@article {pmid40815107,
year = {2026},
author = {Vitiello, F and Vivaldi, C and Rimini, M and Prinzi, FL and Rizzato, MD and Saborowski, A and Antonuzzo, L and Rossari, F and Satake, T and Peeters, F and Salani, F and Pressiani, T and Lucchetti, J and Kim, JW and Abidoye, O and Rapposelli, IG and Gallio, C and Tamberi, S and Finkelmeier, F and Giordano, G and Pircher, C and Chon, HJ and Braconi, C and Qaisar, A and Pastorino, A and Castet, F and Tamburini, E and Yoo, C and Parisi, A and Diana, A and Scartozzi, M and Prager, GW and Avallone, A and Schirripa, M and Kim, IH and Perkhofer, L and Oneda, E and Verrico, M and Couto, N and Adeva, J and Chan, SL and Spinelli, GP and Personeni, N and Garajova, I and Rodriguez, MG and Leo, S and Alvim, CM and Roque, R and Farinea, G and Genovesi, V and De Rosa, A and Lavacchi, D and Camera, S and Ikeda, M and Dekervel, J and Niger, M and Balsano, R and Tonini, G and Kang, M and Tesini, G and Esposito, L and Boccancino, A and Himmelsbach, V and Landriscina, M and Ahcene Djaballah, S and Bekaii-Saab, T and Masi, G and Vogel, A and Lonardi, S and Fornaro, L and Rimassa, L and Casadei-Gardini, A},
title = {Impact of Antibiotic Therapy in Patients with Cholangiocarcinoma Treated with Chemoimmunotherapy.},
journal = {Oncology},
volume = {104},
number = {5},
pages = {575-591},
doi = {10.1159/000546856},
pmid = {40815107},
issn = {1423-0232},
mesh = {Humans ; Female ; Male ; Aged ; Middle Aged ; *Anti-Bacterial Agents/therapeutic use/administration & dosage ; *Cholangiocarcinoma/drug therapy/mortality/pathology ; Prognosis ; *Bile Duct Neoplasms/drug therapy/mortality/pathology ; Immunotherapy/methods ; Aged, 80 and over ; Progression-Free Survival ; Retrospective Studies ; Immune Checkpoint Inhibitors/therapeutic use ; Adult ; },
abstract = {INTRODUCTION: Patients with biliary tract cancers (BTCs) often require antibiotic therapy before starting systemic treatment that includes an immune checkpoint inhibitor. This study aimed to evaluate the prognostic impact of antibiotic therapy administered in the 15 days prior to the start of chemoimmunotherapy in patients with BTC.

METHODS: The study population included patients with metastatic or locally advanced BTC from Western and Eastern populations treated with first-line chemoimmunotherapy. The aim of the study was to evaluate the impact of antibiotic therapy in the 15 days prior to starting oncological treatment (AT population) compared to patients who did not receive antibiotic therapy (NAT). Univariate and multivariate analyses were used to evaluate predictive factors for overall survival (OS) and progression-free survival (PFS), while prognostic factors were analyzed by univariate and multivariate analysis using Cox regression model.

RESULTS: A total of 666 patients were enrolled in the study: 93 (14%) in AT cohort and 573 (86%) in NAT cohort. In the AT population, the incidence of cholangitis (p = 0.0017), alanine aminotransferase elevation (p = 0.0009), fever (p = 0.0021), decreased appetite (p = 0.0007), itching (p = 0.0081), and rash (p = 0.012) was significantly higher compared to the NAT. The median OS was 15.9 months (95% confidence interval [CI]: 13.8-18.3) in NAT cohort versus 10.1 months (95% CI: 7.9-12.4) in AT cohort (NAT vs. AT, hazard ratio [HR]: 0.43, 95% CI: 0.27-0.70, p = 0.0006), while median PFS was 8.5 months in NAT cohort versus 5.4 months in AT cohort (NAT vs. AT, HR: 0.49, 95% CI: 0.34-0.71, p = 0.0001). Multivariate analysis confirmed the prognostic role of antibiotic for OS and PFS. Finally, NAT cohort showed better overall response rate compared with AT cohort (31.4% vs. 20.4%, p = 0.03).

CONCLUSIONS: The use of antibiotic therapy in the 15 days prior to starting chemoimmunotherapy is an independent unfavorable prognostic factor for survival in our cohort of patients with advanced BTC treated with cisplatin, gemcitabine and durvalumab.},
}

Humans
Female
Male
Aged
Middle Aged
*Anti-Bacterial Agents/therapeutic use/administration & dosage
*Cholangiocarcinoma/drug therapy/mortality/pathology
Prognosis
*Bile Duct Neoplasms/drug therapy/mortality/pathology
Immunotherapy/methods
Aged, 80 and over
Progression-Free Survival
Retrospective Studies
Immune Checkpoint Inhibitors/therapeutic use
Adult

@article {pmid42842405,
year = {2026},
author = {Stoner, SN and Larson, ED and Fulte, S and Shaw, SC and Fish, ER and Janoff, EN and Mack, M and Clark, SE},
title = {Myeloid cell reprogramming drives enhanced defense against Streptococcus pneumoniae lung infection following exposure to commensal Prevotella.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {41},
pages = {e2623525123},
doi = {10.1073/pnas.2623525123},
pmid = {42842405},
issn = {1091-6490},
support = {R01AI172958//HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; T32DC012280//HHS | NIH | National Institute on Deafness and Other Communication Disorders (NIDCD)/ ; T32AI007405//HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)/ ; },
mesh = {Animals ; *Streptococcus pneumoniae/immunology ; Mice ; *Myeloid Cells/immunology ; *Prevotella/immunology ; Lung/microbiology/immunology ; *Pneumonia, Pneumococcal/immunology/microbiology ; Neutrophils/immunology ; Macrophages/immunology ; Mice, Inbred C57BL ; Phagocytosis ; },
abstract = {Clinical data link the prevalent respiratory tract anaerobe Prevotella with reduced pneumonia mortality, but the mechanisms directing Prevotella regulation of lung immune homeostasis are unclear. Here, single-cell RNA sequencing was employed to define the transcriptional immune signatures underlying improved clearance of Streptococcus pneumoniae following lung exposure to Prevotella melaninogenica. Overall, we observed a substantial shift in myeloid cell transcriptional programming from interferon-dominant to a more antibacterial profile in S. pneumoniae-infected mice after pre-exposure to P. melaninogenica, correlating with increased macrophage and neutrophil phagocytosis of S. pneumoniae and improved pathogen clearance. In neutrophils, tumor necrosis factor (TNF) signaling through TNFR2 was essential for increased antimicrobial function. Moreover, improved defense required CCR2-dependent monocyte-derived macrophages, with selective enrichment of more a mature Cxcl3+ population which was distinct from the hallmark S. pneumoniae-associated C1qa+ population enriched in the absence of effective clearance. Together, these findings inform the myeloid cell transcriptional changes associated with natural infection resistance mediated by pulmonary microbial exposures.},
}

Animals
*Streptococcus pneumoniae/immunology
Mice
*Myeloid Cells/immunology
*Prevotella/immunology
Lung/microbiology/immunology
*Pneumonia, Pneumococcal/immunology/microbiology
Neutrophils/immunology
Macrophages/immunology
Mice, Inbred C57BL
Phagocytosis

