@article {pmid43005491,
year = {2026},
author = {Fijabi, O and Morenikeji, OB and Ivey, SL and Loest, C and Idowu, M and Ashley, R and Ogunade, IM and Taiwo, G},
title = {Feed additives as systems-level modulators of the ruminant host-microbiome interaction: a multi-omics perspective on efficiency, resistance, and reproduction.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1995937},
pmid = {43005491},
issn = {1664-302X},
abstract = {Ruminant livestock face converging pressures from climatic variation, antimicrobial agents, and the imperative for sustainable intensification. However, the molecular imprints through which nutritional interventions modulate host-microbiome interactions across physiological contexts remain fragmented across disciplinary themes. Here, we synthesize evidence from metagenomics, metatranscriptomics, metabolomics, and host transcriptomics to propose that feed additives operate as systems-level modulators of a functionally integrated rumen-liver-immune-reproductive axis, rather than acting on isolated metabolic pathways. Prevotella, Butyrivibrio, Ruminococcus, and Fibrobacter recurrently emerged across studies to be associated with feed efficiency, immune modulation, resistome dynamics, and reproductive fitness. However, their relationship is context dependent and not causal. Furthermore, hepatic transcriptomic and microRNA (miRNA)-mediated regulatory networks could serve as a molecular bridge connecting ruminal fermentation events to systemic phenotypic outcomes. The ruminant resistome may also represent a potential interface with public health rather than an isolated ecological phenomenon, given the capacity for horizontal gene transfer through mobile genetic elements, although the extent of transmission to humans remains to be quantified. Early-life microbial programming and reproductive tract microbiome composition also represent tractable intervention windows for precision management. This integrated framework could reframe feed additive research from a single pathway to a systems-level perspective, offering a basis for precision ruminant production.},
}

@article {pmid43005495,
year = {2026},
author = {Sanabria, FMLS},
title = {From Prebiotics to Mitochondrial Response: A Critical Narrative Review of Microbiota-Host Metabolic Interactions and Their Implications for Child Neurodevelopment.},
journal = {Cureus},
volume = {18},
number = {11},
pages = {e119347},
pmid = {43005495},
issn = {2168-8184},
abstract = {Prebiotics can modify intestinal microbial fermentation and short-chain fatty acid (SCFA) production, but whether these changes improve mitochondrial bioenergetics or neurodevelopmental outcomes in children remains uncertain. This critical narrative review examines the relationships among prebiotic substrates, microbial metabolism, SCFA availability, host metabolic processing, mitochondrial function, and pediatric clinical outcomes. Literature was identified through PubMed/MEDLINE, journal and publisher websites, and citation tracking, with literature identification completed before October 15, 2026. Evidence was organized by intervention or exposure, biological system, and measured endpoint, distinguishing direct microbial metabolite exposure from oral prebiotic supplementation. Experimental studies show that butyrate supports oxidative energy metabolism in colonocytes and that mitochondrial responses to microbial metabolites vary with concentration, tissue, redox state, and individual metabolic capacity. Increased intestinal fermentation does not necessarily establish greater systemic metabolite availability, enhanced mitochondrial ATP synthesis, or improved neuronal function. Pediatric galactooligosaccharide trials have documented microbial changes without directly measuring mitochondrial ATP production or establishing consistent between-group improvements in behavioral or overall gastrointestinal outcomes. Findings from combined probiotic, prebiotic, and synbiotic interventions cannot establish prebiotic-specific efficacy. A hypothesis-generating framework termed fermentation-bioenergetic response uncoupling is proposed, comprising five potential points of divergence: substrate accessibility, microbial transformation, host exposure, metabolic processing, and mitochondrial functional response. Clinical outcomes are assessed separately. Missing downstream measurements indicate an evidence gap rather than demonstrated biological uncoupling. Future pediatric research should integrate chemically defined nutritional interventions, functional microbiome profiling, metabolomics, validated mitochondrial measurements, and prespecified clinically relevant outcomes. Current evidence does not establish prebiotics as treatments for mitochondrial dysfunction or core neurodevelopmental features; potential gastrointestinal benefits require evaluation for specific clinical indications.},
}

@article {pmid43005677,
year = {2026},
author = {Li, GL and Zhang, ZC and Lyu, XM and Li, MX and Lin, PY and Yu, HS and Zhu, YY and Zhang, GH and Duan, CG and Cheung, Y and Li, W and Zhang, ZJ and Xu, TS and Chen, F and Huang, MW},
title = {Current research status of risk assessment models for oral squamous cell carcinoma based on microbiome databases.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1894946},
pmid = {43005677},
issn = {1664-302X},
abstract = {Oral squamous cell carcinoma (OSCC) is one of the most common oral malignancies. Due to insidious early symptoms, high invasiveness, and frequent cervical lymph node metastasis, patient survival remains poor. Recent studies demonstrate significant associations between oral dysbiosis and OSCC. To address limited early screening and suboptimal survival rates, this review systematically summarizes OSCC microbiome research and disease risk assessment applications. Studies reveal marked oral dysbiosis in patients with OSCC, characterized by enrichment of Fusobacterium and Porphyromonas, reduced Neisseria abundance, and altered community stability. These promote tumorigenesis through chronic pro-inflammatory signaling, the production of carcinogenic metabolites, and direct oncogenic pathway interference. Consequently, the oral microbiome offers non-invasive, sensitive biomarkers for early detection. We identify and distinguish four categories of predictive models in the current literature: (1) detection/discrimination of prevalent OSCC, (2) prediction of malignant transformation from oral potentially malignant disorders, (3) prediction of recurrence or metastasis after treatment, and (4) prognostic models for survival prediction. Existing databases include comprehensive and OSCC-specific collections with multi-omics integration. Risk assessment models encompass traditional statistics, machine learning, deep learning, and multimodal fusion, and have shown promising performance in retrospective cohorts. However, standardized databases are lacking, and existing models face confounding interference, limited generalizability, and insufficient interpretability. Furthermore, current predictive models are predominantly based on 16S rRNA sequencing (bacteriome-centric), whereas comprehensive risk assessment requires integrating interkingdom entities, including fungi, viruses, and archaea, through metagenomic and virome profiling. Critically, the distinction between promising retrospective discrimination and validated prospective clinical utility remains a major translational barrier. Future directions include developing standardized longitudinal databases, integrating multi-omics, using explainable artificial intelligence, and conducting prospective validation studies to achieve personalized precision treatment.},
}

@article {pmid43005720,
year = {2026},
author = {Shree, S and Chaudhary, A and Kumar, S and Singh, K and Dubey, N},
title = {Beneficial microbes in plant salt stress tolerance: mechanisms, antioxidant defense, and multi-omics insights.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1965097},
pmid = {43005720},
issn = {1664-302X},
abstract = {Salinity stress represents a significant environmental challenge that affects plant growth, resulting in adverse impacts on crop productivity and overall yield. Salt accumulation in plants affects cellular homeostasis and provokes osmotic and ionic imbalance. It stimulates higher reactive oxygen species (ROS) production leading to oxidative stress damage and eventual cellular dysfunction. Beneficial microorganisms like plant growth-promoting rhizobacteria, arbuscular mycorrhizal fungi, endophytic fungi, and rhizosphere-associated microbes have recently emerged as resources for sustainable solutions to enhance plant resiliency against salinity stress. Their effects can involve osmotic adjustment, ion sequestration, oxidative-stress mitigation, phytohormone regulation, and rhizosphere-mediated stress buffering. The mechanisms to impart such benefits may include improved nutrients acquisition, assist in osmotic regulation, modulation of phytohormones signaling, and maintenance of cellular ion homeostasis. Often, beneficial microorganisms carry the potential to trigger both enzymatic and non-enzymatic antioxidant defense mechanisms. These responses contribute to oxidative-stress mitigation, yet, their interpretation requires contemplation of fine balance between oxidative damage and plant responses. For example, selected microbial inoculation studies have reported changes in the activity of crucial antioxidant enzymes, like superoxide dismutase, ascorbate peroxidase, catalase, and glutathione reductase. However, the magnitude and the direction of these responses are context dependent. Multi-omics approaches, including amplicon and shotgun metagenomics, metatranscriptomics, host transcriptomics, proteomics, and metabolomics, have expanded our understanding of the taxa, genes, transcripts, proteins, and metabolites associated with plant-microbe interactions under salinity. Therefore, here an effort has been made to present the evidential support for reported microbial effects and their proposed mechanisms of salt tolerance, with a focus on enzymatic and non-enzymatic defense mechanisms and the learnings of multi-omics studies. Frontier integrative mechanisms, including microbiome engineering, synthetic microbial consortia, and systems biology frameworks, are discussed for cultivating climate-resilient crops and sustainable agricultural systems in the salt-affected environments.},
}

@article {pmid43005796,
year = {2026},
author = {Wu, C and Liu, R},
title = {Gut microbiota-host co-metabolism in sepsis and critical illness: source, compartment, immune state, and host defense.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1975307},
pmid = {43005796},
issn = {1664-302X},
abstract = {Critical illness can profoundly disturb the intestinal microbiota-metabolite-host immune axis through the combined effects of shock, hypoxia, altered nutritional intake, antimicrobial exposure, organ dysfunction, and impaired epithelial barrier integrity. These changes can reshape microbial metabolic capacity, host co-metabolism, and systemic metabolite exposure, while the host may simultaneously exhibit overlapping features of hyperinflammation, immune tolerance, lymphocyte dysfunction, impaired antimicrobial defense, and tissue repair. Metabolites generated through microbial metabolism or shared microbial-host pathways may therefore contribute to immune reprogramming, although their effects are highly context dependent and cannot be regarded as uniformly beneficial or detrimental. This narrative review examines short-chain fatty acids, tryptophan-derived indoles, secondary bile acids, succinate, lactate, trimethylamine N-oxide, polyamines, and aromatic metabolites, with particular attention to source attribution, anatomical compartment, host co-metabolism, receptor signaling, and their potential influence on antimicrobial immunity. These metabolites may act through G-protein-coupled receptors, AhR, PXR, FXR, TGR5, VDR, HIF-1α, inflammasome pathways, mitochondrial signaling, and epigenetic mechanisms to modulate macrophages, neutrophils, dendritic cells, innate lymphoid cells, T lymphocytes, epithelial barriers, and endothelial responses. The direction and magnitude of these effects are likely to vary according to timing, concentration, anatomical compartment, immune-cell state, pathogen burden, and renal or hepatic clearance. Within this framework, attenuation of inflammatory signaling may help limit early collateral tissue injury, yet the same response could become disadvantageous when antimicrobial competence is already impaired. Similarly, succinate and lactate may reflect or contribute to distinct inflammatory, regulatory, or reparative programs depending on whether they arise from microbial or host metabolism and whether they act within intracellular or extracellular compartments. Human studies in critically ill populations have linked dysbiosis and metabolomic alterations with secondary infection, prolonged organ support, and mortality; however, most have not been able to resolve microbial source attribution or establish causal mediation. Future work would therefore benefit from integrating longitudinal microbiome, metabolome, immune-function, and organ-clearance measurements with source-resolved approaches, including isotope tracing, as well as state-specific and trajectory-informed clinical endpoints. Microbiome-directed interventions may be most appropriately investigated as context-dependent modulators of host defense rather than as broadly anti-inflammatory strategies.},
}

@article {pmid43005894,
year = {2026},
author = {Wu, L and Yao, HY and Fu, ZJ and Luo, RH and Zhou, S},
title = {The "gut-immune-bone axis": quantitative MRI reveals the microbial-immune-bone metabolic interplay in osteoporosis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1909663},
pmid = {43005894},
issn = {1664-3224},
mesh = {Humans ; *Osteoporosis/metabolism/immunology/diagnostic imaging/microbiology ; Animals ; *Gastrointestinal Microbiome/immunology ; *Bone and Bones/metabolism/immunology/diagnostic imaging ; *Magnetic Resonance Imaging/methods ; Bone Remodeling/immunology ; },
abstract = {Osteoporosis is a systemic skeletal disorder, whose pathogenesis is related to abnormalities in bone metabolism, as well as gut microbiota and immune system dysregulations. This structured narrative review synthesizes recent evidence on the "gut-immune-bone axis" in osteoporosis, with emphasis on studies published from 2020 to 2025 and selected later studies incorporated during manuscript revision when directly relevant. This article first outlines the direct and indirect regulatory roles of gut microbiota and its products (short-chain fatty acids, tryptophan catabolites, etc.) in bone metabolism. It then focuses on immune cells that participate in bone remodeling, including the Th17/Treg balance, B cells, and macrophages, and their interactions with the gut microbiota. The review further discusses recent developments in quantitative magnetic resonance imaging for quantifying bone microarchitecture, marrow composition, and metabolic status and considers how these measures may serve as downstream phenotyping tools in studies of the gut-immune-bone axis. Finally, an integrative model of the microbial-immune-bone metabolic network is proposed and translational strategies, including microbiome-directed interventions, immunomodulatory therapies, and multi-omics approaches, are critically discussed.},
}

Humans
*Osteoporosis/metabolism/immunology/diagnostic imaging/microbiology
Animals
*Gastrointestinal Microbiome/immunology
*Bone and Bones/metabolism/immunology/diagnostic imaging
*Magnetic Resonance Imaging/methods
Bone Remodeling/immunology

@article {pmid43005955,
year = {2026},
author = {Thomson, T and Fusi, M and Prinz, N and Cary, SC and Pilditch, CA and Ellis, JI},
title = {Nutrient enrichment shapes depth-resolved bacterial community assembly in mangrove sediments.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag298},
pmid = {43005955},
issn = {2730-6151},
abstract = {Microbial communities in mangrove sediments are critical for carbon and nutrient cycling; yet despite their importance, responses to eutrophication-a pervasive global threat to coastal ecosystems-remain poorly understood. Here, we tested whether nutrient enrichment restructures mangrove sediment bacterial communities more strongly in the subsurface than at the sediment surface. We assessed bacterial community responses to an in-situ slow-release NPK (Osmocote®) enrichment experiment in a temperate mangrove (Avicennia marina subsp. australasica) forest in Aotearoa New Zealand. Using 16S rRNA gene sequencing, we compared surface (0-2 cm) and subsurface (5-7 cm) community diversity and functional potential, 4.5 months after enrichment. Differences in porewater nutrient concentrations between ambient and enriched plots were subtle and spatially heterogeneous; however, bacterial communities exhibited significant shifts relative to controls. Community shifts in subsurface samples were stronger compared to the surface, with enrichment reducing diversity and altering community composition to Proteobacteria and Bacteroidota favoured communities. Conversely, taxa from Desulfobacterota, Chloroflexi, and Nitrospirota were more abundant in controls. Similarly, shifts in inferred functional potential in the surface remained limited, while the subsurface showed strong, selective changes: a proportional decline of sulphur-cycling and hydrogen-oxidizing taxa and a relative increase of heterotrophic guilds. Community assembly was more deterministic in subsurface compared to surface sediments, and under nutrient addition subsurface assembly shifted, mainly through reduced dispersal limitation, to more closely resemble the surface communities. These results underscore the need to better understand and integrate microbial responses at relevant spatial scales into predictions of ecosystem resilience under increasing anthropogenic pressures.},
}

@article {pmid43005997,
year = {2026},
author = {Benchea, MS and Neamtu, AA and Solomon, CN and Cuc, EA and Pantor, M and Pop, O},
title = {Adjunctive Oral Treatment Improves Helicobacter pylori Eradication Without Evidence of a Dose-Response Gradient: An Updated Meta-Analysis Challenging the Oral Reservoir Hypothesis.},
journal = {Cureus},
volume = {18},
number = {10},
pages = {e117737},
pmid = {43005997},
issn = {2168-8184},
abstract = {Standard antibiotic regimens for Helicobacter pylori are failing more often as resistance rises, and the oral cavity has long been proposed as an extragastric reservoir that seeds gastric recolonization. If so, treating the mouth should improve gastric eradication, a testable clinical claim rather than a correlation. We therefore pooled the randomized evidence on adjunctive periodontal and oral hygiene treatment identified through our search strategy and tested the reservoir hypothesis rather than assuming it. We included randomized and quasi-randomized controlled trials in which adults or children receiving standard eradication therapy for confirmed gastric H. pylori infection were allocated to receive, or not receive, an adjunctive periodontal or oral hygiene intervention. Trials were identified by citation searching of three previous syntheses and by targeted searches for trials published after August 2015, without language restriction. The primary outcome was eradication confirmed at the first post-treatment assessment, at least four weeks after therapy; the co-primary outcome was absence of recurrence at six months or later. We pooled odds ratios and risk ratios using random-effects models with the Hartung-Knapp adjustment, assessed risk of bias with the second version of the Cochrane risk-of-bias tool, and rated certainty using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. Subgroup analyses by intervention intensity, region, publication period, and source verifiability were prespecified, and small-study effects were examined by funnel plot, Egger and Begg tests, and trim-and-fill. Eleven trials contributed data. For eradication, 10 trials, including 1,575 participants, gave a pooled odds ratio of 2.84 (95% confidence interval 1.84 to 4.39; p = 0.0004) with modest heterogeneity (I-squared 34.4%, prediction interval 1.18 to 6.87), corresponding to eradication in 87.1% versus 72.0% and a number needed to treat of six. For recurrence, four trials including 999 participants gave a pooled odds ratio for remaining free of infection of 4.64 (95% confidence interval 2.06 to 10.45); the same trials pooled as risk ratios gave 1.63 (95% confidence interval 0.86 to 3.09), and both are reported with equal prominence because the finding does not survive the change of scale. There was no evidence of small-study effects (Egger p = 0.51; none imputed by trim-and-fill). No gradient with intervention intensity was detected: an antiseptic mouthrinse alone performed at least as well as full-mouth scaling and root planing (test for subgroup differences p = 0.19), although the stratum-level confidence intervals were wide, and the largest single effect in the dataset came from a placebo-controlled trial of an antiseptic mouthrinse with no mechanical component. No trial was at low overall risk of bias. Adjunctive oral treatment is consistently associated with better eradication, but no evidence of a dose-response gradient was detected, which does not support simple mechanical removal of an oral reservoir as the explanation. Certainty was moderate for eradication, downgraded for risk of bias, and low for recurrence, downgraded for risk of bias and imprecision.},
}

@article {pmid43006147,
year = {2026},
author = {Zubairi, I},
title = {Comment on: "Oral Leukoplakia Microbiome Predicts the Degree of Dysplasia and Is Shaped by Smoking and Tooth Loss".},
journal = {Oral diseases},
volume = {},
number = {},
pages = {},
doi = {10.1111/odi.70579},
pmid = {43006147},
issn = {1601-0825},
}

@article {pmid43006633,
year = {2026},
author = {Gutmann, F and Börschel, CS and Markó, L and Löber, U and Bartolomaeus, TUP and Jovanovic, N and Zeller, T and Nauck, M and Friedrich, N and Henning, AK and Forslund-Startceva, SK and Schnabel, RB},
title = {Distinct Gut Microbial and Metabolic Biomarkers Related to Atrial Fibrillation in Low-Risk Patients.},
journal = {Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/europace/euag302},
pmid = {43006633},
issn = {1532-2092},
}

@article {pmid43006873,
year = {2026},
author = {Rebeck, ON and Zhang, A and Mahmud, B and Wallace, MA and Nickel, KB and Johnson, C and Habrock-Bach, T and Zahrah, D and Liao, J and Myckatyn, TM and Tenenbaum, MM and Brandt, KE and Burnham, C-AD and Olsen, MA and Dantas, G},
title = {Comparative genomics of the skin microbiome and associated isolates of patients undergoing mastectomy with immediate breast reconstruction.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0053126},
doi = {10.1128/msphere.00531-26},
pmid = {43006873},
issn = {2379-5042},
abstract = {Mastectomy with immediate breast implant reconstruction (IBIR) is an increasingly common component of breast cancer treatment; however, these procedures carry a substantial risk of surgical site infections (SSIs) and noninfectious wound complications (NIWCs). We hypothesized that the local skin microbiota may contribute to the development of post-operative complications, in part by serving as a reservoir for pathobionts, such as Staphylococcus epidermidis and Cutibacterium acnes. We collected skin and intraoperative samples from 60 patients undergoing mastectomy with IBIR. To evaluate longitudinal shifts in community composition, we performed 16S rRNA gene sequencing of 151 breast and axilla skin swabs collected at pre- and post-operative time points. Using a comprehensive culture approach, we recovered diverse cultivable organisms and selected 232 S. epidermidis and 130 C. acnes isolates from skin swabs, implant swabs, and seroma fluid for whole-genome sequencing and comparative genomic analysis. We observed perturbations to community structure in the breast and axilla following mastectomy. These shifts were characterized by a significant and persistent depletion of Corynebacterium spp., which did not resolve in patients who subsequently developed an SSI. We also uncovered outcome-specific genomic signatures in S. epidermidis isolates, which may offer mechanistic insight into the role of this species in SSI and NIWC development. Importantly, we also identified genomic signatures detectable prior to mastectomy and infection diagnosis that may offer clinical utility toward predicting post-operative complications. Together, these findings illustrate the importance of the skin microbiome in SSI and NIWC development following mastectomy with IBIR.IMPORTANCEAn improved understanding of the relationship between surgical sites and adjacent resident skin microbiota can help identify which patients are at increased risk for developing surgical site infections and noninfectious wound complications. By characterizing bacterial communities before mastectomy with immediate breast reconstruction and during subsequent healing, we sought to evaluate how changes in community composition may contribute to the development of post-operative complications. We also performed in-depth genomic analyses of Staphylococcus epidermidis and Cutibacterium acnes isolates recovered from patients to identify genetic components that may determine whether an isolate protects or predisposes patients toward development of post-operative complications. Last, we identified genomic signatures detectable prior to surgery and infection diagnosis that are correlated with patient outcome, which may serve as informative biomarkers to inform patient care.},
}

@article {pmid43006913,
year = {2026},
author = {Atoom, AM and Allela, OQB and Nayak, PP and Arora, V and Singla, S and Athab, ZH and Urazbaeva, D and Usmanov, R},
title = {Epigenome, Microbiome, and Metabolites: Unraveling the Complex Pathogenesis of Celiac Disease.},
journal = {Cell biology international},
volume = {50},
number = {11},
pages = {},
doi = {10.1002/cbin.70231},
pmid = {43006913},
issn = {1095-8355},
mesh = {Humans ; *Celiac Disease/genetics/microbiology/metabolism ; *Epigenesis, Genetic ; *Epigenome ; *Gastrointestinal Microbiome ; *Microbiota ; Genetic Predisposition to Disease ; Diet, Gluten-Free ; Animals ; DNA Methylation ; HLA-DQ Antigens/genetics ; },
abstract = {Celiac disease (CeD) is a chronic autoimmune disease triggered by gluten consumption in genetically susceptible individuals, primarily those with HLA-DQ2 or HLA-DQ8 haplotypes. Although these genetic factors are responsible for a substantial portion of disease risk, they do not fully explain disease heritability or the rising incidence observed worldwide. Recent clinical studies highlight epigenetic modifications-including DNA methylation, histone modifications, non-coding RNA regulation, and RNA methylation-as critical mediators bridging genetic susceptibility and environmental influences, such as gut microbiota dysbiosis, dietary patterns, early-life exposures, infections, and pharmaceutical interventions. These epigenetic mechanisms modulate immune responses, intestinal barrier function, and inflammatory pathways, contributing to the loss of gluten tolerance and perpetuation of mucosal damage. Key players, including tissue transglutaminase 2 (TG2) and interferon-gamma (IFN-γ), form amplifying feedback loops that exacerbate pathogenesis. Bacterial metabolites and lifestyle factors further influence epigenetic landscapes, offering reversible targets for intervention. This review synthesizes current evidence on epigenetic alterations in CeD, emphasizing their interplay with microbiota and metabolites, tissue-specific patterns, and potential as biomarkers. It also explores implications for novel therapeutic strategies beyond the gluten-free diet, including epigenetic modulators and microbiota-targeted approaches, to advance personalized prevention and management of CeD.},
}

Humans
*Celiac Disease/genetics/microbiology/metabolism
*Epigenesis, Genetic
*Epigenome
*Gastrointestinal Microbiome
*Microbiota
Genetic Predisposition to Disease
Diet, Gluten-Free
Animals
DNA Methylation
HLA-DQ Antigens/genetics

@article {pmid43006985,
year = {2026},
author = {Wang, Q and Fu, D and Ma, Y and Cheng, C and Xu, Y and Agathokleous, E and Feng, Z},
title = {Elevated ozone reshapes wheat root-associated microbiomes through coordinated plant responses and rhizosphere environmental filtering.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0185826},
doi = {10.1128/aem.01858-26},
pmid = {43006985},
issn = {1098-5336},
abstract = {Elevated tropospheric ozone (O3) threatens crop productivity, but how O3-induced changes in plant responses influence root-associated microbiomes remains unclear. We investigated the responses of microbial communities inhabiting the rhizosphere and root endosphere to elevated O3 using four cultivars grown under ambient and 1.5-fold ambient O3 in a field-based free-air O3-concentration enrichment (FACE) system. Plant traits, root-released organic carbon (ROC), rhizosphere properties, extracellular enzyme activities, and bacterial and fungal communities were jointly analyzed. Elevated O3 reduced yield and root biomass, with cultivar-dependent changes in ROC. Elevated O3 consistently increased rhizosphere pH and altered microbial resource allocation, increasing ecoenzymatic vector length by 4.1% and decreasing vector angle by 4.6%. Bacterial communities showed a stronger response than fungal taxonomic communities, particularly in the rhizosphere. However, variation partitioning indicated that soil properties, especially pH, rather than O3 treatment alone, provided the strongest independent explanation for bacterial community variation. Fungal communities showed limited taxonomic turnover but exhibited shifts in predicted trophic guilds, including increased pathotroph- and saprotroph-associated groups and decreased symbiotroph-containing guilds under elevated O3. These results demonstrate that elevated O3 reshapes the wheat root-associated microbiome through coordinated changes in plant performance, rhizosphere environmental filtering, and microbial functional strategies, highlighting the importance of plant-mediated processes in regulating belowground responses to atmospheric change.IMPORTANCEElevated tropospheric O3 is an increasing threat to crop production, but its effects on belowground microbial processes remain poorly understood. This study demonstrates that O3-induced root-associated microbiome changes are closely linked with altered plant carbon allocation and rhizosphere environmental conditions rather than O3 exposure also. By integrating plant traits, soil properties, extracellular enzyme allocation, and microbial community analyses, we reveal a compartment-specific plant-soil-microbiome response to elevated O3. These findings improve our understanding of how atmospheric pollution may reshape crop-associated microbial functions and soil ecological processes under future climate change.},
}

