For TMAO, an endogenous analyte, the calibration curves were determined using a surrogate matrix of 5% bovine serum albumin in phosphate-buffered saline (PBS) for plasma and a surrogate whole-blood matrix for VAMS. Quality control samples were prepared in authentic matrices. The validation process involved examining the calibration curve, LLOQ, accuracy, precision, recovery, matrix effect, stability, incurred sample reanalysis, matrix parallelism, and comparability of plasma-VAMS results. The assay calibration curve was linear from 0.1 to 20 μmol/L. The LLOQ was 0.1 μmol/L for both matrices. The mean calibration R[2] values were 0.9989 ± 0.0007 for plasma and 0.9981 ± 0.0011 for VAMS. The surrogate and true matrices exhibited similar parallelism (slopes of 0.97 and 0.93 for plasma and VAMS, respectively). In the pediatric kidney transplant population, plasma TMAO was highly correlated with serum creatinine (r = 0.964) and inversely correlated with eGFR (r = -0.788). Similar associations were observed between VAMS plasma-estimated TMAO and creatinine (r = 0.951) and eGFR (r = -0.784). The validated method enables reliable quantification of TMAO in both plasma and VAMS microsamples and demonstrates analytical feasibility for future longitudinal biomarker studies in pediatric kidney transplantation. However, these clinical findings should be considered exploratory rather than evidence of clinical utility.
Additional Links: PMID-42863687
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PubMed:
Citation:
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@article {pmid42863687,
year = {2026},
author = {Czarnowski, P and Czajkowska, A and Rubik, J and Kocur, A},
title = {LC-MS/MS quantification of trimethylamine N-oxide in plasma and volumetric absorptive microsamples: analytical validation and feasibility in pediatric kidney transplant recipients.},
journal = {Clinica chimica acta; international journal of clinical chemistry},
volume = {},
number = {},
pages = {122894},
doi = {10.1016/j.cca.2026.122894},
pmid = {42863687},
issn = {1873-3492},
abstract = {Trimethylamine N-oxide (TMAO) is a gut microbiome-related metabolite that may be associated with kidney injury and cardiovascular risk. Measuring TMAO in children after kidney transplantation may support investigation of the gut-kidney-cardiovascular axis; however, repeated venous sampling is often impractical in pediatric longitudinal studies. This study aimed to validate a rapid LC-MS/MS method for measuring TMAO in plasma and 10 μL dried capillary blood samples collected using volumetric absorptive microsampling (VAMS). TMAO was quantified using its stable-isotope-labelled internal standard, TMAO-d9, by hydrophilic interaction chromatography (HILIC) with positive electrospray ionization. For TMAO, an endogenous analyte, the calibration curves were determined using a surrogate matrix of 5% bovine serum albumin in phosphate-buffered saline (PBS) for plasma and a surrogate whole-blood matrix for VAMS. Quality control samples were prepared in authentic matrices. The validation process involved examining the calibration curve, LLOQ, accuracy, precision, recovery, matrix effect, stability, incurred sample reanalysis, matrix parallelism, and comparability of plasma-VAMS results. The assay calibration curve was linear from 0.1 to 20 μmol/L. The LLOQ was 0.1 μmol/L for both matrices. The mean calibration R[2] values were 0.9989 ± 0.0007 for plasma and 0.9981 ± 0.0011 for VAMS. The surrogate and true matrices exhibited similar parallelism (slopes of 0.97 and 0.93 for plasma and VAMS, respectively). In the pediatric kidney transplant population, plasma TMAO was highly correlated with serum creatinine (r = 0.964) and inversely correlated with eGFR (r = -0.788). Similar associations were observed between VAMS plasma-estimated TMAO and creatinine (r = 0.951) and eGFR (r = -0.784). The validated method enables reliable quantification of TMAO in both plasma and VAMS microsamples and demonstrates analytical feasibility for future longitudinal biomarker studies in pediatric kidney transplantation. However, these clinical findings should be considered exploratory rather than evidence of clinical utility.},
}
RevDate: 2026-10-12
Subpopulation networks: a scaling principle for engineering living systems.
Trends in biotechnology pii:S0167-7799(26)00388-4 [Epub ahead of print].
Cell populations underpin applications ranging from bioproduction and biotherapeutics to microbiome engineering and biocomputing. However, treating them as bulk quantities rather than as structured systems limits our understanding of population-level stability, productivity, and robustness. Cellular populations self-organize into coexisting subpopulations (SPs) representing phenotypically distinct states that emerge from the interplay of biological noise and selective pressures. We propose that networks of interacting SPs constitute a fundamental organizational layer for engineering stable cell population dynamics. Surveying published single-cell studies across bacterial, yeast, and mammalian systems, we show that populations consistently self-organize into a limited number of SPs. This dimensional reduction can be captured experimentally by clustering single-cell data and gives rise to scaling laws that link population structure to collective performance.
Additional Links: PMID-42864232
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PubMed:
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@article {pmid42864232,
year = {2026},
author = {Delvigne, F and Roeloffs, F and Josselin, L and Pressé, S and Olsson, L and Grünberger, A},
title = {Subpopulation networks: a scaling principle for engineering living systems.},
journal = {Trends in biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tibtech.2026.09.018},
pmid = {42864232},
issn = {1879-3096},
abstract = {Cell populations underpin applications ranging from bioproduction and biotherapeutics to microbiome engineering and biocomputing. However, treating them as bulk quantities rather than as structured systems limits our understanding of population-level stability, productivity, and robustness. Cellular populations self-organize into coexisting subpopulations (SPs) representing phenotypically distinct states that emerge from the interplay of biological noise and selective pressures. We propose that networks of interacting SPs constitute a fundamental organizational layer for engineering stable cell population dynamics. Surveying published single-cell studies across bacterial, yeast, and mammalian systems, we show that populations consistently self-organize into a limited number of SPs. This dimensional reduction can be captured experimentally by clustering single-cell data and gives rise to scaling laws that link population structure to collective performance.},
}
RevDate: 2026-10-12
CmpDate: 2026-10-12
Gut microbiota shaping fatty liver disease progression.
Life science alliance, 10(1): pii:10/1/e202603756.
The gut-liver axis is an important regulator of homeostasis, and its dysregulation has been implicated in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). In this review, we summarize current knowledge on both compositional alterations of the gut microbiome in MASLD and the functional consequences of these changes. We first discuss changes across major microbial domains, including bacteria, archaea, eukaryota, and bacteriophages, and then focus on microbiota-derived metabolites, such as short-chain fatty acids, trimethylamine and its derivative trimethylamine N-oxide, tryptophan-derived indoles, secondary bile acids, and other bioactive compounds. Their complex impacts on intestinal barrier integrity, inflammation, lipid and glucose metabolism, and immune and hormonal signaling in the liver are highlighted. We further examine mechanisms involving the translocation of microbial products and the modulation of nuclear and membrane receptors. Finally, we outline current challenges and knowledge gaps that need to be addressed to better understand the role of the gut microbiota in MASLD.
Additional Links: PMID-42864263
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PubMed:
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@article {pmid42864263,
year = {2027},
author = {Wysokińska, M and Mysza, M and Uryga, AE and Kołodziejczyk, AA},
title = {Gut microbiota shaping fatty liver disease progression.},
journal = {Life science alliance},
volume = {10},
number = {1},
pages = {},
doi = {10.26508/lsa.202603756},
pmid = {42864263},
issn = {2575-1077},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Fatty Liver/microbiology/metabolism ; Animals ; Disease Progression ; Liver/metabolism ; Intestinal Barrier Function ; Methylamines/metabolism ; Lipid Metabolism ; Bacteria/metabolism ; Bile Acids and Salts/metabolism ; Fatty Acids, Volatile/metabolism ; },
abstract = {The gut-liver axis is an important regulator of homeostasis, and its dysregulation has been implicated in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). In this review, we summarize current knowledge on both compositional alterations of the gut microbiome in MASLD and the functional consequences of these changes. We first discuss changes across major microbial domains, including bacteria, archaea, eukaryota, and bacteriophages, and then focus on microbiota-derived metabolites, such as short-chain fatty acids, trimethylamine and its derivative trimethylamine N-oxide, tryptophan-derived indoles, secondary bile acids, and other bioactive compounds. Their complex impacts on intestinal barrier integrity, inflammation, lipid and glucose metabolism, and immune and hormonal signaling in the liver are highlighted. We further examine mechanisms involving the translocation of microbial products and the modulation of nuclear and membrane receptors. Finally, we outline current challenges and knowledge gaps that need to be addressed to better understand the role of the gut microbiota in MASLD.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/physiology
*Fatty Liver/microbiology/metabolism
Animals
Disease Progression
Liver/metabolism
Intestinal Barrier Function
Methylamines/metabolism
Lipid Metabolism
Bacteria/metabolism
Bile Acids and Salts/metabolism
Fatty Acids, Volatile/metabolism
RevDate: 2026-10-12
Infant microbiome development: a renewed focus on the second six months and complementary feeding.
Pediatric research [Epub ahead of print].
Additional Links: PMID-42864402
PubMed:
Citation:
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@article {pmid42864402,
year = {2026},
author = {Chadwick, BP and Dicker, AJ and Hansen, R},
title = {Infant microbiome development: a renewed focus on the second six months and complementary feeding.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42864402},
issn = {1530-0447},
}
RevDate: 2026-10-13
The Microbiome-Gut-Lung axis in Respiratory Diseases: From Biological Mechanisms to Clinical Translation.
Respirology (Carlton, Vic.) [Epub ahead of print].
Respiratory diseases exhibit substantial heterogeneity in clinical phenotypes and underlying pathobiology that cannot be fully captured by conventional lung-centred frameworks. Accumulating evidence implicates a role for the microbiome-gut-lung axis in respiratory disease pathogenesis. Within this bidirectional axis, gut-derived microbial metabolites and structural components can modulate pulmonary immunity, whereas respiratory infection and exposures can reciprocally influence the gut microbiota. Dysregulation of the microbiome-gut-lung axis may influence respiratory disease susceptibility, progression, and clinical presentation. In this Review, we outline core mechanisms of gut-lung crosstalk, including metabolite-driven immunomodulation, pattern recognition receptor signalling and reciprocal immune-ecological remodelling. We synthesize phenotype-specific evidence linking the axis to major chronic inflammatory airway diseases (asthma, chronic obstructive pulmonary disease, cystic fibrosis and bronchiectasis) and acute respiratory disorders (pneumonia and sepsis-associated acute respiratory distress syndrome), emphasizing mechanistic and clinical evidence. We discuss the translational promise of gut-lung signatures as biomarkers and treatable traits and review current therapies with microbiome effects and emerging microbiome-targeted interventions. Finally, we address key challenges and propose future research priorities to advance clinical management leveraging the gut-lung axis.