@article {pmid42842449,
year = {2026},
author = {Guadano-Procesi, I and García Ramos, A and Gentekaki, E and Tsaousis, AD},
title = {Exploring Blastocystis: hidden complexity in a common intestinal microbe.},
journal = {Journal of medical microbiology},
volume = {75},
number = {10},
pages = {},
pmid = {42842449},
issn = {1473-5644},
mesh = {Humans ; *Blastocystis/genetics/classification/isolation & purification ; *Blastocystis Infections/parasitology/diagnosis/drug therapy/transmission ; Animals ; Genetic Variation ; *Gastrointestinal Microbiome ; Carrier State/parasitology ; },
abstract = {Blastocystis is an anaerobic stramenopile that colonizes the large intestine of humans and many animals worldwide. Small-subunit rRNA-based typing reveals deep genetic diversity: at least 44 genetic variants, namely, subtypes (STs), are recognized, with ST1-ST4 accounting for most human carriage. Its medical relevance remains contested. Blastocystis carriage is frequently asymptomatic, and while associations with non-specific gastrointestinal symptoms (e.g. diarrhoea, abdominal pain and bloating), irritable bowel syndrome and extraintestinal manifestations such as urticaria have been proposed. In parallel, multiple microbiome studies, including a recent population-scale analysis, link Blastocystis carriage to higher bacterial diversity, healthier diets and favourable cardiometabolic profiles, suggesting that in many settings, it may be a marker of a resilient gut ecosystem rather than a primary pathogen. Transmission is primarily faecal-oral, most likely via environmentally resilient cysts, with potential for zoonotic and waterborne spread. Diagnosis using quantitative PCR is the most sensitive method; microscopy has limited sensitivity and can be confounded by morphological plasticity, though its diagnostic accuracy varies considerably according to the experience of the microscopist. Treatment is typically based on excluding alternative causes rather than confirmed causality; while metronidazole is commonly used, clinical outcomes are highly variable due to potential co-infections, inconsistent links between parasite eradication and symptom relief and reports of reduced drug susceptibility.},
}

Humans
*Blastocystis/genetics/classification/isolation & purification
*Blastocystis Infections/parasitology/diagnosis/drug therapy/transmission
Animals
Genetic Variation
*Gastrointestinal Microbiome
Carrier State/parasitology

@article {pmid42842454,
year = {2026},
author = {Tavartkiladze, A and Tavartkiladze, L and Reiter, RJ and Burnier, M and Ulukaya, E and Simonia, G and Kasradze, D and Nozadze, P and Revazishvili, P and Andronikashvili, I and Maisuradze, M},
title = {Lower 24-hour urinary 6-sulfatoxymelatonin and exploratory bile-acid and microbiome associations in adults with dyslipidemia: a prospectively enrolled cross-sectional study.},
journal = {Annals of medicine},
volume = {58},
number = {1},
pages = {2743367},
pmid = {42842454},
issn = {1365-2060},
mesh = {Humans ; Male ; Female ; Cross-Sectional Studies ; Prospective Studies ; Middle Aged ; *Dyslipidemias/urine/microbiology/blood ; *Melatonin/analogs & derivatives/urine ; Adult ; *Bile Acids and Salts/metabolism ; Fibroblast Growth Factors/blood ; *Gastrointestinal Microbiome/physiology ; Aged ; Biomarkers/urine ; },
abstract = {BACKGROUND: We tested the primary hypothesis that lower continuous 24-hour urinary 6-sulfatoxymelatonin (6-SMT) is associated with an adverse lipid and inflammatory profile in adults with dyslipidemia. Associations with FGF19, bile-acid composition, and gut microbiome features were secondary and exploratory.

METHODS: This prospectively enrolled, single-center cross-sectional study included 577 consecutive adults evaluated at the Institute for Personalized Medicine, Tbilisi, Georgia, during 2020-2025. Each participant completed three non-consecutive 24-hour urine collections. Validity required a measured-to-predicted creatinine-excretion ratio of 0.80-1.20, and the participant-level 6-SMT value was the arithmetic mean of three valid collections. Fasting lipids, hs-CRP, FGF19, bile-acid profiles, and 16S rRNA taxonomic composition were assessed. An internal method-matched but unmatched normolipidemic reference comparator (n = 120) was used only for descriptive analyses.

RESULTS: Median 6-SMT was 8.4 μg/24 h (IQR 5.2-12.1). Lower 6-SMT was associated with higher LDL-C (Spearman ρ = -0.38; approximate 95% CI -0.45 to -0.31), triglycerides (ρ = -0.31; -0.38 to -0.23), and hs-CRP (ρ = -0.35; -0.42 to -0.28), and with lower HDL-C (ρ = 0.29; 0.21 to 0.36). FGF19 was above the stated fasting reference range in 489/577 participants (85%; median 312 pg/mL) and correlated inversely with 6-SMT (ρ=-0.42; -0.48 to -0.35). The emphasized microbial taxa correlated positively with 6-SMT. In a post hoc unadjusted statin-stratified sensitivity analysis, the mean difference in 6-SMT for statin users versus non-users was -0.30 μg/24 h (95% CI -0.83 to 0.23; p = 0.26). False-discovery-rate sensitivity analysis across the 14 reported reference-comparator microbiome tests retained q < 0.05 for each reported comparison; this does not resolve comparator confounding. The exploratory complete-case multivariable model had adjusted R[2]=0.40 but was not interpreted causally.

CONCLUSIONS: Lower 24-hour urinary 6-SMT clustered with adverse lipid and inflammatory measures and with exploratory enterohepatic and taxonomic microbiome features. The findings are hypothesis-generating and do not establish a coordinated biological axis, directionality, diagnostic utility, incremental predictive value, or treatment effect.},
}

Humans
Male
Female
Cross-Sectional Studies
Prospective Studies
Middle Aged
*Dyslipidemias/urine/microbiology/blood
*Melatonin/analogs & derivatives/urine
Adult
*Bile Acids and Salts/metabolism
Fibroblast Growth Factors/blood
*Gastrointestinal Microbiome/physiology
Aged
Biomarkers/urine

@article {pmid42842487,
year = {2026},
author = {Miyazawa, T and Toda, M and Hatakeyama, N and Sogame, R and Huang, CY and Yoshioka, T and Nakano, Y and Maejima, D and Ohta, S and Tsuda, T and Iimura, J and Ashida, K and Omae, Y and Ochi, H and Nakada, H and Kusama, K and Matsuda, T and Hattori, K and Aida, T and Sugimoto, K and Miyazawa, T},
title = {A Narrative Review of Integrating Artificial Intelligence and Omics in Food Science and Nutrition: Current Uses, Issues, and Future Perspectives.},
journal = {Nutrition reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/nutrit/nuag143},
pmid = {42842487},
issn = {1753-4887},
support = {//the Tohoku University Fund, Tohoku University, Sendai, Japan/ ; },
abstract = {This narrative review examines how artificial intelligence (AI) and omics are being integrated in food science and nutrition, with particular attention to current applications, practical limitations, and challenges that are specific to foods and dietary exposure. Foods are complex, multicomponent matrices whose composition and biological effects can change during processing, cooking, storage, and consumption. Dietary exposure also varies over time and across individuals. These features make food and nutrition fundamentally more difficult to model than many domains in which AI has advanced rapidly. Relevant literature was identified through searches of PubMed, Google Scholar, and Web of Science. For studies applying AI to foods, reports published in 2023 or later were preferentially selected unless suitable recent studies were unavailable. Selected publications were independently evaluated by the authors and subsequently discussed. The integration of AI and omics approaches are being applied to data integration, feature selection, predictive modeling, network analysis, clustering, interpretation, flavor and taste design, discovery of bioactive ingredients, functional food development, and prediction of dietary responses involving metabolites and the gut microbiome. Across these applications, food- and nutrition-specific difficulties emerged repeatedly, including the partial observability of food composition, changes caused by processing and cooking, mismatches between short-term measurements and long-term health outcomes, nonlinear dose-response relationships, and inter-individual variation. These challenges add to general issues such as data quality, multi-omics integration, model interpretability, and external validation. The integration of AI and omics is expanding the capacity to analyze complex data in food science and nutrition, but reliable translation will require methods adapted to the dynamic and partly observable nature of foods and diets. Improved standardization, exposure assessment, validation, study design, and interpretability will be essential for future research and practical application.},
}