@article {pmid43007215,
year = {2026},
author = {Chakraborty, D and Vanderhyde, M and Camuy-Velez, L and Saha, B and Fayshal, MA and Elvers, R and Dragt, H and Rodriguez, S and Xu, J and Iskander, SM and Banerjee, S},
title = {Longitudinal Multiomics Reveals Core Microbiome Disruption and Potential Keystone-Associated Recovery Following Pesticide Exposure.},
journal = {Environmental science & technology},
volume = {60},
number = {44},
pages = {32021-32033},
doi = {10.1021/acs.est.6c07798},
pmid = {43007215},
issn = {1520-5851},
support = {37000-7690-02442-FARG006387//NDSU Development Foundation/ ; },
mesh = {*Microbiota/drug effects ; *Pesticides ; Multiomics ; Soil Microbiology ; Bacteria ; Fungi ; },
abstract = {Pesticides have become indispensable in modern agriculture, serving as a primary tool to minimize crop loss amid increasing human population pressures. While the negative effects of pesticides on the soil microbiome have been reported, the temporal dynamics of soil microorganisms under pesticide use remain underexplored. Specifically, limited knowledge exists regarding how the soil microbiome responds to pesticides before and after the manufacturer-labeled 'safe period' of 21 days after application. We conducted a longitudinal microcosm study to investigate the temporal impacts of herbicide, fungicide, and insecticide on soil microbial diversity, composition, network complexity, and functional pathways across five time points. Our results show that soil microbial communities are negatively impacted by pesticide applications, but there is a trend of recovery after 21 days. We found a significant impact of the temporal persistence of pesticides on both bacterial and fungal community composition, with a stronger effect on fungi. Network analysis revealed that core microbiome networks were negatively impacted by pesticide applications, with the core microbial nodes, raw associations, and modularity declining in pesticide-treated soils, and this negative effect was particularly strong for pyrethroid insecticides. We identified several differentially abundant taxa, including Xanthobacteraceae and Vicinamibacteriales among bacteria, and Mortierella, Mytilinidales among fungi, which could serve as useful biomarkers for pesticide-affected soils. Results from microbial co-occurrence network analysis revealed that one ASV assigned to the Methyloligellaceae family consistently emerged as a keystone taxon in pesticide-treated soils. Using genome-resolved metagenomics, we assembled the genomes (MAGs) of Methyloligellaceae members and found these taxa harbor putative genes associated with pesticide degradation and antimicrobial resistance, suggesting their possible role in community recovery. Given the remarkably dynamic nature of soil microbial communities, our findings bridge an important knowledge gap regarding the short-term dynamics of microbial structures and functional pathways in response to major pesticides.},
}

*Microbiota/drug effects
*Pesticides
Multiomics
Soil Microbiology
Bacteria
Fungi

@article {pmid43007386,
year = {2026},
author = {Vashishth, S and Ambasta, RK and Kumar, P},
title = {Mechanistic role of functional bacterial amyloids (FuBAs) in inflammatory responses, ubiquitin proteasome system (UPS) impairment, and cross-seedings with host amyloids.},
journal = {Molecular biology reports},
volume = {53},
number = {1},
pages = {},
pmid = {43007386},
issn = {1573-4978},
mesh = {Humans ; *Proteasome Endopeptidase Complex/metabolism ; *Ubiquitin/metabolism ; *Amyloid/metabolism ; *Inflammation/metabolism ; Animals ; Neurodegenerative Diseases/metabolism/microbiology ; *Bacterial Proteins/metabolism ; Amyloid beta-Peptides/metabolism ; alpha-Synuclein/metabolism ; Bacteria/metabolism ; Proteotoxic Stress ; },
abstract = {Neurodegenerative diseases are characterized by disruption of protein homeostasis, aggregation, inflammation, and neuronal resilience, with age affecting disease susceptibility. Bacterial amyloids, such as curli, Fap, TasA, and phenol-soluble modulins, are functional amyloids that aid in biofilm formation and potentially interact with host proteins and innate immune pathways. They are cross-β-sheet proteins that interact with other proteins from different species, and experimental data show that some bacterial amyloids promote the aggregation of amyloid-β and α-synuclein. Various fuBA effects along the gut-brain axis depend on microbial production, retention in the gut, barrier integrity, clearance from the system, immune status, and tissue susceptibility. The activation of innate immune mechanisms, such as Toll-like receptor signaling, by FuBAs or related microbial signals could lead to inflammation and oxidative stress. The ubiquitin-proteasome system (UPS) is another aspect of cellular protein quality control that could be further compromised by increased amyloid burden. To date, direct FuBA-mediated proteasome inhibition remains poorly established. To this end, this review separates direct evidence, indirect effects of aggregation/inflammatory stress, and mechanistic precedents from studies on human amyloid. Structural biology, immunology, and proteostasis research will be combined, and FuBAs will be investigated as potential upstream modulators of the neurodegenerative proteinopathies. We assess whether FuBAs directly influence UPS function in intestinal, peripheral, or neural compartments, and discuss possible therapeutic strategies, including microbiome modulation, barrier repair, immunomodulation, and proteasome stimulation. FuBAs can alter neuronal proteostasis in both amyloid-related disorders and other neurodegenerative processes, but not necessarily act as triggers of these processes.},
}

Humans
*Proteasome Endopeptidase Complex/metabolism
*Ubiquitin/metabolism
*Amyloid/metabolism
*Inflammation/metabolism
Animals
Neurodegenerative Diseases/metabolism/microbiology
*Bacterial Proteins/metabolism
Amyloid beta-Peptides/metabolism
alpha-Synuclein/metabolism
Bacteria/metabolism
Proteotoxic Stress

@article {pmid43007660,
year = {2026},
author = {Pandia, B and Vasudevan, S and Regati, D and Rathod, N and Sankar, S and Sowdhamini, R and Chandra, N},
title = {CAcnesDB: a database of Cutibacterium acnes with integrated functional insights derived from multi-modal genome annotation.},
journal = {Database : the journal of biological databases and curation},
volume = {2026},
number = {},
pages = {},
pmid = {43007660},
issn = {1758-0463},
support = {BT/PR40186/BTIS/137/3/2020//Department of Biotechnology/ ; BT/PR40316/BTIS/137/83/2023//Department of Biotechnology/ ; },
mesh = {*Molecular Sequence Annotation ; *Genome, Bacterial ; *Databases, Genetic ; *Bacterial Proteins/genetics/metabolism/chemistry ; *Propionibacterium acnes/genetics/metabolism ; Biocuration ; Proteome/genetics/metabolism ; Humans ; },
abstract = {Cutibacterium acnes is a predominant member of the human skin microbiome, generally as a beneficial or a benign inhabitant, which under specific conditions transforms into a pathogen, causing acne and associated inflammatory responses. While there is a wealth of data on the microbiology and genomics of the microbe, there is a lack of comprehensive annotation of the proteins coded by the genome, slowing progress in understanding its unique metabolic versatility and survival in host hypoxic sebaceous niches. We configured an integrated pipeline for functional annotation of the C. acnes genome, combining gene calling, domain and ontology mapping, KEGG pathways assignment, proteome-scale structural modeling, predicting pockets and associating the small-molecule metabolites based on binding site similarity to facilitate structure-to-function annotation. Structural predictions using ColabFold covered nearly the full proteome, with 83.7% of models showing high confidence. To infer protein function, ligand-binding sites in the C. acnes modeled proteome were predicted using a consensus of three independent algorithms, PocketDepth, SiteHound, and Fpocket. Small molecule ligands were mapped to the resulting pockets through structural comparison of the pockets with known small-molecule binding sites in PDB where there was direct or indirect evidence for such binding, resulting in the C. acnes predicted ligandome (CApL) comprising 693 protein-ligand pairs across 534 proteins. CAcnesDB is a comprehensive database of the C. acnes genome, hosting functional annotation from multiple levels of input and analyses, covering 2297 protein-coding genes.},
}

*Molecular Sequence Annotation
*Genome, Bacterial
*Databases, Genetic
*Bacterial Proteins/genetics/metabolism/chemistry
*Propionibacterium acnes/genetics/metabolism
Biocuration
Proteome/genetics/metabolism
Humans

@article {pmid43007723,
year = {2026},
author = {Kugelmann, D and García-Ponce, A and Thielemann, N and Radeva, MY and Anders, M and Kang, DE and Siadjeu, C and Burkard, N and Horn, AK and Neubauer, J and Hiermaier, M and Egu, DT and Schmitz, C and Kurzai, O and Vuopala, KS and Kuismin, O and Schlegel, N and Waschke, J},
title = {Dsg2 truncation causes a severe intestinal epithelial barrier breakdown and alters microbiome and immune response.},
journal = {JCI insight},
volume = {},
number = {},
pages = {},
doi = {10.1172/jci.insight.183554},
pmid = {43007723},
issn = {2379-3708},
abstract = {Inflammatory bowel diseases (IBD) including Crohn's disease (CD) are characterized by impaired intestinal epithelial barrier (IEB) function. Alterations in the desmosomal cadherin desmoglein 2 (Dsg2) have been linked to loss of IEB and intestinal inflammation in IBD. We investigated the pathogenic impact of a cytoplasmatic-truncating mutation in the desmosomal cadherin desmoglein 2 gene (DSG2) in an IBD patient. Genetic analysis of a CD patient revealed a likely pathogenic DSG2 mutation leading to a truncated protein lacking part of the intracellular domain. Generation of an enterocyte-specific mouse model to recapitulate the human mutation resulted in a lethal intestinal barrier defect which was evident in homozygous but not in heterozygous mice. In vitro, barrier defects correlated with changes in Dsg2 mobility and upregulation of pore-forming tight junction protein claudin-2. Organoids derived from heterozygous Dsg2 truncated mice exhibited increased epithelial susceptibility to proinflammatory cytokines. Bulk RNAseq followed by gene ontology analysis in homozygous mice revealed a skewed IL17/IL23 response overlapping with transcriptional changes in patients with CD. Furthermore, 16S rRNA sequencing revealed alterations in microbiome composition in animals that carried the Dsg2 truncation. In summary, a patient-derived mutation in the DSG2 gene causing cytoplasmic truncation in homozygous state induced a lethal intestinal barrier breakdown in mice paralleled by altered gut microbiota and intestinal immune response.},
}

@article {pmid43008459,
year = {2026},
author = {Sun, J and Zhao, X and Yan, WJ and Li, WT and Sun, WL and Zhang, PD},
title = {Roots through time: dynamics of the rhizosphere microbiome and its nutrient-cycling potential in Zostera marina meadows with implications for microbiome-based restoration.},
journal = {Marine environmental research},
volume = {223},
number = {},
pages = {108529},
doi = {10.1016/j.marenvres.2026.108529},
pmid = {43008459},
issn = {1879-0291},
abstract = {The seagrass rhizosphere microbiome is critical for sedimentary nutrient turnover, yet the spatiotemporal dynamics of carbon, nitrogen, phosphorus, and sulfur cycling across Zostera marina developmental stages remain poorly understood. Leveraging metagenomic sequencing and 147 metagenome-assembled genomes (MAGs), we resolved functional gene profiles in rhizosphere and bulk sediments across three discrete developmental stage (vegetative, reproductive and dormant). Temporal variation (i.e., sampling period) explained 48.1-57.4% of the variance in nutrient-cycling-associated microbial community composition, whereas spatial partitioning between rhizosphere and bulk compartments accounted for 11.6-20.0%. Carbon fixation genes were significantly enriched in the rhizosphere during reproduction but reached peak abundance in bulk sediments during dormancy. Nitrogen fixation and dissimilatory nitrate reduction to ammonium (DNRA) genes were enriched in the rhizosphere during both vegetative and dormant stages. Phosphorus mobilization-associated genes displayed parallel enrichment patterns, with the regulatory two-component system gene phoR broadly conserved across MAGs. Sulfur oxidation genes were enriched in the rhizosphere during vegetative and dormant stages, yet exhibited higher relative abundance in bulk sediments during reproduction. Critically, multiple Desulfobacterota MAGs co-occurred with nitrogen fixation and sulfate reduction genes, and the alkaline phosphatase gene phoD was identified in several of these genomes. Together, these findings reveal developmentally orchestrated shifts in microbial nutrient-cycling potential, underscoring the importance of protecting the native rhizosphere microbiome in eelgrass restoration, while considering site-specific biogeochemical constraints, particularly nutrient availability and sulfide conditions.},
}

@article {pmid43008658,
year = {2026},
author = {Sun, M and Li, B and Li, T and Li, D and Qin, B and Song, W and Li, X},
title = {Neighbor effects of companion cropping on microbial assembly and potential functions in phthalate-contaminated soils.},
journal = {Journal of environmental management},
volume = {420},
number = {},
pages = {131306},
doi = {10.1016/j.jenvman.2026.131306},
pmid = {43008658},
issn = {1095-8630},
abstract = {Di(2-ethylhexyl) phthalate (DEHP) has emerged as a major contributor to global soil pollution, endangering plant vitality and altering microbial ecosystem balance. However, the ecological mechanisms underlying plant-microbe interactions in response to phthalate stress remain poorly understood. We investigated how interspecific interactions between maize and wheat influence rhizosphere microbial community under varying DEHP concentrations (20, 60, and 100 mg/kg). By analyzing 16S rRNA and ITS amplicon data from soil samples, we explored the mechanisms by which bacteria and fungi contribute to the ecological remediation of DEHP contaminated soils. Here, we found that interspecific planting altered wheat responses to DEHP stress and was associated with shifts in rhizosphere microbial community composition in contaminated soils. The companion crop (maize) played a key role in stabilizing the rhizosphere environment and enriching functional microbial taxa, particularly under high DEHP exposure. Interspecific interactions enhanced the contribution of stochastic processes to the bacterial community in wheat, thereby inducing changes in the core hubs of the bacterial-fungal multi-kingdom network and increasing the potential functional capacity related to DEHP degradation. Hence, interspecific diversity can drive beneficial microbial reorganization, supporting both plant health and pollutant mitigation. Our findings highlight the pivotal role of plant-microbe interactions in restoring DEHP-contaminated soils, demonstrating that intercropping can foster resilient microbial communities and support long-term ecological recovery. This approach offers a promising, nature-based solution for sustainable agriculture.},
}

@article {pmid43008738,
year = {2026},
author = {Schwartz, DJ and Wong, GG and Wardenburg, KE and Erickson, IR and Tung, J and Ning, J and Zhao, L and Shalon, N and D'Souza, AW and Ferreiro, A and Silverstein, RB and Crofts, TS and Hall-Moore, C and Wallace, MA and Robinson, JI and Henderson, JP and Burnham, CD and Warner, BB and Tarr, PI and Dantas, G},
title = {Microbiome-antibiotic-immune interactions influence mortality in preterm infant gut microbiota-humanized gnotobiotic mice.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {103161},
doi = {10.1016/j.xcrm.2026.103161},
pmid = {43008738},
issn = {2666-3791},
abstract = {Infants born preterm are treated with antibiotics when bacterial infection is suspected. Antibiotics disrupt the gut microbiota, leading to unfavorable immune and infectious consequences. However, the impact of specific antibiotics on gut microbial and immune responses is largely unknown. We develop a humanized gnotobiotic mouse model where we gavage preterm infant stool into germ-free dams. We treat microbiota-humanized pups with subcutaneous antibiotics with probenecid to model empiric sepsis treatment regimens. Pups humanized with microbiota including ampicillin-resistant Enterobacteriaceae die during ampicillin with probenecid treatment with increased gut permeability and systemic microbial spread. Conversely, pups with microbiota containing gelatinase-expressing Enterococcus faecalis die during meropenem with probenecid treatment with increased gut E. faecalis and systemic immune dysregulation. Gut E. faecalis, especially strains containing gelE and fsr, increase in human preterm infant gut microbiomes after meropenem. These data raise concerns about the unintended consequences of antibiotic treatment and provide a framework for understanding microbiome-antibiotic-immune interplay.},
}

@article {pmid43009102,
year = {2026},
author = {Bouzid, YY and Oliver, A and Blecksmith, SE and Wilson, SMG and Alkan, Z and Huang, L and Bennett, BJ and Kable, ME and Stephensen, CB and Lemay, DG},
title = {Cross-Sectional Association between Fiber Intake and Gastrointestinal Inflammation is Dependent on FUT2 Secretor Status in Healthy Adults.},
journal = {The Journal of nutrition},
volume = {},
number = {},
pages = {101938},
doi = {10.1016/j.tjnut.2026.101938},
pmid = {43009102},
issn = {1541-6100},
abstract = {BACKGROUND: Gut microbes consume mucins in the absence of dietary fermentable fiber. People with non-secretor alpha-1-2-L-fucosyltransferase 2 (FUT2) genotypes produce gastrointestinal (GI) mucins that lack terminal fucose and have increased risk for inflammatory bowel disease.

OBJECTIVES: This study aimed to determine whether associations between fiber intake and subclinical GI inflammation and/or microbiome function are modified by FUT2 genotype in healthy adults.

METHODS: We assessed interactions between fiber intake, FUT2 genotype, and GI inflammation markers in a cross-sectional observational study of healthy adults. Participants with 24-h dietary recalls and food frequency questionnaires to characterize recent and habitual diet, respectively, and fecal samples, plasma samples and/or shotgun metagenomes (n=297) were included in this analysis. Differences in microbiome composition between secretors and non-secretors were analyzed using PERMANOVA and machine learning. A custom-designed TaqMan[TM] probe was used to genotype a single nucleotide polymorphism (rs601338) to determine secretor status. ELISA was used to measure fecal calprotectin, myeloperoxidase, and neopterin, as well as plasma lipopolysaccharide binding protein. Short-chain fatty acids (SCFAs) were measured in fecal samples. Relationships between fiber intake, FUT2 genotype and outcomes were analyzed using linear mixed effect models.

RESULTS: Higher energy-adjusted total recent fiber, total habitual fiber, and soluble fiber intake was associated with lower calprotectin levels in secretors, but not in non-secretors. Overall microbiome composition did not differ by secretor status. However, the ratio of mucin-degrading to plant-degrading enzymes, Muc2Plant, in the gut microbiome was positively associated with increased fecal calprotectin in secretors, but not in non-secretors. There was no interaction between dietary fiber intake, the FUT2 genotype, and fecal SCFAs.

CONCLUSION: The association of higher dietary fiber intake with lower subclinical GI inflammation and lower mucin-degrading enzymes was observed in secretors, but not in non-secretors. Clinical trials in nutrition are needed to determine if non-secretors are less responsive to dietary fiber.},
}

@article {pmid43009116,
year = {2026},
author = {Zhao, X and Sun, Y and Ding, J and Fei, F and Gu, W and Qu, X and Wang, B and Jiang, X},
title = {Herbicide-based control of Spartina alterniflora disrupts microbial functional potential in a coastal wetland.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {129508},
doi = {10.1016/j.envpol.2026.129508},
pmid = {43009116},
issn = {1873-6424},
abstract = {Herbicide-based control of invasive plants is increasingly implemented in coastal wetlands, yet the ecological consequences of herbicide residues for sediment microbiome-mediated biogeochemical functioning remain poorly understood. Here, we investigated how herbicide exposure associated with Spartina alterniflora management reshapes sediment microbial communities and biogeochemical potentials in Hangzhou Bay, China. Using metagenomic sequencing and a microbe-based Index of Functional Integrity (M-IFI), we quantified alterations in microbial potentials involved in methane, nitrogen, phosphorus, and sulfur cycling. Higher concentrations of haloxyfop and imazapyr were detected in areas subjected to herbicide-based management. Treated sediments exhibited lower α-diversity of methane-cycling genes, and more than 65% of reconstructed biogeochemical pathways had lower relative abundances, with reductions in methanogenesis-associated genes. Nitrogen and sulfur cycling pathways underwent extensive restructuring, whereas phosphorus acquisition, transport, and utilization potentials were broadly impaired. Genome-resolved analyses recovered 300 metagenome-assembled genomes and revealed distinct patterns of functional specialization and metabolic complementarity among microbial populations. Complete methane, nitrogen, and sulfur cycling potentials were sustained through community-level metabolic cooperation, whereas phosphorus cycling was disproportionately supported by a limited number of metabolically versatile populations. Herbicide exposure markedly decreased M-IFI values, with over 70% of treated sediments classified as moderately or severely disturbed. Collectively, our findings reveal that chemical control of invasive plants can impose hidden belowground ecological costs by disrupting microbiome-supported biogeochemical networks and reducing microbial functional integrity, highlighting the need to incorporate microbiome-based indicators into sustainable coastal wetland management.},
}

@article {pmid43009122,
year = {2026},
author = {Hu, SL and Yu, XW and Xue, R and Li, M and Zhou, XZ and Xu, JY and Gong, LK and Li, J and Peng, JJ and Juhasz, AL and Li, HB and Xue, XM},
title = {Arsenic Metabolism and Gut Microbiome Responses Following a Single Meal of Seaweeds in Humans.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {129493},
doi = {10.1016/j.envpol.2026.129493},
pmid = {43009122},
issn = {1873-6424},
abstract = {Seaweeds are increasingly consumed as sustainable foods but contain high concentrations of organoarsenicals. However, their excretion kinetics, metabolic fate, and oral bioavailability in humans remain poorly understood. We conducted a four-day study with 54 volunteers on standardized diets supplemented with a single meal of either nori (Pyropia haitanensis) or kelp (Saccharina japonica). Total arsenic concentrations and arsenic species in urine and feces, gut microbiota composition, and carbohydrate-active enzyme genes were analyzed. Following seaweed consumption, urinary and fecal arsenic concentrations increased markedly during Days 1-2 and declined by Day 3, with urinary arsenic peaking approximately 14-30 h after ingestion. The urinary excretion factor of arsenic from nori was 6.3-fold higher than that from kelp. Phosphate arsenosugar from nori underwent extensive gastrointestinal transformation, with arsenobetaine accounting for 74.0-90.2% of fecal arsenic species. In contrast, sulfonate arsenosugar from kelp was less extensively transformed, with oxo- and thio-sulfonate arsenosugars remaining the predominant fecal arsenic species. This study offers valuable insights into the excretion kinetics, metabolism, and bioavailability of organoarsenicals from seaweeds.},
}

@article {pmid43009128,
year = {2026},
author = {Kain, V and Upadhyay, G and Suraksha, K and Li, S and Sundaraswamy, PM and Jayaprakash, J and Gowda, D and Chainani, N and Krishna, N and Ghobrial, M and Fouad, A and Hui, SP and Mishra, SP and Hall, N and Tan, Z and Soto, NH and Liu, R and Jain, S and Gowda, SGB and Yadav, H and Halade, GV},
title = {Multi-omics analyses of HFpEF progression and regression reveals multi-organ-specific metabolic dysregulation and impaired inflammation resolution.},
journal = {Metabolism: clinical and experimental},
volume = {},
number = {},
pages = {156838},
doi = {10.1016/j.metabol.2026.156838},
pmid = {43009128},
issn = {1532-8600},
abstract = {BACKGROUND: Heart failure with preserved ejection fraction (HFpEF) is a complex cardiometabolic syndrome with limited effective therapies. Given its heterogeneity, whether withdrawal of cardiometabolic stress reverses HFpEF-associated inflammatory, metabolic, and molecular remodeling remains unclear.

OBJECTIVES: To characterize multi-organ metabolic, molecular, and bioactive-lipid remodeling in an obesity-hypertension HFpEF model and determine the extent of recovery during an 8-week combined high-fat diet withdrawal and L-NAME cessation protocol using parallel multi-omics profiling.

METHODS: HFpEF was induced in C57BL/6 mice using a high-fat diet plus nitric oxide synthase inhibition(H + L). A regression cohort(R-H + L) underwent simultaneous return to standard chow and L-NAME cessation for 8 weeks. Multi-omics profiling included targeted and untargeted lipidomics, cardiac transcriptomics, metabolomics, fecal microbiome, and plasma short-chain fatty acid analyses, with detailed assessment of the left ventricle.

RESULTS: H + L mice developed an obesity-hypertension HFpEF phenotype characterized by predominant diastolic dysfunction, concentric remodeling, hypertension, and increased fat mass. The combined regression of H + L protocol attenuated these phenotypic abnormalities but did not restore all measures to control levels. H + L was associated with multi-organ remodeling marked by altered arachidonic acid-derived oxylipid pathways, depletion of triacylglycerols and phospholipids, and enrichment of diacylglycerols and lysophospholipids, consistent with altered resolution-related lipid signaling. Cardiac transcriptomics revealed changes in immune, circadian, vascular, and mitochondrial gene programs, whereas metabolomics revealed altered energy, arginine, and redox metabolism. H + L was also associated with reduced microbial diversity and altered short-chain fatty acids, particularly acetate and propionate. Within the 8-week recovery window, partial reprogramming occurred, but differences remained in lipid signaling, metabolic stress responses, and microbiome-associated measures.

CONCLUSIONS: The HFD/L-NAME model is accompanied by extensive multi-organ metabolic and molecular remodeling. Combined withdrawal of HFD/L-NAME attenuates the HFpEF phenotype however did not fully normalize molecular profiles within the 8-week recovery period. Persistent lipid-remodeling and metabolic dysregulation may represent potential therapeutic targets thus warrants pathway specific investigation.},
}

@article {pmid43009395,
year = {2026},
author = {Einarsson, GG and Elborn, JS and Sherrard, LJ and Carson, JP and Vardy, N and Adler, FR and Tunney, MM and Liou, TG and , },
title = {Airway microbial-inflammatory endotypes are associated with disease severity and predicted survival in cystic fibrosis.},
journal = {Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jcf.2026.11.005},
pmid = {43009395},
issn = {1873-5010},
abstract = {BACKGROUND: The airway microbiome and host inflammatory response synergistically drive cystic fibrosis (CF) lung disease. We hypothesized that integrating airway microbial community structures with inflammatory biomarker profiles would reveal distinct ecological-inflammatory endotypes associated with clinical outcome measures.

METHODS: We performed a cross-sectional secondary analysis of 112 clinically stable people with CF. Baseline sputum microbial communities were profiled via 16S rRNA sequencing, clustered using partitioning around medoids and linked with previously quantified inflammatory biomarker data. Co-occurrence network analyses assessed microbial community organisation. Associations with time-to-next pulmonary exacerbation (PEx) and 5-year prognostic survival scores were evaluated utilizing Cox proportional hazards models and multivariable regression.

RESULTS: Two distinct ecological-inflammatory endotypes were identified. Endotype 1 (n = 65) exhibited higher microbial diversity, enrichment of oral-associated commensals (e.g., Prevotella, Veillonella), a highly interconnected co-occurrence network, and a moderated inflammatory milieu. Endotype 2 (n = 47) was characterized by Pseudomonas dominance, elevated neutrophilic inflammation (e.g., neutrophil elastase, IL-1β), and more advanced lung disease. The two-cluster solution was highly stable under repeated subsampling. Higher microbial diversity was independently associated with a more favourable 5-year prognostic survival score, including after adjustment for endotype membership. Endotype membership itself was not associated with time to subsequent PEx, and associations between ecological measures and PEx were attenuated after additional adjustment for baseline lung function.