Additional Links: PMID-42864764
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PubMed:
Citation:
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@article {pmid42864764,
year = {2026},
author = {Yang, Y and Tang, X and Chen, R and Wang, Z},
title = {The Microbiome-Gut-Lung axis in Respiratory Diseases: From Biological Mechanisms to Clinical Translation.},
journal = {Respirology (Carlton, Vic.)},
volume = {},
number = {},
pages = {},
doi = {10.1002/resp.70329},
pmid = {42864764},
issn = {1440-1843},
support = {2022YFA1304300//National Key Research and Development Program of China/ ; 82495200//National Natural Science Foundation of China/ ; 82495201//National Natural Science Foundation of China/ ; 82404633//National Natural Science Foundation of China/ ; GZNL2023A02001//Major Project of Guangzhou National Laboratory/ ; 2024ZD0528400//Noncommunicable Chronic Diseases-National Science and Technology Major Project/ ; 2026ZD0555400//Noncommunicable Chronic Diseases-National Science and Technology Major Project/ ; SKLRD-Z-202507//Open Project of State Key Laboratory of Respiratory Disease/ ; 2026A1515011144//Basic and Applied Basic Research Foundation of Guangdong Province/ ; },
abstract = {Respiratory diseases exhibit substantial heterogeneity in clinical phenotypes and underlying pathobiology that cannot be fully captured by conventional lung-centred frameworks. Accumulating evidence implicates a role for the microbiome-gut-lung axis in respiratory disease pathogenesis. Within this bidirectional axis, gut-derived microbial metabolites and structural components can modulate pulmonary immunity, whereas respiratory infection and exposures can reciprocally influence the gut microbiota. Dysregulation of the microbiome-gut-lung axis may influence respiratory disease susceptibility, progression, and clinical presentation. In this Review, we outline core mechanisms of gut-lung crosstalk, including metabolite-driven immunomodulation, pattern recognition receptor signalling and reciprocal immune-ecological remodelling. We synthesize phenotype-specific evidence linking the axis to major chronic inflammatory airway diseases (asthma, chronic obstructive pulmonary disease, cystic fibrosis and bronchiectasis) and acute respiratory disorders (pneumonia and sepsis-associated acute respiratory distress syndrome), emphasizing mechanistic and clinical evidence. We discuss the translational promise of gut-lung signatures as biomarkers and treatable traits and review current therapies with microbiome effects and emerging microbiome-targeted interventions. Finally, we address key challenges and propose future research priorities to advance clinical management leveraging the gut-lung axis.},
}
RevDate: 2026-10-13
Wheat straw biochar enhances rhizosphere colonization of Bacillus amyloliquefaciens B1408 for biocontrol of cucumber Fusarium wilt.
Pest management science [Epub ahead of print].
BACKGROUND: Plant growth-promoting rhizobacteria (PGPR) offer a sustainable alternative for managing soilborne diseases, yet their field efficacy is often compromised by poor rhizosphere persistence. Here, we tracked the spatiotemporal colonization dynamics of a GFP-labeled Bacillus amyloliquefaciens B1408 strain and developed a wheat straw biochar-based formulation to overcome this bottleneck.
RESULTS: At 120 days post-inoculation, the biochar formulation increased B1408 populations from 7.49 × 10[3] to 4.96 × 10[4] CFU g[-1] in the rhizosphere soil and from 1.41 × 10[4] to 7.58 × 10[4] CFU g[-1] on the rhizoplane, corresponding to 6.62- and 5.36-fold increases, respectively. In pot trials, the formulation reduced the cucumber Fusarium wilt disease index from 73.33% to 20%. The WSBA treatment was associated with enhanced soil nutrient-cycling enzyme and plant antioxidant enzyme activities, altered rhizosphere microbial community structure, reduced the connectivity of FOC-associated microbial co-occurrence networks, and enriched several indigenous bacterial genera, including Allorhizobium and Sphingomonas. In validation assays, Allorhizobium sp. 813 and Ensifer sp. 4724 isolated from the WSBA-treated rhizosphere significantly increased cucumber plant height and fresh weight.
CONCLUSION: These findings demonstrate that wheat straw biochar enhances the rhizosphere persistence and biocontrol efficacy of B1408 and is associated with changes in rhizosphere microbial composition and network connectivity. This formulation provides a promising strategy for improving the stability and performance of B. amyloliquefaciens-based biocontrol agents. © 2026 Society of Chemical Industry.
Additional Links: PMID-42864827
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@article {pmid42864827,
year = {2026},
author = {Yu, H and Feng, J and Li, M and Zhao, Y and Wang, Y},
title = {Wheat straw biochar enhances rhizosphere colonization of Bacillus amyloliquefaciens B1408 for biocontrol of cucumber Fusarium wilt.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.71400},
pmid = {42864827},
issn = {1526-4998},
support = {32072474//the Natural Science Foundation of China/ ; 2017YFD0201203//National Key Research and Development Program of China/ ; 2020zdzx03-03-01//major Science and Technology Projects of Shaanxi Province/ ; },
abstract = {BACKGROUND: Plant growth-promoting rhizobacteria (PGPR) offer a sustainable alternative for managing soilborne diseases, yet their field efficacy is often compromised by poor rhizosphere persistence. Here, we tracked the spatiotemporal colonization dynamics of a GFP-labeled Bacillus amyloliquefaciens B1408 strain and developed a wheat straw biochar-based formulation to overcome this bottleneck.
RESULTS: At 120 days post-inoculation, the biochar formulation increased B1408 populations from 7.49 × 10[3] to 4.96 × 10[4] CFU g[-1] in the rhizosphere soil and from 1.41 × 10[4] to 7.58 × 10[4] CFU g[-1] on the rhizoplane, corresponding to 6.62- and 5.36-fold increases, respectively. In pot trials, the formulation reduced the cucumber Fusarium wilt disease index from 73.33% to 20%. The WSBA treatment was associated with enhanced soil nutrient-cycling enzyme and plant antioxidant enzyme activities, altered rhizosphere microbial community structure, reduced the connectivity of FOC-associated microbial co-occurrence networks, and enriched several indigenous bacterial genera, including Allorhizobium and Sphingomonas. In validation assays, Allorhizobium sp. 813 and Ensifer sp. 4724 isolated from the WSBA-treated rhizosphere significantly increased cucumber plant height and fresh weight.
CONCLUSION: These findings demonstrate that wheat straw biochar enhances the rhizosphere persistence and biocontrol efficacy of B1408 and is associated with changes in rhizosphere microbial composition and network connectivity. This formulation provides a promising strategy for improving the stability and performance of B. amyloliquefaciens-based biocontrol agents. © 2026 Society of Chemical Industry.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Targeting the Tumor Microenvironment Network to Overcome Immunotherapy Resistance in Non-Small Cell Lung Cancer: Mechanisms to Clinical Translation.
Cancer medicine, 15(10):e72335.
BACKGROUND: Immunotherapy has transformed the treatment landscape for advanced non-small cell lung cancer (NSCLC), yet resistance mediated by the tumor microenvironment (TME) limits its efficacy in most patients. This review aims to synthesize the current understanding of the TME as an integrated network driving immunotherapy resistance and to evaluate emerging therapeutic strategies aimed at overcoming it.
METHODS: We conducted a comprehensive narrative review of key literature in the field, sourced from PubMed and major conference proceedings. The focus was on mechanistic studies elucidating immunosuppressive cell circuits, metabolic reprogramming, epigenetic regulation, spatial heterogeneity, and microbiome interactions within the lung cancer TME. Preclinical and clinical evidence for TME-targeted combination therapies and biomarker development was also critically analyzed.
RESULTS: The TME orchestrates resistance through highly interconnected axes: (1) cellular circuits including myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), and M2-polarized tumor-associated macrophages (M2-TAMs), (2) metabolic barriers (lactate acidosis, nutrient depletion), (3) epigenetic reprogramming, and (4) systemic communication via exosomes and the microbiome. Spatial transcriptomics reveals that driver mutations (e.g., EGFR, KRAS) shape distinct immune-excluded architectures. To disrupt this network, rational combination strategies-such as immune checkpoint inhibitors with metabolic modulators (LDHAi), epigenetic drugs, targeted agents (METi), or microbiome interventions-show synergistic potential in early-phase trials. Furthermore, a tiered biomarker system integrating spatial, metabolic, and microbial features is proposed to guide patient stratification.
CONCLUSION: Overcoming immunotherapy resistance requires a paradigm shift from single-target to network-targeted therapy. This review provides an integrated framework for understanding TME-mediated resistance and translates these insights into a roadmap for clinical translation. Future efforts must prioritize biomarker-validated, rationally designed combination therapies to improve outcomes for patients with resistant NSCLC.
Additional Links: PMID-42864833
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PubMed:
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@article {pmid42864833,
year = {2026},
author = {Wang, Z and Luo, Z and Wang, L and Tang, J and Zhang, Z and Fan, X},
title = {Targeting the Tumor Microenvironment Network to Overcome Immunotherapy Resistance in Non-Small Cell Lung Cancer: Mechanisms to Clinical Translation.},
journal = {Cancer medicine},
volume = {15},
number = {10},
pages = {e72335},
doi = {10.1002/cam4.72335},
pmid = {42864833},
issn = {2045-7634},
support = {202301AY070001-090//The Science and Technology Department of Yunnan Province-Kunming Medical University Joint Special Project/ ; 202501AS070099//The Basic Research Key Project of Science and Technology Department of Yunnan Province/ ; RLMY20220004//The Yunnan Xingdian Talent Support Program-Famous Doctor Training Object/ ; RLMY20220011//The Yunnan Xingdian Talent Support Program-Famous Doctor Training Object/ ; //The National Collaborative "Flagship" Department of Chinese and Western Medicine/ ; 2025-TD-03//The Kunming Medical University First Affiliated Hospital Undergraduate Education Teaching High-Quality Development Research Project-Respiratory Medicine Teaching Master Team/ ; },
mesh = {Humans ; *Tumor Microenvironment/immunology/drug effects ; *Carcinoma, Non-Small-Cell Lung/immunology/drug therapy/therapy/pathology ; *Lung Neoplasms/immunology/drug therapy/therapy/pathology ; *Immunotherapy/methods ; *Drug Resistance, Neoplasm/drug effects ; Animals ; Translational Research, Biomedical ; Metabolic Reprogramming ; },
abstract = {BACKGROUND: Immunotherapy has transformed the treatment landscape for advanced non-small cell lung cancer (NSCLC), yet resistance mediated by the tumor microenvironment (TME) limits its efficacy in most patients. This review aims to synthesize the current understanding of the TME as an integrated network driving immunotherapy resistance and to evaluate emerging therapeutic strategies aimed at overcoming it.
METHODS: We conducted a comprehensive narrative review of key literature in the field, sourced from PubMed and major conference proceedings. The focus was on mechanistic studies elucidating immunosuppressive cell circuits, metabolic reprogramming, epigenetic regulation, spatial heterogeneity, and microbiome interactions within the lung cancer TME. Preclinical and clinical evidence for TME-targeted combination therapies and biomarker development was also critically analyzed.
RESULTS: The TME orchestrates resistance through highly interconnected axes: (1) cellular circuits including myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), and M2-polarized tumor-associated macrophages (M2-TAMs), (2) metabolic barriers (lactate acidosis, nutrient depletion), (3) epigenetic reprogramming, and (4) systemic communication via exosomes and the microbiome. Spatial transcriptomics reveals that driver mutations (e.g., EGFR, KRAS) shape distinct immune-excluded architectures. To disrupt this network, rational combination strategies-such as immune checkpoint inhibitors with metabolic modulators (LDHAi), epigenetic drugs, targeted agents (METi), or microbiome interventions-show synergistic potential in early-phase trials. Furthermore, a tiered biomarker system integrating spatial, metabolic, and microbial features is proposed to guide patient stratification.
CONCLUSION: Overcoming immunotherapy resistance requires a paradigm shift from single-target to network-targeted therapy. This review provides an integrated framework for understanding TME-mediated resistance and translates these insights into a roadmap for clinical translation. Future efforts must prioritize biomarker-validated, rationally designed combination therapies to improve outcomes for patients with resistant NSCLC.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Tumor Microenvironment/immunology/drug effects
*Carcinoma, Non-Small-Cell Lung/immunology/drug therapy/therapy/pathology
*Lung Neoplasms/immunology/drug therapy/therapy/pathology
*Immunotherapy/methods
*Drug Resistance, Neoplasm/drug effects
Animals
Translational Research, Biomedical
Metabolic Reprogramming
RevDate: 2026-10-13
The Gut Microbiota-inflammation-immune Axis in Cancer: Anti-inflammatory Mechanisms and Therapeutic Implications.
Anti-inflammatory & anti-allergy agents in medicinal chemistry pii:AIAAMC-EPUB-159031 [Epub ahead of print].