@article {pmid42842625,
year = {2026},
author = {Deng, J and Chen, D and Shen, S and Zhou, Y and Cui, H and Qiu, Y and Li, Q and Hu, YQ},
title = {A joint mixture Tobit method with latent microbial abundance improves detection of microbiome-disease associations in zero-inflated data.},
journal = {PLoS computational biology},
volume = {22},
number = {10},
pages = {e1014844},
doi = {10.1371/journal.pcbi.1014844},
pmid = {42842625},
issn = {1553-7358},
abstract = {Zero inflation remains a major challenge in microbiome differential abundance analysis, often resulting in inflated type I error rates or reduced statistical power. Although numerous methods have been proposed to address excess zeros, many existing approaches do not explicitly distinguish between distinct zero-generating mechanisms, and censoring-based modeling perspectives remain relatively underexplored in microbiome data analysis. To advance methodological development in this area, we introduce a novel censoring-based modeling perspective for microbiome differential abundance analysis. Specifically, we develop a joint mixture Tobit (joint mTobit) method for zero-inflated microbiome data. Building on a mixture Tobit formulation, the model incorporates a point-mass component to represent structural zeros, while modeling latent microbial abundance via a Tobit regression component. The proposed framework jointly links disease status, latent true microbial abundance, and relevant covariates within a unified probabilistic model, allowing appropriate adjustment for confounding factors and facilitating more reliable statistical inference. By explicitly modeling the latent abundance underlying observed counts, the joint mTobit method improves estimation stability and enhances detection power under zero inflation. Extensive simulation studies demonstrate that the joint mTobit method achieves effective type I error control while maintaining high statistical power and stable coefficient estimation across a wide range of settings. Application to a real-world colorectal cancer and adenoma microbiome dataset further illustrates its ability to identify biologically meaningful differentially abundant taxa. Overall, this work develops a joint mTobit modeling framework for zero-inflated microbiome data, enabling inference on latent microbial abundance and providing a censoring-based statistical framework for investigating disease-microbiome associations in differential abundance analysis.},
}

@article {pmid42843190,
year = {2026},
author = {Chan, CWK},
title = {Recurrence is not the same as robustness: Refining reproducibility in the multiple sclerosis gut microbiome.},
journal = {Multiple sclerosis and related disorders},
volume = {115},
number = {},
pages = {107964},
doi = {10.1016/j.msard.2026.107964},
pmid = {42843190},
issn = {2211-0356},
}

@article {pmid42843232,
year = {2026},
author = {Biţă, A and Scorei, IR and Mogoşanu, GD and Gheonea, DI},
title = {From boron symbiotaxis to symbiogenic nutrients: extending the concept of ecological essentiality.},
journal = {Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)},
volume = {98},
number = {},
pages = {127974},
doi = {10.1016/j.jtemb.2026.127974},
pmid = {42843232},
issn = {1878-3252},
abstract = {Nutritional science has traditionally interpreted the biological functions of nutrients according to their metabolic roles within the host organism. Microbiome-oriented concepts, including prebiotics, probiotics, synbiotics, and postbiotics, have substantially expanded this perspective by recognizing the biological importance of microbial communities. However, existing nutritional classifications remain largely centered on either the host or the microbiota, without explicitly considering the functional organization emerging from their continuous interaction. In this review, we propose the concept of symbiogenic nutrients (SNs) as a complementary functional classification of nutrients defined according to their demonstrated capacity to preserve, restore, or enhance host-microbiome functional organization (HMFO). Building upon the concepts of ecological essentiality and boron (B) symbiotaxis, we introduce a systems-oriented framework in which nutritional function is interpreted not only through direct metabolic activities or microbial modulation but also through preservation of the structural, communicative, ecological, and metabolic processes that collectively sustain functional symbiosis. To facilitate operational implementation, we propose explicit principles and criteria for the classification of SNs and illustrate their application using B as the first experimentally supported prototype. Current evidence indicates that B contributes to biological interface integrity, microbial communication, ecological regulation, and host metabolic integration, thereby fulfilling the proposed operational framework. The concept is further extended from individual SNs to symbiogenic compositions, interface-active compositions, and symbiogenic nutrition, as a systems-oriented nutritional strategy aimed at preserving HMFO. This framework provides new perspectives for healthy longevity, metabolic health, chronic inflammation, and precision nutrition, establishing a conceptual foundation for future interface-targeted nutritional interventions.},
}

@article {pmid42843234,
year = {2026},
author = {Su, K and Wu, D and Xia, Y and Tian, S and Li, C and Ji, J and Guo, Y and Zhao, X and Huang, J and Hu, S and Ye, J},
title = {Prediction of age using shotgun metagenomic sequencing and random forest algorithm based on cadaveric colon.},
journal = {Forensic science international},
volume = {390},
number = {},
pages = {113154},
doi = {10.1016/j.forsciint.2026.113154},
pmid = {42843234},
issn = {1872-6283},
abstract = {Age estimation is important for the identification of unknown cadavers in forensic practice. Previous studies have shown that gut microbiota is associated with host age, but most evidence has been derived from fecal samples of living individuals. In this study, shotgun metagenomic sequencing was performed on mid-colon tissue samples from 76 cadavers to explore age-associated taxonomic and predicted functional patterns in cadaveric colon microbiota and to evaluate their potential value for forensic age estimation. After quality control and taxonomic annotation, 3980 microbial species were identified. Descriptive differences among age groups were observed in microbial composition, alpha diversity, species-enrichment patterns, co-occurrence network structure, and KEGG functional profiles; however, a multivariable PERMANOVA did not detect a statistically significant association between age group and overall species-level community composition after accounting for postmortem sampling interval, cause-of-death category, and sex. The complete random forest pipeline was re-evaluated using repeated nested five-fold cross-validation, with all data-dependent filtering, transformation, feature selection, and hyperparameter tuning restricted to the outer training data. The resulting out-of-fold performance was limited (R[2] = 0.005, MAE = 13.686 years, and RMSE = 17.741 years), and predictions showed regression toward the cohort mean. Overall, this study provides preliminary evidence that cadaveric colon microbiota contains age-associated microbial signals, but these findings should be interpreted as exploratory. Larger cohorts and independent external validation are needed before microbiome-based age prediction can be applied in forensic practice.},
}