CONCLUSIONS: Distinct ecological-inflammatory endotypes in the CF airway reflect differences in microbial community structure, inflammatory state and underlying disease severity. Longitudinal studies are required to determine the stability of these states and their relationship with subsequent clinical disease.},
}

@article {pmid43009614,
year = {2026},
author = {Wu, J and Li, L and Lai, Y and Li, J and Asthana, P and Zhai, L and Chen, L and Chen, M and Chen, B and Gurung, S and Lyu, J and Zhang, Y and Lu, L and Huang, S and Kuang, W and Shi, H and Luo, Y and Gou, Z and Kong, X and Wong, SH and Chan, KM and Yuan, S and Kwan, HY and Yuan, X and Huang, W and Ruan, Y and Lu, H and Wong, CC and Su, Y and Koohi-Moghadam, M and Lyu, A and Bian, Z and Ren, Y and Hu, X and Ma, Y and Wong, HLX},
title = {Microbiota-based modulation of intratumoral cholesterol metabolism for colorectal cancer treatment.},
journal = {Nature metabolism},
volume = {},
number = {},
pages = {},
pmid = {43009614},
issn = {2522-5812},
support = {12102020//Research Grants Council, University Grants Committee (RGC, UGC)/ ; 08793626//Food and Health Bureau of the Government of the Hong Kong Special Administrative Region | Health and Medical Research Fund (HMRF)/ ; ITS/058/22MS//Innovation and Technology Commission (ITF)/ ; 32322091//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82070535//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82370601//National Natural Science Foundation of China (National Science Foundation of China)/ ; RC-RSRG/23-24/SCM/01//Hong Kong Baptist University (HKBU)/ ; RC-SFCRG/23-24/R2/SCM/01//Hong Kong Baptist University (HKBU)/ ; 2022A1515011302//Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation)/ ; },
abstract = {Excess cholesterol accumulates in colorectal cancer (CRC) and promotes its progression, yet systemic cholesterol-lowering has limited benefits and safety concerns. Here we show that redirecting intestinal cholesterol metabolism through the gut microbiota generates a metabolite, 4-cholesten-3-one (4-C-3), which suppresses CRC growth. A screen of microbial cholesterol metabolites showed that 4-C-3 is depleted in faecal and tumour samples from patients with CRC. 4-C-3 suppresses tumour growth in CRC cell lines, patient-derived organoids and xenografts. Mechanistically, 4-C-3 suppresses two major oncogenic drivers of CRC by inhibiting epidermal growth-factor receptor activation and stabilizing mutant oncogenic KRAS in an inactive state, thereby overcoming KRAS-driven resistance to anti-epidermal growth-factor receptor therapy. As proof of concept, restoring 4-C-3 using either Oscillibacter ruminantium, a natural 4-C-3 producer reduced in CRC, or a non-pathogenic Escherichia coli engineered to convert intestinal cholesterol into 4-C-3, lowered intratumoral cholesterol and induced tumour regression in preclinical models without overt toxicity. These findings uncover a microbiota-cholesterol metabolic pathway that can be harnessed through microbiome engineering to selectively target CRC and overcome therapy resistance.},
}

@article {pmid43009621,
year = {2026},
author = {Nachman, EJ and Wozniak, KJ and Danhof, HA and Di Rienzi, SC and Britton, RA},
title = {The small intestine microbiome: composition, host interactions and therapeutic potential.},
journal = {Nature reviews. Microbiology},
volume = {},
number = {},
pages = {},
pmid = {43009621},
issn = {1740-1534},
abstract = {The human microbiome, the collection of microorganisms that inhabit the human body, has been extensively studied over the past two decades and has been shown to play a critical part in health and disease. These research efforts renewed interest in developing microbial therapeutics to promote human health and treat disease. However, the vast majority of human gut microbiome research has been focused on fecal microbial strains and communities, leaving most of the gastrointestinal tract understudied. The dynamic environment of the small intestine provides distinct opportunities for microorganisms to interact with the host and diet. In this Review, we discuss the current state of research on the microbiome of the small intestine, how interactions between the small intestine and its microbiome influence host physiology, and we posit that small intestinal microorganisms are a unique source of novel therapeutics for treating human disease. Next-generation microbial therapeutics that emerge from the small intestinal microbiome are anticipated to be relevant to improving small intestinal diseases as well as systemic human health.},
}

@article {pmid43009709,
year = {2026},
author = {Damgaard, F and Justesen, US},
title = {Metagenomic evidence for persistent gut colonization of colibactin-producing Escherichia coli in colorectal cancer patients.},
journal = {Cancer causes & control : CCC},
volume = {37},
number = {12},
pages = {},
pmid = {43009709},
issn = {1573-7225},
mesh = {Humans ; *Polyketides/metabolism ; *Colorectal Neoplasms/microbiology ; *Escherichia coli/genetics/metabolism ; *Peptides/metabolism ; Female ; Male ; Metagenomics/methods ; *Gastrointestinal Microbiome/genetics ; *Escherichia coli Infections/microbiology ; Middle Aged ; Aged ; },
abstract = {Colibactin-producing Escherichia coli (pks[+] E. coli) has been linked to colorectal cancer (CRC) through double-strand DNA breaks and distinct mutational signatures. Whether gut colonization by pks[+] E. coli is persistent and has direct implications for whether it represents a modifiable risk factor in diagnosed patients. Based on whole-genome metagenomic sequencing data from 638 individuals it was found that pks[+] E. coli was significantly more prevalent in CRC patients (34.7%) than in controls (17.2%; OR = 2.76, 95% CI 1.86-4.09, p < 0.001). These findings indicate that colonization by pks[+] E. coli might not be confined to early carcinogenesis but may persist in a substantial proportion of CRC patients.},
}

Humans
*Polyketides/metabolism
*Colorectal Neoplasms/microbiology
*Escherichia coli/genetics/metabolism
*Peptides/metabolism
Female
Male
Metagenomics/methods
*Gastrointestinal Microbiome/genetics
*Escherichia coli Infections/microbiology
Middle Aged
Aged

@article {pmid43009760,
year = {2026},
author = {Li, S and Yu, Z and Jin, Y and Ma, K and Sha, L and Qian, M and Chen, X and Han, S},
title = {Gut microbiome and metabolite profiling in term SGA infants: a multi-omics approach to physical development.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {43009760},
issn = {1471-2180},
mesh = {Humans ; *Gastrointestinal Microbiome ; Feces/microbiology/chemistry ; Female ; Male ; Multiomics ; Infant, Newborn ; Case-Control Studies ; Prospective Studies ; *Infant, Small for Gestational Age/growth & development/metabolism ; Infant ; *Bacteria/classification/genetics/isolation & purification/metabolism ; *Metabolome ; Metabolomics/methods ; Metagenomics/methods ; },
abstract = {INTRODUCTION: Early-life gut microbial composition and fecal metabolic profiles may be altered in infants born small for gestational age (SGA), but evidence specifically concerning term SGA infants remains limited.

OBJECTIVES: To characterize gut microbial composition, predicted microbial functions, and fecal metabolite profiles in term SGA infants and explore their associations with early growth.

METHODS: This prospective nested case-control study included 62 term infants (31 SGA and 31 appropriate for gestational age [AGA]). Fecal samples were collected at 3 months. Untargeted metabolomics was performed in the full cohort, and shotgun metagenomic sequencing was conducted in a nested subset of 20 infants (10 SGA and 10 AGA). Differential taxa, KEGG orthologs (KOs), metabolites, and cross-omics correlations were analyzed.

RESULTS: Alpha diversity did not differ significantly between groups, whereas microbial composition and species-level abundance patterns differed between SGA and AGA infants. Functional analysis identified 135 differential KOs, including 36 with higher and 99 with lower abundance in the SGA group. These KOs were mapped to 25 metabolic pathways, including galactose, butanoate, D-amino acid, aromatic amino acid, fructose-mannose, pyruvate, propanoate, and lipid metabolism. Twelve fecal metabolite features differed between groups, including 5'-methylthioadenosine, taurocholate, β-alanine, and 17α-hydroxypregnanolone. Exploratory integration identified connections among microbial species, KOs, and metabolites. Several microbial and metabolite features showed nominal associations with 6-month growth indices, but most cross-omics and metabolite-growth associations did not remain significant after false discovery rate correction.

CONCLUSIONS: Term SGA infants showed differences in gut microbial composition, predicted metabolic potential, and fecal metabolite profiles at 3 months. Associations with subsequent growth were exploratory and require validation in larger longitudinal studies.},
}

Humans
*Gastrointestinal Microbiome
Feces/microbiology/chemistry
Female
Male
Multiomics
Infant, Newborn
Case-Control Studies
Prospective Studies
*Infant, Small for Gestational Age/growth & development/metabolism
Infant
*Bacteria/classification/genetics/isolation & purification/metabolism
*Metabolome
Metabolomics/methods
Metagenomics/methods

@article {pmid43009769,
year = {2026},
author = {Li, Y and Chen, Y and Pu, R and Zhu, Z and Wang, T and Li, Y and Liu, J},
title = {Machine learning-based analysis of behavioral and dental plaque microbiome features associated with dental caries in 5-year-old children from urban and rural Yunnan.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {43009769},
issn = {1471-2180},
support = {2022QN001//Youth Research Fund of Yunnan Provincial Clinical Research Center for Oral Diseases/ ; XDYC-YLWS-2023-0047//Xingdian Talent Support Plan of Yunnan Province-Medical and Health Talents Special Project/ ; },
mesh = {Humans ; *Dental Caries/microbiology/epidemiology ; Child, Preschool ; *Dental Plaque/microbiology ; *Machine Learning ; China/epidemiology ; *Microbiota ; Female ; Rural Population/statistics & numerical data ; Male ; RNA, Ribosomal, 16S/genetics ; *Bacteria/classification/genetics/isolation & purification ; Urban Population ; Surveys and Questionnaires ; Oral Hygiene ; Feeding Behavior ; },
abstract = {BACKGROUND: This study aimed to integrate questionnaire-based oral health behavior data with dental plaque microbiome profiles to identify behavioral and microbiological factors associated with dental caries among 5-year-old children from urban and rural areas of Yunnan Province. It also evaluated the performance of these features in machine learning classification models.

METHODS: This study included children from Fengqing County (rural) and Hongta District (urban) in Yunnan Province, who were categorized into a caries-free (CF) group and a dental caries (DC) group based on their caries status. Dietary habits, oral hygiene practices, and regional background data were collected using a questionnaire. Dental plaque samples were collected simultaneously for 16 S rRNA gene sequencing. Based on the relative abundances of the microbial community at the phylum and genus levels, differences in microbial profiles were compared between children with different caries statuses and across regions. Random forest, least absolute shrinkage and selection operator (LASSO), and other machine learning models were employed to identify key microbial features and evaluate the performance of these features, together with relevant behavioral variables, in classifying caries status.

RESULTS: Questionnaire analysis revealed significant differences between the DC and CF groups in location, frequency of dessert consumption, and nighttime post-brushing sugar intake (NPSI). By location, Fengqing County and Hongta District differed significantly in NPSI and use of fluoridated toothpaste. Plaque microbiome analysis revealed significant phylum-level differences between the DC and CF groups, particularly in Bacteroidetes, Fusobacteria, and Proteobacteria. A phylum-level diagnostic model identified Fusobacteria as a key discriminative variable (area under the curve [AUC] = 0.737). LASSO analysis identified three genera-Capnocytophaga, Haemophilus, and Comamonas-with Capnocytophaga contributing to diagnostic performance (AUC = 0.720). Incorporating location, dessert consumption, and NPSI further improved model performance (AUC = 1.000).

CONCLUSION: Behavioral factors, regional background, and dental plaque microbial characteristics are jointly associated with the risk of dental caries in 5-year-old children, suggesting that regional differences may partially reflect underlying socioeconomic conditions. However, as these findings are correlational, further validation is required.},
}

Humans
*Dental Caries/microbiology/epidemiology
Child, Preschool
*Dental Plaque/microbiology
*Machine Learning
China/epidemiology
*Microbiota
Female
Rural Population/statistics & numerical data
Male
RNA, Ribosomal, 16S/genetics
*Bacteria/classification/genetics/isolation & purification
Urban Population
Surveys and Questionnaires
Oral Hygiene
Feeding Behavior

@article {pmid43009984,
year = {2026},
author = {Lu, Q and Zhou, D and Yang, R and Ban, Y and Gao, C and Li, P and Wang, J and Dai, Y and Yang, Y and Chen, R and Xie, S and Tian, X},
title = {Effects of different feeding regimes on growth performance, antioxidant activity, rumen fermentation, rumen microbiota and rumen metabolism in beef cattle.},
journal = {BMC veterinary research},
volume = {22},
number = {1},
pages = {},
pmid = {43009984},
issn = {1746-6148},
support = {Qiankehe Foundation [2024] Youth 106//Basic Research Program (Natural Science) Youth Guidance Project of Guizhou Province/ ; Qianjiaoji [2024] 33//Youth Science and Technology Talent Development Project of Guizhou Province/ ; none//the Agriculture and Rural Affairs Department Project of Guizhou Province (Exploration and Utilization of Excellent Germplasm Resources of Guanling Cattle)/ ; Qiankexie KJLYRC-[2026] 078//Science and Technology Project of Guizhou Province/ ; 32260849 and 32302779//National Natural Science Foundation of China/ ; },
mesh = {Animals ; Cattle/growth & development/microbiology/metabolism/physiology ; *Rumen/microbiology/metabolism ; *Antioxidants/metabolism ; Fermentation ; *Diet/veterinary ; Animal Feed/analysis ; *Gastrointestinal Microbiome ; Male ; Animal Nutritional Physiological Phenomena ; },
abstract = {BACKGROUND: The feeding regime significantly impacts on the production performance, ruminal fluid microbiota, and metabolites of ruminants. However, studies comparing the microbial metagenomics and metabolites in ruminal fluid of beef cattle fed pasture-based grazing and housed total mixed ration (TMR) feeding regimes have rarely been reported.

METHODS: Forty healthy Guanling beef cattle were divided into two equal groups according to a randomized complete block design. The pasture-based grazing group (BG) was allowed to the grazing period was 08:00-18:00 at a natural ranch. The housed TMR feeding group (BB) was reared under a housed feeding system and fed a TMR diet. Each treatment consisted of 20 beef cattle, and the experimental period lasted for 90 d. The metagenomics and metabolomics were used analysis ruminal fluid microbiota and metabolism.

RESULTS: The results indicated that the BB group showed significantly higher levels of average daily gain, total antioxidant capacity, catalase, 2,2-diphenyl-1-picrylhydrazyl scavenging activity, ammonia nitrogen, and volatile fatty acid (P < 0.05), whereas it had significantly lower levels of malondialdehyde and hydroxyl free radical relative to the BG group (P < 0.05). Compared with the BB group, the BG group exhibited a significantly increased (P < 0.05) abundance of Bacillota at the phylum level but a significantly decreased (P < 0.05) abundance of Prevotella at the genus level. The modules associated with these relative abundance levels (Reductive citrate cycle (Arnon-Buchanan cycle), and Guanine ribonucleotide degradation, GMP = > Urate) were significantly more important in the BG group (P < 0.05) than in the BB group. Glycosyltransferase 2_Glycos_transf_2 was significantly enriched in the BB group, whereas glycoside hydrolase (GH)3, GH78, and GH36 were significantly enriched in the BG group. Metabolomic analysis revealed that linoleic acid metabolism was the dominant pathway in the rumen.

CONCLUSION: Overall, the housed TMR-fed cattle enhanced growth performance, antioxidant activity, rumen fermentation, and Prevotella abundance, whereas the pasture-based grazing fed cattle enhanced Bacillota abundance and linoleic acid metabolism.},
}

Animals
Cattle/growth & development/microbiology/metabolism/physiology
*Rumen/microbiology/metabolism
*Antioxidants/metabolism
Fermentation
*Diet/veterinary
Animal Feed/analysis
*Gastrointestinal Microbiome
Male
Animal Nutritional Physiological Phenomena

@article {pmid43009990,
year = {2026},
author = {Jia, Z and Zheng, P and Zhang, H and Zhang, J and Lin, Y and Wu, J and Pan, T and Song, Y and Liu, W and Wu, M},
title = {Longitudinal metagenomic profiling of gut microbiome dynamics in B-cell lymphoma patients receiving CAR-T cell therapy.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
pmid = {43009990},
issn = {1479-5876},
mesh = {Humans ; Female ; *Gastrointestinal Microbiome/genetics ; Longitudinal Studies ; *Metagenomics ; Male ; *Lymphoma, B-Cell/microbiology/therapy/immunology ; *Immunotherapy, Adoptive ; Middle Aged ; Treatment Outcome ; *Receptors, Chimeric Antigen/metabolism ; Aged ; },
abstract = {BACKGROUND: Chimeric antigen receptor T-cell (CAR-T) therapy has improved outcomes in B-cell malignancies, but treatment response and immune-related toxicities remain heterogeneous. We characterized peri-infusion gut microbiome dynamics and examined their associations with subsequent response and toxicity.

METHODS: We performed shotgun metagenomic sequencing of 103 fecal samples from 21 patients with B-cell lymphoma collected on days -7, 0, 7, 14 and 28 relative to CAR-T infusion. We assessed pre-infusion stability, longitudinal microbiome remodeling, and associations with treatment response, cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). Longitudinal data were analyzed using mixed-effects models, and composition-aware sensitivity analyses incorporated centered log-ratio transformation and false-discovery-rate correction. Day -7 clinical and microbial features were also evaluated using exploratory nested cross-validation for response and CRS.

RESULTS: The gut microbiome remained broadly stable at the community level before infusion but underwent early, patient-specific remodeling after CAR-T therapy, characterized by a transient decline in alpha diversity and increased within-patient compositional deviation from baseline. Against this dynamic background, pre-infusion microbial variation was associated with subsequent clinical outcomes. Responders differed from non-responders in baseline microbial diversity, community structure and selected Sutterella and Segatella taxa. Patients who developed CRS showed lower microbial diversity and distinct community composition, whereas no comparable association was detected for ICANS. Exploratory nested cross-validation yielded AUCs of 0.51, 0.55 and 0.72 for the clinical, microbiome and combined response models, respectively, and 0.44, 0.85 and 0.83 for the corresponding CRS models.

CONCLUSIONS: CAR-T therapy was accompanied by early, patient-specific gut microbiome remodeling, while pre-infusion microbial variation was associated with subsequent treatment response and CRS occurrence. These hypothesis-generating findings require confirmation in larger, independent prospective cohorts.},
}

Humans
Female
*Gastrointestinal Microbiome/genetics
Longitudinal Studies
*Metagenomics
Male
*Lymphoma, B-Cell/microbiology/therapy/immunology
*Immunotherapy, Adoptive
Middle Aged
Treatment Outcome
*Receptors, Chimeric Antigen/metabolism
Aged

@article {pmid43010047,
year = {2026},
author = {Luo, Y and Yang, J and Chen, C},
title = {Genomic variant features of gut microbes among distinct pig populations and identification of microbial variants associated with fatness traits.},
journal = {Animal microbiome},
volume = {8},
number = {1},
pages = {},
pmid = {43010047},
issn = {2524-4671},
abstract = {BACKGROUND: The gut microbiota is involved in host metabolism, immunity, and energy homeostasis. Stressors, such as diets and environments, can cause changes in microbial compositions and genomic variations.

RESULTS: Here, we performed a population genomic analysis to reveal the genetic landscape of the pig gut microbiome and identified microbial single-nucleotide variants (SNVs) associated with host fatness traits. We characterized genomic variant features of gut microbiota across three pig populations having distinct genetics background and raised in dramatically different environments: wild boars (free-range and natural diets), Tibetan pigs (semi-free, high-altitude, and hypoxic environment), and Duroc pigs (intensive farming, and commercial diets). At the population level, gut microbiome of wild boars harbored the lowest SNV density, but the highest pN/pS ratios, in contrast to the elevated SNV density and recombination rates observed in Duroc and Tibetan pigs. Functional profiles of genes under selection in microbial genomes also differed across populations: purifying selected genes were enriched in the pathway of simple sugar metabolism in Duroc pigs, but secondary bile acid biosynthesis in wild boars, with Tibetan pigs exhibiting an intermediate pattern that included additional flavonoid metabolism pathways. Positively selected genes were involved in carbohydrate metabolism and proteolysis in Duroc pigs, adhesion in wild boars, and mucin-binding functions in Tibetan pigs. To further investigate whether microbial SNVs affected pig fatness traits, we performed an association analysis in well-phenotyped F6 pigs from a designed mosaic pig population. We identified 11 microbial SNVs in Lactobacillus amylovorus, Limosilactobacillus reuteri, Streptococcus faecavium, and CAG-177 sp003514385 that were significantly associated with pig fatness-related traits. These SNVs were predicted to be involved in energy metabolic enzymes and epigenetic modification. All associations were independent of bacterial abundance, highlighting the value of SNV-based analyses beyond traditional abundance approaches.

CONCLUSIONS: Our findings revealed distinct genomic signatures of gut microbiota across three pig populations and established a framework for linking microbial genetic variation to host phenotypes, moving beyond taxonomic composition.},
}

@article {pmid43010098,
year = {2026},
author = {Keohane, E and Poehlein, L and Chaparro, JM and Wrigley, SD and Graham, EL and Wahl, D and Espinosa, P and Bayer, R and Hart, R and Gentile, CL and Weir, TL and Prenni, JE},
title = {A human microbiota-associated translational mouse model reveals sex-specific responses to cannabidiol and cannabigerol.},
journal = {Journal of cannabis research},
volume = {8},
number = {1},
pages = {},
pmid = {43010098},
issn = {2522-5782},
abstract = {Cannabidiol (CBD) and cannabigerol (CBG) are non-psychoactive phytocannabinoids with therapeutic potential, yet their effects on host physiology and interactions with the gut microbiome remain poorly defined. Here, we used a translational mouse model colonized with human-associated microbiotas to investigate the effects of oral CBD and CBG intervention on microbial composition, endocannabinoid signaling, and intestinal protein expression. While neither phytocannabinoids altered overall gut microbiome diversity, both induced sex-specific shifts in bacterial taxa associated with mucin utilization and short-chain fatty acid production. Circulating concentrations of CBD were higher than those of CBG, and females exhibited higher plasma phytocannabinoid concentrations than males. Males treated with CBD had elevated anandamide (AEA) levels, potentially reflecting inhibition of fatty acid amide hydrolase, consistent with upregulation of serine protease inhibitors observed in ileal proteomes. Females also accumulated more subcutaneous adipose tissue with both CBD and CBG treatment resulting in greater total CBD storage in this depot. Collectively, these findings suggest sex-specific interactions between phytocannabinoids, the endocannabinoid system, and the gut microbiome, underscoring the importance of considering biological sex in cannabinoid research and informing personalized therapeutic strategies.},
}

@article {pmid43010113,
year = {2026},
author = {Na, SW and Zhou, M and Choi, Y and Kim, H and Chen, Y and Bork, EW and Fitzsimmons, C and Guan, LL},
title = {Shifts in rumen prokaryotic communities of grazing beef cows with divergent feed efficiency in response to seasonal grazing.},
journal = {Animal microbiome},
volume = {8},
number = {1},
pages = {},
pmid = {43010113},
issn = {2524-4671},
abstract = {BACKGROUND: Cow-calf operations represent a major component of beef production, typically relying on seasonal grazing of perennial forages. While understanding the role of the rumen microbiome in improving feed efficiency in grazing systems is essential for sustainable beef production, most studies have focused on cattle in confined systems such as feedlots. There is limited understanding of how rumen microbial communities change across feeding regimens in cow-calf operations with seasonal grazing. This study characterized rumen prokaryotic communities of beef cows across four feeding regimens, drylot (DL), planted pasture (PP), summer native rangeland (SNR), and fall native rangeland (FNR) within a year-round cow-calf production cycle, aiming to determine their relationships with feed efficiency.

RESULTS: Prokaryotic communities in rumen samples collected from breeding beef cows under DL, PP, SNR, and FNR were assessed using metataxonomic sequencing and quantitative PCR. Feed efficiency was evaluated using residual feed intake adjusted for backfat thickness (RFIf) under DL. The microbial profiling and quantification revealed significant shifts in microbial composition and diversity across the four regimens. Bacterial diversity was highest in DL and declined during grazing, while archaeal diversity increased in SNR compared to PP and FNR. Several taxa were differentially enriched under distinct feeding regimens: Thermobifida, Saccharomonospora, Corynebacterium, and Methanoculleus thermophilus appeared only in DL, while Patescibacteria and Olsenella were more abundant during grazing. Further analysis of microbial fermentation profiles revealed that concentrations of major volatile fatty acids (VFAs) were higher in PP than in the other regimens. Heritable bacteria (p-251-o5 and Pirellula) were enriched in native rangelands and negatively correlated with VFA concentrations. In FNR, the abundance of the dominant bacterial taxon Christensenellaceae R-7 group increased, while Prevotella declined. Differential abundance analysis identified RFIf-associated taxa, including Eubacterium cellulosolvens group, Colidextrobacter, and Methanosphaera sp. ISO3-F5 regardless of feeding regime variation.