Through its mediation between inflammatory and immune pathways, the gut microbiota has proved to be a key regulator of cancer development, progression, and treatment response. Changes in microbial composition known as dysbiosis might facilitate chronic inflammation, immune dysregulation, and genomic instability, thereby facilitating carcinogenesis. Conversely, positive commensal microbes can generate short-chain fatty acids, bile acids, and tryptophan derivatives, which help maintain the epithelial barrier, cytokine signaling, and innate and adaptive immune responses. These microbial metabolites regulate immune cell differentiation, including regulatory T cells, dendritic cells, macrophages, and cytotoxic CD8+ T cells, thereby impacting the tumor microenvironment and tumor progression. Recent research highlights the microbiota as an outcome of response to cancer therapies, particularly immune checkpoint inhibitors, chemotherapy, and targeted therapies. Certain microbial genera, e.g., Akkermansia muciniphila, Bifidobacterium species, and Faecalibacterium prausnitzii, have been linked to augmented antitumor immunity and treatment efficacy. To enhance treatment outcomes and minimize toxicity during therapy, therapeutic interventions that target the regulation of the gut microbiome, such as dietary interventions, probiotics, prebiotics, fecal microbiota transplantation, and engineered microbial platforms, are under investigation. Moreover, improvements in metagenomics, metabolomics, and immunomics are now enabling the discovery of microbiome-based biomarkers to inform precision oncology. Knowledge of the gut microbiota-inflammation-immune axis thus presents promising possibilities in creating new treatment modalities and in designing individualized treatments in cancer management.
Additional Links: PMID-42864924
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PubMed:
Citation:
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@article {pmid42864924,
year = {2026},
author = {Suresh, N and Singh, V and Rathore, A and Dwivedi, S and Bansal, A},
title = {The Gut Microbiota-inflammation-immune Axis in Cancer: Anti-inflammatory Mechanisms and Therapeutic Implications.},
journal = {Anti-inflammatory & anti-allergy agents in medicinal chemistry},
volume = {},
number = {},
pages = {},
doi = {10.2174/0118715230502786261001104534},
pmid = {42864924},
issn = {1875-614X},
abstract = {Through its mediation between inflammatory and immune pathways, the gut microbiota has proved to be a key regulator of cancer development, progression, and treatment response. Changes in microbial composition known as dysbiosis might facilitate chronic inflammation, immune dysregulation, and genomic instability, thereby facilitating carcinogenesis. Conversely, positive commensal microbes can generate short-chain fatty acids, bile acids, and tryptophan derivatives, which help maintain the epithelial barrier, cytokine signaling, and innate and adaptive immune responses. These microbial metabolites regulate immune cell differentiation, including regulatory T cells, dendritic cells, macrophages, and cytotoxic CD8+ T cells, thereby impacting the tumor microenvironment and tumor progression. Recent research highlights the microbiota as an outcome of response to cancer therapies, particularly immune checkpoint inhibitors, chemotherapy, and targeted therapies. Certain microbial genera, e.g., Akkermansia muciniphila, Bifidobacterium species, and Faecalibacterium prausnitzii, have been linked to augmented antitumor immunity and treatment efficacy. To enhance treatment outcomes and minimize toxicity during therapy, therapeutic interventions that target the regulation of the gut microbiome, such as dietary interventions, probiotics, prebiotics, fecal microbiota transplantation, and engineered microbial platforms, are under investigation. Moreover, improvements in metagenomics, metabolomics, and immunomics are now enabling the discovery of microbiome-based biomarkers to inform precision oncology. Knowledge of the gut microbiota-inflammation-immune axis thus presents promising possibilities in creating new treatment modalities and in designing individualized treatments in cancer management.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Context-dependent TREM2 signalling in myeloid cells: Molecular mechanisms and immunotherapeutic divergence in neurodegeneration and cancer.
Clinical and translational medicine, 16(10):e70863.
BACKGROUND: Triggering receptor expressed on myeloid cells 2 (TREM2) is a pivotal lipid-sensing receptor that governs the functional plasticity and metabolic fitness of mononuclear phagocytes, including microglia, osteoclasts, dendritic cells and tissue-resident macrophages. While originally identified as a genetic risk factor for Alzheimer's disease (AD), TREM2 functions as a context-dependent immunometabolic checkpoint rather than a uniform phenotypic driver, exerting divergent biological outputs dictated by distinct tissue microenvironments and ligand repertoires.
SUMMARY OF KEY CONTENTS: This review provides a comprehensive synthesis of TREM2 immunobiology, detailing how ligand engagement-including cell-surface phospholipids and apolipoprotein E (ApoE)-activates the DAP12/DAP10-SYK-PI3K-mTOR signalling axis. This coordinated intracellular cascade instructively drives myeloid adaptation towards metabolically competent disease-associated microglia (DAM) and lipid-associated macrophage (LAM) states, sustaining bioenergetics and debris clearance under pathological stress. Across neurodegenerative proteinopathies and acute cerebral ischemia, TREM2 signalling is predominantly neuroprotective by promoting aggregate compaction and mitigating secondary excitotoxicity, although chronic dysregulated activation may drive stage-dependent neuroinflammation. In peripheral inflammatory pathologies such as rheumatoid arthritis and sepsis, TREM2 fine-tunes macrophage efferocytosis and systemic metabolic thresholds. In oncology, TREM2 displays a complex, microenvironment-dependent divergence: in central nervous system malignancies such as glioblastoma (GBM), TREM2 exerts controversial, stage-dependent effects, spanning microglial tumour containment in early stages versus pro-tumoural myelin recycling and immunosuppression by monocyte-derived macrophages in post-treatment recurrence; conversely, in peripheral solid tumours, monocyte-derived TREM2+ tumour-associated macrophages (TAMs) predominantly orchestrate an immunosuppressive, nutrient-deprived niche that impairs cytotoxic T-cell function. Furthermore, we synthesise emerging paradigms along the bidirectional microbiome-gut-brain-tumour axis, elucidating how commensal and intra-tumoural microbial cues dynamically calibrate myeloid signalling tone and therapeutic susceptibility.
CONCLUSION: We address translation bottlenecks-including blood-brain barrier (BBB) shuttles, human trial scarcity and soluble TREM2 (sTREM2) biomarker harmonisation-outlining a biomarker-guided, context-tailored precision therapeutic framework for targeting the TREM2 axis.
Additional Links: PMID-42865133
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PubMed:
Citation:
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@article {pmid42865133,
year = {2026},
author = {Lv, Y and Shi, M and Zhao, Y and Yu, Y and Lv, J and Zhao, H},
title = {Context-dependent TREM2 signalling in myeloid cells: Molecular mechanisms and immunotherapeutic divergence in neurodegeneration and cancer.},
journal = {Clinical and translational medicine},
volume = {16},
number = {10},
pages = {e70863},
doi = {10.1002/ctm2.70863},
pmid = {42865133},
issn = {2001-1326},
support = {ZR2022QH372//Shandong Province Natural Science Foundation/ ; },
mesh = {Humans ; *Receptors, Immunologic/metabolism ; *Membrane Glycoproteins/metabolism ; *Signal Transduction ; *Myeloid Cells/metabolism/immunology ; *Neoplasms/therapy/immunology ; Animals ; *Immunotherapy/methods ; *Neurodegenerative Diseases/therapy/immunology ; },
abstract = {BACKGROUND: Triggering receptor expressed on myeloid cells 2 (TREM2) is a pivotal lipid-sensing receptor that governs the functional plasticity and metabolic fitness of mononuclear phagocytes, including microglia, osteoclasts, dendritic cells and tissue-resident macrophages. While originally identified as a genetic risk factor for Alzheimer's disease (AD), TREM2 functions as a context-dependent immunometabolic checkpoint rather than a uniform phenotypic driver, exerting divergent biological outputs dictated by distinct tissue microenvironments and ligand repertoires.
SUMMARY OF KEY CONTENTS: This review provides a comprehensive synthesis of TREM2 immunobiology, detailing how ligand engagement-including cell-surface phospholipids and apolipoprotein E (ApoE)-activates the DAP12/DAP10-SYK-PI3K-mTOR signalling axis. This coordinated intracellular cascade instructively drives myeloid adaptation towards metabolically competent disease-associated microglia (DAM) and lipid-associated macrophage (LAM) states, sustaining bioenergetics and debris clearance under pathological stress. Across neurodegenerative proteinopathies and acute cerebral ischemia, TREM2 signalling is predominantly neuroprotective by promoting aggregate compaction and mitigating secondary excitotoxicity, although chronic dysregulated activation may drive stage-dependent neuroinflammation. In peripheral inflammatory pathologies such as rheumatoid arthritis and sepsis, TREM2 fine-tunes macrophage efferocytosis and systemic metabolic thresholds. In oncology, TREM2 displays a complex, microenvironment-dependent divergence: in central nervous system malignancies such as glioblastoma (GBM), TREM2 exerts controversial, stage-dependent effects, spanning microglial tumour containment in early stages versus pro-tumoural myelin recycling and immunosuppression by monocyte-derived macrophages in post-treatment recurrence; conversely, in peripheral solid tumours, monocyte-derived TREM2+ tumour-associated macrophages (TAMs) predominantly orchestrate an immunosuppressive, nutrient-deprived niche that impairs cytotoxic T-cell function. Furthermore, we synthesise emerging paradigms along the bidirectional microbiome-gut-brain-tumour axis, elucidating how commensal and intra-tumoural microbial cues dynamically calibrate myeloid signalling tone and therapeutic susceptibility.
CONCLUSION: We address translation bottlenecks-including blood-brain barrier (BBB) shuttles, human trial scarcity and soluble TREM2 (sTREM2) biomarker harmonisation-outlining a biomarker-guided, context-tailored precision therapeutic framework for targeting the TREM2 axis.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Receptors, Immunologic/metabolism
*Membrane Glycoproteins/metabolism
*Signal Transduction
*Myeloid Cells/metabolism/immunology
*Neoplasms/therapy/immunology
Animals
*Immunotherapy/methods
*Neurodegenerative Diseases/therapy/immunology
RevDate: 2026-10-13
Pathophysiology and Pharmacological Management of Chronic Liver Injury: Current Challenges and Future Directions.
Current drug research reviews pii:CDRR-EPUB-159060 [Epub ahead of print].
INTRODUCTION: Chronic liver injury results from persistent hepatic injuries such as metabolic disorders, alcohol consumption, viral infections, drug toxicity, autoimmune conditions, and genetic factors. It is a major global health concern due to its progression to fibrosis, cirrhosis, and hepatocellular carcinoma. This review aims to summarize key pathophysiological mechanisms and evaluate current and emerging pharmacological strategies.
METHODS: A narrative review of preclinical and clinical studies was conducted, focusing on inflammation, oxidative stress, immune dysfunction, fibrogenesis, and therapeutic approaches, including conventional drugs, antifibrotics, metabolic modulators, and advanced drug delivery systems. A total of 352 records were identified, of which 158 studies were included in the review.
RESULTS: Chronic liver injury is characterized by persistent inflammation, oxidative stress, hepatocyte death, impaired regeneration, and activation of hepatic stellate cells, leading to extracellular matrix accumulation and fibrosis. Current therapies are largely etiology-based and slow disease progression but rarely reverse fibrosis. Emerging therapies targeting nuclear receptors, metabolic pathways, gene-based interventions, microbiome modulation, and nanocarrier-based systems show promising potential.
DISCUSSION: These findings indicate that chronic liver injury is a complex, multifactorial process involving interconnected molecular pathways, limiting the effectiveness of single-target therapies. The gap between mechanistic insights and clinical translation remains a key challenge. Multi-targeted, combination, and precision-based therapeutic approaches, along with targeted drug delivery systems, may enhance treatment efficacy and overcome current limitations.
CONCLUSION: Despite advances in understanding disease mechanisms, effective diseasemodifying therapies remain limited. The development of combination and personalized treatment strategies is essential for improving outcomes and preventing disease progression.