@article {pmid42843243,
year = {2026},
author = {Pu, G and Han, Q and Liu, Y and Zheng, M and Shang, J and Shao, J and Yun, K and Yan, J and Guo, Z},
title = {Biogenic maturation of mineral-encrusted plastispheres overrides ecological drift to orchestrate multi-kingdom assembly and nitrogen reprogramming in agroecosystems.},
journal = {Journal of hazardous materials},
volume = {517},
number = {},
pages = {143809},
doi = {10.1016/j.jhazmat.2026.143809},
pmid = {42843243},
issn = {1873-3336},
abstract = {The quantitative assembly rules and multi-kingdom functional gateways of the soil plastisphere remain poorly resolved. We integrated multi-omics with high-resolution surface deconvolution to decode the ecological signatures of weathered polyethylene (PE) films in intensive agroecosystems. Surface characterization revealed an interfacial metamorphosis where biogenic maturation facilitated the formation of a dense mineral organic crust, transforming inert polymers into reactive metabolic islands. Ecological modeling identifies a distinct departure from neutral assembly, demonstrating that niche-based selection driven by polymer surface remodeling overrides ecological drift in shaping microbial consortia. Machine learning and structural equation modeling identify ammonia oxidizing archaea as the primary functional keystone taxa orchestrating the global interactome. This archaeal-bacterial axis, regulated by protistan assemblages that exhibit significant topological densification, catalyzes a cross-kingdom metabolic relay synchronized with nitrogenous biomarker accumulation and intensified enzymatic mineralization. Functional decoupling across taxonomic domains reveals a metabolic lag where rapid deterministic recruitment outpaces steady-state nutrient stabilization. While promoting local alpha-diversity, the bacterial core exhibits structural fragmentation and elevated antagonistic interactions, signaling an asynchronous regime shift that may trigger positive priming effects on native soil organic carbon. These findings establish a mechanistic blueprint for how weathered PE residues redirect terrestrial nutrient fluxes via deterministic multi-kingdom assembly, pinpointing specific organo-mineral signatures and archaeal keystone taxa as critical targets for precision microbiome engineering in the Anthropocene.},
}

@article {pmid42843345,
year = {2026},
author = {Zhao, S and Haryono, MAS and Lai, CWM and Seah, F and Tang, YL and Lim, M and Febriana, E and Lee, MH and Tan, KS and Fu, JH and Yip, JK and Preshaw, PM and Williams, RBH and Toh, SA and Lee, JWJ and Goh, CE},
title = {Oral microbial nitrate metabolism is associated with lower prevalence of prediabetes.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {103092},
doi = {10.1016/j.xcrm.2026.103092},
pmid = {42843345},
issn = {2666-3791},
abstract = {The oral microbiome is a key microbial interface for dietary or oral nitrate metabolism, yet its role in early glycemic dysregulation remains poorly defined. In a population-based cohort (n = 472), we perform metagenomic profiling of tongue dorsum microbiomes and identify 11 taxa and nine microbial pathways associated with prediabetes. Among these, Rothia mucilaginosa and microbial nitrate reduction emerge as the only taxon and the strongest pathway associated with lower prediabetes prevalence. Individuals without prediabetes show higher salivary nitrate and nitrite concentrations, supporting enhanced oral nitrate bioavailability. Functional characterization of an isolated Rothia mucilaginosa strain demonstrates its capacity to mediate both nitrate-nitrite-NO and nitrate-nitrite-NH4[+] pathways under oxygen-limited conditions. Incorporating nitrate metabolism-associated microbial features into clinical risk factors improves risk stratification for progression to prediabetes. These findings support oral nitrate metabolism as a microbial pathway linking oral ecology to systemic metabolic health and suggest that tongue cleaning may modulate microbial functions involved in this pathway.},
}

@article {pmid42843354,
year = {2026},
author = {Hasanuzzaman, M and Bang, CS and Lee, JJ and Gong, EJ},
title = {Fecal Microbiota Transplantation Beyond Clostridioides difficile Infection: Expanding Indications, Mechanisms, and Future Directions.},
journal = {Journal of Korean medical science},
volume = {41},
number = {38},
pages = {e335},
pmid = {42843354},
issn = {1598-6357},
support = {RS-2023-00223501/NRF/National Research Foundation of Korea/Korea ; /Hallym/Hallym University/Korea ; },
mesh = {*Fecal Microbiota Transplantation ; Humans ; *Clostridium Infections/therapy/microbiology ; Inflammatory Bowel Diseases/therapy ; Clostridioides difficile ; Irritable Bowel Syndrome/therapy ; Dysbiosis/therapy ; Gastrointestinal Microbiome ; Nervous System Diseases/therapy ; Metabolic Diseases/therapy ; Animals ; },
abstract = {Fecal microbiota transplantation (FMT) has emerged as a transformative therapeutic approach to restore gut microbial homeostasis. The most established indication is recurrent Clostridioides difficile infection (CDI), demonstrating that restoring ecosystem-level microbiota has substantial clinical benefits. Building on this success, FMT is now being investigated across a broader range of indications associated with gut dysbiosis and altered microbiome-host signaling, including inflammatory bowel disease, irritable bowel syndrome, metabolic, and neurological disorders. Mechanistic insights into the gut-organ axes provide biological plausibility for this expansion; gut dysbiosis can function as a modifiable upstream driver of host metabolism, immune-neural signaling, and barrier function. However, the clinical benefits beyond CDI remain heterogeneous and often modest, highlighting the need for further research on patient stratification, standardized protocols, and mechanistic biomarkers. Furthermore, regulatory frameworks remain heterogeneous worldwide, and recent approvals of standardized microbiota-based products for recurrent CDI represent a transition toward treating microbiome therapeutics as regulated biologics. This review synthesizes the mechanistic rationale and current evidence for FMT beyond CDI and outlines future directions for personalized and next-generation microbiome therapeutics.},
}

*Fecal Microbiota Transplantation
Humans
*Clostridium Infections/therapy/microbiology
Inflammatory Bowel Diseases/therapy
Clostridioides difficile
Irritable Bowel Syndrome/therapy
Dysbiosis/therapy
Gastrointestinal Microbiome
Nervous System Diseases/therapy
Metabolic Diseases/therapy
Animals

@article {pmid42843466,
year = {2026},
author = {Huang, J and Ji, L and Jin, H and Shi, Z and Song, X and Cai, Y and Tong, X},
title = {Nanoparticle-based senolytic and senomorphic therapies for healthy aging: design principles, translational evidence, and challenges.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {103398},
doi = {10.1016/j.arr.2026.103398},
pmid = {42843466},
issn = {1872-9649},
abstract = {Cellular senescence contributes to age-associated tissue dysfunction through persistent growth arrest, metabolic remodeling, and altered communication with immune and stromal cells. Senolytic therapies preferentially eliminate susceptible senescent cells, while senomorphic therapies modulate harmful senescence-associated activities. Nanoparticle engineering can improve the delivery of these agents through cargo protection, surface functionalization, and controlled release. Surface ligands can promote cellular uptake, and components responsive to lysosomal β-galactosidase, acidic pH, reactive oxygen species, or protease activity can regulate cargo release. The selectivity of these mechanisms depends on biological features that vary among senescent populations and also occur in other cellular states. This review examines how material composition and physicochemical properties influence target recognition, intracellular transport, therapeutic activity, and safety. Representative platforms are evaluated across fibrotic, musculoskeletal, metabolic, oncologic, and neurodegenerative disease models, with particular attention to mitochondrial delivery, immune-mediated clearance, nucleic-acid modulation, and microbiome interactions. Preclinical findings are considered alongside human senotherapy studies, which have primarily evaluated small-molecule drug regimens and yielded preliminary or mixed outcomes. Clinical development requires reproducible manufacturing, pharmacokinetic characterization of both carrier and cargo, and assessment of immunotoxicity and delayed organ injury in older hosts. Progress depends on matching a defined pathological cell population to an appropriate delivery strategy and demonstrating an advantage in therapeutic index or sustained functional outcomes against relevant comparators, including clinically feasible non-nanoparticle treatments where available.},
}