CONCLUSIONS: This study provides a comprehensive assessment of rumen prokaryotic dynamics across seasonal feeding regimens in cow-calf production, revealing varied shifts between bacteria and archaea. We further identified feeding regimen-specific associations between microbial taxa and feed efficiency, suggesting diet-microbiome interactions influencing grazing cow's feed efficiency. These findings enhance the understanding of host-microbe interactions in confined and grazing environments, offering insights for sustainable beef production strategies.},
}

@article {pmid43010175,
year = {2026},
author = {Ibrahim, R and Aranjani, JM},
title = {Engineered bacteriophages as precision antimicrobials against multidrug-resistant ESKAPE pathogens: molecular engineering strategies, clinical translation, and the crystallizing global regulatory landscape.},
journal = {Future science OA},
volume = {12},
number = {1},
pages = {2755467},
doi = {10.1080/20565623.2026.2755467},
pmid = {43010175},
issn = {2056-5623},
abstract = {The global antimicrobial resistance crisis, driven primarily by the ESKAPE pathogen consortium has catalyzed the translation of engineered bacteriophage therapeutics from experimental platforms to clinical-stage precision medicines. Unlike their wild-type counterparts, which are constrained by narrow host ranges, susceptibility to reticuloendothelial clearance, and limited biofilm penetrability, synthetically engineered phages exploit receptor-binding protein remodeling, phage-derived enzymatic depolymerases, CRISPR-Cas3 chromosomal shredding payloads, sequence-independent SASPject delivery vectors, and in vivo microbiome base editors to overcome the multilayered resistance arsenals of MDR ESKAPE organisms. Recent clinical development has generated human evidence across both genetically engineered phage platforms and advanced fixed phage-cocktails. Engineered programmes include CRISPR-Cas3-based LBP-EC01 and SNIPR001, while AP-SA02 represents an analytically characterized fixed multi-phage cocktail targeting Staphylococcus aureus. This review examines engineering strategies, pharmacokinetics, immune-mediated clearance, delivery challenges, clinical evidence, manufacturing, and regulatory pathways. It also discusses emerging regulatory approaches and distinctions between natural and genetically modified phage products. The literature search was conducted from January-June 2026 using PubMed, Scopus, and Google Scholar, supplemented by searches of ClinicalTrials.gov and the websites of the US-FDA and EMA. Overall, this review evaluates the translational potential of engineered phages, identifies barriers to clinical adoption, and considers future developments in precision antimicrobial therapy against multidrug-resistant pathogens.},
}

@article {pmid43010179,
year = {2026},
author = {Tracey, H and Antolín, A and Teichenne, J and Jones, OAH and Van, TTH and Puig, J and Ramos, R and Garre-Olmo, J and Fernández-Real, JM and Mayneris-Perxachs, J and Del Bas, JM},
title = {Human cognitive performance-associated gut microbiota influences learning and memory in mice through arginine and pterin metabolism.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2750588},
doi = {10.1080/19490976.2026.2750588},
pmid = {43010179},
issn = {1949-0984},
mesh = {Animals ; Humans ; Male ; Mice, Inbred C57BL ; Mice ; *Cognition ; *Gastrointestinal Microbiome/physiology ; *Arginine/metabolism ; *Memory ; Fecal Microbiota Transplantation ; Feces/microbiology ; Aged ; Hippocampus/metabolism ; Bacteria/classification/isolation & purification/genetics/metabolism ; *Learning ; },
abstract = {The human gut microbiome undergoes changes across the lifespan and has been implicated in age-related decline. The symbol digit modalities test (SDMT) is a measure of information processing speed and is sensitive to mild cognitive impairment. Here, we assessed SDMT scores and fecal shotgun metagenomics in older individuals from the Imageomics cohort (n = 867) and performed fecal microbiota transplantation (FMT) from human donors to male C57BL/6 mouse recipients. In mice, we evaluated cognitive performance using the Morris water maze (MWM) and measured neurone density, fecal shotgun metagenomics, hippocampal metabolomics, and cortical gene expression to identify microbial-derived functional properties related to cognitive performance. In humans, both microbial species composition and functional profiles were associated with cognitive performance. FMT from high-SDMT donors improved cognitive performance and increased neuronal density in recipient mice compared with FMT from low-SDMT donors. In both humans and mice, higher cognitive performance was associated with arginine and proline metabolism and pterin-related pathways. In mice receiving microbiota from high-SDMT donors, cortical gene expression showed enrichment of dopamine receptor pathways and reduced dopamine reuptake and catecholamine biosynthesis. Our findings highlight the potential role of the gut microbiome in cognitive performance among older individuals, particularly information processing speed, and identify potential mechanisms involving alterations in arginine and pterin metabolism. Integrating human and mouse data supports a model in which microbiota-associated metabolic remodeling influences cognitive performance.},
}

Animals
Humans
Male
Mice, Inbred C57BL
Mice
*Cognition
*Gastrointestinal Microbiome/physiology
*Arginine/metabolism
*Memory
Fecal Microbiota Transplantation
Feces/microbiology
Aged
Hippocampus/metabolism
Bacteria/classification/isolation & purification/genetics/metabolism
*Learning

@article {pmid43010182,
year = {2026},
author = {Sharma, R and Holcomb, LE and Ishaq, SL and O'Doherty, KC},
title = {Microbiome changes following immigration: Rethinking "Westernization" as an explanatory concept.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2756705},
doi = {10.1080/19490976.2026.2756705},
pmid = {43010182},
issn = {1949-0984},
mesh = {Humans ; *Emigrants and Immigrants ; *Emigration and Immigration ; *Microbiota ; *Gastrointestinal Microbiome ; Diet ; Life Style ; Australia ; Canada ; Bacteria/classification/isolation & purification/genetics ; Terminology as Topic ; },
abstract = {An emerging focus in microbiome science is on changes to people's microbiomes following immigration, particularly to so-called Western countries, such as the USA, Canada, and Australia. Moving to these regions has been linked to microbiome changes that may increase immigrants' susceptibility to health problems, including obesity and Inflammatory Bowel Disease. The term "Westernization" (and adjacent terminology) is frequently used to describe changes in diet, lifestyle, and built environment - and the consequent microbiome shifts - associated with immigration. However, what Westernization means in this context, and whether it is an appropriate descriptor, is often unclear. The purpose of this article is to provide a review of the diverse meanings associated with the terms "West", "Western", "Westernization" (and similar) across microbiome-related research and broader uses. We argue that these terms can obscure the specific structural, environmental, and cultural factors shaping microbiome changes. We discuss the consequences of this imprecision and provide recommendations for future research. Avoiding oversimplified conclusions about what impacts immigrants' microbiome and health can contribute to more accurate targets for public health interventions for these groups in the long term.},
}

Humans
*Emigrants and Immigrants
*Emigration and Immigration
*Microbiota
*Gastrointestinal Microbiome
Diet
Life Style
Australia
Canada
Bacteria/classification/isolation & purification/genetics
Terminology as Topic

@article {pmid43010602,
year = {2026},
author = {Mønsted, MØ and Bilgin, M and Krych, L and Wiedenbein, ES and Hansen, CHF and Haupt-Jorgensen, M},
title = {Microbiota Regulates Phosphatidylcholine in the Intestinal Mucus Lipidome of Mice in a Strain- and Segment-Dependent Manner.},
journal = {Endocrinology, diabetes & metabolism},
volume = {9},
number = {6},
pages = {},
pmid = {43010602},
issn = {2398-9238},
support = {//Poul og Erna Sehested Hansens Fond/ ; //Skibsreder Per Henriksen, R. og hustrus fond/ ; },
mesh = {Animals ; *Phosphatidylcholines/metabolism ; Mice ; *Intestinal Mucosa/metabolism/microbiology ; Mice, Inbred C57BL ; Female ; *Gastrointestinal Microbiome/physiology ; Mice, Inbred BALB C ; Mice, Inbred NOD ; Colon/metabolism/microbiology ; Lipidomics ; *Diabetes Mellitus, Type 1/metabolism/microbiology ; *Mucus/metabolism ; Jejunum/metabolism/microbiology ; Intestinal Barrier Function ; },
abstract = {BACKGROUND: Type 1 diabetes (T1D) is associated with intestinal barrier dysfunction, which depends on an intact mucus layer. Phosphatidylcholine (PC) is a major lipid of intestinal mucus that likely exerts an important barrier function due to its hydrophobic and anti-inflammatory properties. Recently, we showed that PC is reduced in jejunal and colonic mucus in pre-diabetic non-obese diabetic (NOD) mice compared to C57BL/6 (B6) mice. As such, PC may play a protective role in T1D. Some bacteria produce PC. However, it is unknown whether T1D-associated dysbiosis (i.e., altered microbial composition) is behind the reduced PC content in the intestine.

METHODS: Here, we examined the impact of gut microbiota on jejunal and colonic mucus PC composition. This was done by treating 4 weeks old pre-diabetic NOD and B6 mice with a broad-spectrum antibiotic cocktail and by breeding germ-free BALB/c mice, which were then compared with untreated barrier-housed NOD, B6 and BALB/c mice. The intestinal mucus lipid profile was analysed by quantitative shotgun lipidomics, while the relative composition of the faecal microbiota was assessed by 16S rRNA gene amplicon sequencing and verified by absolute quantifications using qPCR.

RESULTS: Comparing jejunum and colon from the mice revealed that the overall intestinal mucus lipidome was segment- but not strain-specific. Antibiotic treatment reduced colonic PC levels in the NOD and B6 mice, whereas germ-free conditions did not in the BALB/c mice, which, independent of the presence of microbiota, had the lowest levels of colon PC. The faecal microbiome composition also differed between the three strains of untreated barrier-housed mice, including reduced abundance of phyla with PC-containing bacteria in the BALB/c mice.

CONCLUSIONS: Results suggest that gut microbiota perturbation is an important determinant of intestinal mucus PC content, although the effect seems to depend on the host-specific baseline microbiota composition.},
}

Animals
*Phosphatidylcholines/metabolism
Mice
*Intestinal Mucosa/metabolism/microbiology
Mice, Inbred C57BL
Female
*Gastrointestinal Microbiome/physiology
Mice, Inbred BALB C
Mice, Inbred NOD
Colon/metabolism/microbiology
Lipidomics
*Diabetes Mellitus, Type 1/metabolism/microbiology
*Mucus/metabolism
Jejunum/metabolism/microbiology
Intestinal Barrier Function

@article {pmid43010669,
year = {2026},
author = {Cifuentes, MP and Young, GR and Nelson, A and Palmer, J and Nunes Dos Santos, R and Tanou, T and Chapman, JA and Hazledine, EL and Beck, L and Smith, DL and Johnson, MJ and Garg, S and Lamb, CA and Embleton, ND and Stewart, CJ and Berrington, JE},
title = {Microbiome and immune development in preterm infants receiving powdered human milk-based fortification from the PUFFIN trial.},
journal = {Journal of pediatric gastroenterology and nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1002/jpn3.70662},
pmid = {43010669},
issn = {1536-4801},
support = {//Neokare Ltd/ ; //NIHR Newcastle Biomedical Research Centre/ ; //Newcastle upon Tyne Hospitals NHS Foundation Trust/ ; //MRC Discovery Medicine North Doctoral Training Partnership/ ; },
abstract = {OBJECTIVE: To determine the impact of powdered human milk-based fortification (PHMF) compared to powdered bovine milk-based fortification on gut microbiome and inflammation in preterm infants.

METHODS: Mechanistic study within randomised controlled trial in infants <32 weeks gestation or <1500 g birthweight, only receiving human milk and fully enterally fed without previous fortification, in two UK neonatal intensive care units (NICU). Stool and urine at recruitment (D0), weekly until day 21 (D21) and discharge. Microbiota (stool) and secretory immunoglobulin A (sIgA)/IgA (stool and urine) were evaluated at all time points and immune related proteins (IRP) (stool) at day 7 (D7) and D21.

RESULTS: Twenty-eight patients (14 per arm; median gestation 27.18 ± 2.42 weeks) participated. One hundred and twenty-nine stools and 109 urines were collected. Analysis of gut microbiota (111 stools), sIgA (113 stools and 108 urines), and IRPs (52 stools) was performed. Fortifier type did not significantly impact stool alpha or beta diversity or specific taxa and explained <5% of variance at any time point, with site being most influential (14.7% at day 14 [D14], p = 0.04; 25.7% at D21, p = 0.007). Stool but not urine sIgA was higher in PHMF recipients. Whilst fortifier type was not associated with IRPs from D7 to D21, NICU site impacted IRPs.

CONCLUSIONS: Fortifier type did not have a large impact on microbiota or IRPs but stool sIgA was higher in PHMF recipients. An association between NICU site and other outcomes was observed.

TRIAL REGISTRATION: ClinicalTrials.gov identifier: The Preterm milk fortification in neonates (PUFFIN) study was prospectively registered ISRCTN 22484792.},
}

@article {pmid43010940,
year = {2026},
author = {Li, Y and Shan, M and Liu, Q and Jing, X and Wang, Z and Mao, T and Qi, X and Cao, B and Tian, Z and Han, R},
title = {Fucoidan attenuates metabolic dysfunction-associated fatty liver disease in mice and is associated with gut microbiota remodeling and AMPK/PPARγ signaling.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1936901},
pmid = {43010940},
issn = {1664-302X},
abstract = {BACKGROUND: Metabolic dysfunction-associated fatty liver disease (MAFLD) is a growing metabolic disorder closely linked to gut micro biota dysbiosis and impaired gut-liver communication. Dietary interventions targeting the gut micro biota represent a promising strategy for MAFLD management. Fucoidan (FUC), a marine-derived bioactive polysaccharide with limited host digestibility, is primarily metabolized by intestinal microorganisms. However, whether FUC protects against MAFLD in association with micro biota-mediated mechanisms remains incompletely understood.

METHODS: C57BL/6J mice were fed a high-fat diet (HFD) for 14 weeks, while the FUC intervention group received FUC by oral gavage at a dose of 200 mg/kg/day over the same period. Body weight, adiposity, serum lipid and glucose metabolism, liver function, and histopathology were evaluated. Gut micro biota composition was analyzed by 16S rRNA sequencing, and serum metabolomic profiling was performed using untargeted metabolomics combined with KEGG enrichment and Spearman correlation analyses.

RESULTS: FUC supplementation markedly attenuated HFD-induced obesity, impaired glucose tolerance, dyslipidemia, hepatic steatosis, and HFD-associated alterations in intestinal barrier-related structural and molecular features. Microbiome analysis revealed that FUC administration was associated with changes in gut microbial diversity and community composition, including altered relative abundances of Akkermansia, Adlercreutzia, and Dubosiella. Metabolomic analysis further demonstrated changes in systemic metabolic profiles, particularly tricarboxylic acid (TCA) cycle-related metabolites. Correlation analyses identified associations among microbial features, circulating metabolites, and MAFLD-related phenotypes. FUC administration was associated with gut micro biota remodeling and altered hepatic AMPK/PPARγ signaling, accompanied by improved metabolic homeostasis and reduced hepatic inflammation.

CONCLUSION: Our findings demonstrate that FUC alleviates HFD-induced MAFLD and is associated with remodeling of the gut micro biota, alterations in circulating TCA cycle-related metabolites, and changes in hepatic AMPK/PPARγ signaling. Integrated analyses suggest a potential gut micro biota-metabolism-liver regulatory network associated with the hepato protective effects of FUC. These findings provide potential mechanistic insights into the beneficial effects of FUC and support further investigation of marine-derived polysaccharides as dietary strategies for metabolic disease management.},
}

@article {pmid43010976,
year = {2026},
author = {Zhao, Z and Dai, J and Zou, Y and An, X and Zhang, Y and Zhu, C and Hao, L and Jia, L},
title = {Paired metabolomics identify associations between fecal and serum metabolites in cardiovascular-kidney-metabolic syndrome.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1982623},
pmid = {43010976},
issn = {1664-2392},
mesh = {Humans ; *Feces/chemistry/microbiology ; *Metabolic Syndrome/metabolism/blood ; *Metabolomics/methods ; Male ; Female ; Cross-Sectional Studies ; Middle Aged ; *Cardio-Renal Syndrome/metabolism/blood ; *Biomarkers/analysis/metabolism/blood ; *Metabolome ; Adult ; Proteomics ; },
abstract = {BACKGROUND: Whether fecal metabolic alterations are associated with circulating metabolic changes in cardiovascular-kidney-metabolic (CKM) syndrome remains unclear. We compared serum and fecal metabolites between different CKM stages and investigated fecal-serum associations.

METHODS: Forty-four participants participated in the cross-sectional study, including 19 subjects in CKM stages 1-2 and 25 subjects in CKM stages 3-4. All participants underwent untargeted serum and fecal metabolomics and fecal microbiome profiling. Exploratory serum proteomics was available for 35 participants. Candidate metabolites were selected according to group differences, annotation confidence and redundancy. CKM-adjusted partial Spearman correlations were calculated for paired metabolites. Bootstrap and leave-one-participant-out analyses assessed stability. Serum-fecal KEGG pathway scores and clinical associations were also examined.

RESULTS: Serum analysis identified 470 annotated, non-exogenous features. Different features were involved in lipid-related, organic acid and steroid-related metabolites. Fecal analysis identified six features after Benjamini-Hochberg (BH) correction. Paired analysis of 17 fecal and 48 serum metabolites identified exploratory eight associations. Serum uridine was associated with fecal 1-palmitoyl lysophosphatidic acid, Asp Ala Phe and PE (16:0/0:0). Serum and fecal pyrimidine metabolism scores were positively correlated after adjustment for CKM group (partial rho = 0.429, P = 0.0041, BH-FDR = 0.0246). Selected metabolites were mainly associated with renal function indicators. The fecal microbiome showed greater genus-level dispersion in stages 3-4. Proteomic analysis identified 221 differential proteins enriched in complement and coagulation, inflammatory and lipid-related pathways.

CONCLUSIONS: Paired serum and fecal metabolomics identified a positive association between serum and fecal pyrimidine metabolism scores in CKM syndrome, accompanied by the uridine as an exploratory candidate associated with multiple fecal metabolites.},
}

Humans
*Feces/chemistry/microbiology
*Metabolic Syndrome/metabolism/blood
*Metabolomics/methods
Male
Female
Cross-Sectional Studies
Middle Aged
*Cardio-Renal Syndrome/metabolism/blood
*Biomarkers/analysis/metabolism/blood
*Metabolome
Adult
Proteomics

@article {pmid43011049,
year = {2026},
author = {Dhandapani, S},
title = {Tropical peatland microbiomes as a One Health nexus: linking soil, plant, and climate health across land-use transitions.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1931180},
pmid = {43011049},
issn = {1664-302X},
abstract = {The One Health framework recognizes the intrinsic connections among environmental, plant, animal and human health. While soils and soil microbes have received substantial attention in the recent years, tropical peatlands still remain largely overlooked despite representing globally important reservoirs of carbon, biodiversity, freshwater. Microorganisms are central regulators of peat accumulation, nutrient cycling, greenhouse gas exchange and ecosystem resilience, yet their role as mediators of One Health outcomes has received limited attention. Emerging evidence from tropical peatlands demonstrates that land-use change, drainage, fire and agricultural conversion substantially alter microbial community composition and function, with cascading effects on ecosystem processes. In this Perspective, peatland microbiomes are proposed as critical but neglected One Health nexus linking soil health, vegetation dynamics, wildlife habitat quality, climate regulation and human wellbeing. Considering, oil palm plantations that produce the most consumed vegetable oil in the world, cover substantial portion of tropical peatlands, tropical peat also plays a crucial role in food security and safety. The perspective argues that microbial communities should move from being considered ecological indicators to becoming policy-relevant components of peatland governance. Furthermore, incorporation of microbiome informed indicators into restoration, carbon accounting and ecosystem health frameworks is proposed as a necessity. By integrating microbial ecology with One Health principles, tropical peatlands can serve as an impactful model system for understanding how belowground biodiversity underpins ecosystem services and planetary health.},
}

@article {pmid43011059,
year = {2026},
author = {Meneses, CHSG and Simoes-Araujo, JL and Szczyglowski, K and Vidal, MS},
title = {Editorial: Enhancing plant stress resilience: innovative roles of plant growth-promoting bacteria (PGPB) in sustainable agriculture and crop protection.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {2023684},
doi = {10.3389/fpls.2026.2023684},
pmid = {43011059},
issn = {1664-462X},
}

@article {pmid43011315,
year = {2026},
author = {Suzuki, K and Vidra, N and Kajita, C and Pot, BDF},
title = {The gut, conductor of our health: putting the microbiota in the spotlight, a symposium report.},
journal = {Gut microbiome (Cambridge, England)},
volume = {7},
number = {},
pages = {e15},
pmid = {43011315},
issn = {2632-2897},
abstract = {This report summarizes key takeaways from the 11th International Yakult Symposium held in Amsterdam, the Netherlands, in October 2024. It provides an overview of insights obtained by the latest basic and clinical research, meta-analyses, and omics research, underscoring the relevance of the exposome, the outer and inner factors to which our bodies are exposed throughout our entire lifespan, in shaping the microbiota. The symposium addressed external factors such as diet (including probiotics and novel fermented foods), additives, pharmacologic agents, and physical environment, as well as the internal crosstalk between tissue or organ-specific microbial communities and their interactions with immune mediators, metabolic and neuroendocrine hormones, and their receptors. Collectively, the data presented during the symposium reinforced the understanding that health and disease are the result of the (im)balance of a tightly interconnected network rather than isolated axes. This was illustrated using examples of inflammatory and infectious diseases of the brain, mouth, gynaecologic tract, lungs, as well as of metabolic and mental states. Finally, a roundtable discussion on the current state of clinical trials in nutrition, including challenges and solutions was featured. The conclusion indicated that there is room for new developments and that hurdles need to be overcome, requiring continued collaboration across scientific disciplines.},
}

@article {pmid43011332,
year = {2026},
author = {Tyagi, A and Tayal, R and Bhatt, DN and Srivastava, S and Kumar, A and Kumar, A and Kumar, V},
title = {Gut epithelial barriers as regulators of metabolite-driven immune responses.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1959305},
pmid = {43011332},
issn = {1664-3224},
mesh = {Humans ; Animals ; Intestinal Barrier Function ; *Intestinal Mucosa/immunology/metabolism/microbiology ; *Gastrointestinal Microbiome/immunology ; },
abstract = {Immunometabolism provides a framework for understanding how metabolic cues shape immune cell fate and function. While traditionally centered on cell-intrinsic pathways, emerging evidence highlights a critical role for epithelial barrier regulation in shaping immune responses by controlling exposure to microbiome derived metabolites. Microbial metabolites including short-chain fatty acids, bile acid derivatives, tryptophan catabolites, and polyamines engage conserved metabolic checkpoints such as mTOR, AMPK, PPARs, SIRT1, and HIF-1α to influence immune activation, tolerance, and inflammatory tone. Critically, epithelial barriers regulate immune exposure to these signals, positioning barrier integrity as an upstream determinant of immunometabolic reprogramming. Altered epithelial metabolism compromises tight junction stability and metabolite flux, contributing to dysregulated immune activation and chronic inflammation. In this review, we synthesize current evidence supporting the concept that epithelial barriers act as metabolic gatekeepers of immunity, integrating microbial signals with host metabolic pathways to regulate immune function and disease susceptibility.},
}

Humans
Animals
Intestinal Barrier Function
*Intestinal Mucosa/immunology/metabolism/microbiology
*Gastrointestinal Microbiome/immunology

@article {pmid43011350,
year = {2026},
author = {Schmidt, MA and Schmidt, CM and Schmidt, JC and Meydan, C and Afshin, EE and Overbey, EG and Kim, J and Singh, RS and Beheshti, A and Mason, CE},
title = {Correction: Systemic elevation of gut derived p-cresol during one year in space: implications for brain, heart, bone, liver and microbiome in astronauts.},
journal = {Frontiers in physiology},
volume = {17},
number = {},
pages = {2034151},
doi = {10.3389/fphys.2026.2034151},
pmid = {43011350},
issn = {1664-042X},
abstract = {[This corrects the article DOI: 10.3389/fphys.2026.1878680.].},
}

@article {pmid43011505,
year = {2026},
author = {Hao, L and Li, L and Chen, Y and Gao, J and Xie, Y and Li, Q and Lu, J and Zhang, Z},
title = {Harnessing the Immune System in Hepatocellular Carcinoma Targeting: Mechanistic Insights and Therapeutic Potential of Natural Products and Traditional Chinese Medicine.},
journal = {Drug design, development and therapy},
volume = {20},
number = {},
pages = {646082},
pmid = {43011505},
issn = {1177-8881},
mesh = {Humans ; *Liver Neoplasms/immunology/drug therapy/pathology/therapy ; *Carcinoma, Hepatocellular/immunology/drug therapy/pathology/therapy ; *Biological Products/pharmacology/therapeutic use/chemistry ; *Medicine, Chinese Traditional ; Tumor Microenvironment/drug effects/immunology ; *Drugs, Chinese Herbal/pharmacology ; Animals ; Immunotherapy ; *Immune System/drug effects/immunology ; },
abstract = {Hepatocellular carcinoma (HCC) is highly malignant, and most patients are diagnosed at intermediate or advanced stages. Current regimens, including surgery, targeted therapy and immune checkpoint inhibitors (ICIs), are limited by low response rates, drug resistance, prominent toxicities and high costs, so safe and effective combination strategies are urgently needed. Natural products and traditional Chinese medicine (TCM) exert multi-target, multi-pathway and bidirectional immunomodulatory effects, remodel the immunosuppressive tumor microenvironment (TME) of liver cancer, and synergize with immunotherapy, with promising clinical significance as adjuncts to standard treatments. This review systematically summarizes the cellular and non-cellular components of the HCC immune microenvironment and the molecular mechanisms by which natural medicines reverse tumor immune escape and improve immunotherapy sensitivity, covering regulation of immune cells, interference with PD-1/PD-L1, CTLA-4 and TIM-3 pathways, targeting of cancer-associated fibroblasts (CAFs) and the extracellular matrix, modulation of chemokine networks, and inhibition of tumor angiogenesis. Preclinical evidence supporting efficacy enhancement and toxicity reduction upon combination of natural medicines with targeted agents, ICIs, radiotherapy and chemotherapy is also summarized. Current challenges, including tumor heterogeneity, low bioavailability, lack of unified quality standards and insufficient translational evidence, are analyzed, and future directions such as single-cell and spatial multi-omics, nano-delivery systems and gut microbiome analysis are proposed to accelerate mechanism-driven personalized combinations and standardized clinical trials, providing a theoretical basis for the clinical application of natural products and TCM in liver cancer immunotherapy.},
}

Humans
*Liver Neoplasms/immunology/drug therapy/pathology/therapy
*Carcinoma, Hepatocellular/immunology/drug therapy/pathology/therapy
*Biological Products/pharmacology/therapeutic use/chemistry
*Medicine, Chinese Traditional
Tumor Microenvironment/drug effects/immunology
*Drugs, Chinese Herbal/pharmacology
Animals
Immunotherapy
*Immune System/drug effects/immunology

@article {pmid43011567,
year = {2026},
author = {Orozco-Mosqueda, MDC and Carrión, VJ and Babalola, OO and Schoebitz, M and Santoyo, G},
title = {Harnessing stress-tolerant plant growth-promoting rhizobacteria for climate-resilient rice agroecosystems.},
journal = {Frontiers in systems biology},
volume = {6},
number = {},
pages = {1998786},
pmid = {43011567},
issn = {2674-0702},
abstract = {Environmental stresses pose a serious threat to global rice production. Drought, flooding, salinity, heavy metal contamination, and the excessive use of synthetic pesticides are among the major stressors affecting rice production, with some of these pressures being exacerbated by climate change. This review examines the ecological roles, mechanisms, and potential applications of stress-tolerant plant growth-promoting rhizobacteria (PGPR) as a sustainable strategy to enhance the resilience of rice agroecosystems under adverse environmental conditions. Particular emphasis is placed on the ecological responses of the rice rhizosphere microbiome and the molecular and physiological responses of rice plants to abiotic stress, together with the adaptive mechanisms associated with stress-tolerant PGPR activity. These include modulation of stress-responsive genes, enhanced antioxidant responses, osmoprotectant production, exopolysaccharide synthesis, and biofilm formation. The role of bacterial ACC deaminase in modulating stress-induced ethylene accumulation in rice is also reviewed. In addition, the potential contribution of stress-tolerant PGPR to mitigating methane emissions from paddy fields is explored, together with the potential of saline and heavy metal-contaminated soils as reservoirs of novel multi-stress-tolerant PGPR. Finally, recent advances in the bioformulation and delivery of stress-tolerant PGPR are discussed, highlighting their potential to improve bacterial survival, rhizosphere colonization, and field performance and to support more sustainable and climate-resilient rice production.},
}

@article {pmid43011569,
year = {2026},
author = {Akif, A and Sultana, N and Mikrani, I},
title = {The Microbiota-Metabolism Axis: Mechanistic Insights and Translational Targets Across Diabetes and Gastrointestinal Disorders.},
journal = {International journal of endocrinology},
volume = {2026},
number = {},
pages = {7761643},
pmid = {43011569},
issn = {1687-8337},
abstract = {The gut microbiota (GM) modulates host energy balance, glucose-lipid metabolism, and enteroendocrine signaling through metabolite-receptor axes that include short-chain fatty acids (SCFAs) acting on FFAR2/FFAR3 (GPR43/GPR41), microbially transformed bile acids signaling via FXR/TGR5, and amino-acid/choline-derived compounds such as imidazole propionate (ImP) and trimethylamine N-oxide (TMAO). These pathways regulate incretin biology (GLP-1/PYY), insulin sensitivity, hepatic glucose output, adipose lipolysis, and appetite, thereby shaping risk and progression of Type 2 diabetes mellitus (T2DM), obesity, inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), and related conditions. Here, we synthesize mechanistic and translational evidence, highlight bidirectional drug-microbiome interactions (GLP-1 receptor agonists), and review interventions spanning diet, pre/probiotics, fecal microbiota transplantation (FMT), and pharmacologic targeting of bile-acid and SCFA pathways. Together, these findings support precision strategies that profile GM-metabolite signatures (e.g., SCFAs, secondary bile acids, and ImP TMAO) to guide prevention and therapy in metabolic and gastrointestinal disease.},
}

@article {pmid43011581,
year = {2026},
author = {Hribernik, N and Maan, H and Povolotsky, TL},
title = {A translational-readiness framework for natural and engineered probiotics.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1965075},
pmid = {43011581},
issn = {2235-2988},
mesh = {*Probiotics/therapeutic use ; Humans ; Microbiota ; Vagina/microbiology ; *Translational Research, Biomedical ; Female ; Animals ; Biological Therapy/methods ; },
abstract = {The human microbiome has become a major source of therapeutic candidates, yet clinical translation has progressed far more slowly than mechanistic and preclinical discovery. In this review we ask: what determines whether a microbial therapeutic reaches the clinic? We compare traditional probiotics, next-generation probiotics and engineered live biotherapeutics using representative examples from metabolic disease, oncology and the vaginal microbiome. Together, these examples show that translational success depends less on biological sophistication than on the ability to achieve durable colonization, demonstrate meaningful clinical benefit and satisfy biocontainment and regulatory requirements. We explore the vaginal niche as a case study because it illustrates these challenges particularly well. Its relatively simple microbial community, local delivery and measurable ecological and clinical endpoints allow colonization, activity and recurrence to be assessed together. We integrate these observations into a translational-readiness framework that evaluates microbial therapeutics according to target specificity, colonization durability, biocontainment and safety, demonstrated benefit and regulatory precedent. This framework provides a practical approach for comparing emerging microbial therapeutic candidates and for identifying the factors most likely to accelerate their progression from promising biological discoveries to reliable clinical translation.},
}