Additional Links: PMID-42865179
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PubMed:
Citation:
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@article {pmid42865179,
year = {2026},
author = {Parveen, N and Kumar, M and Das, M and Singh, N and Patel, AK and Kumar, D and Singh, LP and Goswami, PK},
title = {Pathophysiology and Pharmacological Management of Chronic Liver Injury: Current Challenges and Future Directions.},
journal = {Current drug research reviews},
volume = {},
number = {},
pages = {},
doi = {10.2174/0125899775508122261001092450},
pmid = {42865179},
issn = {2589-9783},
abstract = {INTRODUCTION: Chronic liver injury results from persistent hepatic injuries such as metabolic disorders, alcohol consumption, viral infections, drug toxicity, autoimmune conditions, and genetic factors. It is a major global health concern due to its progression to fibrosis, cirrhosis, and hepatocellular carcinoma. This review aims to summarize key pathophysiological mechanisms and evaluate current and emerging pharmacological strategies.
METHODS: A narrative review of preclinical and clinical studies was conducted, focusing on inflammation, oxidative stress, immune dysfunction, fibrogenesis, and therapeutic approaches, including conventional drugs, antifibrotics, metabolic modulators, and advanced drug delivery systems. A total of 352 records were identified, of which 158 studies were included in the review.
RESULTS: Chronic liver injury is characterized by persistent inflammation, oxidative stress, hepatocyte death, impaired regeneration, and activation of hepatic stellate cells, leading to extracellular matrix accumulation and fibrosis. Current therapies are largely etiology-based and slow disease progression but rarely reverse fibrosis. Emerging therapies targeting nuclear receptors, metabolic pathways, gene-based interventions, microbiome modulation, and nanocarrier-based systems show promising potential.
DISCUSSION: These findings indicate that chronic liver injury is a complex, multifactorial process involving interconnected molecular pathways, limiting the effectiveness of single-target therapies. The gap between mechanistic insights and clinical translation remains a key challenge. Multi-targeted, combination, and precision-based therapeutic approaches, along with targeted drug delivery systems, may enhance treatment efficacy and overcome current limitations.
CONCLUSION: Despite advances in understanding disease mechanisms, effective diseasemodifying therapies remain limited. The development of combination and personalized treatment strategies is essential for improving outcomes and preventing disease progression.},
}
RevDate: 2026-10-13
Dietary and Microbial Determinants of Intestinal Sulfur Gas and Malodor: Mechanisms, Phenotypes, and Nutritional Mitigation.
Journal of gastroenterology and hepatology [Epub ahead of print].
Intestinal gas and malodor are common nutrition-related concerns that may influence dietary adherence, gastrointestinal symptoms, and quality of life. Although gas volume and odor are often treated as a single outcome, they arise from partly distinct processes. Bulk intestinal gas is generated principally through swallowed air, acid-bicarbonate reactions, and microbial fermentation, whereas malodor is determined mainly by trace volatile sulfur compounds, including hydrogen sulfide, methanethiol, and dimethyl sulfide. Their production depends on dietary sulfur amino acids, sulfate, taurine, host-derived substrates, microbial cross-feeding, intestinal transit, luminal chemistry, and gas-liquid partitioning. This review integrates evidence concerning dietary determinants of intestinal gas, gut microbial sulfur metabolism, nutritional and microbiome-directed interventions, and downstream odor-control strategies. The concept of conditional sound-odor discordance is retained as a secondary framework illustrating that gas volume, acoustic intensity, and odor burden should not be considered interchangeable endpoints. Human dietary trials indicate that low-FODMAP diets and substrate-specific enzymes may reduce fermentation-related symptoms or total gas production, but they do not necessarily suppress sulfur-derived odorants. Probiotic evidence remains strain-specific and largely indirect, whereas sulfide-binding compounds and external adsorptive devices target odor-active molecules more directly. Future nutritional studies should combine controlled dietary exposure with measurements of gas volume, volatile sulfur compounds, microbial functional pathways, intestinal transit, and perceived odor.
Additional Links: PMID-42865215
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PubMed:
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@article {pmid42865215,
year = {2026},
author = {Ullah, A},
title = {Dietary and Microbial Determinants of Intestinal Sulfur Gas and Malodor: Mechanisms, Phenotypes, and Nutritional Mitigation.},
journal = {Journal of gastroenterology and hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jgh.70806},
pmid = {42865215},
issn = {1440-1746},
abstract = {Intestinal gas and malodor are common nutrition-related concerns that may influence dietary adherence, gastrointestinal symptoms, and quality of life. Although gas volume and odor are often treated as a single outcome, they arise from partly distinct processes. Bulk intestinal gas is generated principally through swallowed air, acid-bicarbonate reactions, and microbial fermentation, whereas malodor is determined mainly by trace volatile sulfur compounds, including hydrogen sulfide, methanethiol, and dimethyl sulfide. Their production depends on dietary sulfur amino acids, sulfate, taurine, host-derived substrates, microbial cross-feeding, intestinal transit, luminal chemistry, and gas-liquid partitioning. This review integrates evidence concerning dietary determinants of intestinal gas, gut microbial sulfur metabolism, nutritional and microbiome-directed interventions, and downstream odor-control strategies. The concept of conditional sound-odor discordance is retained as a secondary framework illustrating that gas volume, acoustic intensity, and odor burden should not be considered interchangeable endpoints. Human dietary trials indicate that low-FODMAP diets and substrate-specific enzymes may reduce fermentation-related symptoms or total gas production, but they do not necessarily suppress sulfur-derived odorants. Probiotic evidence remains strain-specific and largely indirect, whereas sulfide-binding compounds and external adsorptive devices target odor-active molecules more directly. Future nutritional studies should combine controlled dietary exposure with measurements of gas volume, volatile sulfur compounds, microbial functional pathways, intestinal transit, and perceived odor.},
}
RevDate: 2026-10-13
Oral and Fecal Microbial Dysbiosis as Non-Invasive Diagnostic Biomarkers for Gastrointestinal Cancers: A Systematic Review and Meta-Analysis of Diagnostic Accuracy.
International journal of cancer [Epub ahead of print].
Gastrointestinal (GI) cancers, including esophageal (EC), gastric (GC), and colorectal cancer (CRC), impose a substantial global burden, with early detection remaining crucial for improving patient outcomes. The oral and gut microbiota are increasingly implicated in cancer development and hold promise as sources of non-invasive biomarkers. However, current evidence on microbiome-based diagnostics remains fragmented, and a systematic comparison of the diagnostic accuracy between oral and fecal sampling across multiple GI cancer types is lacking. To address this gap, a systematic search of PubMed, Embase, and Scopus up to December 31, 2025, identified 43 case-control studies (59 cohorts) comprising 4452 cancer patients and 5809 controls. The pooled area under the curve (AUC) was 0.846 (95% CI: 0.824-0.867), though with substantial heterogeneity (I[2] = 86.5%). By cancer type, pooled AUCs were 0.746 for EC (5 cohorts), 0.886 for GC (8 cohorts), and 0.850 for CRC (46 cohorts). A bivariate analysis of 20 cohorts comparing sample types found no statistically significant difference in diagnostic performance between oral (sAUC = 0.863) and fecal sampling (sAUC = 0.820; p = 0.369). While these exploratory findings suggest that oral and fecal microbial biomarkers may offer comparable diagnostic accuracy for GI cancers, with oral sampling presenting a more practical option for screening, the results are preliminary. Significant heterogeneity, a limited number of oral cohorts, and the absence of clinical control groups highlight the need for large-scale prospective studies with direct comparisons and real-world validation to validate these biomarkers for clinical translation.
Additional Links: PMID-42865226
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PubMed:
Citation:
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@article {pmid42865226,
year = {2026},
author = {Hu, S and Chen, Z and Li, Y and Liao, Q and Luo, M and Song, D and Yu, H and Gao, Y and Yang, S and Wan, S and Zhang, S and Luo, C and Zhao, LY},
title = {Oral and Fecal Microbial Dysbiosis as Non-Invasive Diagnostic Biomarkers for Gastrointestinal Cancers: A Systematic Review and Meta-Analysis of Diagnostic Accuracy.},
journal = {International journal of cancer},
volume = {},
number = {},
pages = {},
doi = {10.1002/ijc.70779},
pmid = {42865226},
issn = {1097-0215},
abstract = {Gastrointestinal (GI) cancers, including esophageal (EC), gastric (GC), and colorectal cancer (CRC), impose a substantial global burden, with early detection remaining crucial for improving patient outcomes. The oral and gut microbiota are increasingly implicated in cancer development and hold promise as sources of non-invasive biomarkers. However, current evidence on microbiome-based diagnostics remains fragmented, and a systematic comparison of the diagnostic accuracy between oral and fecal sampling across multiple GI cancer types is lacking. To address this gap, a systematic search of PubMed, Embase, and Scopus up to December 31, 2025, identified 43 case-control studies (59 cohorts) comprising 4452 cancer patients and 5809 controls. The pooled area under the curve (AUC) was 0.846 (95% CI: 0.824-0.867), though with substantial heterogeneity (I[2] = 86.5%). By cancer type, pooled AUCs were 0.746 for EC (5 cohorts), 0.886 for GC (8 cohorts), and 0.850 for CRC (46 cohorts). A bivariate analysis of 20 cohorts comparing sample types found no statistically significant difference in diagnostic performance between oral (sAUC = 0.863) and fecal sampling (sAUC = 0.820; p = 0.369). While these exploratory findings suggest that oral and fecal microbial biomarkers may offer comparable diagnostic accuracy for GI cancers, with oral sampling presenting a more practical option for screening, the results are preliminary. Significant heterogeneity, a limited number of oral cohorts, and the absence of clinical control groups highlight the need for large-scale prospective studies with direct comparisons and real-world validation to validate these biomarkers for clinical translation.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Patterns of Functional Redundancy and Anaerobic Metabolic Potential Characterise the Skin Microbiome of a Critically Endangered Sawfish.
Environmental microbiology, 28(10):e70442.
Using shotgun metagenomics of largetooth sawfish (Pristis pristis) skin and paired pool water samples, we provide the first taxonomic and functional characterisation of a sawfish skin microbiome and assess its ecological distinctiveness, assembly, and resilience relative to the surrounding water column. The skin microbiome was strongly host-associated and compositionally distinct, with lower taxonomic richness than the water column but dominated by Bacillota, particularly spore-forming Bacilli. Functional profiling revealed genes associated with sporulation, dormancy, anaerobic metabolism, and peptide transport, consistent with low-oxygen, low-flow conditions. In contrast, water-column microbiomes were more taxonomically diverse and enriched in phototrophic and polysaccharide-utilisation pathways. Sawfish skin communities exhibited patterns consistent with greater functional redundancy, with gene functions accumulating more rapidly per taxon. Together with greater among-individual taxonomic dispersion, this pattern is consistent with a host-filtered, lottery-like assembly process in which taxonomically variable communities maintain similar functional potential. The enrichment of dormancy and anaerobic pathways suggests the skin microbiome persists through periods of host quiescence and environmental stress while maintaining metabolic potential. Together, these results demonstrate that the sawfish skin supports a resilient, functionally robust microbiome distinct from ambient aquatic communities, highlighting the potential for integrating microbial functional data into conservation strategies for Critically Endangered vertebrates.