@article {pmid42843574,
year = {2026},
author = {Wen, Y and Sun, H and Xiong, N and Xu, X and Ye, Y and Shen, Z and Wang, C},
title = {Glycosylation in colorectal cancer: From tumor-intrinsic signaling to the host-microbiome glyco-interface.},
journal = {Biochimica et biophysica acta. Reviews on cancer},
volume = {1881},
number = {6},
pages = {189735},
doi = {10.1016/j.bbcan.2026.189735},
pmid = {42843574},
issn = {1879-2561},
abstract = {Aberrant glycosylation is increasingly recognized as a key regulatory layer in colorectal cancer (CRC), extending beyond tumor-cell-intrinsic signaling to shape the tumor microenvironment and host-microbiome interactions. In the immune compartment, glycosylation modulates the stability and activity of classical checkpoints, including PD-L1, while tumor-associated glycans engage MGL, DC-SIGN, Siglecs, and galectins to form glyco-immune checkpoints that influence T-cell dysfunction, macrophage polarization, dendritic-cell tolerance, and NK-cell activity. These mechanisms support emerging glyco-immunotherapeutic strategies such as targeted desialylation, glycoform-specific targeting, and combination with immune checkpoint blockade. Glycosylation also functions as a molecular language at the host-microbiome interface. Site-specific epithelial glycoproteins, mucin O-glycoforms, bidirectional host-bacterial fucosylation, IgA-associated glycan recognition, and microbial glycan utilization may collectively shape CRC-associated dysbiosis and mucosal inflammation. Integrating stool glycoproteomics with microbiome profiling may further enable noninvasive screening and patient stratification. This review highlights glycosylation as a multidimensional interface linking tumor biology, antitumor immunity, and microbiome ecology, with implications for biomarker development and precision therapy in CRC.},
}

@article {pmid42843699,
year = {2026},
author = {Ye, J and Deng, M and Liao, Y and Li, J and Jia, X and Li, C and Wu, K},
title = {The Immunomodulatory Landscape of Anesthetic Agents: Mechanisms, Clinical Implications, and Therapeutic Potential.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {179401},
doi = {10.1016/j.ejphar.2026.179401},
pmid = {42843699},
issn = {1879-0712},
abstract = {The pharmacological actions of anesthetic agents extend far beyond neurodepression, encompassing complex immunomodulatory effects with implications for perioperative immune function, surgical outcomes, infection risk, and cancer biology. This review critically evaluates current evidence on how different anesthetic classes influence innate and adaptive immunity, examining cellular targets and signaling mechanisms. Rather than viewing anesthesia as monolithically immunosuppressive, current evidence supports a nuanced understanding in which immunological effects vary according to anesthetic agent, dose, timing, and clinical context. Volatile anesthetics (isoflurane, sevoflurane) attenuate natural killer cell cytotoxicity and neutrophil function, promote lymphocyte apoptosis with T helper 2 cell skewing, and exhibit context-dependent anti-inflammatory properties. Propofol preserves immune function by attenuating ROS-mediated cellular damage and maintaining Th1/Th2 balance. Ketamine exerts concentration-dependent immunomodulatory effects including anti-inflammatory actions on macrophages and biphasic lymphocyte modulation. We discuss clinical implications in oncological surgery, sepsis, and autoimmune disorders, emphasizing strengths and limitations of current evidence. Emerging frontiers include personalized anesthesia guided by immune phenotyping, novel targeted agents, and the gut microbiome as a modulator of anesthetic-immune interactions, though these remain promising directions rather than established practice. This review integrates mechanistic insights with clinical evidence and identifies priorities for translational research.},
}

@article {pmid42843892,
year = {2026},
author = {Hu, B and Liu, Y and Zhang, X and Manickam, S},
title = {Microbial Metabolic Messengers from Fermented Foods: Multi-Organ Regulation of Energy Homeostasis and Obesity.},
journal = {Nutrition reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/nutrit/nuag146},
pmid = {42843892},
issn = {1753-4887},
support = {2025S075//Ningbo Public Welfare Research/ ; Y202557618//General Scientific Research Project of Zhejiang Provincial Department of Education/ ; UTB/GSR/2/2025 (5)//Universiti Teknologi Brunei (UTB)/ ; },
abstract = {Mechanistic evidence was systematically reviewed on how major metabolites produced during fermentation of foods modulate obesity through gut microbiota remodeling and multiorgan metabolic regulation, with emphasis on the gut-brain axis, immunometabolic pathways, and epigenetic mechanisms. Obesity remains a major global public health challenge, and conventional management strategies are frequently limited by poor long-term efficacy, low adherence, and undesirable side effects. Increasing evidence positions the gut microbiome as a central metabolic organ that profoundly influences host energy homeostasis and adiposity. Individuals with obesity commonly have a disrupted intestinal microbial ecosystem characterized by reduced microbial diversity, depletion of health-promoting taxa, and enrichment of facultative pathogens, which compromise intestinal barrier function, promote chronic low-grade inflammation, and disturb systemic metabolic regulation. Fermented foods, integral to traditional diets, provide a rich source of live microorganisms and a diverse repertoire of bioactive metabolites produced through fermentation. A narrative review was conducted by synthesizing evidence from experimental, mechanistic, and preclinical studies on fermented foods, gut microbial ecology, fermentation-derived metabolites, and obesity-related metabolic pathways. Current evidence indicates that the anti-obesity effects of fermented foods are mediated not only by transient microbial colonization but, more importantly, by fermentation-derived metabolites such as short-chain fatty acids, conjugated linoleic acid, and indole derivatives (eg, indole-3-propionic acid). These metabolites exert multiorgan physiological effects through the gut-brain axis, immunometabolic pathways, and epigenetic regulation. Collectively, they modulate key processes, including enteroendocrine hormone secretion, hepatic glucose and lipid metabolism, browning of white adipose tissue, and central appetite control, ultimately contributing to metabolic restoration. This review provides a systematic and mechanistic evaluation of how major fermentation-derived metabolites counteract obesity by reshaping gut microbiota composition and functional activity across interconnected organ systems. The insights provide a strengthened conceptual framework for designing microbiota-directed nutritional strategies to sustain body-weight regulation.},
}

@article {pmid42843943,
year = {2026},
author = {Daulat, S},
title = {Early nutrition and the infant microbiome: Implications for atopy.},
journal = {The journal of allergy and clinical immunology. In practice},
volume = {14},
number = {10},
pages = {2437},
doi = {10.1016/j.jaip.2026.07.029},
pmid = {42843943},
issn = {2213-2201},
}