*Probiotics/therapeutic use
Humans
Microbiota
Vagina/microbiology
*Translational Research, Biomedical
Female
Animals
Biological Therapy/methods

@article {pmid43011731,
year = {2026},
author = {Lei, Y and Liu, Q and Lu, Q},
title = {The skin microbiome in aging from ecological dysbiosis to molecular therapeutics.},
journal = {Microbiome research reports},
volume = {5},
number = {3},
pages = {25},
pmid = {43011731},
issn = {2771-5965},
abstract = {Skin aging is a progressive process driven by cumulative alterations in skin structure and function, resulting in a distinct clinical phenotype characterized by wrinkles, loss of elasticity, pigmentary changes, and impaired barrier integrity. Although intrinsic aging and environmental stressors are well-established contributors, the skin microbiome is increasingly recognized as an important regulator of cutaneous homeostasis through its roles in modulating immune responses, maintaining barrier function, and regulating metabolic homeostasis. Age-associated physiological changes in the host selectively reshape the composition and function of the skin microbiome, while the resulting microbial dysbiosis may, in turn, contribute to the development of skin aging phenotypes. Here, we summarize the mechanistic crosstalk between the aging host and the skin microbiome, with particular emphasis on how these bidirectional interactions contribute to the pathogenesis of geriatric dermatoses. We further evaluate emerging microbiome-based therapeutic strategies, ranging from ecological restoration to precision microbial modulation. Viewing skin aging through this ecological framework may provide a foundation for developing translational strategies aimed at promoting healthier skin aging.},
}

@article {pmid43011761,
year = {2026},
author = {Sun, C and Han, F and Xu, W and Wang, X and Wang, X},
title = {Deciphering the gut-lung axis in non-small cell lung cancer: from immune microenvironment crosstalk to clinical translation.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1975256},
pmid = {43011761},
issn = {2234-943X},
abstract = {Immune checkpoint inhibitors (ICIs) targeting the PD-1/PD-L1 axis have established a new standard of care for non-small cell lung cancer (NSCLC); however, clinical efficacy is frequently limited by primary resistance, acquired (secondary) resistance, and immune-related adverse events. The heterogeneity of the tumor immune microenvironment (TIME) is a critical determinant of therapeutic response, a state effectively regulated by the gut microbiota via the gut-lung axis. This review systematically examines the mechanistic crosstalk between intestinal commensals and the pulmonary TIME. We first delineate how specific bacterial metabolites, such as short-chain fatty acids and indole-3-acetic acid, alongside bacterial-fungal trans-kingdom interactions, modulate innate and adaptive immune responses within the lung through epigenetic remodeling and metabolic signaling, and we map the discrete points at which these gut-derived signals converge on the intrinsic metabolic programmes of pulmonary tumor cells. Furthermore, we analyze the dual role of the microbiome as a predictive biomarker, discussing the evolution from simple taxonomic abundance profiling to complex ecological topology scores and the identification of therapeutic toxicity driven by molecular mimicry, and we examine whether pre-intervention alpha or beta diversity metrics are required for patient selection. Finally, we evaluate emerging therapeutic strategies, including next-generation probiotics, bacterial-derived extracellular vesicles, and combinational interventions that aim to overcome ICI resistance by restructuring the host-microbe ecosystem, with particular attention to acquired resistance to PD-1 blockade. We also critically appraise the barriers that currently impede clinical translation, including the inter-cohort non-reproducibility of taxonomic biomarkers, methodological heterogeneity between 16S amplicon and shotgun metagenomic profiling, and the safety and regulatory constraints on fecal microbiota transplantation in immunocompromised patients. This synthesis underscores the necessity of integrating microbiome profiling into standard oncological practice to facilitate precision immunotherapy.},
}

@article {pmid43011763,
year = {2026},
author = {Shah, AA and Madan, A and Pazhani, S and Singh, DP and Nazir, I and Thakur, S and Bhardwaj, R and Gupta, A},
title = {Dietary modulation of gut immunophysiology in food-producing animals: mechanistic links between the microbiota, mucosal immunity, and product quality.},
journal = {Frontiers in physiology},
volume = {17},
number = {},
pages = {1987339},
pmid = {43011763},
issn = {1664-042X},
abstract = {In food-producing animals, the gastrointestinal tract is an immunometabolic interface where nutrients, microbial communities, epithelial barriers, and mucosal immune systems converge to regulate nutrient utilization, barrier integrity, host defense, and physiological adaptation. This review critically evaluates how dietary inputs are translated through the diet-microbiota-host axis into intestinal phenotypes, host-microbiota responses, animal performance, and animal-food characteristics. Evidence from ruminants as well as non-ruminants is synthesized, with emphasis on studies in food-producing animals that directly evaluate dietary interventions and mechanistic investigations linking dietary substrates with microbial metabolism, epithelial-immune interactions, and host immunometabolic responses. Evidence from non-livestock models is considered primarily to clarify biological mechanisms and is distinguished from livestock outcomes. Evidence indicates that dietary modulation can alter microbial ecology and metabolite production, thereby influencing epithelial sensing, mucosal immune regulation, redox homeostasis, inflammatory signaling, and cellular metabolism. Microbial metabolites, including short-chain fatty acids, indole derivatives, and bile-acid metabolites, emerge as intermediates linking nutritional inputs with epithelial and immune function. These processes provide mechanistic connections between intestinal homeostasis, nutrient partitioning, stress resilience, and, in some experimental contexts, productive phenotypes and animal-product characteristics. However, the magnitude and direction of these responses are context dependent and vary with species, gastrointestinal anatomy, developmental or production stage, dietary composition, microbial community structure, and environmental challenge. Mechanistic and intervention evidence is more developed in swine and poultry, whereas extrapolation to ruminants requires consideration of foregut fermentation and altered delivery of substrates and metabolites to the intestine. Importantly, alterations in microbial composition, barrier markers, or immune signaling should not be interpreted as evidence of improved production performance or product quality unless these outcomes are directly demonstrated. The review therefore distinguishes established livestock evidence from mechanistic inference, association, and proposed biological frameworks, while identifying unresolved causal relationships between gut processes and whole-animal phenotypes. Emerging approaches, including microbiome profiling, multi-omics, sensor-based phenotyping, and artificial intelligence, may support biomarker discovery and nutrition decision-making, but their predictive and intervention value requires prospective validation across species and production environments. Overall, current evidence supports the gut as a regulatory interface between nutrition and host physiology, while highlighting species-specific, contextual, and causal limitations that constrain predictive precision nutrition.},
}

@article {pmid43011769,
year = {2026},
author = {Sohail, M and Hassan, AT and Gulzar, M and Numan, N and Mafe, AN and Büsselberg, D},
title = {Gut dysbiosis and brain cancer: exploring the emerging role of sweeteners and food additives.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1960004},
pmid = {43011769},
issn = {2813-4338},
abstract = {Glioblastoma (GBM) remains the most aggressive primary brain malignancy, with a median survival of approximately 15 months, and its rising incidence has increased interest in modifiable dietary risk factors. Despite growing evidence that food additives disrupt gut microbial ecology and that gut dysbiosis influences neuro-oncological pathways, no previous review has systematically integrated these findings through the gut-brain axis. This narrative review synthesizes evidence from studies on food additives, gut microbiome, and glioblastoma to identify shared mechanistic pathways. Across five additive categories (artificial sweeteners, food colorants, preservatives, nanoparticles, and emulsifiers), a common dysbiotic signature emerged, characterized by depletion of short-chain fatty acid-producing bacteria, increased lipopolysaccharide (LPS) production, disruption of tryptophan metabolism, and impairment of intestinal and blood-brain barrier integrity. These changes converged on neuroinflammatory, immunosuppressive, and oncogenic pathways, including NF-κB, PI3K/AKT, and m[6]A-mediated epigenetic reprogramming. Among all additives reviewed, aspartame provided the most complete hypothesized mechanistic sequence linking gut dysbiosis, epithelial barrier dysfunction, and m[6]A-mediated upregulation of glioblastoma-associated genes, highlighting a plausible microbiome-epigenetic axis that warrants further investigation. These findings position food additives as biologically active modulators of the gut-brain axis with potential relevance to glioblastoma pathogenesis and provide a mechanistic framework to guide future microbiome-informed prevention, biomarker discovery, and therapeutic research.},
}

@article {pmid43011779,
year = {2026},
author = {Sheng, W and Yang, X and Yu, Z and Yang, Y and Chen, H and Cheng, Y and Wang, W},
title = {Juvenile idiopathic arthritis and rheumatoid arthritis: a narrative review of age-dependent, subtype-specific immune mechanisms, biomarkers, and treatment strategies.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1873473},
pmid = {43011779},
issn = {1664-3224},
mesh = {Humans ; *Arthritis, Juvenile/immunology/drug therapy/diagnosis/therapy ; *Arthritis, Rheumatoid/immunology/drug therapy/diagnosis/therapy ; Biomarkers ; Age Factors ; Antirheumatic Agents/therapeutic use ; Child ; Animals ; Autoantibodies/immunology ; },
abstract = {BACKGROUND: Juvenile idiopathic arthritis (JIA) and adult rheumatoid arthritis (RA) share chronic inflammatory arthritis, but their biological drivers and implications vary by developmental stage and phenotype. JIA arises during immune and skeletal maturation and encompasses heterogeneous conditions, whereas adult RA develops after skeletal maturity. Existing reviews have considered the diseases separately or focused on polyarticular JIA, leaving uncertain which adult RA-derived mechanisms, biomarkers, and treatment principles transfer to JIA phenotypes.

MAIN BODY: A targeted search of PubMed/MEDLINE and Web of Science through 25 September 2026 informed an age-by-endotype framework comparing JIA phenotypes with adult RA across immune and tissue mechanisms, structural consequences, biomarker function and evidence maturity, and treatment mechanism, exposure, and safety. Systemic JIA, conceptualized within the Still's disease spectrum, diverges most from adult RA because of myeloid-cell activation, macrophage activation syndrome risk, and inflammation associated with interleukin-1, interleukin-6, and interleukin-18. Rheumatoid factor (RF)-positive polyarticular JIA shows partial convergence with adult seropositive RA through autoantibody-associated adaptive immunity, chronic synovitis, and erosive potential, but development and pediatric safety preclude equivalence. Oligoarticular JIA is distinguished by synovitis and uveitis, whereas enthesitis-related arthritis and juvenile psoriatic arthritis align more closely with entheseal and psoriatic-spectrum biology than with RA. Biomarker interpretation and treatment are phenotype-specific: ferritin, interleukin-18, and S100 proteins inform systemic hyperinflammation; RF and anti-citrullinated protein antibodies characterize RA-like polyarthritis; antinuclear antibodies inform uveitis surveillance; and human leukocyte antigen B27 supports classification in enthesitis-related arthritis. Treatment ranges from early interleukin-1 or interleukin-6 inhibition in systemic JIA to methotrexate, biologic disease-modifying antirheumatic drugs, and selected Janus kinase inhibitor use in RA-like polyarthritis after consideration of regulatory approval and individualized risk, and therapy directed at tumor necrosis factor or interleukin-17 in entheseal or psoriatic disease. Tissue, imaging, multi-omic, microbiome, and treatment-response biomarkers remain investigational.

CONCLUSIONS: The relationship between JIA and adult RA is phenotype- and domain-specific rather than universal. This framework identifies where adult-derived evidence can inform pediatric interpretation and where direct pediatric validation is required. Longitudinal, subtype-defined pediatric cohorts integrating tissue, imaging, and multi-omic data are needed to support mechanism-based, developmentally appropriate care.},
}

Humans
*Arthritis, Juvenile/immunology/drug therapy/diagnosis/therapy
*Arthritis, Rheumatoid/immunology/drug therapy/diagnosis/therapy
Biomarkers
Age Factors
Antirheumatic Agents/therapeutic use
Child
Animals
Autoantibodies/immunology

@article {pmid43011784,
year = {2026},
author = {Kumbhare, SV and Pedroso, I and Sinha, R and Almonacid, DE},
title = {Pharmacomicrobiomics of GLP-1 receptor agonist gastrointestinal tolerability: integrating host genetics and the gut microbiome.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {2016564},
pmid = {43011784},
issn = {2813-4338},
abstract = {Gastrointestinal (GI) adverse events, such as nausea, vomiting, diarrhea, and constipation, remain a dominant barrier to the sustained use of GLP-1 receptor agonists (GLP-1 RAs), driving discontinuation independently of the drug's metabolic benefits. Two host-side biological systems have been independently established as determinants of this variability. The first is host genetics, anchored by a 2026 genome-wide association study in which GLP1R variants predicted both weight-loss efficacy and nausea or vomiting risk, while a GIPR signal for vomiting was restricted to tirzepatide users. The second system is the gut microbiome, which regulates endogenous GLP-1 secretion through short-chain fatty acid and bile acid signaling and is itself reshaped by GLP-1 RA exposure. Pharmacomicrobiomics integrates host genetic and microbiome data to explain drug response. In the literature surveyed for this review, these two determinants are consistently examined in parallel rather than jointly: we did not identify a study, in GLP-1 RA therapy or in another drug class, that fit a 'host-genotype-by-microbiome' interaction model against a drug tolerability outcome. Published methodological studies have suggested why such a study would be challenging: both interaction detection and the measurement unreliability associated with single-timepoint microbiome profiling impose substantial sample size penalties. This review summarizes what host genetics and the microbiome individually do and do not explain about GLP-1 RA tolerability, and describes the study design features, paired genotyping, repeat-sample metagenomics, and prospective symptom capture that a future joint analysis would require.},
}

@article {pmid43011801,
year = {2026},
author = {Zhu, G and Huang, Y and Huang, Y and Yang, W},
title = {Predicting response to GLP-1-based therapy in MASLD/MASH: an evidence-tiered, endpoint-specific framework built on host genotype and gut microbial features.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1962068},
pmid = {43011801},
issn = {1664-2392},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; Genotype ; *Glucagon-Like Peptide 1/therapeutic use ; Semaglutide ; *Incretins/therapeutic use ; *Fatty Liver/drug therapy/genetics/microbiology ; *Non-alcoholic Fatty Liver Disease/drug therapy/genetics/microbiology ; Glucagon-Like Peptides/therapeutic use ; },
abstract = {Incretin-based therapy is now central to treating metabolic dysfunction-associated steatohepatitis (MASH), but the benefit is uneven. In the ESSENCE trial, semaglutide resolved steatohepatitis without worsening fibrosis in 62.9% of patients; placebo did so in 34.3%. No one can yet tell in advance which patient will respond. Weight loss explains most of the difference between trials, but it cannot be prescribed. This review asks whether biology measured before the first dose can predict who will benefit. Hepatocytes carry almost no GLP-1 receptor, so the liver benefit arrives indirectly, through weight loss and through gut-liver signaling. Both routes can be influenced from outside the liver, which points to two measurable domains: host genotype, fixed and assayable at baseline, and gut microbial features. For a dietary prebiotic, baseline microbial features have already forecast response, with an externally validated area under the curve of 0.74 (95% CI 0.66-0.81). Nothing equivalent has been tested for a GLP-1 receptor agonist. The genotype evidence comes from dietary weight loss rather than from a drug. Both pillars therefore rest on interventions other than incretin therapy, and the framework grades them accordingly. We assemble this evidence into a framework with two rules. Findings are graded by how mature the evidence behind them is. Liver and cardiovascular benefits are predicted separately, because the two do not track together. The output is a probability rather than a label. One conclusion is already usable: a predicted poor liver response is not, on its own, a reason to withhold or stop a GLP-1 receptor agonist.},
}

Humans
*Gastrointestinal Microbiome/drug effects
Genotype
*Glucagon-Like Peptide 1/therapeutic use
Semaglutide
*Incretins/therapeutic use
*Fatty Liver/drug therapy/genetics/microbiology
*Non-alcoholic Fatty Liver Disease/drug therapy/genetics/microbiology
Glucagon-Like Peptides/therapeutic use

@article {pmid43011805,
year = {2026},
author = {Aliberti, A and Coppola, N and Gasparro, R and Trosino, O and Sammartino, JC and Sammartino, G},
title = {The oral exposome and environment-related diseases of hard and soft oral tissues: a comprehensive review.},
journal = {Frontiers in oral health},
volume = {7},
number = {},
pages = {1976898},
pmid = {43011805},
issn = {2673-4842},
abstract = {BACKGROUND: The oral cavity is continuously exposed to environmental, lifestyle-related, microbial, and systemic influences capable of altering tissue homeostasis and contributing to chronic oral disease. Environmental exposures may interact through inflammatory, microbial, and metabolic pathways affecting both hard and soft oral tissues. This review critically synthesizes current evidence on environment-related oral diseases within the framework of the oral exposome, focusing on environmental determinants, biological mechanisms, tissue alterations, and implications for oral surgery, implantology, regenerative procedures, and precision oral medicine.

MATERIALS AND METHODS: A comprehensive narrative review was conducted through electronic searches of PubMed, Scopus, and Web of Science for studies published up to April 2026. English-language articles evaluating relationships between environmental exposure and oral tissue alterations were included. Evidence regarding environmental pollutants, smoking, alcohol consumption, dietary factors, occupational exposures, and other external determinants was critically analyzed together with host-related modifiers, including salivary dysfunction, microbial dysbiosis, systemic disease, and chronic inflammatory conditions. The review considered exposure-associated alterations involving dental hard tissues, periodontal and peri-implant structures, oral mucosa, salivary homeostasis, and oral microbial ecology.

RESULTS: The strength of evidence varied substantially across exposure-outcome relationships. The most mature human evidence concerned conventional tobacco smoking and selected carcinogenic exposures, whereas associations involving air pollution, heavy metals, occupational toxicants, electronic cigarettes, endocrine-disrupting chemicals, and emerging contaminants showed greater heterogeneity and, for several outcomes, relied substantially on observational, experimental, or mechanistic evidence. Across these different levels of evidence, recurrent pathways included oxidative stress, inflammation, microbial dysbiosis, epithelial dysfunction, and altered tissue homeostasis.

CONCLUSIONS: The oral exposome provides a useful framework for understanding the multifactorial nature of oral disease and the interaction among environmental exposure, microbial ecology, host response, and tissue homeostasis.},
}

@article {pmid43011890,
year = {2026},
author = {Islam, MM and Yang, G and Kang, KS},
title = {Gut microbiome and aging-related disorders: mechanistic insights and emerging microbiome-targeted therapies for healthy aging.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1839461},
pmid = {43011890},
issn = {2296-861X},
abstract = {BACKGROUND: The human gut harbors a diverse and dense microbial community that maintains metabolic, immune, and intestinal homeostasis through a symbiotic relationship with the host. Aging is a complex biological process that involves alterations in the gut microbiome, including decreased microbial diversity and a decline in beneficial microbiota that produce useful metabolites, which impair intestinal barrier function and enhance chronic low-grade inflammation (inflammaging).

SCOPE: This review explores current evidence on the interaction between aging and the gut microbiome, emphasizing its impact on age-associated diseases, such as frailty and sarcopenia, cardiovascular issues, type 2 diabetes, obesity, osteoporosis, and neurodegenerative conditions. It further delves into the distinct microbial profiles of centenarians and evaluates microbiome-targeted interventions, such as dietary approaches, probiotics, prebiotics, synbiotics, fecal microbiota transplants, caloric restriction, intermittent fasting, and pharmaceutical agents, by synthesizing evidence from both human and animal research to emphasize their potential in fostering healthy aging and increased longevity.

KEY FINDINGS: Evidence from human and preclinical studies suggests that alterations in the gut microbiome associated with aging facilitate immune dysregulation, metabolic dysfunction, and the progression of various chronic diseases. Whereas, centenarians possess distinctive microbial signatures rich in beneficial metabolites that could promote healthy aging and prolonged life. Additionally, microbiome-targeted interventions have demonstrated promise in enhancing gut microbial diversity and host wellbeing, though their clinical effectiveness needs additional validation.

CONCLUSION: The gut microbiome is a potential focus for supporting healthy aging and warding off age-related illnesses. Nonetheless, its significant inter-individual variability emphasizes the necessity for personalized microbiome-based approaches, which require validation through extensive longitudinal studies and properly structured randomized controlled trials to demonstrate causality and verify long-term effectiveness.},
}

@article {pmid43012069,
year = {2026},
author = {Wang, Y and Zeng, M and Yang, H and Peng, K and Xu, S and Zhao, S and Zhang, Q and Zhou, Y and Yue, X and Tang, X and Wu, R and Wang, R and Wang, T and Wu, Q and Gan, R and Wang, B and Wu, R and Jin, H and Fang, X and Liu, Y and Ren, Y and Wang, J and Jeon, CO and Shi, X and Chen, J and Yuan, Z and Zheng, Z and Shen, X and Cui, J and Wan, Z and Zhang, Y and Jia, G and Sun, Z and Zhang, D and Wu, J and Li, P and Ma, P and Liu, YX},
title = {Food Microbiome Project.},
journal = {Innovation (Cambridge (Mass.))},
volume = {7},
number = {11},
pages = {101573},
pmid = {43012069},
issn = {2666-6758},
}

@article {pmid43012185,
year = {2026},
author = {Molefe-Madlaliso, RR and Amoo, AE and Babalola, OO},
title = {Unveiling Microbial Gene Functions in Maize Cultivars With Varying Drought Resistance.},
journal = {Journal of basic microbiology},
volume = {66},
number = {11},
pages = {},
doi = {10.1002/jobm.70213},
pmid = {43012185},
issn = {1521-4028},
support = {UID123634//National Research Foundation of South Africa/ ; UID132595 OOB//National Research Foundation of South Africa/ ; },
mesh = {*Zea mays/microbiology/genetics/physiology ; *Drought Resistance/genetics ; Rhizosphere ; *Microbiota/genetics ; Stress, Physiological/genetics ; Droughts ; *Bacteria/genetics/classification/isolation & purification ; Soil Microbiology ; Metagenomics ; Genotype ; Plant Roots/microbiology ; },
abstract = {The rhizosphere microbiome is recognized as a "biological tool" for mitigating drought stress on plant development. However, the functional genes involved in plant-microbe interactions, particularly in drought-sensitive and drought-tolerant cultivars, remain poorly understood. This study comparatively evaluated the functional gene set of the maize rhizosphere microbiome in Monsanto DKC 72-70 (drought-tolerant) and CRN-3505 (drought-sensitive) maize genotypes at water holding capacity (WHC) values of 60, 80, and 100% via shotgun metagenomics. The findings revealed that both cultivars contained a variety of microbial taxa, such as Actinobacteria, Alphaproteobacteria, Gammaproteobacteria, and Bacilli, with plant stress tolerance genes. The analysis of beta diversity indicated significant differences between drought-stressed (60% WHC) and well-watered (100% WHC) conditions in both cultivars (R ≈ 0.57, 0.58; p < 0.01), which implies that the functional gene composition is different and that there are intermediate patterns at 80% WHC. In terms of functional responses, drought-sensitive maize presented increased expression of genes related to sulfur oxidation (soxA, soxB, soxD) and osmoprotectant synthesis (BetI, betC, CHCH), indicating a reactive stress response. Conversely, drought- tolerant maize presented regulated expression of the nitrogen metabolism (glnA) and iron homeostasis (FUR) genes in all the WHCs, thus indicating efficient adaptation. In addition, the drought-tolerant maize cultivar selectively expressed stress-response genes (SigB, AhpC) and protein protection genes (dnaJ, dnaK), whereas the drought-sensitive maize cultivar constitutively expressed these genes across conditions. This study provides novel evidence of cultivar-specific functional microbial signatures and demonstrates how microbial gene functions underpin drought tolerance in maize under varying water availability conditions.},
}

*Zea mays/microbiology/genetics/physiology
*Drought Resistance/genetics
Rhizosphere
*Microbiota/genetics
Stress, Physiological/genetics
Droughts
*Bacteria/genetics/classification/isolation & purification
Soil Microbiology
Metagenomics
Genotype
Plant Roots/microbiology

@article {pmid43012319,
year = {2026},
author = {Saiyawong, JNS and Watrous, KM and Buchmann, S and Melin, A and Hammer, TJ},
title = {Sparse gut microbiomes in solitary bees and wasps.},
journal = {Biology letters},
volume = {22},
number = {11},
pages = {},
pmid = {43012319},
issn = {1744-957X},
support = {DGE-1839285//U.S. National Science Foundation Graduate Research Fellowship/ ; //Sea and Sage Audubon Society/ ; //California Native Plant Society Orange County Chapter/ ; //University of California Nature/ ; //Mapula Trust/ ; },
mesh = {Animals ; Bees/microbiology ; *Wasps/microbiology ; *Gastrointestinal Microbiome ; Bacteria/classification/isolation & purification/genetics ; Symbiosis ; },
abstract = {Bees and wasps are ecologically vital, but many species are declining owing to anthropogenic stressors. Social bees harbour host-specific and dense gut microbiomes that affect their resilience to stress. However, there are tens of thousands of other bee and wasp species that vary in sociality and diet (including pollen-feeding and predatory guilds), traits known to influence host-microbe symbioses. The role of gut microbes in the biology of these species is largely unknown. Here, we measured the composition and absolute abundance of bacterial communities in adult metasomas across 61 genera and 14 families of field-collected bees, predatory wasps and pollen wasps. We found that solitary bees and both wasp guilds harbour distinct bacterial taxa and lower bacterial abundances as compared with social bees. Bacterial abundances also varied extensively among and within genera of solitary bees, with little variation explained by body size, diet breadth or nesting ecology. Furthermore, microbiome composition was only weakly differentiated among solitary bees and the two wasp groups, even when comparing herbivorous (pollen-feeding) and omnivorous taxa. We suggest that the sparse and somewhat stochastic microbiomes of solitary bees and wasps reflect weak host dependence on microbially mediated functions, a trait that may influence their responses to environmental change.},
}

Animals
Bees/microbiology
*Wasps/microbiology
*Gastrointestinal Microbiome
Bacteria/classification/isolation & purification/genetics
Symbiosis

@article {pmid43000596,
year = {2026},
author = {Su, Z and Zhang, Y and Li, S and Liu, G and Wang, S},
title = {Panax notoginseng alleviates obesity and insulin resistance involving the Enterocloster clostridioformis-IRS-PI3K-AKT axis.},
journal = {Science China. Life sciences},
volume = {},
number = {},
pages = {},
pmid = {43000596},
issn = {1869-1889},
abstract = {In this study, supplementation with Panax notoginseng (PN) in obese mice reversed excessive weight gain, improved glucose homeostasis and insulin sensitivity, and significantly reversed hepatic steatosis. Concurrently, PN treatment normalized the intestinal microecosystem, reflected in a decreased Firmicutes-to-Bacteroidetes ratio (F/B ratio) and an enrichment of the commensal species Enterocloster clostridioformis (EC). Of particular note, oral administration of EC alone largely reproduced the major beneficial phenotypes observed with PN-namely, reduced fat mass, improved glycaemic regulation, and attenuated hepatic triglyceride deposition. Mechanistically, EC intervention suppressed the pathological overactivation of the hepatic insulin receptor substrate (IRS)-phosphatidylinositol-3 kinase (PI3K)-AKT kinase (AKT) pathway and inhibited the phosphorylation of IRS. This recalibration of the insulin signaling cascade improved insulin sensitivity and effectively counteracted the metabolic disturbances provoked by the high-fat diet (HFD). Taken together, these results suggest that the anti-obesity effects of PN are at least partially mediated by gut microbiota-driven EC enrichment, with consequent modulation of the IRS-PI3K-AKT pathway. Collectively, our findings identify EC as a potential candidate commensal bacterium and highlight the importance of the PN-EC-IRS-PI3K-AKT regulatory axis in counteracting obesity and its associated comorbidities.},
}