Additional Links: PMID-42865259
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@article {pmid42865259,
year = {2026},
author = {Doane, MP and Martin, B and Kerr, E and Dinsdale, EA and Rangers, MM and Guida, L and Kyne, PM},
title = {Patterns of Functional Redundancy and Anaerobic Metabolic Potential Characterise the Skin Microbiome of a Critically Endangered Sawfish.},
journal = {Environmental microbiology},
volume = {28},
number = {10},
pages = {e70442},
doi = {10.1111/1462-2920.70442},
pmid = {42865259},
issn = {1462-2920},
support = {//Charles Darwin University 2021 Institute of Advanced Studies (IAS) Rainmaker Start Up/ ; //Australian Marine Conservation Society (AMCS)/ ; //Flinders Accelerator for Microbiome Exploration/ ; },
mesh = {Animals ; *Skin Microbiome ; Anaerobiosis ; *Bacteria/classification/genetics/isolation & purification/metabolism ; Endangered Species ; *Microbiota ; Metagenomics ; *Skin/microbiology ; Phylogeny ; },
abstract = {Using shotgun metagenomics of largetooth sawfish (Pristis pristis) skin and paired pool water samples, we provide the first taxonomic and functional characterisation of a sawfish skin microbiome and assess its ecological distinctiveness, assembly, and resilience relative to the surrounding water column. The skin microbiome was strongly host-associated and compositionally distinct, with lower taxonomic richness than the water column but dominated by Bacillota, particularly spore-forming Bacilli. Functional profiling revealed genes associated with sporulation, dormancy, anaerobic metabolism, and peptide transport, consistent with low-oxygen, low-flow conditions. In contrast, water-column microbiomes were more taxonomically diverse and enriched in phototrophic and polysaccharide-utilisation pathways. Sawfish skin communities exhibited patterns consistent with greater functional redundancy, with gene functions accumulating more rapidly per taxon. Together with greater among-individual taxonomic dispersion, this pattern is consistent with a host-filtered, lottery-like assembly process in which taxonomically variable communities maintain similar functional potential. The enrichment of dormancy and anaerobic pathways suggests the skin microbiome persists through periods of host quiescence and environmental stress while maintaining metabolic potential. Together, these results demonstrate that the sawfish skin supports a resilient, functionally robust microbiome distinct from ambient aquatic communities, highlighting the potential for integrating microbial functional data into conservation strategies for Critically Endangered vertebrates.},
}
MeSH Terms:
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Animals
*Skin Microbiome
Anaerobiosis
*Bacteria/classification/genetics/isolation & purification/metabolism
Endangered Species
*Microbiota
Metagenomics
*Skin/microbiology
Phylogeny
RevDate: 2026-10-13
CmpDate: 2026-10-13
The archibiome: extending engineered living materials to multiscale built environments.
Frontiers in systems biology, 6:1943876.
The integration of living systems into architecture is advancing rapidly through developments in biotechnology, materials science, and design approaches grounded in regenerative principles. Engineered Living Materials (ELMs) and living artefacts demonstrate how microbial systems can be embedded within materials to enable responsiveness, metabolic activity, and adaptive functionality. However, current applications remain largely confined to discrete material components, overlooking the complex and dynamic microbial ecosystems already present within buildings. This opinion paper introduces the concept of the archibiome as a framework for extending ELMs from isolated systems to interconnected architectural environments. The archibiome conceptualizes buildings as dynamic microbial ecosystems in which engineered systems, material interfaces, and native microbial communities interact across spatial and temporal scales. While this shift offers opportunities for adaptive and regenerative design, it also introduces challenges related to system stability, environmental variability, biosafety, and regulatory constraints. Addressing these challenges requires interdisciplinary approaches that integrate microbial ecology, materials engineering, architectural design, and regulatory science. Ultimately, the archibiome positions microbial life as a design variable, enabling a transition toward predictive, systems-level strategies for living architecture.
Additional Links: PMID-42865466
PubMed:
Citation:
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@article {pmid42865466,
year = {2026},
author = {Sandak, A and Pajerski, W and Gubenšek, A and Butina Ogorelec, K and Černoša, A},
title = {The archibiome: extending engineered living materials to multiscale built environments.},
journal = {Frontiers in systems biology},
volume = {6},
number = {},
pages = {1943876},
pmid = {42865466},
issn = {2674-0702},
abstract = {The integration of living systems into architecture is advancing rapidly through developments in biotechnology, materials science, and design approaches grounded in regenerative principles. Engineered Living Materials (ELMs) and living artefacts demonstrate how microbial systems can be embedded within materials to enable responsiveness, metabolic activity, and adaptive functionality. However, current applications remain largely confined to discrete material components, overlooking the complex and dynamic microbial ecosystems already present within buildings. This opinion paper introduces the concept of the archibiome as a framework for extending ELMs from isolated systems to interconnected architectural environments. The archibiome conceptualizes buildings as dynamic microbial ecosystems in which engineered systems, material interfaces, and native microbial communities interact across spatial and temporal scales. While this shift offers opportunities for adaptive and regenerative design, it also introduces challenges related to system stability, environmental variability, biosafety, and regulatory constraints. Addressing these challenges requires interdisciplinary approaches that integrate microbial ecology, materials engineering, architectural design, and regulatory science. Ultimately, the archibiome positions microbial life as a design variable, enabling a transition toward predictive, systems-level strategies for living architecture.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Effects of trait stacking on the maize phyllosphere microbiome: a shotgun metagenomic comparison.
Frontiers in microbiology, 17:1904641.
Current safety assessments for stacked-trait transgenic crops underrepresent the phyllosphere, a critical interface directly exposed to transgenic products, warranting strengthened risk evaluation. Here, we employed metagenomics to characterize the phyllosphere of three maize lines under herbicide-free conditions: wild-type (Corn.CK), herbicide-resistant single-trait (transgene of cp4-epsps, Corn.S), and insect- and herbicide-resistant stacked-trait (transgene of cry1Ab and cp4-epsps, Corn.D). Shannon diversity showed a consistent trend toward higher values in the cp4-epsps single-trait line than in the wild type (not significant after correction for multiple comparisons), whereas the stacked-trait line showed an intermediate increase. Transgenic events were associated with bidirectional taxonomic remodeling, characterized by the depletion of Enterobacterales and enrichment of environmentally adapted taxa. Functionally, transgenic lines displayed pervasive metabolic depletion across KEGG pathways and CAZyme categories, alongside reduced abundance of virulence-associated gene homologs (e.g., T6SS and Enterobactin) and lower antibiotic resistance gene diversity (wild-type > stacked-trait > single-trait), driven by the concomitant loss of Enterobacterales hosts. Notably, in most of the taxonomic, functional, virulence, and resistome dimensions examined, the stacked-trait line exhibited an intermediate microbiome profile between the wild-type and single-trait lines. These findings suggest that, for this genotype combination under these controlled conditions, trait stacking was not associated with microbiome perturbation greater than that observed for the single trait, and provide a preliminary, genotype- and stage-specific reference for phyllosphere biosafety assessment, pending field validation.
Additional Links: PMID-42865524
PubMed:
Citation:
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@article {pmid42865524,
year = {2026},
author = {Yan, JY and Zhou, Y and Ni, L and Ding, ZJ and Lin, C},
title = {Effects of trait stacking on the maize phyllosphere microbiome: a shotgun metagenomic comparison.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1904641},
pmid = {42865524},
issn = {1664-302X},
abstract = {Current safety assessments for stacked-trait transgenic crops underrepresent the phyllosphere, a critical interface directly exposed to transgenic products, warranting strengthened risk evaluation. Here, we employed metagenomics to characterize the phyllosphere of three maize lines under herbicide-free conditions: wild-type (Corn.CK), herbicide-resistant single-trait (transgene of cp4-epsps, Corn.S), and insect- and herbicide-resistant stacked-trait (transgene of cry1Ab and cp4-epsps, Corn.D). Shannon diversity showed a consistent trend toward higher values in the cp4-epsps single-trait line than in the wild type (not significant after correction for multiple comparisons), whereas the stacked-trait line showed an intermediate increase. Transgenic events were associated with bidirectional taxonomic remodeling, characterized by the depletion of Enterobacterales and enrichment of environmentally adapted taxa. Functionally, transgenic lines displayed pervasive metabolic depletion across KEGG pathways and CAZyme categories, alongside reduced abundance of virulence-associated gene homologs (e.g., T6SS and Enterobactin) and lower antibiotic resistance gene diversity (wild-type > stacked-trait > single-trait), driven by the concomitant loss of Enterobacterales hosts. Notably, in most of the taxonomic, functional, virulence, and resistome dimensions examined, the stacked-trait line exhibited an intermediate microbiome profile between the wild-type and single-trait lines. These findings suggest that, for this genotype combination under these controlled conditions, trait stacking was not associated with microbiome perturbation greater than that observed for the single trait, and provide a preliminary, genotype- and stage-specific reference for phyllosphere biosafety assessment, pending field validation.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Trust your gut: the neuro-gastroenteric mechanics of prediction and expectation.
Frontiers in human neuroscience, 20:1956182.
Living organisms constantly make probabilistic predictions about what they expect to see in their external environment, and actively solicit information from the environment to inform their predictions. This process is foundational for many frameworks including Active Inference and Predictive Processing. It relies on organisms having prior expectations, entailed by an internal generative model of the environment. Posterior expectations are updated based on the selected data, driven by prediction error minimization. However, failures to contextualize the precision or confidence placed in predictions, can give rise to perceptual abnormalities that are at the basis of various psychiatric conditions. Different factors can influence this process. Notably, disruptions in the gut microbiome have been implicated in some psychotic disorders. Gut microbial dysregulation has also been associated with alterations in neurotransmitter synthesis, metabolism, and turnover, which may affect processes involved in the encoding of precision of prediction errors. On the basis of this gut-brain connection, this Hypothesis and Theory article hypothesizes that the gut microbiome plays a role as a modulator of predictive processing, influencing how predictions are formed and expectations updated. Specifically, this article explores the importance of "mental model" embodiment, and considers the role of hippocampal activity in predictive coding and its modulation by the gut microbiome. Finally, it offers a novel perspective on the use of cortico-hippocampal-gastroenteric frameworks for inferring personalized dietary interventions in nutritional psychiatry.
Additional Links: PMID-42865525
PubMed:
Citation:
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@article {pmid42865525,
year = {2026},
author = {Caccamo, A},
title = {Trust your gut: the neuro-gastroenteric mechanics of prediction and expectation.},
journal = {Frontiers in human neuroscience},
volume = {20},
number = {},
pages = {1956182},
pmid = {42865525},
issn = {1662-5161},
abstract = {Living organisms constantly make probabilistic predictions about what they expect to see in their external environment, and actively solicit information from the environment to inform their predictions. This process is foundational for many frameworks including Active Inference and Predictive Processing. It relies on organisms having prior expectations, entailed by an internal generative model of the environment. Posterior expectations are updated based on the selected data, driven by prediction error minimization. However, failures to contextualize the precision or confidence placed in predictions, can give rise to perceptual abnormalities that are at the basis of various psychiatric conditions. Different factors can influence this process. Notably, disruptions in the gut microbiome have been implicated in some psychotic disorders. Gut microbial dysregulation has also been associated with alterations in neurotransmitter synthesis, metabolism, and turnover, which may affect processes involved in the encoding of precision of prediction errors. On the basis of this gut-brain connection, this Hypothesis and Theory article hypothesizes that the gut microbiome plays a role as a modulator of predictive processing, influencing how predictions are formed and expectations updated. Specifically, this article explores the importance of "mental model" embodiment, and considers the role of hippocampal activity in predictive coding and its modulation by the gut microbiome. Finally, it offers a novel perspective on the use of cortico-hippocampal-gastroenteric frameworks for inferring personalized dietary interventions in nutritional psychiatry.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Intratumoral microbiota-host gene associations characterize stage-associated microecological patterns in colorectal cancer.
Frontiers in microbiology, 17:1934580.
INTRODUCTION: Intratumoral microbiota are emerging as important ecological components of the colorectal cancer (CRC) microenvironment. However, their stage-associated patterns and coordination with host gene expression remain poorly understood. This study aimed to characterize stage-associated associations between intratumoral microbiota and the host transcriptome in CRC.