@article {pmid42843944,
year = {2026},
author = {Robbins, E and Koueik, J and Singh, AM and Frischmeyer-Guerrerio, PA and Hourigan, SK},
title = {Reply to "Early nutrition and the infant microbiome: implications for atopy".},
journal = {The journal of allergy and clinical immunology. In practice},
volume = {14},
number = {10},
pages = {2437-2438},
doi = {10.1016/j.jaip.2026.07.030},
pmid = {42843944},
issn = {2213-2201},
}

@article {pmid42843978,
year = {2026},
author = {Mueller, T and Kueneman, J and Fordyce, R and McArt, S and Danforth, B},
title = {Landscape-associated pesticide contamination shapes pollen provision microbiomes in Osmia cornifrons (Hymenoptera: Megachilidae).},
journal = {Journal of insect science (Online)},
volume = {26},
number = {5},
pages = {},
pmid = {42843978},
issn = {1536-2442},
support = {NSF-DEB 1929499//National Science Foundation/ ; },
mesh = {Animals ; *Pollen/microbiology ; Bees/microbiology ; *Microbiota/drug effects ; *Pesticides/analysis/adverse effects ; New York ; Bacteria ; Ecosystem ; },
abstract = {Bees live and forage across a landscape increasingly altered by human activity, collecting pollen, nectar, and an essential microbiome from the local environment as well as chemical contamination from surrounding human activities. The increasing frequency and intensity of antimicrobial chemical use in agricultural systems disrupts the environmental microbial community and has been linked to bee declines. However, it remains largely unknown how pesticides and antimicrobial agents vary across the landscape, and in turn, cascade to alter microbiome assembly in solitary bees. To evaluate landscape-level effects of pesticide contamination on the pollen microbiome of solitary bees, we surveyed Osmia cornifrons (Hymenoptera: Megachilidae Radoszkowski, 1887) pollen provisions across 3 contrasting land use types in central upstate New York: forest, urban, and orchard habitats. Pollen provisions were screened for 94 common pesticides and sequenced to characterize their bacterial community. We found pesticide concentrations and risk varied significantly across land use types and was highest at orchard sites. Microbial communities also differed across landscapes, with increased surrounding forest cover corresponding to higher abundances of Apilactobacillus, a beneficial bee-associated genus in the family Lactobacilliacea. We found a significant correlation between increased pesticide concentration and decreased pollen-associated microbial diversity. These results indicate links between land use, pesticide exposure, and the microbiome of solitary bees.},
}

Animals
*Pollen/microbiology
Bees/microbiology
*Microbiota/drug effects
*Pesticides/analysis/adverse effects
New York
Bacteria
Ecosystem

@article {pmid42844060,
year = {2026},
author = {Kim, BR and Blair, EM and Howard, JP and Gois, IM and Flick, R and Lankiewicz, TS and Mondo, S and Pangilinan, J and Lipzen, A and Guo, J and Hundley, H and Lee, R and Talag, J and Bunting, V and Rajasekar, S and Barry, K and Grigoriev, IV and O'Malley, MA and Lawson, CE},
title = {Engineering anaerobic fungal-bacterial consortia for direct conversion of lignocellulosic biomass into medium-chain fatty acids.},
journal = {Trends in biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tibtech.2026.09.013},
pmid = {42844060},
issn = {1879-3096},
abstract = {Lignocellulosic biomass is a renewable feedstock for sustainable fuels and chemicals, yet industrial conversion remains constrained by carbohydrate solubilization. Inspired by herbivore rumen microbiomes, we engineered an anaerobic fungal-bacterial consortium thatconverts native lignocellulose into medium-chain fatty acids (MCFAs) without pretreatment. Systematic screening identified the anaerobic fungus isolated here, Neocallimastix sp. FC1, togetherwith Megasphaerahexanoica, as a top-performing consortium, achieving a lignocellulose-to-MCFA yield of 21.0% (carbon-to-carbon basis) through tight lactate cross-feeding without competition for soluble sugars. Fungal lactate production limited the growth of M. hexanoica in co-culture, and the bacterium reallocated protein from growth toward chain elongation, resulting in increased MCFA production. These findings identify fungal lactate production as the primary biological constraint, and balancing lactate production and consumption as a key engineering strategy for improving lignocellulose-to-MCFA conversion. Techno-economic analysis identified high cultivation medium costs as the primary economic constraint and established quantitative cost-yield targets for profitable MCFA production.},
}

@article {pmid42844155,
year = {2026},
author = {Khosrofar, R and Morshedi, I and Behzadpour, M and Afzali, N and Hosseini, RS and Aghili, A},
title = {Recent Advances in Autism Spectrum Disorder Research on Epigenetics and Personalised Medicine.},
journal = {International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience},
volume = {86},
number = {6},
pages = {e70184},
doi = {10.1002/jdn.70184},
pmid = {42844155},
issn = {1873-474X},
mesh = {Humans ; *Autism Spectrum Disorder/genetics/therapy/diagnosis ; *Epigenesis, Genetic ; *Precision Medicine/methods ; Pregnancy ; Animals ; Female ; },
abstract = {BACKGROUND: Autism spectrum disorder (ASD) is a multifaceted neurodevelopmental condition characterised by impairments in social interaction and communication, repetitive and restricted patterns of behaviour and atypical sensory processing. Although genetic susceptibility accounts for a substantial proportion of ASD risk, increasing evidence indicates that epigenetic modifications and environmental exposures play pivotal roles in disease development and progression.

PURPOSE: This review provides an updated overview of the current understanding of ASD pathogenesis, focusing on the interplay between epigenetic regulation, maternal health and the gut microbiome. It also highlights emerging diagnostic biomarkers and therapeutic strategies that have the potential to enhance early diagnosis and improve clinical management.

MAIN FINDINGS: Recent studies indicate that maternal immune dysregulation, nutritional status, metabolic disorders and alterations in the maternal gut microbiota during pregnancy may contribute to ASD risk by inducing epigenetic changes and disrupting neurodevelopmental pathways. At the same time, novel pharmacological interventions aimed at alleviating behavioural symptoms and targeting epigenetic mechanisms are being actively explored. Advances in diagnostic technologies, including saliva-based microRNA profiling and epigenetic biomarkers, offer promising opportunities for earlier and more accurate ASD detection. Furthermore, genome-wide analyses and multi-omics approaches are facilitating the development of personalised diagnostic and therapeutic strategies.