@article {pmid43000727,
year = {2026},
author = {Steenkamp, I and Pillay, L},
title = {Hidradenitis suppurativa in primary care: From early recognition to modern management.},
journal = {South African family practice : official journal of the South African Academy of Family Practice/Primary Care},
volume = {68},
number = {1},
pages = {e1-e6},
doi = {10.4102/safp.v68i1.6318},
pmid = {43000727},
issn = {2078-6204},
mesh = {Humans ; *Hidradenitis Suppurativa/diagnosis/therapy/epidemiology ; *Primary Health Care ; Early Diagnosis ; },
abstract = {Hidradenitis suppurativa (HS), also known as acne inversa, is a heterogeneous, chronic, relapsing inflammatory disease of the pilo-sebaceous unit, primarily affecting intertriginous areas such as the axillae, groin and anogenital region. Despite its relatively low global prevalence, HS remains underdiagnosed, especially in primary care settings, where it is often mistaken for recurrent boils. The pathogenesis is multifactorial, involving follicular occlusion, immune dysregulation, genetic susceptibility, microbiome imbalance, hormonal influences and lifestyle factors. Hidradenitis suppurativa typically presents after puberty with a peak incidence during the second and third decades of life. The condition is characterised by painful nodules, abscesses and in advanced stages of the disease, forms sinus tracts and scars that greatly impair quality of life. Early recognition and a multidisciplinary management approach, including lifestyle modification, long-term medical therapy and surgical intervention when indicated, are essential to prevent disease progression and complications. This article provides an evidence-based overview of HS and practical guidance for family practitioners on its recognition, classification and management within the South African context.},
}

Humans
*Hidradenitis Suppurativa/diagnosis/therapy/epidemiology
*Primary Health Care
Early Diagnosis

@article {pmid43000839,
year = {2026},
author = {Xie, YS and Wu, ZL and Wei, FQ and Zheng, SG},
title = {[Characterization of the caries-associated oral microbiome across age groups based on global metagenomic species-level genome bins data].},
journal = {Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology},
volume = {61},
number = {11},
pages = {1622-1632},
doi = {10.3760/cma.j.cn112144-20260122-00038},
pmid = {43000839},
issn = {1002-0098},
support = {82501126//National Natural Science Foundation of China/ ; },
abstract = {Objective: Based on the analysis of global multicenter metagenomic species-level genome bin (SGB), this study aims to identify core cariogenic SGBs across all age groups and provide a basis for the precise diagnosis and age-stratified prevention and treatment of dental caries. Methods: Eight published studies available in the National Center for Biotechnology Information database before August 2024 were included, with a total of 496 oral metagenomic samples enrolled. Samples were stratified into saliva and dental plaque groups across three age segments (<6, 6 to<13, and≥13 years). Taxonomic profiling, core microbiota identification, and differential analysis of strains were conducted. Results: Analysis at the SGB level revealed that 652 SGBs were detected in plaque samples and 931 SGBs in saliva samples. Specific core SGB clusters were identified in each age group (<6, 6 to<13, and≥13 years), with 13 SGBs consistently detected across all groups (detection rate>50%). Differential analysis indicated that caries was accompanied by marked ecological dysbiosis. These differential patterns were highly age-and sample-specific. Saliva samples in the group aged<6 years identified the most numerous differential SGBs (227). In plaque samples of aged 6 to<13 years, the caries group was characterized by Streptococcus enrichment versus Capnocytophaga in the healthy group. Notably, in the≥13-year-old group, the caries-associated microbiome shifted to anaerobic Prevotella species alongside Streptococcus. Heatmap analysis confirmed clear ecological turnovers across all ages, with the sharpest demarcation found in the youngest age group. Conclusions: Analysis at the SGB level unveils microbial dysbiosis patterns with greater precision than traditional species-level profiling, providing a novel theoretical basis for the precision diagnosis and age-specific management of dental caries.},
}

@article {pmid43000952,
year = {2026},
author = {Ha, S and Lv, C and Cui, J and Yu, H and Sun, L},
title = {A validated low-abundance uterine microbial signature associated with chronic endometritis.},
journal = {Zygote (Cambridge, England)},
volume = {},
number = {},
pages = {1-15},
doi = {10.1017/S0967199426100677},
pmid = {43000952},
issn = {1469-8730},
abstract = {BACKGROUND: Chronic endometritis (CE) is a persistent inflammatory endometrial disorder associated with infertility, recurrent implantation failure, and pregnancy loss. While previous microbiome studies have focused on Lactobacillus depletion and common genital tract bacteria, low-abundance microbial lineages remain poorly characterised.

OBJECTIVE: To identify reproducible low-abundance microbial signatures associated with CE and evaluate their robustness through external validation and complementary analyses.

METHODS: Uterine lavage specimens from infertile women with CE (n = 29) and non-CE controls (n = 16) were analysed by 16S rRNA sequencing in a discovery cohort. An independent cohort of 58 participants was used for external validation. CE was diagnosed by hysteroscopy and CD138 immunohistochemistry (≥5 stromal plasma cells/10 high-power fields). Multiple negative controls were included, and contaminants were assessed using decontam. Prespecified analyses included cervicovaginal source tracking, shotgun metagenomics in a subset, cytokine profiling, and post-treatment follow-up.

RESULTS: CE samples exhibited increased richness and modestly higher diversity. Presence/absence-based beta diversity demonstrated clearer separation between CE and controls. CE was associated with enrichment of Patescibacteria, Planctomycetota, Bdellovibrionota, and selected archaeal-lineage signals. After contaminant filtering, major rare-lineage features remained enriched. Patescibacteria and Bdellovibrio-related signals correlated with CD138-positive plasma-cell counts and inflammatory cytokines. A nested discovery model achieved an area under the receiver operating characteristic curve (AUC) of 0.84, and the locked marker panel achieved an AUC of 0.81 in external validation.

CONCLUSIONS: CE is associated with a reproducible low-abundance microbial signature in uterine lavage samples. These findings highlight candidate microbial lineages for further investigation but do not establish causality or uterine residency.},
}

@article {pmid43000968,
year = {2026},
author = {Jia, J and Zhang, J and Zhang, W and Zhang, F and Yun, K and Yan, J},
title = {[Microbiomics‑Based Prediction of Postmortem Interval in Rats with Ethanol Exposure Combined with CO Poisoning].},
journal = {Fa yi xue za zhi},
volume = {42},
number = {4},
pages = {295-301},
doi = {10.12116/j.issn.1004-5619.2024.440903},
pmid = {43000968},
issn = {1004-5619},
mesh = {Animals ; *Postmortem Changes ; *Ethanol/toxicity ; Rats ; *Carbon Monoxide Poisoning/microbiology ; RNA, Ribosomal, 16S/genetics ; Male ; Rats, Sprague-Dawley ; *Bacteria/genetics/classification/isolation & purification ; Disease Models, Animal ; *Gastrointestinal Microbiome ; Time Factors ; },
abstract = {OBJECTIVES: To investigate the temporal changes of intestinal bacterial communities in rats that died from combined ethanol and carbon monoxide (CO) poisoning using microbiome analysis techniques, and to explore potential correlations between these changes and the postmortem interval (PMI).

METHODS: Four experimental groups were established：fatal CO poisoning, fatal CO poisoning following ethanol exposure, ethanol exposure, and blank controls. Rectal specimens were collected at 0, 1, 3, 7, and 14 days postmortem. High-throughput sequencing of the 16S rRNA gene was employed to analyze bacterial communities. Bacterial diversity, relative abundance, and community differences were analyzed. A predictive model for PMI estimation using bacterial community succession patterns was constructed using a random forest algorithm.

RESULTS: The intestinal bacterial community structure of rats changed at both the phylum and genus levels within 14 days postmortem in the experimental groups. The PMI estimation model based on bacterial characteristics demonstrated good predictive performance across different experimental groups, with model fitting accuracies of 0.60, 0.59, 0.61 and 0.60 for each of the four groups. The average prediction error across all groups was approximately 1 day.

CONCLUSIONS: Ethanol exposure, CO poisoning, and the combined effects of ethanol exposure and CO poisoning all affect postmortem bacterial succession in rat cadavers. In forensic practice, it is recommended to adopt a predictive model specifically developed for the corresponding poisoning condition to improve the accuracy of PMI estimation.},
}

Animals
*Postmortem Changes
*Ethanol/toxicity
Rats
*Carbon Monoxide Poisoning/microbiology
RNA, Ribosomal, 16S/genetics
Male
Rats, Sprague-Dawley
*Bacteria/genetics/classification/isolation & purification
Disease Models, Animal
*Gastrointestinal Microbiome
Time Factors

@article {pmid43001270,
year = {2026},
author = {Kallapura, G and Prakash, AS and Prasad, R and Josphine, I and Maurya, M and Dhar, D},
title = {Gut microbiota composition of India's Baiga tribe: Insights from an indigenous particularly vulnerable tribal group.},
journal = {iScience},
volume = {29},
number = {11},
pages = {118082},
pmid = {43001270},
issn = {2589-0042},
abstract = {The transition from traditional foraging lifestyles to modernized urban environments is associated with reduced human gut microbiome diversity. To examine this shift within the Indian subcontinent, we used shotgun metagenomics to compare the gut microbiota of 50 adults: 25 from the indigenous, foraging, and particularly vulnerable Baiga tribe and 25 from an urban population in Bhopal, Central India. The Baiga maintained a diverse ecosystem enriched with fiber-degrading bacteria such as Roseburia and Faecalibacterium, forming networks suited to complex carbohydrate fermentation. The urban microbiome showed lower phylogenetic diversity and evenness, with higher relative abundance of Prevotella copri and dairy-adapted taxa. Functionally, the tribal gut retained pathways for environmental sensing and complex plant metabolism, whereas the urban gut was enriched in pathways associated with potential inflammation. These findings identify the Baiga as a reservoir of preserved human microbial diversity relevant to metabolic health.},
}

@article {pmid43001315,
year = {2026},
author = {Zhou, X and Zhao, C and Jia, R and He, Z and Lin, Z and Cao, J and Luo, Y and Yang, S and Liu, D and Li, Y},
title = {Effects of andrographolide on growth performance, serum indices, and multi-site microbial communities in weaned calves.},
journal = {Animal nutrition (Zhongguo xu mu shou yi xue hui)},
volume = {27},
number = {},
pages = {474-492},
pmid = {43001315},
issn = {2405-6383},
abstract = {Weaning stress frequently induces systemic inflammation and oxidative stress in calves, thereby impairing growth performance and increasing susceptibility to gastrointestinal and respiratory diseases. Andrographolide (AG) is a natural active compound extracted from the medicinal plant Andrographis paniculata. It exhibits potent anti-inflammatory and antioxidant properties, but its impacts on calf physiological health and multi-site microbial ecosystems remain poorly understood. This study aimed to evaluate the effects of AG supplementation on growth performance, serum anti-inflammatory and antioxidant levels, and microbial communities across multiple sites (rumen, rectum, and nasal cavity) in weaned calves. Eighteen healthy Angus calves (age 90 ± 3 d, initial body weight 88.25 ± 4.98 kg) were randomly assigned to three groups (n = 6 per group): 0 mg/kg AG group (CON), 8 mg/kg AG group (L-AG), and 16 mg/kg AG group (H-AG). The trial lasted for 42 d. Results indicated that AG supplementation linearly increased calf average daily gain (ADG; P = 0.011); however, the L-AG group exhibited the most significant weight gain advantage during the latter phase (22-42 d) (P = 0.026). Serum analysis revealed that AG supplementation significantly enhanced calves' antioxidant (e.g., superoxide dismutase [SOD] and glutathione peroxidase [GSH-Px]) and anti-inflammatory (e.g., interleukin [IL]-4 and IL-10) capacities (P < 0.05), while markedly reducing pro-inflammatory factors (e.g., IL-1β, IL-2, and IL-6) and the oxidative stress marker (malondialdehyde) (P < 0.05); the H-AG group exhibited the most pronounced anti-inflammatory and antioxidant effects. Microbiome analysis revealed that AG treatment consistently remodeled microbial communities across all sites (P < 0.05). In the rumen, the L-AG group specifically enriched beneficial genera associated with volatile fatty acid (VFA) synthesis, including Pseudoscardovia, CAG-238, CAG-127, and CAG-793 (P adj < 0.05). In the nasal cavity, AG significantly reduced the abundance of multiple potential pathogenic microorganisms, including Pasteurella, Moraxella_C, Brevundimonas, and Exiguobacterium_A (P adj < 0.05). Furthermore, AG enhanced cross-site microbial interactions, with a numerical increase in cross-site edges (CON = 529, L-AG = 741, H-AG = 866). The AG treatments significantly altered the network topological structure (P < 0.05), suggesting a strengthening of the gut-lung axis. In summary, AG supplementation during calf weaning effectively suppressed inflammation and oxidative stress responses while improving growth performance and health status through multi-site microbial regulation. Based on the observed phenotypic and microbiome differences, L-AG appears to favor long-term growth benefits by optimizing rumen microbial communities, whereas H-AG maximizes short-term improvements through more potent anti-inflammatory and antioxidant effects.},
}

@article {pmid43001780,
year = {2026},
author = {Fang, H and Shu, Y and Zhou, Z and Li, Y and Gong, T and Yang, M and Zhang, B and Jin, Y and Liu, Y and Wang, C and Zhao, L and Liu, Y and Chen, P},
title = {Identification of ebastine and ceritinib as effective inhibitors of Fusobacterium nucleatum FtsZ.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0132626},
doi = {10.1128/spectrum.01326-26},
pmid = {43001780},
issn = {2165-0497},
abstract = {UNLABELLED: The role of microorganisms in cancer is not a new concept-bacteria, parasites, and viruses have all been implicated in cancer development. Fusobacterium nucleatum, a member of the oral microbiota, has emerged as an important cancer-associated bacterium. Unbiased global genomic analyses have demonstrated that F. nucleatum is enriched in human colorectal cancer (CRC) tissues compared with noncancerous colorectal tissues, underscoring the urgent need for specific antimicrobial agents targeting F. nucleatum for CRC prevention and treatment. In this study, structure-based virtual screening successfully identified ebastine and ceritinib as antimicrobial agents targeting Fusobacterium nucleatum FtsZ (FnFtsZ). Their potent anti-F. nucleatum activity was confirmed through in vitro assays, including minimum inhibitory concentration determination and microscopic observation of filamentous morphology. Both ebastine and ceritinib exhibited significant antibacterial effects. Enzyme activity and polymerization assays demonstrated that their mechanism of action involves inhibition of FnFtsZ GTPase activity and disruption of FnFtsZ polymerization. Scanning electron microscopy (SEM) and light microscopy further confirmed that these compounds effectively disrupt cell division, leading to abnormal or halted division and inhibiting F. nucleatum proliferation. Overall, our findings identified ebastine and ceritinib as potential drugs against F. nucleatum proliferation, although further structural optimization is required. Additionally, our results demonstrate the effectiveness of an integrated computational-experimental approach targeting bacterial cell division in microbiome-associated pathologies.

IMPORTANCE: Colorectal cancer (CRC) is strongly driven by the enrichment of the oncogenic bacterium Fusobacterium nucleatum in gut lesions. However, the lack of targeted anti-F. nucleatum drugs significantly limits microbe-related interventions for CRC. In this study, we repurposed two clinically approved drugs, ebastine and ceritinib, as highly effective inhibitors of FnFtsZ, the key protein responsible for bacterial cell division. We demonstrated that both drugs inhibit bacterial proliferation by suppressing FnFtsZ function and disrupting the cell division process. Our work offers safe, readily available candidate agents for controlling CRC-associated pathogenic bacteria and establishes a reliable computational-experimental workflow to screen division-targeted antimicrobials for microbiome-related cancers.},
}

@article {pmid43001783,
year = {2026},
author = {Paris, ER and Salcedo, RSR and Buessecker, S and Pozarycki, C and Desmarais, M and Sephus, CD and Schartup, AT and Bartlett, DH and Ingall, ED and Doran, PT and Andersson, A and Glass, JB and Quartini, E and Schmidt, BE and Bowman, JS and Dekas, AE},
title = {Free-living autotrophs drive a carbon fixation peak within the Orca Basin chemocline while heterotrophs dominate total activity from seawater to brine.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag279},
pmid = {43001783},
issn = {1751-7370},
abstract = {Deep hypersaline anoxic basins (DHABs) are stratified, polyextreme environments found within enclosed and semi-enclosed seas worldwide. Here, we quantified microbial activity in Orca Basin, the largest known DHAB, to investigate carbon cycling across its steep chemical and salinity gradients. We measured total anabolic activity and dissolved inorganic carbon (DIC) fixation as a function of metabolic lifestyle (autotroph or heterotroph) and spatial niche (free-living or particle-associated) using dual-isotope labeling experiments and single-cell analysis by nanoscale secondary ion mass spectrometry (nanoSIMS). Activity was detected within all ten depths investigated from seawater to hypersaline brine, including by most cells within the brine. DIC fixation and total anabolic activity peaked within the oxic-anoxic interface, notably separate from the peak in cell and particle density deeper in the halocline. Autotrophs drove the peak in DIC fixation, but heterotrophs drove that of total activity; autotrophs were more abundant than heterotrophs at this depth but on average smaller and slower growing. Particle-associated heterotrophs, but not autotrophs, were significantly more active than their free-living counterparts within the interface. Heterotrophic communities derived an average of 4% to 10% of their biomass from DIC across the vertical transect, contributing just 2% of total DIC fixation within the peak but the majority within overlying seawater. Metagenomic analysis of catabolically active, sorted cells indicated members of at least five phyla were active within the oxic-anoxic interface, including putatively autotrophic Thermoproteota. These data provide high-sensitivity microbial activity measurements in Orca Basin and highlight the widespread viability of the resident microbiome.},
}

@article {pmid43001800,
year = {2026},
author = {Tang, Y and Sun, Y},
title = {Benchmarking gut microbiome health indices by their sensitivity to subclinical risk in 12,561 adults.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0331626},
doi = {10.1128/spectrum.03316-26},
pmid = {43001800},
issn = {2165-0497},
abstract = {A growing number of indices claim to summarize gut "microbiome health," yet they are routinely treated as interchangeable, even though their relative sensitivity to host risk remains undefined. In 12,561 adults from the American Gut Project (16S rRNA gene profiles), we benchmarked five indices spanning distinct constructs-taxonomic composition (Gut Microbiome Wellness Index 2 [GMWI2] and ZOE), diversity (Shannon), functional redundancy index (FRI), and reference-based structural deviation (microbiome deviation index [MDI])-along a cumulative lifestyle-risk gradient and against four chronic disease clusters. Shannon diversity, abundance-weighted ZOE, and MDI each shifted dose-dependently from the earliest risk increments (Jonckheere-Terpstra P < 0.001), and pathway-level composites moved in the expected directions; FRI and GMWI2 did not. Disease associations were index specific and cluster specific: Shannon (protective direction) and ZOE (risk direction) were associated with all four clusters, MDI with metabolic/systemic disease, and FRI with gastrointestinal disease, whereas GMWI2 showed no association throughout. The five indices were only moderately intercorrelated (Spearman |ρ| ≤0.52). Shannon and ZOE-the most consistent performers-showed only modest effects (per standard deviation, odds ratios 0.84-0.94 and 1.08-1.22, respectively), and neither captured the structural-deviation signal indexed by MDI. Associations between environmental stressors (including PM10, heptachlor, and ozone) and microbiome outcomes were concentrated in higher-risk hosts, consistent with host vulnerability gating the microbiome's environmental stress response. Together, these results show that widely used microbiome health indices are not interchangeable: they detect overlapping but non-identical facets of dysbiosis, and their sensitivity to subclinical risk depends on index formulation and data resolution. An interpretable, complementary panel rather than any single score may therefore best support early stratification.IMPORTANCEGut microbiome "health" is increasingly summarized using single numerical scores, yet these scores are often treated as equivalent despite measuring different biological features. By comparing five widely used indices in 12,561 adults, we show that they differ substantially in their ability to detect early, subclinical changes associated with cumulative lifestyle risk. Measures of microbial diversity, abundance-weighted taxonomic composition, and deviation from a healthy reference changed progressively from the earliest risk increments, whereas a functional redundancy measure and a presence/absence-based taxonomic index were comparatively insensitive, and pairwise correlations between indices were only moderate (|ρ| ≤0.52). We also found that associations between environmental pollutants and microbiome disruption were strongest among individuals with higher baseline lifestyle risk. These findings argue against relying on a single universal microbiome health score and support the use of complementary indices for early risk stratification and future microbiome-based prevention research.},
}

@article {pmid43001898,
year = {2026},
author = {Mazzoni, C and Yassour, M},
title = {IBD is associated with species-specific changes in gut microbial gene diversity.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0082726},
doi = {10.1128/msystems.00827-26},
pmid = {43001898},
issn = {2379-5077},
abstract = {UNLABELLED: Intra-species genomic variation provides the raw material for natural selection and can reflect the recent diversification history of microbial populations. Environmental stress may be regarded as the ultimate accelerator of the evolutionary process, especially for microorganisms, which can alter their DNA if presented with nutrient limitation, toxins, or pathogen attack. Chronic intestinal inflammation, as in inflammatory bowel disease (IBD), represents prolonged environmental stress for gut commensal bacteria, bringing many enteric species down to undetectable levels. However, it remains unclear how microbes that colonize IBD patients actually respond to IBD-associated stressors and whether stress-driven bacterial dynamics may be identified at the population level from the bacterial gut metagenome. To investigate IBD-associated strain-level population dynamics, we performed metagenomic analyses focusing on measuring within-individual bacterial diversity for a panel of gut commensals present across IBD patients and Controls. First, we found species-specific differences in genome-level bacterial diversity. Then, we found that certain genes and functions may harbor different levels and kinds of genetic divergence within the same species across IBD patients and Controls. Functions that were enriched in IBD with both neutral divergence and functional divergence were associated with motility and iron-scavenging, among others. These results may point toward functions that are under selection in the context of IBD stress and could inform future mechanistic work, exploring previously unknown routes of bacterial diversification and adaptation to stress in the gut microbiome.

IMPORTANCE: Inflammatory bowel disease (IBD) is characterized by profound alterations in the gut microbiome composition, and most research so far has focused on changes in species-level abundance to understand gut microbiome contributions to disease dynamics. However, investigating strain-level variation has the potential to uncover previously unknown factors underlying bacterial persistence during gut inflammation, hence revealing key aspects driving gut dysbiosis. Here, we showed that IBD is associated with species-specific changes in gut microbial population-level genetic diversity and identified individual genes and functions that seem to harbor differential genetic diversity within IBD-associated strains. More broadly, our results highlight how intra-species population- and gene-level diversity could be used as sensors of environmental stress in the gut microbiome, and further studies could follow up on the functions highlighted in this work to establish causal links between gut inflammatory conditions and processes of bacterial adaptation to stress.},
}

@article {pmid43002042,
year = {2026},
author = {Liu, S and Chen, W and Chen, L and Wang, Y and Zhou, L and Yin, Q and Wang, Z and Wang, D and Lu, Z},
title = {Targeted Dual-Responsive Probiotic Microspheres for Sequential Protection, Adhesion, and On-Demand Release in Ulcerative Colitis Therapy.},
journal = {Biomacromolecules},
volume = {27},
number = {11},
pages = {7377-7387},
doi = {10.1021/acs.biomac.6c01432},
pmid = {43002042},
issn = {1526-4602},
support = {52273060//National Natural Science Foundation of China (NSFC)/ ; },
mesh = {*Probiotics/administration & dosage/chemistry/pharmacology ; Animals ; *Microspheres ; *Colitis, Ulcerative/drug therapy/chemically induced/microbiology/pathology ; Mice ; Dextran Sulfate/toxicity ; Mice, Inbred C57BL ; Humans ; },
abstract = {Oral probiotics show promise for inflammatory bowel disease but are limited by poor gastrointestinal viability, targeting, and colonization. We developed a multi-targeting probiotic composite microsphere (PCM) via scalable solution blow-spinning, with >20-fold higher throughput than electrospinning. PCMs provide three key functions: (1) pH-triggered probiotic protection: PCMs contract in gastric acid, shielding probiotics and increasing survival 2162-fold over free probiotics; (2) charge-mediated adhesion: negatively charged microspheres adhere to positively charged mucin overexpressed at inflamed colonic lesions; and (3) enzyme-triggered release: overexpressed hyaluronidase degrades hyaluronic acid, releasing viable bacteria via the "Trojan horse" mechanism. This sequential mechanism ensures high local probiotic density at inflamed sites. In DSS-induced mouse colitis, PCMs outperformed 5-aminosalicylic acid in alleviating inflammation, repairing the mucosal barrier, and restoring microbial homeostasis. 16S rRNA sequencing showed selective enrichment of beneficial genera and suppression of inflammation-associated pathobionts. This scalable, multi-responsive platform offers next-generation oral therapy for IBD and microbiome-associated gastrointestinal diseases.},
}

*Probiotics/administration & dosage/chemistry/pharmacology
Animals
*Microspheres
*Colitis, Ulcerative/drug therapy/chemically induced/microbiology/pathology
Mice
Dextran Sulfate/toxicity
Mice, Inbred C57BL
Humans

@article {pmid43002081,
year = {2026},
author = {Irfan, B and Ghafarian, AM and Salahie, A and Shihabi, K and Ewidat, O and Riyad, N and Kamel, M and Khan, I and Tesfaye, B},
title = {Nutrition's Impact on Recovery in Craniofacial and Otorhinolaryngological Injuries: Considering Areas of Armed Conflict and Humanitarian Emergencies.},
journal = {The Journal of craniofacial surgery},
volume = {37},
number = {1-2},
pages = {383-388},
pmid = {43002081},
issn = {1536-3732},
mesh = {Humans ; *Armed Conflicts ; *Craniocerebral Trauma/physiopathology ; *Facial Injuries ; *Malnutrition/physiopathology/complications ; Emergencies ; *Neck Injuries ; Wound Healing/physiology ; *Nutritional Status ; Recovery of Function ; },
abstract = {Head-and-neck trauma can often create a double burden wherein metabolic demand surges just as oral intake is curtailed by pain, dysphagia, fixation, airway protection, and procedure-related restrictions. This article argues that nutrition often becomes the rate-limiting step of recovery in craniofacial and otorhinolaryngological injuries. We synthesize how the neuroendocrine stress-metabolic response drives hypercatabolism and immune activation, and how malnutrition can derail these adaptive programs by impairing collagen deposition, angiogenesis, leukocyte function, and the oral microbiome, and thereby raising the risk of infection and potentially delaying wound closure, speech, mastication, swallowing, and psychosocial reintegration. We then map some of the compounding effects of armed conflict and humanitarian crises, wherein the absence of robust medical and humanitarian aid and coupled with resource shortages, patients may be pushed into states of poorer health outcomes.},
}