METHODS: We profiled 73 regional tumor specimens from 30 independent, treatment-naïve CRC patients using full-length 16S rRNA gene sequencing and mRNA sequencing. Microbial diversity, predicted functional profiles, co-occurrence networks, differential abundance, and microbiota-host transcriptome associations were analyzed. Regularized canonical correlation analysis and machine-learning modeling with SHAP-based feature interpretation were performed to identify stage-discriminative features. Candidate associations were evaluated in two independent public microbiome datasets. Mendelian randomization and immune-infiltration analyses were further conducted to explore the potential biological relevance of representative microbiota-gene associations.
RESULTS: Disease stage was a major factor shaping intratumoral microbial composition. Advanced-stage CRC exhibited increased microbial α-diversity, distinct predicted functional profiles, and altered microbial co-occurrence patterns. Integrated microbiota-transcriptome analysis identified ten genus-level and six species-level candidate microbiota-gene association pairs. Core genera showed reproducible stage-discriminative signals in two independent public microbiome datasets. SHAP analysis identified the principal microbial and host transcriptomic features contributing to stage classification. Integrating microbial and host gene signatures improved classification performance, with the combined model achieving an AUROC greater than 0.90. The Alloprevotella-MDH1 pair was selected as a representative association axis. Alloprevotella abundance was negatively correlated with MDH1 expression, while low MDH1 expression was associated with poorer survival and distinct metabolic-immune states in CRC. Exploratory Mendelian randomization analysis provided preliminary genetic epidemiological support for an association between Alloprevotella abundance and CRC risk.
DISCUSSION: Intratumoral microbiota and host transcriptional profiles exhibit coordinated, stage-associated alterations in CRC. The identified microbiota-gene associations, particularly the Alloprevotella-MDH1 axis, provide potential biological links between tumor microbial ecology, host metabolism, immune states, and CRC progression. These findings support the value of integrated microbiome-transcriptome analysis for characterizing the intratumoral microenvironment and identifying candidate microbial-host regulatory relationships.
Additional Links: PMID-42865545
PubMed:
Citation:
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@article {pmid42865545,
year = {2026},
author = {Chen, Z and Gan, W and Cao, F and Yu, F and Lin, W and Wang, X and Hong, Y and Yang, M and Hong, L and Chen, C and Wu, J and Liu, X and Zhang, W and Lian, Y},
title = {Intratumoral microbiota-host gene associations characterize stage-associated microecological patterns in colorectal cancer.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1934580},
pmid = {42865545},
issn = {1664-302X},
abstract = {INTRODUCTION: Intratumoral microbiota are emerging as important ecological components of the colorectal cancer (CRC) microenvironment. However, their stage-associated patterns and coordination with host gene expression remain poorly understood. This study aimed to characterize stage-associated associations between intratumoral microbiota and the host transcriptome in CRC.
METHODS: We profiled 73 regional tumor specimens from 30 independent, treatment-naïve CRC patients using full-length 16S rRNA gene sequencing and mRNA sequencing. Microbial diversity, predicted functional profiles, co-occurrence networks, differential abundance, and microbiota-host transcriptome associations were analyzed. Regularized canonical correlation analysis and machine-learning modeling with SHAP-based feature interpretation were performed to identify stage-discriminative features. Candidate associations were evaluated in two independent public microbiome datasets. Mendelian randomization and immune-infiltration analyses were further conducted to explore the potential biological relevance of representative microbiota-gene associations.
RESULTS: Disease stage was a major factor shaping intratumoral microbial composition. Advanced-stage CRC exhibited increased microbial α-diversity, distinct predicted functional profiles, and altered microbial co-occurrence patterns. Integrated microbiota-transcriptome analysis identified ten genus-level and six species-level candidate microbiota-gene association pairs. Core genera showed reproducible stage-discriminative signals in two independent public microbiome datasets. SHAP analysis identified the principal microbial and host transcriptomic features contributing to stage classification. Integrating microbial and host gene signatures improved classification performance, with the combined model achieving an AUROC greater than 0.90. The Alloprevotella-MDH1 pair was selected as a representative association axis. Alloprevotella abundance was negatively correlated with MDH1 expression, while low MDH1 expression was associated with poorer survival and distinct metabolic-immune states in CRC. Exploratory Mendelian randomization analysis provided preliminary genetic epidemiological support for an association between Alloprevotella abundance and CRC risk.
DISCUSSION: Intratumoral microbiota and host transcriptional profiles exhibit coordinated, stage-associated alterations in CRC. The identified microbiota-gene associations, particularly the Alloprevotella-MDH1 axis, provide potential biological links between tumor microbial ecology, host metabolism, immune states, and CRC progression. These findings support the value of integrated microbiome-transcriptome analysis for characterizing the intratumoral microenvironment and identifying candidate microbial-host regulatory relationships.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Short-term clinical outcomes of nasoduodenal tube versus feeding jejunostomy after minimally invasive esophagectomy: a retrospective cohort study with exploratory microbiome analysis.
Journal of thoracic disease, 18(9):1024.
BACKGROUND: Esophagectomy remains an effective treatment for esophageal cancer but is associated with severe postoperative complications, in which nutritional status plays a critical role. The optimal route for enteral feeding remains uncertain. To address this uncertainty, we compared the short-term clinical outcomes of the two approaches and exploratorily analyzed the differences in gut microbiota.
METHODS: This retrospective cohort study enrolled patients who underwent minimally invasive esophagectomy (MIE) for esophageal squamous cell carcinoma (ESCC) between July 2018 and June 2021. Primary outcomes were surgery-related complications (including anastomotic leakage, anastomotic stenosis, pneumonia, respiratory failure, cardiac events, chylothorax, intestinal fistula and bowel obstruction) and catheter-related outcomes (including occlusion, accidental removal, displacement and retention time). Baseline data were extracted from medical records. Propensity score matching (PSM) was applied to control for potential confounders. Intestinal fluid and fecal samples were collected after enteral nutrition for 16S ribosomal DNA (16S rDNA) sequencing.
RESULTS: After PSM, a total of 381 patients (nasoduodenal tube: 282; feeding jejunostomy: 153) was finally included. The feeding jejunostomy group exhibited a higher incidence of pneumonia (21.49% vs. 33.99%, P=0.007), respiratory failure (3.07% vs. 13.07%, P<0.001), anastomotic stenosis (1.32% vs. 5.23%, P=0.03) and bowel obstruction (0% vs. 2.16%, P=0.03). Nasoduodenal tube placement was associated with more accidental removal (13.16% vs. 0.65%, P<0.001) and catheter displacement (13.60% vs. 6.54%, P=0.03). The catheter retention time {37 [interquartile range (IQR): 15-40] days vs. 39 (IQR: 37-42) days, P<0.001} was also shorter in nasoduodenal tube group.
CONCLUSIONS: In this study, nasoduodenal tube placement was associated with a higher incidence of catheter-related complications, whereas feeding jejunostomy was linked to more surgery-related complications. Nasoduodenal tube placement also showed potential functional advantages for the gut microbiome. However, future multi-center randomized controlled trials are still needed to minimize potential confounders and validate the differences between the two enteral nutrition routes.
Additional Links: PMID-42865837
PubMed:
Citation:
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@article {pmid42865837,
year = {2026},
author = {Ge, QY and Wang, CY and Zheng, C and Zheng, HT and Wen, YX and Luo, J and Qiang, Y and Wang, YQ and Cong, ZZ and Shen, Y},
title = {Short-term clinical outcomes of nasoduodenal tube versus feeding jejunostomy after minimally invasive esophagectomy: a retrospective cohort study with exploratory microbiome analysis.},
journal = {Journal of thoracic disease},
volume = {18},
number = {9},
pages = {1024},
pmid = {42865837},
issn = {2072-1439},
abstract = {BACKGROUND: Esophagectomy remains an effective treatment for esophageal cancer but is associated with severe postoperative complications, in which nutritional status plays a critical role. The optimal route for enteral feeding remains uncertain. To address this uncertainty, we compared the short-term clinical outcomes of the two approaches and exploratorily analyzed the differences in gut microbiota.
METHODS: This retrospective cohort study enrolled patients who underwent minimally invasive esophagectomy (MIE) for esophageal squamous cell carcinoma (ESCC) between July 2018 and June 2021. Primary outcomes were surgery-related complications (including anastomotic leakage, anastomotic stenosis, pneumonia, respiratory failure, cardiac events, chylothorax, intestinal fistula and bowel obstruction) and catheter-related outcomes (including occlusion, accidental removal, displacement and retention time). Baseline data were extracted from medical records. Propensity score matching (PSM) was applied to control for potential confounders. Intestinal fluid and fecal samples were collected after enteral nutrition for 16S ribosomal DNA (16S rDNA) sequencing.
RESULTS: After PSM, a total of 381 patients (nasoduodenal tube: 282; feeding jejunostomy: 153) was finally included. The feeding jejunostomy group exhibited a higher incidence of pneumonia (21.49% vs. 33.99%, P=0.007), respiratory failure (3.07% vs. 13.07%, P<0.001), anastomotic stenosis (1.32% vs. 5.23%, P=0.03) and bowel obstruction (0% vs. 2.16%, P=0.03). Nasoduodenal tube placement was associated with more accidental removal (13.16% vs. 0.65%, P<0.001) and catheter displacement (13.60% vs. 6.54%, P=0.03). The catheter retention time {37 [interquartile range (IQR): 15-40] days vs. 39 (IQR: 37-42) days, P<0.001}
was also shorter in nasoduodenal tube group.
CONCLUSIONS: In this study, nasoduodenal tube placement was associated with a higher incidence of catheter-related complications, whereas feeding jejunostomy was linked to more surgery-related complications. Nasoduodenal tube placement also showed potential functional advantages for the gut microbiome. However, future multi-center randomized controlled trials are still needed to minimize potential confounders and validate the differences between the two enteral nutrition routes.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Decoding host-microbiome interactions through integrative multi-omics and artificial intelligence: from biological mechanisms to predictive modelling.
Frontiers in microbiomes, 5:1906484.
The mutual communication between the human host and its microbiome plays a fundamental role in maintaining metabolic and immunological homeostasis. Disruptions in this delicate ecosystem are heavily linked to severe pathologies like inflammatory bowel disease (IBD), metabolic syndromes, and cancer. Whilst traditional single-omics approaches offer limited taxonomic snapshots, multi-omics strategies are bridging the gap by mapping the complex, multi-layered networks driving host-microbe interactions. However, integrating these highly dimensional, heterogeneous datasets creates significant computational bottlenecks. Artificial Intelligence (AI), spanning machine learning and deep learning architectures, has emerged as a critical catalyst to resolve this crisis. AI transforms complex data into predictive models for early diagnosis, clinical biomarker discovery, and personalised therapeutics. Despite persistent hurdles in model generalisation and data standardisation, the convergence of multi-omics and AI is actively driving the future of precision medicine.
Additional Links: PMID-42865919
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Citation:
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@article {pmid42865919,
year = {2026},
author = {Krishna S, G and Reeja, N and Sadanandan, S and Mappurath, B and Chatterjee, A and Antony, G and Grace, T},
title = {Decoding host-microbiome interactions through integrative multi-omics and artificial intelligence: from biological mechanisms to predictive modelling.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1906484},
pmid = {42865919},
issn = {2813-4338},
abstract = {The mutual communication between the human host and its microbiome plays a fundamental role in maintaining metabolic and immunological homeostasis. Disruptions in this delicate ecosystem are heavily linked to severe pathologies like inflammatory bowel disease (IBD), metabolic syndromes, and cancer. Whilst traditional single-omics approaches offer limited taxonomic snapshots, multi-omics strategies are bridging the gap by mapping the complex, multi-layered networks driving host-microbe interactions. However, integrating these highly dimensional, heterogeneous datasets creates significant computational bottlenecks. Artificial Intelligence (AI), spanning machine learning and deep learning architectures, has emerged as a critical catalyst to resolve this crisis. AI transforms complex data into predictive models for early diagnosis, clinical biomarker discovery, and personalised therapeutics. Despite persistent hurdles in model generalisation and data standardisation, the convergence of multi-omics and AI is actively driving the future of precision medicine.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Seminal dysbiosis in idiopathic male infertility: toward a seminal dysbiosis-inflammatory/oxidative endophenotype-SDF axis.