CONCLUSION: Despite considerable progress in elucidating the genetic and environmental factors associated with ASD, the disorder remains highly heterogeneous and biologically complex. Future research integrating epigenetic insights, microbiome investigations and precision medicine approaches will be crucial for uncovering the underlying molecular mechanisms and translating these discoveries into more effective diagnostic tools and targeted therapies.},
}

Humans
*Autism Spectrum Disorder/genetics/therapy/diagnosis
*Epigenesis, Genetic
*Precision Medicine/methods
Pregnancy
Animals
Female

@article {pmid42844446,
year = {2026},
author = {Kozlov, M},
title = {Revealed: how this common gut microbe protects against heart disease.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42844446},
issn = {1476-4687},
}

@article {pmid42844483,
year = {2026},
author = {Carter, MM and Liu, Z and Olm, MR and Martin, M and Sprockett, DD and Ghadermazi, P and Trumble, BC and Kaplan, H and Stieglitz, J and Rodriguez, DE and Relman, DA and Sonnenburg, ED and Gurven, M and Good, BH and Sonnenburg, JL},
title = {Prehistoric global migration of vanishing gut microbes with humans.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42844483},
issn = {1476-4687},
abstract = {The gut microbiome is crucial for health and is affected strongly by lifestyle[1]. Many microorganisms commonly found in non-industrialized populations are disappearing or have become extinct in industrialized populations[2-6]. Studying which microorganisms have been long-term residents of the human gut and may have co-evolved with humans[2,7,8] could provide insights into how microbial biodiversity loss affects human health. However, the genetic complexities of microbial evolution and the plasticity of gut microbiome composition have made it challenging to resolve the evolutionary history of these long-term associations. Here we performed deep metagenomic sequencing of the Tsimane horticulturalists of Bolivia and compared their gut microbiomes with those of the Hadza hunter-gatherers of Tanzania[3]. These two populations, whose ancestors have been separated for tens of thousands of years, share 1,231 microbial species, most of which are rare in or absent from industrialized populations. Population genetic analyses of 636 of the shared species revealed patterns of microbial divergence and gene flow consistent with prehistoric human co-migration, with estimated split times that approximately align with human migration out of Africa and into the Americas. Our findings indicate that a diverse gut microbiome co-migrated with humans worldwide and has persisted over millennia. However, many of these species are now vanishing from industrialized populations and the consequences for human health remain uncertain.},
}

@article {pmid42844513,
year = {2026},
author = {Shruti, and Bala, K},
title = {The Gut-Insulin Axis in Polycystic Ovary Syndrome: A Narrative Review of Gut Dysbiosis, Inflammation, and Emerging Therapeutic Strategies.},
journal = {Reproductive sciences (Thousand Oaks, Calif.)},
volume = {},
number = {},
pages = {},
pmid = {42844513},
issn = {1933-7205},
abstract = {Polycystic ovary syndrome (PCOS) is a complicated, endocrine-endemic disorder with a prevalence rate of 8-13% in reproductive-age women in the world, which manifests through insulin resistance, hyperandrogenism, and reproductive dysfunction. Despite its high global prevalence, existing therapeutic interventions focus predominantly on symptom management rather than targeting the heterogeneous and multifactorial pathophysiology of the syndrome. Intestinal barrier integrity is destroyed by dysbiosis of the gut microbiota and induces endotoxemia and chronic low-grade inflammation through signalling pathways, such as LPS-TLR4-NF-kB signalling, which contribute to increased insulin resistance and androgen excess. These mechanistic pathways we dissect include changes in short-chain fatty acids (SCFAs), bile acid metabolism, involvement of FXR and TGR5 receptors, neuroendocrine regulation of the gut-brain axis, and microbial metabolites (tryptophan and agmatine), which altogether alter metabolic and reproductive abnormalities in PCOS. The preclinical evidence in the area of fecal microbiota transplantation proves the causal component of microbiota imbalance in the phenotype of PCOS. Dietary interventions that have been reviewed are fiber and resistant starch modulation, probiotics, prebiotics, synbiotics, fecal microbiota transplantation, and pharmacotherapies like metformin, which also alter the microbiome. They are heading towards individualized microbiome-based therapies and diagnostics, aided by artificial intelligence and standardized biomarkers. This review explains the emerging role of the gut-insulin axis as an important factor in the pathogenesis of PCOS and uses a novel way of combining them as a radical intervention for personalized and innovative PCOS treatment, which has the potential to enhance metabolic and endocrine health, as well as reproductive outcomes.},
}

@article {pmid42844624,
year = {2026},
author = {Yoon, J and Lee, B and Yoo, KC and Kwak, MJ and Song, HJ and Hwang, CY and Chung, Y and Kim, K and Kwon, SK and Song, JY and Yoon, HS and Kim, JF},
title = {Novel Antarctic chemolithotroph drives iron biomineralization.},
journal = {Microbiome},
volume = {14},
number = {1},
pages = {},
pmid = {42844624},
issn = {2049-2618},
mesh = {*Iron/metabolism ; *Geologic Sediments/microbiology/chemistry ; Antarctic Regions ; *Biomineralization ; Oxidation-Reduction ; *Bacteria/classification/genetics/metabolism/isolation & purification ; *Microbiota ; *Chemoautotrophic Growth ; RNA, Ribosomal, 16S/genetics ; Phylogeny ; Metagenomics/methods ; Seawater/microbiology ; },
abstract = {BACKGROUND: Iron, the most abundant redox-active metal in the Earth's crust, is coupled to numerous biogeochemical cycles. However, the mechanisms of iron oxidation and the organisms involved remain incompletely understood. Banded iron formations (BIFs) are a major reservoir of iron ore in the Precambrian sedimentary record, yet the biological contribution to their genesis remains a subject of unresolved debate. While large-scale BIF deposition largely ceased after the Proterozoic, microbial activity in modern Holocene sediments under fluctuating redox conditions provides a unique opportunity to examine mechanisms reminiscent of ancient iron cycling. Here, we report the stratigraphic sequence of microbiome profiles recorded in laminated facies with iron-containing crystalline illite in the embayment sediments beneath the Larsen C Ice Shelf (LCIS) in Antarctica during the Holocene.

RESULTS: LCIS sediments record microbial community shifts tightly coupled to environmental changes throughout the Holocene. Metagenomic analyses revealed three dominant microbial phases corresponding to geological facies boundaries. The open marine setting (phase A) showed higher taxonomic richness, whereas the sub-ice shelf sediments (phases B and C) were largely anoxic and characterized by diverse chemolithoautotrophic metabolisms. Keystone taxa including uncultured members of Thermodesulfovibrionia, as well as unique microbial communities and metabolisms, were evident in the aphotic, anoxic seawater; metagenomic analyses further revealed chemolithotrophy. The Thermodesulfovibrionia bacterium, visualized using fluorescence in situ hybridization and designated as "Candidatus Mariimomonas ferrooxydans", formed a novel clade in the phylum Nitrospirota. Metagenome-assembled genome analysis identified a putative outer-membrane Fe(II) oxidase, Cyc2, whose Fe(II)-oxidation activity was experimentally confirmed.