Humans
*Armed Conflicts
*Craniocerebral Trauma/physiopathology
*Facial Injuries
*Malnutrition/physiopathology/complications
Emergencies
*Neck Injuries
Wound Healing/physiology
*Nutritional Status
Recovery of Function

@article {pmid43002096,
year = {2026},
author = {Radlinski, LC and Bäumler, AJ},
title = {Beyond association: pathogenesis models reveal ecological drivers of vaginal dysbiosis.},
journal = {Infection and immunity},
volume = {},
number = {},
pages = {e0028726},
doi = {10.1128/iai.00287-26},
pmid = {43002096},
issn = {1098-5522},
abstract = {Despite its critical importance to health, our understanding of the vaginal microbiome lags far behind other mucosal sites, reflecting both the distinct biology of the human vaginal microenvironment and the historic neglect of women's reproductive health in biomedical research. Recent investment in this area, coupled with the widespread use of high-throughput omics technologies, has greatly expanded our understanding of vaginal microbiota states and their associations with health and disease. However, associative studies that correlate community composition with clinical outcomes are limited in their ability to define causal, modifiable host-microbe relationships that support a protective microbiota. Consequently, broad probiotic strategies based on descriptive findings show limited success in restoring lasting homeostasis in the female reproductive tract. Murine infection models provide tractable systems for identifying evolutionarily conserved physiological processes that influence microbial growth. Here, we highlight studies across pathogenesis fields that leverage murine models to identify ecological factors controlling infection susceptibility in the vaginal microenvironment. Rather than treating pathogen colonization as an endpoint alone, we emphasize how genetically tractable microbes reveal the resources, barriers, and immune responses mediating microbial persistence, ascension, and inflammation. Where possible, we integrate these findings with clinical observations to assess their relevance to human reproductive health. Together, these studies illustrate how imperfect but tractable models reveal causal drivers of vaginal dysbiosis in women and help ground large-scale associative studies in a more clinically relevant way.},
}

@article {pmid43002309,
year = {2026},
author = {Jasur, R and Abdujalilovich, BS and Bakhodirjon, S and Narziyev, Z and Kamol, K},
title = {Microbiome-associated metabolites as emerging biomarkers of cancer immunotherapy response: from mechanistic networks to clinical validation.},
journal = {Folia microbiologica},
volume = {},
number = {},
pages = {},
pmid = {43002309},
issn = {1874-9356},
abstract = {Immune checkpoint blockade has improved outcomes across several cancers, yet many patients experience primary or acquired resistance. The gut microbiome may contribute to this variation through metabolic activities that influence systemic and tumor-associated immunity. This narrative review examines microbiome-associated metabolites as potential markers of immunotherapy response, with particular attention to their biological origins, immune effects, and clinical validation. We distinguish metabolites produced directly by microorganisms, such as fermentation-derived short-chain fatty acids and bacterial indoles, from host substrates transformed by microbial enzymes, including secondary bile acids. We also consider host-microbial co-metabolites and predominantly host- or tumor-derived mediators, such as kynurenine and CD39/CD73-generated adenosine, whose regulation may be influenced by the microbiome. Evidence concerning inosine, polyamines, and lipid mediators is interpreted according to their specific metabolic sources. These compounds have been linked to epithelial barrier function, antigen presentation, T-cell activity, and immunosuppressive signaling, although their effects vary across biological compartments and clinical settings. We examine the limitations of stool and circulating measurements, pre-analytical variability, metabolomic assays, and the distinction between mechanistic findings and clinically validated associations. Current evidence supports further investigation of selected metabolite signatures, but few have undergone independent clinical validation. Reliable biomarker development will require source-aware interpretation, standardized quantitative methods, longitudinal clinical studies, and evidence that metabolite measurements improve decisions about immunotherapy.},
}

@article {pmid43002367,
year = {2026},
author = {Tiwari, S and Bhattacharya, S},
title = {Sodium Butyrate: A Microbiota-Derived Short-Chain Fatty Acid Regulating Inflammation, Gut Barrier Function, and Colorectal Cancer Progression.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {43002367},
issn = {1867-1314},
abstract = {Colorectal cancer (CRC) is a polyetiologic disease related to genetic changes, chronic inflammation, dysregulation of the intestinal barrier, diet and gut microbiota dysbiosis. Butyrate is a short-chain fatty acid (SCFA) produced by the microbiota that plays a crucial role in energy metabolism, epithelial homeostasis and mucosal immunity. Sodium butyrate (NaB), the sodium salt of butyric acid, has therefore been the subject of experimental investigation and appears to be a therapeutic option of potential interest. This review critically explores the biological, pharmacological and translational significance of butyrate and NaB in CRC. It details the origins and physicochemical properties, pharmacokinetics, effects on the intestinal barrier, and interactions with the intestinal microbiota, alongside immunomodulatory actions, molecular pathways underlying anti-cancer efficacy, clinical evidence, and patent holdings, and further explores prospective formulation and delivery methods. Butyrate/NaB exerts pleiotropic effects via inhibition of HDAC and activation of free fatty acid receptors (FFARs), such as GPR41/FFAR3, GPR43/FFAR2 and GPR109A/HCAR2.These processes regulate various inflammatory and oncogenic signaling pathways, including NF-κB, NLRP3, Wnt/β-catenin, PI3K/Akt, MAPK, and STAT3, as well as mitochondrial metabolism, oxidative stress, cell-cycle progression, apoptosis, epithelial-mesenchymal transition, and immune-cell function. Additionally, butyrate helps preserve gut barrier function and can influence CRC biology by interacting with the tumour microenvironment, microbial metabolism, and epithelial cells. There is extensive preclinical evidence of the barrier-protective, anti-inflammatory, immunomodulatory, and anticancer properties of butyrate/NaB in cell- and animal-based models. The strength of evidence, however, depends on the model, concentration/dose, duration of treatment and endpoint. The mechanistic and preclinical results should therefore not be interpreted as being equivalent to actual clinical efficacy. There is limited available human evidence for specific therapeutic uses of CRC. Various factors limit its translational application, including rapid metabolism, a short biological half-life, and low systemic exposure, as well as inherent butyrate fluctuations, formulation challenges, and a scarcity of stringent clinical trials tailored to CRC. Colon-targeted delivery systems, microencapsulation, nanotechnology-based delivery systems, microbiome-directed interventions, patient selection by biomarkers, and rational combination strategies may overcome these limitations. Butyrate/NaB offers a promising multitarget strategy for CRC research; however, further investigation into its mechanisms, pharmacokinetics, dosing, formulation, and large-scale clinical trials is necessary to validate its therapeutic efficacy and define its translational potential.},
}

@article {pmid43002368,
year = {2026},
author = {Kshirsagar, S and Narwal, N and Rajendran, V and Vinchurkar, RV and Kelkar, S and Kadyan, S and Vishweswaraiah, RH and Vij, S and Pradhan, D},
title = {From Phenotype to Phylogenomics: Evolution of Lactobacillaceae Taxonomy, the 2020 Reclassification and its Technological and Regulatory Implications.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {43002368},
issn = {1867-1314},
abstract = {Lactic acid bacteria (LAB) are a diverse group of microorganisms with major importance in food fermentation, biopreservation, probiotic development, and biotechnology. Advances in molecular biology and whole-genome sequencing have revealed limitations of traditional phenotype-based classification, driving a transition toward genome-based taxonomy and fundamentally reshaping the classification of the family Lactobacillaceae. This review traces the evolution of LAB taxonomy from classical phenotypic classification through the molecular era to contemporary phylogenomic approaches. It examines the genomic methodologies underpinning modern bacterial systematics, including whole-genome sequencing, Average Nucleotide Identity (principally a species-level measure), Average Amino Acid Identity, and core-genome phylogenetics, which culminated in the landmark 2020 reclassification of the former genus Lactobacillus into 25 phylogenetically coherent genera. The review further evaluates the scientific evidence supporting this reclassification and its validation through subsequent phylogenomic, pangenomic, and ecological studies. Genome-based taxonomy has established a more evolutionarily coherent and biologically informative classification of Lactobacillaceae, improving our understanding of ecological adaptation, metabolic diversity, and functional potential. Genus-level taxonomy provides a useful framework for comparative research, but its predictive value is limited by the strain-specific nature of many functional and safety traits. The revised taxonomy has nevertheless strengthened comparative genomics, microbiome research, strain selection, and communication across scientific, industrial, and regulatory domains. Although the nomenclatural transition has created challenges for product labeling, regulatory documentation, database harmonization, and scientific communication, it provides a more robust evolutionary framework for future research and industrial innovation. Remaining challenges, including limitations of 16 S rRNA-based identification, uncertainty surrounding genomic thresholds, and incorporation of uncultured diversity through metagenomics and pangenomics, indicate that Lactobacillaceae taxonomy will continue to evolve as genomic resources and analytical approaches advance.},
}

@article {pmid43002640,
year = {2026},
author = {da Silva Santos, A and Teixeira, JP and Boiago, MM and Brancalion, CA and da Silva, AS and de Lima Neto, DF and da Rosa, JG and Bajay, MM},
title = {Temporal Dynamics of the Faecal Microbiota and Physiological Responses to Phytobiotics and Organic Acids in Broiler Chickens.},
journal = {Journal of animal physiology and animal nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1111/jpn.70126},
pmid = {43002640},
issn = {1439-0396},
support = {//Coordenação de Aperfeiçoamento de Pessoal de Nível Superior-Brasil (CAPES)/ ; },
abstract = {This study compared three alternative feed-additive blends with an antibiotic control to assess growth performance, physiological responses and age-related variation in the faecal microbiota of broiler chickens. A total of 240 male Cobb 500 broilers were allocated to four treatments with four replicate pens each: antibiotic control, organic acids (OA), plant extracts and essential oils (PE+EO), and essential oils combined with prebiotic/probiotic components and minerals (EO+PRE/PRO). Faecal bacterial profiles were assessed by 16S ribosomal RNA gene sequencing in 16 pooled libraries representing the four treatments at 7, 21, 35 and 42 days. Microbiome analyses were exploratory because only one library was available per treatment-age combination. Alpha diversity did not differ significantly by treatment or age. Permutational multivariate analysis of variance identified an age effect on Bray-Curtis community composition (R[2] = 0.312, p = 0.0139), but no treatment effect (R[2] = 0.201, p = 0.221). No genus showed a treatment effect after false-discovery-rate correction. Predicted functional analysis identified 31 pathways with a global age effect and no robust treatment effect. The PE + EO blend improved feed conversion relative to the antibiotic control during Days 1-21 and 1-35. Physiological, meat-quality and intestinal-morphometry responses varied among treatments. Thus, host responses to these additives occurred alongside predominantly age-associated faecal microbial variation; the data do not establish that microbiota changes mediated the host responses.},
}

@article {pmid43002692,
year = {2026},
author = {Margalida, A and Castellano-Hinojosa, A and Oliva-Vidal, P and Boutin, S and María Martínez, J and Braun, M and Sauer-Gürth, H and Schulze-Hagen, K and Wink, M},
title = {Host and anatomical filters prevent microbiome convergence in avian scavengers.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {47},
pages = {e2626358123},
doi = {10.1073/pnas.2626358123},
pmid = {43002692},
issn = {1091-6490},
support = {PID2022-142328OB-I00//Ministry of Science and Innovation/ ; },
mesh = {Animals ; *Microbiota ; Bacteria/classification/genetics ; *Falconiformes/microbiology ; Male ; Female ; Cloaca/microbiology ; *Host Microbial Interactions ; },
abstract = {How host-associated microbiomes assemble under intense environmental microbial exposure remains a central question in microbial ecology. Vultures represent a unique natural system because these species differ markedly in feeding ecology and carcass use. We characterized bacterial communities across four anatomical niches (facial, buccal, tracheal, and cloacal) in 155 individuals spanning all four European obligate vulture species (subfamily Gypaetinae: Gypaetus barbatus, Neophron percnopterus, and Aegypiinae: Aegypius monachus and Gyps fulvus) and the facultative scavenger Milvus milvus. Microbiome composition was jointly structured by host species and anatomical niche, with host identity explaining more variation than anatomical compartment and a significant interaction indicating that interspecific differentiation depended on body site. Each niche supported distinct bacterial assemblages and core microbiomes: Cloacal communities were enriched in anaerobic gut-associated taxa, whereas facial and tracheal communities contained more environmental and respiratory-associated bacteria. Host-specific taxonomic signatures persisted within anatomical niches despite recurrent exposure to the same carrion-associated microbial pool. Age further influenced community composition, whereas sex had little detectable effect. The facultative scavenger showed the same broad anatomical compartmentalization observed in obligate scavengers, although taxonomic signatures differed among species. Thus, sustained exposure to a shared, microbially rich resource was insufficient to produce a common scavenger microbiome. Instead, microbiome assembly reflected hierarchical filtering by host identity, anatomical environment, and ontogeny. These findings distinguish microbial exposure from microbial persistence, establishing avian scavengers as a natural model for understanding how host-associated communities remain differentiated, despite recurrent exposure to shared environmental microbial reservoirs across ecological and anatomical scales in vertebrate hosts.},
}

Animals
*Microbiota
Bacteria/classification/genetics
*Falconiformes/microbiology
Male
Female
Cloaca/microbiology
*Host Microbial Interactions

@article {pmid43002898,
year = {2026},
author = {Yu, X and He, J and Liu, M},
title = {Critical advances and translational bottlenecks of gut microbiota-gut-brain axis targeted therapy for neurodegenerative and neurodevelopmental disorders.},
journal = {Journal of neuroimmunology},
volume = {423},
number = {},
pages = {579117},
doi = {10.1016/j.jneuroim.2026.579117},
pmid = {43002898},
issn = {1872-8421},
abstract = {Neurological diseases have become a major global public health burden. Existing central nervous system-targeted therapies can only alleviate clinical symptoms but fail to halt the progression of neurodegenerative diseases, presenting mechanistic limitations and therapeutic bottlenecks. The gut microbiota participates in the regulation of central nervous system (CNS) homeostasis and neuropathological processes via the microbiota-gut-brain axis (MGBA). Notably, dysbiosis may induce damage to the blood-brain barrier, neurotransmitter dysregulation, and immune imbalance, thereby mediating the onset and progression of various neurological diseases, including Parkinson's disease, Alzheimer's disease (AD), autism spectrum disorder (ASD), and multiple sclerosis (MS). This article provides a systematic review of the core mechanisms by which the gut microbiome regulates neurological diseases, including inflammation regulation, oxidative stress responses, and neuroendocrine remodeling mediated by microbial metabolites. It also comprehensively summarizes the research progress, application advantages, and existing limitations of novel gut-targeted interventions, such as probiotics, prebiotics, fecal microbiota transplantation (FMT), dietary interventions, and live biological therapies. At the same time, the article critically examines key bottlenecks prevalent in the field: the causal relationship between the microbiota and disease remains unclear; there is a significant translational gap between animal and human studies; there is a lack of unified standards for multi-omics analysis systems; and interference from confounding factors such as age, diet, and medications is significant. Existing research indicates that gut microbiota interventions complement traditional symptomatic treatments and hold promising prospects for early disease intervention and adjunctive therapy for refractory patients. Future efforts should integrate multi-omics and artificial intelligence technologies to decipher the causal networks governing gut-central nervous system regulation, establish standardized research frameworks, advance the clinical translation of precision gut microbiota therapies, and provide new approaches for the comprehensive prevention, control, and personalized treatment of neurological disorders.},
}

@article {pmid43003072,
year = {2026},
author = {Kotlarova, A and Vlasak, J and Wald, M and Stolz, A},
title = {Skin Microbiome in Lymphatic Insufficiency And Lymphedema: A Systematic Review of Clinical Sequencing Studies.},
journal = {Lymphology},
volume = {59},
number = {3},
pages = {153-160},
pmid = {43003072},
issn = {2522-7963},
mesh = {Humans ; *Skin Microbiome ; *Lymphedema/microbiology ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Lymphatic insufficiency predisposes to chronic edema, barrier dysfunction, and recurrent cellulitis/erysipelas. Because the skin microbiome interacts with cutaneous immunity, dysbiosis may contribute to infectious complications and lymphatic insufficiency progression. We performed a PRISMA 2020-guided systematic review of studies indexed in PubMed/MEDLINE, Scopus, and Web of Science from inception to 31 December 2025. Studies included adult clinical studies that profiled the skin microbiome in lymphatic insufficiency/lymphedema using molecular methods (primarily 16S rRNA sequencing) and compared affected skin with contralateral sites and/or healthy controls. Four studies with 292 subjects met inclusion criteria and encompassed cancer‑related upper‑limb lymphedema and endemic lower‑limb lymph-edema (filarial lymphedema and podoconiosis). Methodological quality assessment using the Newcastle-Ottawa Scale demonstrated moderate-to-high quality across the included studies. All studies reported differences between affected and control skin, but no consistent taxonomic "signature" emerged. Reported changes included greater microbial heterogeneity, relative enrichment of potentially pathogenic taxa (notably Staphylococcus and Streptococcus), depletion of common commensals (Corynebacterium and Cutibacterium), and greater representation of anaerobes with increasing clinical severity. Standardized longitudinal studies are needed to establish causality and clinical utility.},
}

Humans
*Skin Microbiome
*Lymphedema/microbiology
RNA, Ribosomal, 16S/genetics

@article {pmid43003155,
year = {2026},
author = {Levin, G and Peláez-Vico, MÁ and Fichman, Y and Schuster, G and Mittler, R},
title = {H2O2 as a universal interspecies signaling molecule.},
journal = {Free radical biology & medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.freeradbiomed.2026.11.015},
pmid = {43003155},
issn = {1873-4596},
abstract = {Hydrogen peroxide (H2O2) plays a central role in cells, serving as important signal transduction molecule but also potentially causing oxidative stress, leading to cell death. Recent studies reveal that in addition to its many intracellular redox-driven signaling roles, H2O2 can mediate different cell-to-cell, organism-to-organism, and even interspecies communication, with major consequences for the health, symbiosis, and/or survival of the involved organisms. While new research has revealed some of the mechanisms and outcomes of interspecies H2O2 signaling, the effects of H2O2-driven interspecies communication routes on entire communities and ecosystems remain largely unknown. Here, we summarize current research on interspecies H2O2 signaling. We present examples from multiple biological systems to demonstrate the universality of H2O2/redox-driven communication mechanisms and discuss their effects on participating organisms. Finally, we highlight the potential contributions interspecies H2O2 signaling may have to communities and ecosystems and how studying interspecies H2O2 signaling can help us prevent long-term agricultural, ecological, and human health damages.},
}

@article {pmid43003303,
year = {2026},
author = {Ovaskainen, O and Łukasik, P and Roslin, T},
title = {Joint species distribution modelling of insect microbiota: Time to jump onto a new opportunity.},
journal = {Current opinion in insect science},
volume = {},
number = {},
pages = {101650},
doi = {10.1016/j.cois.2026.101650},
pmid = {43003303},
issn = {2214-5753},
abstract = {How microbes and insects influence each other is a topical question in insect science. With this contribution, we highlight joint species distribution models (JSDMs) - which model all microbial taxa in a community jointly rather than one at a time - as a statistical framework particularly well suited for resolving the drivers of host-microbe associations. While JSDM has been widely applied to microbiota of organisms other than insects, only a handful of studies have applied them thus far to insect systems. To encourage insect microbiota researchers to catch up with the benefits of JSDM, we outline the statistical and ecological basics of JSDM and give flesh to the modelling framework by reviewing how it has so far been applied to insect microbiota. We highlight the power of JSDMs in separating host, environmental and microbial drivers of community assembly, and in generating hypotheses about how different microbes influence each other. We further propose a predictive framework for identifying and characterizing five ecological categories of insect-associated microbes: (1) obligate nutritional symbionts; (2) facultative endosymbionts; (3) specialized gut associates; (4) transient microbes; and (5) pathogens and parasites. In particular, we hypothesize how the ecological characteristics of these different microbial categories are reflected in the statistical signatures recovered by JSDMs. We further suggest how JSDM can be applied to address the phylogenetic and ecological scales at which microbiome patterns are structured and to uncover how global environmental changes may reshape insect microbiota.},
}

@article {pmid43003314,
year = {2026},
author = {Xiang, J and Lian, B and Li, H and Bai, W and Wang, J},
title = {Valorization of livestock biogas slurry through indigenous Oocystis sp. cultivation for nutrient recovery and production of plant-beneficial biomass.},
journal = {Bioresource technology},
volume = {},
number = {},
pages = {136214},
doi = {10.1016/j.biortech.2026.136214},
pmid = {43003314},
issn = {1873-2976},
abstract = {Livestock biogas slurry contains abundant nitrogen and phosphorus resources, but requires effective strategies for nutrient recovery and high-value utilization. This study isolated an indigenous Oocystis sp. strain from livestock biogas slurry and evaluated its potential for coupling wastewater treatment with the production of value-added algal biomass. The nutrient-removal performance of Oocystis sp. in the sequential bacteria-microalgae coupling system was evaluated, while its growth, biochemical composition, and IAA-equivalent content were compared among different cultivation backgrounds. The sequential bacteria-Oocystis sp. coupling system achieved overall removal efficiencies of 96.68 %, 84.72 %, 72.07 %, and 87.13 % for PO4[3-]-P, total phosphorus, NH4[+]-N, and NO3[-]-N, respectively. Compared to BG11 cultivation, cultivation in microbially treated slurry increased soluble protein and IAA-equivalent contents of Oocystis sp. biomass by 57.60 % and 142.57 %, respectively. Furthermore, application of the Oocystis sp. culture produced in microbially treated slurry increased plant dry weight, root length, and root activity by 53.84 %, 44.13 %, and 154.18 %, respectively. Moreover, within the microbially treated slurry background, the WBO treatment was associated with altered rhizosphere bacterial community composition, and several WBO-enriched taxa showed positive correlations with plant growth traits. Therefore, indigenous Oocystis sp. cultivation provides a promising route for nutrient recovery from livestock biogas slurry and subsequent agricultural utilization of the resulting microalgal culture.},
}

@article {pmid43003693,
year = {2026},
author = {Niedobová, J and Wijacki, T and Faltýnková, A},
title = {Predator-associated microbiomes as hidden modulators of pesticide-compatible biological control in agroecosystems.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.71483},
pmid = {43003693},
issn = {1526-4998},
support = {RO1526//Ministerstvo Zemědělství/ ; },
abstract = {Beneficial arthropod predators are central components of integrated pest management, yet their performance in crop systems is often variable because predator efficacy depends on interactions among host traits, prey availability, intraspecific and interspecific interactions, pesticide exposure and environmental stressors. Predator-associated microbiomes, including gut microbiota, tissue-resident bacteria and facultative or obligate endosymbionts, represent an overlooked functional layer that may influence predator nutrition, stress physiology, reproduction, behaviour, dispersal and pesticide tolerance. This review synthesizes evidence from spiders, ladybird beetles, green lacewings, earwigs and predatory Heteroptera, with emphasis on traits that determine biological pest control under agroecosystem pressure. A central contribution is an evidence hierarchy that distinguishes descriptive, associative, experimental, mechanistic and field-level evidence. The strongest predator-specific associations currently come from spiders, where tissue-resident microbial assemblages have been linked to the spider insecticide survival, predicted detoxification pathways and physiological resilience under chemical stress; however, causal microbial mechanisms remain insufficiently tested. In other predator groups, microbiome-associated patterns suggest plausible microbial contributions to predator performance, but experimentally validated microbiome-mediated effects remain limited and are often inferred from symbiont surveys, diet-induced shifts in predator-associated microbiomes, reproductive manipulation and functional prediction. We argue that pest management research should move from descriptive microbiome profiling toward causal tests linking microbial taxa and functions to predator performance, pesticide compatibility and field-scale pest suppression. Incorporating microbiome information and experimentally validated microbial traits into ecotoxicology, mass rearing and conservation biological control could improve the reliability and resilience of predator-based pest suppression in agricultural landscapes. © 2026 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.},
}

@article {pmid43003811,
year = {2026},
author = {Kayongo, A and Bartolomaeus, TUP and Hecker, J and Birkner, T and Vila, E and Ntayi, ML and Markó, L and Löber, U and Olweny, G and Kyalo, E and Kyamulabi, D and Ndawula, J and Ssengooba, W and Nabatanzi, R and Kyobe, S and Nassali, F and Kigozi, E and Kalyesubula, R and Munana, R and Namaganda, J and Musiime, CJ and Sekibira, R and Bagaya, BS and Kateete, DP and Joloba, ML and Jjingo, D and Lusiba, J and Worodria, W and Mayanja-Kizza, H and Lalitha, R and Ham, W and Sanyu, I and Zawedde, J and Robertson, NM and Obondo, JS and Weidinger, C and Kunkel, D and Kirenga, BJ and Siddharthan, T and Hurst, JR and Checkley, W and Cookson, WB and Moffatt, MF and Forslund-Startceva, SK},
title = {Microbial ecological instability and non-linear host interactions shape airway inflammation in HIV-associated COPD.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {43003811},
issn = {2041-1723},
support = {R21TW012354//U.S. Department of Health & Human Services | NIH | Fogarty International Center (FIC)/ ; 3R21TW012354-S1/S2//U.S. Department of Health & Human Services | NIH | Fogarty International Center (FIC)/ ; K43TW013092//U.S. Department of Health & Human Services | NIH | Fogarty International Center (FIC)/ ; },
mesh = {Humans ; *Pulmonary Disease, Chronic Obstructive/microbiology/immunology/complications ; *HIV Infections/complications/microbiology/immunology ; Sputum/microbiology ; RNA, Ribosomal, 16S/genetics ; *Microbiota/genetics ; *Inflammation/microbiology ; Female ; Male ; Adult ; *Host Microbial Interactions/immunology ; Middle Aged ; Longitudinal Studies ; Cytokines/metabolism ; Multiomics ; Bronchoalveolar Lavage Fluid ; },
abstract = {Chronic obstructive pulmonary disease (COPD) is increasingly recognized among people living with HIV in sub-Saharan Africa, yet the mechanisms linking airway microbial ecology to chronic inflammation remain poorly understood. Here, we study 200 adults stratified by HIV and COPD status, including 160 participants with two-year longitudinal follow-up, using an integrated multi-omics framework combining sputum 16S rRNA profiling, bacterial outer membrane vesicle quantification, airway cytokine profiling, CyTOF immune phenotyping, bulk transcriptomics of induced sputum, bronchoalveolar lavage and peripheral blood, and bronchoalveolar lavage single-cell RNA sequencing-guided deconvolution. We find that sputum microbial communities are shaped predominantly by temporal ecological turnover rather than HIV or COPD status. Although microbial diversity, microbiome instability, outer membrane vesicle burden and inferred airway cellular composition remain largely preserved, HIV-associated COPD exhibits disease-specific microbial signatures together with inflammatory transcriptional remodeling concentrated in induced sputum. Integrated analyses identify selective host-microbe interaction networks linking discrete microbial taxa with inflammatory, immune and transcriptional programmes.},
}

Humans
*Pulmonary Disease, Chronic Obstructive/microbiology/immunology/complications
*HIV Infections/complications/microbiology/immunology
Sputum/microbiology
RNA, Ribosomal, 16S/genetics
*Microbiota/genetics
*Inflammation/microbiology
Female
Male
Adult
*Host Microbial Interactions/immunology
Middle Aged
Longitudinal Studies
Cytokines/metabolism
Multiomics
Bronchoalveolar Lavage Fluid