Frontiers in endocrinology, 17:1943471.
Idiopathic male infertility (IMI) usually refers to abnormal semen parameters after known causes have been excluded. However, its clinical stratification and intervention evidence remain difficult to reconcile. Based on low biomass in semen, this review proposes an SD-IO-SDF axis linking seminal dysbiosis (SD), inflammatory/oxidative endophenotype (IO), and sperm DNA fragmentation (SDF) in subsets of IMI. It integrates three mechanisms of evidence strength: (i) inflammation-oxidative injury pathway (leukocyte-dependent); (ii) leukocyte-independent redox imbalance; and (iii) a metabolic-epigenetic route (SAM cycle, butyrate) as a testable hypothesis. Existing evidence suggests that the association between SD and SDF concentrates in specific IO activation states and IMI subtypes. IO stratification may reduce effect dilution across mixed populations and make the hypothesis more directly testable. For research implementation, we propose IO indicators grouped by measurement type (inflammatory: leukocytospermia and/or PMN-elastase; oxidative: sORP), with validation against SDF platforms as a subsequent step. This approach provides a falsifiable structure for IMI and provides a template for future trial designs based on SD×IO stratification.
Additional Links: PMID-42865978
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Citation:
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@article {pmid42865978,
year = {2026},
author = {Gao, Y and Lv, X and Sun, Z},
title = {Seminal dysbiosis in idiopathic male infertility: toward a seminal dysbiosis-inflammatory/oxidative endophenotype-SDF axis.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1943471},
pmid = {42865978},
issn = {1664-2392},
mesh = {Humans ; Male ; *Infertility, Male/metabolism/pathology/etiology ; *Semen/microbiology/metabolism ; *Dysbiosis/metabolism ; *Oxidative Stress ; *Inflammation/pathology/metabolism ; *Endophenotypes ; *DNA Fragmentation ; *Spermatozoa/pathology/metabolism ; },
abstract = {Idiopathic male infertility (IMI) usually refers to abnormal semen parameters after known causes have been excluded. However, its clinical stratification and intervention evidence remain difficult to reconcile. Based on low biomass in semen, this review proposes an SD-IO-SDF axis linking seminal dysbiosis (SD), inflammatory/oxidative endophenotype (IO), and sperm DNA fragmentation (SDF) in subsets of IMI. It integrates three mechanisms of evidence strength: (i) inflammation-oxidative injury pathway (leukocyte-dependent); (ii) leukocyte-independent redox imbalance; and (iii) a metabolic-epigenetic route (SAM cycle, butyrate) as a testable hypothesis. Existing evidence suggests that the association between SD and SDF concentrates in specific IO activation states and IMI subtypes. IO stratification may reduce effect dilution across mixed populations and make the hypothesis more directly testable. For research implementation, we propose IO indicators grouped by measurement type (inflammatory: leukocytospermia and/or PMN-elastase; oxidative: sORP), with validation against SDF platforms as a subsequent step. This approach provides a falsifiable structure for IMI and provides a template for future trial designs based on SD×IO stratification.},
}
MeSH Terms:
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Humans
Male
*Infertility, Male/metabolism/pathology/etiology
*Semen/microbiology/metabolism
*Dysbiosis/metabolism
*Oxidative Stress
*Inflammation/pathology/metabolism
*Endophenotypes
*DNA Fragmentation
*Spermatozoa/pathology/metabolism
RevDate: 2026-10-13
CmpDate: 2026-10-13
New insights into the gut-heart axis: microbial metabolite biomarkers, multi-omics, and engineered bacterial delivery systems.
Frontiers in microbiology, 17:1987882.
Despite rapid growth in gut-heart axis research, clinical translation remains limited. This review addresses that gap by critically synthesizing recent evidence on microbiota-derived metabolites, biomarkers, multi-omics workflows, and engineered bacterial interventions in cardiovascular disease (CVD). We examine how TMAO, short-chain fatty acids, bile acids, indole derivatives, and phenylacetylglutamine exert context-dependent cardiovascular effects, and why functional microbial gene markers and integrated biomarker panels may outperform single-taxon signatures. We then evaluate multi-omics strategies, metagenomics, metabolomics, proteomics, single-cell and spatial omics, and bioinformatics integration, for causal inference and biomarker validation. Finally, we assess engineered bacterial delivery systems, including gene circuit design, colonization control, biocontainment, and safety, and outline short-, medium-, and long-term milestones for clinical translation, cost-effectiveness, and intellectual property. The key takeaway is that precision microbiome medicine in CVD will require standardized assays, prospective validation, robust regulatory pathways, and equitable commercialization. By linking mechanistic insights with translational requirements, this review provides a framework for developing microbiome-targeted diagnostics and therapeutics in CVD.
Additional Links: PMID-42865986
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Citation:
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@article {pmid42865986,
year = {2026},
author = {Chen, Y and Li, Y and Lu, H and Jia, S and Jiang, Y},
title = {New insights into the gut-heart axis: microbial metabolite biomarkers, multi-omics, and engineered bacterial delivery systems.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1987882},
pmid = {42865986},
issn = {1664-302X},
abstract = {Despite rapid growth in gut-heart axis research, clinical translation remains limited. This review addresses that gap by critically synthesizing recent evidence on microbiota-derived metabolites, biomarkers, multi-omics workflows, and engineered bacterial interventions in cardiovascular disease (CVD). We examine how TMAO, short-chain fatty acids, bile acids, indole derivatives, and phenylacetylglutamine exert context-dependent cardiovascular effects, and why functional microbial gene markers and integrated biomarker panels may outperform single-taxon signatures. We then evaluate multi-omics strategies, metagenomics, metabolomics, proteomics, single-cell and spatial omics, and bioinformatics integration, for causal inference and biomarker validation. Finally, we assess engineered bacterial delivery systems, including gene circuit design, colonization control, biocontainment, and safety, and outline short-, medium-, and long-term milestones for clinical translation, cost-effectiveness, and intellectual property. The key takeaway is that precision microbiome medicine in CVD will require standardized assays, prospective validation, robust regulatory pathways, and equitable commercialization. By linking mechanistic insights with translational requirements, this review provides a framework for developing microbiome-targeted diagnostics and therapeutics in CVD.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Applications of artificial intelligence in personalized nutrition interventions.
Frontiers in nutrition, 13:1974199.
Unhealthy dietary patterns remain a major modifiable contributor to the global burden of obesity, type 2 diabetes mellitus (T2DM), cardiovascular disease, and cancer. However, individuals can respond markedly differently to identical foods, limiting the effectiveness of one-size-fits-all dietary guidance. This review examines the application of artificial intelligence (AI) to personalized nutrition interventions across three interconnected layers. At the biological level, inter-individual variability can be characterized by three mechanistic dimensions: nutrigenomic variation, which influences nutrient metabolism and disease susceptibility; metabolomic biomarkers, which objectively capture dietary exposure and early metabolic alterations; and the gut microbiome, which bidirectionally mediates diet-host interactions. At the technological level, AI integrates these dimensions into multimodal digital profiles. Machine learning models predict individual postprandial glycemic and lipemic responses, with reported correlations of up to r = 0.77 in large cohorts; deep learning and computer vision automate dietary assessment; natural language processing and large language models (LLMs) support nutrition counseling; knowledge graphs enable constraint-aware food recommendations; and digital-twin and adaptive closed-loop systems incorporating continuous glucose monitoring and wearable-device data support real-time nutritional interventions. However, the strength of clinical evidence varies across disease domains. Glycemic management in T2DM and prediabetes currently has the most mature randomized controlled trial evidence: an AI-enabled personalized intervention combining algorithmic dietary personalization with CGM-linked feedback improved glycemic endpoints compared with a Mediterranean diet, while a fully automated AI-delivered diabetes prevention program achieved outcomes non-inferior to those of human coaching. In obesity, cardiovascular disease, oncology, and gastrointestinal disorders, the evidence remains mixed or preliminary. Clinical translation also faces substantial challenges, including biased and inconsistently standardized dietary and multi-omics data; the underrepresentation of non-European populations, which limits model generalizability and raises concerns about health equity; limited model explainability; privacy and data-governance challenges; immature regulatory pathways for adaptive software as a medical device; and specific risks associated with LLMs, such as hallucinated or guideline-discordant dietary advice. AI-enabled personalized nutrition is therefore progressing from proof of concept toward clinical translation. Realizing its potential equitably will require multi-ethnic nutrition-omics cohorts, privacy-preserving multicenter collaboration, dietitian-led human-AI collaboration, and lifecycle safety governance for generative models.
Additional Links: PMID-42865996
PubMed:
Citation:
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@article {pmid42865996,
year = {2026},
author = {Zhang, Y and Feng, M and Xue, Q and Ma, R and Liu, F},
title = {Applications of artificial intelligence in personalized nutrition interventions.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1974199},
pmid = {42865996},
issn = {2296-861X},
abstract = {Unhealthy dietary patterns remain a major modifiable contributor to the global burden of obesity, type 2 diabetes mellitus (T2DM), cardiovascular disease, and cancer. However, individuals can respond markedly differently to identical foods, limiting the effectiveness of one-size-fits-all dietary guidance. This review examines the application of artificial intelligence (AI) to personalized nutrition interventions across three interconnected layers. At the biological level, inter-individual variability can be characterized by three mechanistic dimensions: nutrigenomic variation, which influences nutrient metabolism and disease susceptibility; metabolomic biomarkers, which objectively capture dietary exposure and early metabolic alterations; and the gut microbiome, which bidirectionally mediates diet-host interactions. At the technological level, AI integrates these dimensions into multimodal digital profiles. Machine learning models predict individual postprandial glycemic and lipemic responses, with reported correlations of up to r = 0.77 in large cohorts; deep learning and computer vision automate dietary assessment; natural language processing and large language models (LLMs) support nutrition counseling; knowledge graphs enable constraint-aware food recommendations; and digital-twin and adaptive closed-loop systems incorporating continuous glucose monitoring and wearable-device data support real-time nutritional interventions. However, the strength of clinical evidence varies across disease domains. Glycemic management in T2DM and prediabetes currently has the most mature randomized controlled trial evidence: an AI-enabled personalized intervention combining algorithmic dietary personalization with CGM-linked feedback improved glycemic endpoints compared with a Mediterranean diet, while a fully automated AI-delivered diabetes prevention program achieved outcomes non-inferior to those of human coaching. In obesity, cardiovascular disease, oncology, and gastrointestinal disorders, the evidence remains mixed or preliminary. Clinical translation also faces substantial challenges, including biased and inconsistently standardized dietary and multi-omics data; the underrepresentation of non-European populations, which limits model generalizability and raises concerns about health equity; limited model explainability; privacy and data-governance challenges; immature regulatory pathways for adaptive software as a medical device; and specific risks associated with LLMs, such as hallucinated or guideline-discordant dietary advice. AI-enabled personalized nutrition is therefore progressing from proof of concept toward clinical translation. Realizing its potential equitably will require multi-ethnic nutrition-omics cohorts, privacy-preserving multicenter collaboration, dietitian-led human-AI collaboration, and lifecycle safety governance for generative models.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
From gut to lung: the microbiome-directed causal mechanisms and therapeutic horizons in asthma.
Frontiers in immunology, 17:1935791.