@article {pmid43003812,
year = {2026},
author = {Kong, L and Wenyue, M and Tingting, L and Jiani, W and Ziyi, L and Yongfang, L and Jingqi, Y and Qinmiao, Y and Yingting, L},
title = {The gut microbiota dietary index reveals a modifiable diet-depression association varying by BMI and possibly linked to inflammation: a hypothesis-generating modified diet for future intervention research.},
journal = {Translational psychiatry},
volume = {16},
number = {1},
pages = {},
pmid = {43003812},
issn = {2158-3188},
mesh = {Humans ; Female ; *Inflammation ; *Gastrointestinal Microbiome/physiology ; Male ; *Diet ; Cross-Sectional Studies ; *Depression/microbiology ; *Body Mass Index ; Adult ; Middle Aged ; },
abstract = {In the context of the microbiota-gut-brain axis, diet represents a critical yet still debated component of translational psychiatry. However, population-based evidence linking microbiota-supportive dietary patterns to depressive symptoms remains limited. This research leverages the Dietary Index for Gut Microbiota (DI-GM) to examine the associations between a gut-microbiota-friendly diet and depression, providing a theoretical framework for future research on practical applications. Using data from 28,884 adults, this cross-sectional study evaluated the association between DI-GM and PHQ-9 using survey-compatible descriptive and conventional regression analyses, ordinary-weighted generalized additive models (GAMs), XGBoost with SHAP for exploratory feature ranking, and an exploratory mediation-type analysis of systemic inflammation. Participants with depression had lower DI-GM scores than those without depression. Model-based analyses suggested an inverse predicted pattern between DI-GM and PHQ-9, especially with the interaction GAM indicating significant BMI-related heterogeneity (a more pronounced inverse association at higher BMI). XGBoost with SHAP analyses identified fiber, refined grains, percent energy from fat and whole grains as dietary features with relatively larger contributions to model predictions. Exploratory mediation-type analysis suggested that inflammation may partially explain the DI-GM-PHQ-9 association. However, a high DI-GM diet lacks depression-related nutrients like vitamin D, omega-3 fatty acids, and zinc. Based on these hypothesis-generating findings, we propose a conceptual framework for a Modified Gut Microbiota-Friendly Diet (MGFD) with high DI-GM score, caloric control, and targeted nutrient supplementation, requiring validation via prospective cohorts, randomized trials, and gut microbiome/metabolomic studies.},
}

Humans
Female
*Inflammation
*Gastrointestinal Microbiome/physiology
Male
*Diet
Cross-Sectional Studies
*Depression/microbiology
*Body Mass Index
Adult
Middle Aged

@article {pmid43003844,
year = {2026},
author = {Wang, Y and Xu, X and Chen, X and Zhang, Y and Zheng, W and Zhang, T},
title = {Scellmate enables contamination aware curation and host mobilome linkage analysis of large SAG datasets.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {43003844},
issn = {2041-1723},
support = {17212124//Research Grants Council, University Grants Committee (RGC, UGC)/ ; },
mesh = {*Genome, Bacterial/genetics ; *Microbiota/genetics ; Single-Cell Analysis/methods ; Metagenome/genetics ; *Bacteria/genetics/classification ; *Data Curation/methods ; Biocuration ; Metagenomics/methods ; Phylogeny ; },
abstract = {Single-cell genomics enables cell-resolved insights into in-situ microbial communities, yet single amplified genomes (SAGs) are often fragmented, taxonomically ambiguous, and prone to contamination, limiting their biological interpretation. Here, we present Scellmate, a scalable, semi-supervised framework that integrates whole-SAG curation, species-level taxonomic anchoring and SAG-mobilome linkage analysis for large-scale SAG datasets. Following benchmarking of its SAG curation and SAG-eMGE linkage modules using in silico and four-strain mock SAG datasets, respectively, Scellmate was applied to 11,976 sewage-derived SAGs. This approach yielded 4,198 SAGs passing Scellmate's whole-SAG curation, which captured pronounced heterogeneity masked by bulk methods. At the species level, we resolved extensive hidden diversity within abundant taxa such as Aliarcobacter that was unresolved by matched metagenome-assembled genomes; at the strain level, we pinpointed a distinct Agathobacter rectalis cluster carrying specialized carbon-utilization pathways, suggesting niche differentiation. Leveraging these curated SAGs, we identified 6,474 host-mobilome linkages across 2,378 SAGs; these linkages not only showed high concordance with host-association data within the Integrated Microbial Genomes (IMG) system but also significantly expanded species-level host assignments. Furthermore, we detected frequent inter-species sharing patterns of diverse cryptic plasmids within the order Bacteroidales. Together, this work demonstrates that high-throughput single-cell genomics, empowered by the robust framework, resolves fine-scale heterogeneity and host-mobilome dynamics, advancing culture-independent microbiome research.},
}

*Genome, Bacterial/genetics
*Microbiota/genetics
Single-Cell Analysis/methods
Metagenome/genetics
*Bacteria/genetics/classification
*Data Curation/methods
Biocuration
Metagenomics/methods
Phylogeny

@article {pmid43003899,
year = {2026},
author = {Kumpitsch, C and Bauer, E and Arora, B and Schmitz, RA and Moissl-Eichinger, C},
title = {The mammalian archaeome: diversity, function and emerging roles in health and disease.},
journal = {Nature reviews. Microbiology},
volume = {},
number = {},
pages = {},
pmid = {43003899},
issn = {1740-1534},
abstract = {Archaea are a fundamental yet historically overlooked part of the mammalian microbiome. Once thought to be limited to extreme environments, archaea, particularly methanogenic archaea, are now recognized as widespread colonizers of mammalian hosts, with key roles in gut metabolism, microbial syntrophy and host interaction. In this Review, we summarize current knowledge on the distribution, diversity and function of the mammalian archaeome, with a focus on humans and ruminants. We explore the ecological and physiological roles of Methanobrevibacter spp. as key gastrointestinal colonizers, archaeal interactions with bacterial communities and the host, and the impact of external factors such as diet, age and health status on the archaeome. We further highlight the translational potential of archaeome research, including methane mitigation strategies in cattle and emerging associations between the archaeome and human disease. By integrating insights across host species, we argue that understanding the archaeome is essential to fully comprehend mammalian microbiome function, evolution and its relevance to health and disease.},
}

@article {pmid43003900,
year = {2026},
author = {Javaid, N and Mateeva, T},
title = {The microbiome's voyage beyond Earth.},
journal = {Nature reviews. Microbiology},
volume = {},
number = {},
pages = {},
pmid = {43003900},
issn = {1740-1534},
}

@article {pmid43004013,
year = {2026},
author = {Scholten, J and El Aater, K and Bakker, CMD and Stockmann, HBAC and van Egmond, M and Kazemier, G and Tuynman, JB and Oosterling, SJ},
title = {Oral antibiotic prophylaxis in colorectal surgery and perioperative microbiota composition: a systematic review.},
journal = {International journal of colorectal disease},
volume = {41},
number = {1},
pages = {},
pmid = {43004013},
issn = {1432-1262},
support = {Uit2023/ad/2023.10//Spaarne Gasthuis Academie/ ; },
mesh = {Humans ; *Antibiotic Prophylaxis ; Colorectal Surgical Procedures ; Administration, Oral ; *Gastrointestinal Microbiome/drug effects ; *Anti-Bacterial Agents/administration & dosage ; Surgical Wound Infection/prevention & control/microbiology ; },
abstract = {PURPOSE: Oral antibiotic bowel prophylaxis (OAP) is used to reduce infectious complications in colorectal surgery, but its effects on perioperative gut microbiota composition remain unclear. This systematic review evaluated the impact of OAP on intestinal microbiota composition in adults undergoing colorectal surgery.

METHODS: A systematic search of PubMed, Cochrane Library, and Google Scholar was conducted up to November 18th, 2025, following PRISMA guidelines. Studies were eligible if they included adult colorectal surgery patients receiving OAP and reported microbiota composition using 16S rRNA sequencing and/or qPCR. Primary outcomes were changes in microbial diversity and taxonomic composition. Secondary outcomes were surgical site infection (SSI) and anastomotic leakage (AL).

RESULTS: Eleven studies involving over 1500 microbiota samples met inclusion criteria. OAP regimens varied widely in agents, duration, and combination with mechanical bowel preparation (MBP) or probiotics. Across studies, OAP consistently reduced microbial diversity and altered taxonomic composition, some shifts, such as increased Enterococcus or decreased Bacteroides, persisted postoperatively. Only a minority of studies assessed microbiota recovery beyond the early postoperative phase. Clinical outcomes such as SSI and anastomotic leakage were inconsistently reported, with limited direct correlations to microbiota data.

CONCLUSION: OAP substantially alters perioperative gut microbiota composition in colorectal surgery patients. Heterogeneity in sampling, analysis, and clinical correlation limits definitive conclusions. Standardized study designs are needed to clarify the relationship between OAP and microbiota composition changes.},
}

Humans
*Antibiotic Prophylaxis
Colorectal Surgical Procedures
Administration, Oral
*Gastrointestinal Microbiome/drug effects
*Anti-Bacterial Agents/administration & dosage
Surgical Wound Infection/prevention & control/microbiology

@article {pmid43004014,
year = {2026},
author = {Unno, T and Choi, G and Hwang, H and Cheon, NJ and Jeong, SE and Lee, TW and Kim, K and Park, S and Seo, J and Kang, JY and Choi, YS and Ahn, US and Kim, L and Han, D and Kim, SS and Jang, J},
title = {Ecological Variation in Bacterial Community Composition and Zoonotic Genus Distribution Across Body Sites, Host Species, and Seasonal Life-History Stages in Insectivorous Bats.},
journal = {Microbial ecology},
volume = {89},
number = {1},
pages = {},
pmid = {43004014},
issn = {1432-184X},
support = {NIE-B-2024-38//National Institute of Ecology/ ; No. 2022R1C1C1003384//National Research Foundation of Korea/ ; },
mesh = {Animals ; *Chiroptera/microbiology/physiology ; *Bacteria/classification/isolation & purification/genetics ; Seasons ; RNA, Ribosomal, 16S/genetics ; *Microbiota ; Phylogeny ; Skin Microbiome ; Republic of Korea ; Zoonoses/microbiology ; Feces/microbiology ; },
abstract = {Bats harbour diverse genera containing zoonotic species, yet whether colonisation by these genera reflects stable host-microbe associations or transient environmental exposure remains unresolved. We propose that bat bacterial communities are shaped by three axes of variation: body site defines the microbial niche, host species imposes ecological and phylogenetic constraints, and seasonal life-history transitions alter exposure regimes. We tested four predictions: (1) each body site would (2) host species would show different bacterial profiles associated with differences in roosting ecology, colony density, and foraging behavior; (3) active and hibernation periods would differ in community structure and predicted metabolic function; and (4) zoonotic genera would show predominantly transient detection across years within individuals. Using 16 S rRNA gene amplicon sequencing of 2,747 oral, skin, and gut (stool) samples from eight insectivorous bat species across four seasons (2021-2024) in South Korea, all four predictions were supported. Body site was the strongest determinant of community structure: mean zoonotic genus relative abundance was 10-fold higher in gut (6.91%) than in oral samples (0.69%), dominated by Helicobacter and Chlamydia, while skin carried Rickettsia and Bartonella. Host species structured oral communities most strongly (PERMANOVA R[2] = 0.295), with interspecific variation in zoonotic genus composition. PICRUSt2 predicted that hibernation-associated oral taxa were enriched in fatty acid β-oxidation pathway genes, paralleling the host's metabolic switch from carbohydrate to lipid catabolism during torpor. Longitudinal tracking of 80 recaptured individuals over 2-3 years confirmed predominantly transient carriage, supporting seasonal environmental acquisition rather than chronic colonisation.},
}

Animals
*Chiroptera/microbiology/physiology
*Bacteria/classification/isolation & purification/genetics
Seasons
RNA, Ribosomal, 16S/genetics
*Microbiota
Phylogeny
Skin Microbiome
Republic of Korea
Zoonoses/microbiology
Feces/microbiology

@article {pmid43004160,
year = {2026},
author = {Ndiaye, PA and Saidi, R and Sellami, W and Ibnyasser, A and Kadmiri, IM and Idbella, M and Houasli, C and Daoui, K and Bargaz, A},
title = {Chickpea responsiveness to contrasting P fertilization reveals agro-physiological and genotypic variability in P use efficiency and rhizosphere microbial communities.},
journal = {BMC plant biology},
volume = {26},
number = {1},
pages = {},
pmid = {43004160},
issn = {1471-2229},
mesh = {*Cicer/genetics/microbiology/growth & development/metabolism/physiology ; *Rhizosphere ; *Phosphorus/metabolism ; Genotype ; Soil Microbiology ; *Fertilizers ; *Microbiota ; },
abstract = {BACKGROUND: Phosphorus (P) is crucial for grain legumes including chickpea, however P use efficiency (PUE) for both chickpea symbiosis and plant growth strongly relies on chickpea genotypic variability and responsiveness to contrasting P conditions including source, availability and application rate. In this study, three winter Moroccan chickpea (Cicer arientinum L.) varieties (Arifi, Bochra and Taounate) were assessed for plant growth, PUE and rhizosphere soil-associated microbiome composition under both available "ortho-P" and unavailable P sources (rock-P) at increasing rates (0, 40, 80 and 120 kg P2O5 ha[- 1]).

RESULTS: Chickpea growth traits related to shoot dry weight (SDW), leaf area index (LAI), branches number and plant height were significantly enhanced under ortho-P (120 kg ha[- 1]). The highest pod DW (PDW) (108%) and Harvest Index (HI) (55%) were obtained under rock-P (120 kg ha[- 1]) as compared to unfertilized treatment, which is the case of Taounate variety that exhibited the highest PDW (2.33 g plant[- 1]), pod number (9.5 per plant), LAI (321), high PUE and P harvest index (PHI) as a consequence of improved root traits (biomass, length and surface-area). Meanwhile, Bochra variety responded more favorably to rock-P (40, 80 and 120 kg ha[- 1]) showing a higher PUE concomitantly to a lower root traits. Furthermore, chickpea varieties and P sources influenced the rhizosphere-associated microbial community with a notable abundance of Actinobacteria under rock-P in Bochra variety and Chytridiomycota phylum in Taounate variety under ortho-P, while Bochra and Arifi varieties had more Basidiomycota and Mortierellomycota under ortho-P.

CONCLUSIONS: Findings revealed that ortho-P-fertilized Taounate and rock-P-fertilized Bochra exhibited high PUE and yielded superior agro-physiological performance concomitantly with specific rhizosphere microbial modifications. Such a genotype-P specific pattern indicates a differential responsiveness to P fertilization suggesting tight relationships between chickpea genotypic diversity, responsiveness to P and modulation of the rhizosphere microbiota that needs to be deciphered.},
}

*Cicer/genetics/microbiology/growth & development/metabolism/physiology
*Rhizosphere
*Phosphorus/metabolism
Genotype
Soil Microbiology
*Fertilizers
*Microbiota

@article {pmid43004180,
year = {2026},
author = {Aldeyarbi, S and Elhanafy, E and Saber-Ayad, M and Abu Almaaty, AH and Sagheer, A and Hassan, MK},
title = {Molecular mechanisms of colorectal cancer: from carcinogenesis and molecular classification to targeted therapy.},
journal = {Molecular medicine (Cambridge, Mass.)},
volume = {32},
number = {1},
pages = {},
pmid = {43004180},
issn = {1528-3658},
support = {23_828//ARICA/ ; },
mesh = {Humans ; *Colorectal Neoplasms/etiology/metabolism/genetics/diagnosis/therapy/pathology/drug therapy ; Molecular Targeted Therapy ; Tumor Microenvironment ; Animals ; *Carcinogenesis/genetics ; Biomarkers, Tumor ; Chromosomal Instability ; Microsatellite Instability ; Cell Transformation, Neoplastic/genetics/metabolism ; Gene Expression Regulation, Neoplastic ; DNA Methylation ; },
abstract = {Colorectal cancer (CRC) is a heterogeneous disease that results from the progressive accumulation and interactions at multiple levels of genetic alterations, which lead to the transformation of normal colonic epithelium into malignant colorectal tumors. Understanding the molecular basis of CRC pathogenesis, together with the interactions between genetic alterations, epigenetic modifications, environmental and lifestyle factors, is essential for improving prevention, diagnosis, prognosis, and treatment strategies. This review aims to provide a critical reference point for understanding the temporal dynamics of colorectal carcinogenesis, the evolution of molecular classification systems, including their computational and machine-learning foundations and emerging image-based prediction approaches, molecular drivers and the tumor microenvironment (TME) of CRC by summarizing the most investigated molecular pathways involved in CRC pathogenesis and their role as biomarkers for early CRC diagnosis based on the three main molecular mechanisms of colorectal carcinogenesis: chromosomal instability (CIN), microsatellite instability (MSI), and CpG island methylator phenotype (CIMP). Importantly, emerging evidence reveals that the TME acts as an important factor in driving CRC progression by regulating the immune system through dynamic cellular and molecular interactions. In particular, tumor metabolic reprogramming and microbiota-driven alterations act as major drivers of therapy resistance and immune escape. Combining these mechanisms will enhance biomarker discovery and aid in developing precision medicine for patients with CRC. This review also highlights the regulatory roles of key signaling pathways, including Wnt/β-catenin, epidermal growth factor receptor (EGFR), tumor protein p53 (TP53), and transforming growth factor-beta (TGF-β) signaling, during CRC initiation and progression, while further addressing current targeted therapies and emerging precision-based and experimental therapeutic strategies.},
}

Humans
*Colorectal Neoplasms/etiology/metabolism/genetics/diagnosis/therapy/pathology/drug therapy
Molecular Targeted Therapy
Tumor Microenvironment
Animals
*Carcinogenesis/genetics
Biomarkers, Tumor
Chromosomal Instability
Microsatellite Instability
Cell Transformation, Neoplastic/genetics/metabolism
Gene Expression Regulation, Neoplastic
DNA Methylation

@article {pmid43004182,
year = {2026},
author = {Luo, G and Pan, Z and Yu, T and Xie, Y and Liu, Q and Yang, X and Yan, Z and Xia, C and Su, J},
title = {Altered circulating blood microbiota in unexplained recurrent spontaneous abortion.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {43004182},
issn = {1471-2180},
support = {2220001004427//Foshan Self-funded Science and Technology Innovation Projects/ ; 2024LZ-B1001//Guangdong Provincial Medical Association Clinical Research Fund/ ; },
mesh = {Humans ; Female ; *Microbiota/genetics ; RNA, Ribosomal, 16S/genetics ; Pregnancy ; *Abortion, Habitual/microbiology/blood ; Adult ; Cytokines/blood ; *Dysbiosis/microbiology/blood ; *Bacteria/classification/genetics/isolation & purification ; },
abstract = {BACKGROUND: The etiology of unexplained recurrent spontaneous abortion (URSA) remains poorly understood. Emerging evidence implies that URSA is closely related to dysbiosis of the symbiotic microbiota, while the characteristics of blood microbiome in URSA remain unclear.

METHODS: In the present preliminary exploratory study, 20 patients with URSA and 11 healthy postpartum controls were enrolled for blood microbiome analysis by full-length 16 S rRNA gene sequencing and cytokines profiling by Luminex assay.

RESULTS: It was found that although alpha diversity was similar between the two groups, beta diversity analysis revealed a significantly distinct overall microbiota structure in URSA patients. It was found that Blautia wexlerae was remarkably enriched in URSA, while Hydrogenophaga sp. HaHa333 and Zoogloea resiniphila were significantly depleted. Co-occurrence network analysis by topological properties suggested a more pronounced compartmentalized structure with stronger intra‑module associations within the blood microbiome of URSA as indicated by the higher modularity index, which exhibited a predominantly positive and monotonous correlation pattern. Concurrently, the decreased IL-1β and IL-8 in serum co-existed with enrichment of B. wexlerae in URSA. However, IL-27 and IL-13 was elevated, and the level of IL-27 was negatively associated with the URSA-depleted H. sp. HaHa333.

CONCLUSIONS: In this proof-of-concept investigation, it is the first time to systematically characterize the blood microbiome in URSA patients with cross-sectional clinical observation. These hypothesis-generating findings suggested that URSA is associated with a distinct blood microbiota and an altered cytokine profile, which requires future large-scale validation.},
}

Humans
Female
*Microbiota/genetics
RNA, Ribosomal, 16S/genetics
Pregnancy
*Abortion, Habitual/microbiology/blood
Adult
Cytokines/blood
*Dysbiosis/microbiology/blood
*Bacteria/classification/genetics/isolation & purification

@article {pmid43004363,
year = {2026},
author = {Trivett, H and Dalby, MJ and Peel, N and Heavens, D and Kiu, R and Acuna-Gonzalez, A and Mohamad, M and Humayun, G and Leggett, RM and Patel, VC and Hall, LJ},
title = {Decoding the microbiome and resistome of advanced chronic liver disease through long-read metagenomics.},
journal = {Genome medicine},
volume = {18},
number = {1},
pages = {},
pmid = {43004363},
issn = {1756-994X},
support = {BBX011089/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; BB/R012490/1; BB/X011054/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; 220876/Z/20/Z/WT_/Wellcome Trust/United Kingdom ; },
mesh = {Humans ; *Metagenomics/methods ; Metagenome ; *Gastrointestinal Microbiome ; *Microbiota ; Liver Cirrhosis/microbiology ; Chronic Disease ; Male ; Female ; Enterococcus faecium/genetics ; Acute-On-Chronic Liver Failure/microbiology ; Drug Resistance, Bacterial/genetics ; Bacteria/genetics ; *Liver Diseases/microbiology ; Middle Aged ; },
abstract = {BACKGROUND: Patients with advanced chronic liver disease (ACLD) and underlying cirrhosis frequently require repeated courses of antimicrobial therapy, with both the frequency and spectrum of antimicrobial exposure increasing alongside disease progression. In this population, impaired immune function and increased intestinal barrier dysfunction contribute to a heightened susceptibility of multidrug-resistant bacterial infections.

METHODS: To comprehensively characterise the gastrointestinal microbiome and antimicrobial resistance gene (ARG) landscape across the clinical spectrum of ACLD, and to identify microbial and resistome signatures associated with disease severity, we employed long-read metagenomic sequencing (Oxford Nanopore Technologies) to profile the gastrointestinal microbiome and resistome in patients with acute-on-chronic liver failure (ACLF), decompensated cirrhosis (DC), and stable cirrhosis (SC), compared to healthy controls (HC).

RESULTS: ACLF patients showed marked enrichment of Enterococcus faecium, with six of 28 samples showing >95% relative abundance, highlighting its potential as a bacterial biomarker of advanced cirrhosis. We reconstructed 28 high-quality metagenome-assembled genomes (MAGs) of E. faecium from cirrhosis patients, 17 from ACLF cases. E. faecium dominance was associated with substantially reduced microbial diversity and a marked depletion of key commensal taxa, including Blautia, Akkermansia, Faecalibacterium, and Bifidobacterium. Consistent with these compositional shifts, resistome analysis revealed significant enrichment of clinically relevant antimicrobial resistance genes (ARGs) in DC and ACLF, including determinants conferring resistance to aminoglycosides, beta-lactams, and glycopeptides, consistent with prior antimicrobial exposure.

CONCLUSION: Long-read metagenomics enables high-resolution characterisation of microbial and resistome dynamics across ACLD severities. By capturing taxonomic shifts, functional potential, and ARG enrichment, this approach provides valuable insights into microbiome trajectories linked with disease severity, informing mechanistic research and potential clinical interventions.},
}

Humans
*Metagenomics/methods
Metagenome
*Gastrointestinal Microbiome
*Microbiota
Liver Cirrhosis/microbiology
Chronic Disease
Male
Female
Enterococcus faecium/genetics
Acute-On-Chronic Liver Failure/microbiology
Drug Resistance, Bacterial/genetics
Bacteria/genetics
*Liver Diseases/microbiology
Middle Aged

@article {pmid43004378,
year = {2026},
author = {Liu, W and Zhang, H and Zhang, L and Wang, W and Liu, B and Li, R and Yao, Y and Xie, L},
title = {Bacterial lipopolysaccharide mediates the interplay between tumor microbiome and immune microenvironment in breast cancer: development of a prognostic risk score.},
journal = {Breast cancer research : BCR},
volume = {28},
number = {1},
pages = {},
pmid = {43004378},
issn = {1465-542X},
support = {ZDXK202233//Jiangsu Provincial Medical Key Discipline/ ; 2022-LCYJ-DBZ-07//Nanjing Drum Tower Hospital/ ; NDYGN2023030//Project of Chinese Hospital Reform and Development Institute, Nanjing University/ ; },
mesh = {*Tumor Microenvironment/immunology ; *Lipopolysaccharides/metabolism/immunology ; Female ; *Breast Neoplasms/immunology/microbiology/pathology/genetics/mortality ; Humans ; Prognosis ; Animals ; *Microbiota/immunology ; Mice ; Biomarkers, Tumor/genetics ; Gene Expression Regulation, Neoplastic ; },
abstract = {BACKGROUND: The immunosuppressive microenvironment of breast cancer drives a 'cold' tumor phenotype characterized by limited immune cell infiltration and poor response to immunotherapy. While intratumoral microbiota and circulating lipopolysaccharide (LPS) have the potential to remodel immunity, the specific mechanisms and prognostic impact of LPS-driven immunomodulation in breast cancer remain unclear.

METHODS: We utilized the Comparative Toxicogenomics Database (CTD) to systematically identify LPS-related genes. Prognosis-associated LPS-related genes (PALRGs) were identified via Cox regression analyses. Subsequently, we applied LASSO-Cox regression to construct an LPS-related risk score (LPSRS) and evaluated its predictive performance and associations with immune microenvironment characteristics in TCGA-BRCA (n = 1,196) and GEO (n = 525) cohorts. For further validation, we recruited an independent clinical cohort of 56 breast cancer patients and confirmed differential expression of LPSRS genes and tumor microenvironment (TME) heterogeneity between high- and low-risk groups. We integrated RNA sequencing with 2bRAD-M sequencing to explore potential interactions between the tumor microbiome and host gene expression. Finally, we conducted mechanistic validation using 4T1 tumor-bearing mice, with treatment groups receiving either Pseudomonas. putida or purified LPS.

RESULTS: We identified 26 PALRGs and constructed an 8-gene LPSRS signature as Risk Score which demonstrated strong prognostic performance (C-index = 0.750, 95% CI 0.712-0.788) across multiple independent cohorts and our clinical cohort. Notably, low-risk patients exhibited significant Pseudomonas enrichment (median abundance: 4.3% vs. 2.4%, P = 0.04). Correlation analysis revealed significant associations between Pseudomonas abundance and transcriptome (P = 6.36 × 10[-6]). In mechanistic validation experiments, Pseudomonas-treated mice showed an significant reduction in tumor volume (P = 0.0009), accompanied by a 2- fold increase in M1 macrophage polarization (P < 0.0001), confirming the beneficial remodeling of the TME.

CONCLUSIONS: Intratumoral microbiota-related LPS is associated with microbiome-immunity crosstalk in breast cancer. LPSRS serves as a promising prognostic marker with therapeutic insights.},
}

*Tumor Microenvironment/immunology
*Lipopolysaccharides/metabolism/immunology
Female
*Breast Neoplasms/immunology/microbiology/pathology/genetics/mortality
Humans
Prognosis
Animals
*Microbiota/immunology
Mice
Biomarkers, Tumor/genetics
Gene Expression Regulation, Neoplastic