The gut-lung axis represents a predominantly gut-to-lung communication network through which gut microbiota and their metabolites influence pulmonary immunity. In asthma, gut dysbiosis-characterized by reduced microbial diversity, depletion of short-chain fatty acid (SCFA)-producing taxa, and expansion of pro-inflammatory pathobionts-has been consistently associated with disease severity and type 2 inflammation. While the axis is conceptually bidirectional, the vast majority of mechanistic evidence to date describes unidirectional gut to lung regulation. This review critically synthesizes evidence on the gut-lung axis in asthma. We evaluate multi-kingdom microbial ecology, evaluating contributions from bacterial, fungal, protozoan, and phage. We examine metabolite-specific immune reprogramming via SCFAs, bile acids, and tryptophan derivatives, explicitly acknowledging unresolved controversies including the SCFA concentration paradox. We integrate causal inference frameworks that combine Mendelian randomization, gnotobiotic models, and experimental triangulation. We also present precision therapeutic pipelines with evidence-based grading of interventions ranging from probiotics to engineered live biotherapeutics. We propose that targeting the gut-lung axis represents a foundational strategy for asthma modification and outline a roadmap from multi-omics discovery to biomarker-guided clinical trials. Distinguishing this review from prior work, we explicitly separate established mechanisms from speculative pathways and provide actionable criteria for clinical translation. We also critically identify the reverse (lung to gut) pathway as a major knowledge gap requiring urgent investigation.
Additional Links: PMID-42866007
PubMed:
Citation:
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hide bibtex listing
@article {pmid42866007,
year = {2026},
author = {Ni, FX and Pan, CF and Chen, HH and Huang, DH and Jiang, ZB},
title = {From gut to lung: the microbiome-directed causal mechanisms and therapeutic horizons in asthma.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1935791},
pmid = {42866007},
issn = {1664-3224},
mesh = {Humans ; *Asthma/therapy/microbiology/immunology/metabolism/etiology ; Animals ; *Lung/immunology/microbiology/metabolism ; *Gastrointestinal Microbiome/immunology ; Dysbiosis/immunology ; Probiotics/therapeutic use ; },
abstract = {The gut-lung axis represents a predominantly gut-to-lung communication network through which gut microbiota and their metabolites influence pulmonary immunity. In asthma, gut dysbiosis-characterized by reduced microbial diversity, depletion of short-chain fatty acid (SCFA)-producing taxa, and expansion of pro-inflammatory pathobionts-has been consistently associated with disease severity and type 2 inflammation. While the axis is conceptually bidirectional, the vast majority of mechanistic evidence to date describes unidirectional gut to lung regulation. This review critically synthesizes evidence on the gut-lung axis in asthma. We evaluate multi-kingdom microbial ecology, evaluating contributions from bacterial, fungal, protozoan, and phage. We examine metabolite-specific immune reprogramming via SCFAs, bile acids, and tryptophan derivatives, explicitly acknowledging unresolved controversies including the SCFA concentration paradox. We integrate causal inference frameworks that combine Mendelian randomization, gnotobiotic models, and experimental triangulation. We also present precision therapeutic pipelines with evidence-based grading of interventions ranging from probiotics to engineered live biotherapeutics. We propose that targeting the gut-lung axis represents a foundational strategy for asthma modification and outline a roadmap from multi-omics discovery to biomarker-guided clinical trials. Distinguishing this review from prior work, we explicitly separate established mechanisms from speculative pathways and provide actionable criteria for clinical translation. We also critically identify the reverse (lung to gut) pathway as a major knowledge gap requiring urgent investigation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Asthma/therapy/microbiology/immunology/metabolism/etiology
Animals
*Lung/immunology/microbiology/metabolism
*Gastrointestinal Microbiome/immunology
Dysbiosis/immunology
Probiotics/therapeutic use
RevDate: 2026-10-13
CmpDate: 2026-10-13
Gut microbiota and health-related quality of life in paediatric inherited metabolic disorders: a narrative review and conceptual framework.
Frontiers in microbiology, 17:1928657.
Inherited metabolic disorders (IMDs) comprise more than 1,400 rare genetic conditions affecting paediatric patients worldwide. Despite advances in newborn screening and dietary management, many children experience chronic complications, gastrointestinal symptoms, and reduced health-related quality of life (HRQoL). Emerging evidence-predominantly from phenylketonuria (PKU)-suggests that gut microbiota may influence metabolic homeostasis and patient-centred outcomes in affected children. Because of substantial methodological heterogeneity and the rarity of individual disorders, we elected a narrative review format to synthesise current evidence rather than a formal quantitative synthesis. Electronic searches were performed in PubMed, Embase, and Web of Science from inception to February 2026. We synthesise current evidence regarding gut microbiota composition in major paediatric IMDs, including PKU, organic acidemias, glycogen storage diseases, lysosomal storage disorders, and mitochondrial diseases. For PKU, controlled studies report reduced microbial diversity and depletion of butyrate-producing taxa associated with long-term dietary treatment. For the remaining disorders, direct paediatric microbiome data are sparse or absent, and proposed links rely on mechanistic extrapolation from non-IMD populations. We present the gut microbiota-metabolism-quality of life axis as a conceptual framework that integrates microbial metabolites, intestinal barrier function, immune signalling, and patient-reported outcomes, while emphasising that direct causal evidence linking microbiota alterations to HRQoL in paediatric IMDs is currently lacking. Microbiota-directed interventions remain preliminary. Future multicentre longitudinal studies integrating microbiome profiling, multi-omics technologies, and validated patient-reported outcomes are needed to clarify causal mechanisms and therapeutic potential. Importantly, the available evidence is heterogeneous: direct paediatric microbiome evidence is strongest for PKU, whereas evidence for other IMDs is sparse and often observational, preclinical, or extrapolated from non-IMD populations. The proposed microbiota-metabolism-HRQoL axis is therefore presented as a hypothesis-generating framework rather than an established causal pathway.
Additional Links: PMID-42866012
PubMed:
Citation:
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@article {pmid42866012,
year = {2026},
author = {Dumbuya, JS and Li, Y and He, B and Li, G and Liu, Y and Zhong, Y and Huang, S and Chen, X},
title = {Gut microbiota and health-related quality of life in paediatric inherited metabolic disorders: a narrative review and conceptual framework.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1928657},
pmid = {42866012},
issn = {1664-302X},
abstract = {Inherited metabolic disorders (IMDs) comprise more than 1,400 rare genetic conditions affecting paediatric patients worldwide. Despite advances in newborn screening and dietary management, many children experience chronic complications, gastrointestinal symptoms, and reduced health-related quality of life (HRQoL). Emerging evidence-predominantly from phenylketonuria (PKU)-suggests that gut microbiota may influence metabolic homeostasis and patient-centred outcomes in affected children. Because of substantial methodological heterogeneity and the rarity of individual disorders, we elected a narrative review format to synthesise current evidence rather than a formal quantitative synthesis. Electronic searches were performed in PubMed, Embase, and Web of Science from inception to February 2026. We synthesise current evidence regarding gut microbiota composition in major paediatric IMDs, including PKU, organic acidemias, glycogen storage diseases, lysosomal storage disorders, and mitochondrial diseases. For PKU, controlled studies report reduced microbial diversity and depletion of butyrate-producing taxa associated with long-term dietary treatment. For the remaining disorders, direct paediatric microbiome data are sparse or absent, and proposed links rely on mechanistic extrapolation from non-IMD populations. We present the gut microbiota-metabolism-quality of life axis as a conceptual framework that integrates microbial metabolites, intestinal barrier function, immune signalling, and patient-reported outcomes, while emphasising that direct causal evidence linking microbiota alterations to HRQoL in paediatric IMDs is currently lacking. Microbiota-directed interventions remain preliminary. Future multicentre longitudinal studies integrating microbiome profiling, multi-omics technologies, and validated patient-reported outcomes are needed to clarify causal mechanisms and therapeutic potential. Importantly, the available evidence is heterogeneous: direct paediatric microbiome evidence is strongest for PKU, whereas evidence for other IMDs is sparse and often observational, preclinical, or extrapolated from non-IMD populations. The proposed microbiota-metabolism-HRQoL axis is therefore presented as a hypothesis-generating framework rather than an established causal pathway.},
}
RevDate: 2026-10-13
CmpDate: 2026-10-13
Oral microbiome and postmenopausal breast cancer risk: findings from the NIH-AARP diet and health study.
Journal of oral microbiology, 18(1):2728745.
INTRODUCTION: Breast cancer is the most frequently diagnosed cancer among women worldwide. Some case-control studies have reported associations between the oral microbiome and breast cancer, but the temporality of the association remains unclear. Therefore, we examined this association prospectively in the NIH-AARP Diet and Health Study.
METHODS: In 2005, oral wash samples were collected from a subset of the NIH-AARP cohort. We identified 318 women who developed breast cancer after collection and 318 controls, incidence-density matched on age at collection, race/ethnicity and smoking. DNA was extracted using the DNeasy PowerSoil Pro Kit, followed by shotgun metagenomic sequencing. Conditional logistic regression was used to calculate the odds ratios (OR) for associations between alpha- and beta-diversity and species- and gene-level metrics with breast cancer risk, adjusting for potential confounders.
RESULTS: Cases developed breast cancer on average 3.4 years after sample collection. Overall, the majority of the microbial metrics, including species and genes, showed largely null associations with the exception of Pielou's evenness (OR = 0.82; 95% CI = 0.70-0.95). When stratified by time to diagnosis, the inverse association with Pielou's evenness was only detected among women diagnosed within 2 years (29% of cases). In this subgroup, some previously reported associations, like the inverse association with the presence of Treponema (OR = 0.37; 95% CI = 0.17-0.78), were replicated. Null associations were predominantly observed for cases diagnosed more than 2 years after sample collection.
CONCLUSIONS: The oral microbiome was generally not prospectively associated with postmenopausal breast cancer in a US population and results suggested previous findings may reflect reverse causation.
Additional Links: PMID-42866017
PubMed:
Citation:
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@article {pmid42866017,
year = {2026},
author = {Herrera, G and Hua, X and Wu, Z and Liao, LM and Wan, Y and Dagnall, CL and Jones, K and Hicks, BD and Hutchinson, A and Gail, MH and Shi, J and Gierach, GL and Sinha, R and Vogtmann, E},
title = {Oral microbiome and postmenopausal breast cancer risk: findings from the NIH-AARP diet and health study.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2728745},
pmid = {42866017},
issn = {2000-2297},
abstract = {INTRODUCTION: Breast cancer is the most frequently diagnosed cancer among women worldwide. Some case-control studies have reported associations between the oral microbiome and breast cancer, but the temporality of the association remains unclear. Therefore, we examined this association prospectively in the NIH-AARP Diet and Health Study.
METHODS: In 2005, oral wash samples were collected from a subset of the NIH-AARP cohort. We identified 318 women who developed breast cancer after collection and 318 controls, incidence-density matched on age at collection, race/ethnicity and smoking. DNA was extracted using the DNeasy PowerSoil Pro Kit, followed by shotgun metagenomic sequencing. Conditional logistic regression was used to calculate the odds ratios (OR) for associations between alpha- and beta-diversity and species- and gene-level metrics with breast cancer risk, adjusting for potential confounders.
RESULTS: Cases developed breast cancer on average 3.4 years after sample collection. Overall, the majority of the microbial metrics, including species and genes, showed largely null associations with the exception of Pielou's evenness (OR = 0.82; 95% CI = 0.70-0.95). When stratified by time to diagnosis, the inverse association with Pielou's evenness was only detected among women diagnosed within 2 years (29% of cases). In this subgroup, some previously reported associations, like the inverse association with the presence of Treponema (OR = 0.37; 95% CI = 0.17-0.78), were replicated. Null associations were predominantly observed for cases diagnosed more than 2 years after sample collection.
CONCLUSIONS: The oral microbiome was generally not prospectively associated with postmenopausal breast cancer in a US population and results suggested previous findings may reflect reverse causation.},
}
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