CONCLUSION: Our findings document the interaction between microbiome and environment, illustrating how LCIS sediments preserve a dynamic record of microbial community responses to environmental transitions. These results provide critical insights into microbial iron mineralization, echoing the biogeochemistry of the geologic past, particularly synglacial iron formation during the Neoproterozoic Snowball Earth. Video Abstract.},
}

*Iron/metabolism
*Geologic Sediments/microbiology/chemistry
Antarctic Regions
*Biomineralization
Oxidation-Reduction
*Bacteria/classification/genetics/metabolism/isolation & purification
*Microbiota
*Chemoautotrophic Growth
RNA, Ribosomal, 16S/genetics
Phylogeny
Metagenomics/methods
Seawater/microbiology

@article {pmid42844853,
year = {2026},
author = {Chen, J and Deng, W and He, J and Niu, S and Xing, S and Liao, X},
title = {Source tracking and transmission of antibiotic resistance genes mediated by core microbiota in black soldier fly larvae bioconversion of doxycycline-contaminated hen manure.},
journal = {Insect science},
volume = {},
number = {},
pages = {},
doi = {10.1111/1744-7917.70366},
pmid = {42844853},
issn = {1744-7917},
support = {32072783//National Natural Science Foundation of China/ ; 2020B1212060060//Science and Technology Program of Guangdong Province, China/ ; CARS-40//Modern Agro-industry Technology Research System/ ; },
abstract = {Black soldier fly larvae (BSFL) bioconversion of doxycycline-contaminated hen manure raises concerns about antibiotic resistance gene (ARG) transmission. Although core microbiota in gut may participate in ARG dynamics, the relative contributions of microbiota from manure and baseline larval gut to the BSFL gut resistome remain unclear. Using metagenomics, amplicon sequencing, and cultivable bacteria analysis, we found that: (1) Providencia, Klebsiella, Enterococcus, and Escherichia-Shigella dominated the BSFL gut and served as primary ARG hosts; (2) Fecal filtrate intervention drastically altered gut microbiota and ARG profiles, suppressing Klebsiella (by 95.56%) and Escherichia-Shigella (to < 0.5%) while enriching Providencia (3.53 fold increase) and Enterococcus, with increased ARGs such as tet(59) and qnrD1. Long-read metagenomic analysis indicated that viable manure-borne bacteria, rather than cell-free fecal filtrate, delivered structurally intact ARG-MGE units as key carrier of mobile resistance cassettes; (3) Source tracking (FEAST) assigned the majority of ARBs (> 90%) and their ARGs in the BSFL gut to the baseline BSFL gut source, with manure-derived ARBs contributing 4.80%. Culture-based 16S rRNA gene homology provided evidence consistent with possible manure-to-gut transfer of selected Escherichia-Shigella and Enterococcus. The BSFL gut resistome was more strongly associated with the baseline BSFL microbiota than with manure, but manure still represented a detectable source of ARB and ARG introduction. FEAST source assignments should be interpreted as composition-based bioinformatic estimates rather than definitive proof of origin, due to lack of direct functional tracing. These findings have critical implications for assessing the ecological safety of BSFL-based waste valorization.},
}

@article {pmid42845110,
year = {2026},
author = {Scheperjans, F and Borghammer, P and Pfeiffer, RF and Appel-Cresswell, S and Keshavarzian, A},
title = {The Gut-Brain Axis in Parkinson's Disease: From Clinical Observation toward Mechanism-Based Precision Medicine.},
journal = {Movement disorders : official journal of the Movement Disorder Society},
volume = {},
number = {},
pages = {},
doi = {10.1002/mds.70566},
pmid = {42845110},
issn = {1531-8257},
support = {//Sigrid Juséliuksen Säätiö/ ; 1U01DK140923-01/NH/NIH HHS/United States ; //Pacific Parkinson's Research Institute/ ; },
abstract = {Gastrointestinal dysfunction is increasingly recognized as a core feature of Parkinson's disease (PD), affecting quality of life, nutrition, medication response, and potentially the earliest stages of pathogenesis. This perspective traces the evolution of the gut from a neglected source of non-motor symptoms to a central component of biological models of PD. Gastrointestinal manifestations are physiologically heterogeneous and require objective phenotyping to distinguish dysphagia, gastroparesis, slow transit, defecatory dysfunction, and overlapping mechanisms. The body-first/brain-first framework further suggests that Lewy pathology may follow distinct anatomical trajectories, with early enteric and autonomic involvement defining a subgroup in which gut-directed biomarkers and therapies may be especially relevant. Alterations of the gut microbiome are reproducibly associated with PD, although geography, constipation, medication, diet, disease stage, and reverse causation complicate interpretation. Emerging work is shifting from taxonomy toward microbial functions and host pathways, including barrier integrity, immune and enteroendocrine signaling, short-chain fatty acids, glucagon-like peptide-1 (GLP-1), host genetic susceptibility, α-synuclein aggregation and propagation, and microbial levodopa metabolism. Trials of probiotics, fecal microbiota transplantation, and dietary interventions remain heterogeneous and have not established disease-modifying efficacy. Progress will require longitudinal studies in prodromal and subtype-defined populations, objective gastrointestinal measurements, integrated microbial, host-genetic and other multi-omics, mechanistic human and animal models, and clinical trials combining target-engagement markers with meaningful outcomes. Such an approach may enable precision gut-brain medicine for appropriately selected patients with PD. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.},
}

@article {pmid42845171,
year = {2026},
author = {Lee, HY and Kim, JH},
title = {Tissue Level and Intratumoral Microbiome: A Missing Piece in the Prostate Cancer Microbiome Landscape.},
journal = {The world journal of men's health},
volume = {},
number = {},
pages = {},
doi = {10.5534/wjmh.260229},
pmid = {42845171},
issn = {2287-4208},
support = {/SCH/Soonchunhyang University/Korea ; },
}

@article {pmid42845172,
year = {2026},
author = {Xu, Q and Song, Y and Yu, H and Wang, Y and Gu, HF},
title = {Gut Microbiota Modulation by Abelmoschus manihot (L.) Improves Circulating Metabolites and Alleviates Diabetic Nephropathy in db/db Mice.},
journal = {BioMed research international},
volume = {2026},
number = {1},
pages = {e5630909},
pmid = {42845172},
issn = {2314-6141},
support = {CPU20200228//Suzhong Pharmaceutical Group Co. Ltd/ ; },
mesh = {Animals ; *Diabetic Nephropathies/drug therapy/microbiology/blood/metabolism ; Mice ; *Gastrointestinal Microbiome/drug effects ; *Abelmoschus/chemistry ; Male ; Metabolomics ; Metabolome/drug effects ; Diabetes Mellitus, Experimental/drug therapy ; *Plant Extracts/pharmacology ; Diabetes Mellitus, Type 2/drug therapy ; Disease Models, Animal ; Mice, Inbred C57BL ; *Drugs, Chinese Herbal/pharmacology ; },
abstract = {BACKGROUND: Huangkui capsule (HKC), derived from the ethanol extract of Abelmoschus manihot (L.) flowers, is widely used in China for treating kidney diseases, including diabetic nephropathy (DN). Our previous study demonstrated that HKC modulates the intestinal microbiota and circulating metabolites in non-obese diabetic mice, a type 1 diabetes model. To further explore its efficacy, we evaluated HKC in db/db mice, a well-established type 2 diabetes and DN model.

METHODS: An HKC cohort studied in 2022 was compared with historical Ctrl and DN cohorts studied in 2021. Shotgun metagenomic sequencing was performed to characterize intestinal microbiota changes, while liquid chromatography-mass spectrometry (LC-MS)-based plasma metabolomics was used to identify alterations in circulating metabolites. The biological functions of the altered microbiota and plasma metabolites were analyzed, and the potential association between the intestinal microbiome and plasma metabolome was evaluated.

RESULTS: Compared with the historical DN cohort, the HKC cohort had higher abundances of Streptococcaceae, Streptococcus, and Massilimaliae and lower abundances of Alloprevotella and Prevotellamassilia in exploratory comparisons. In the HKC-versus-DN comparison, the archived gene set enrichment analysis reported 15 pathways with nominal positive enrichment. Additionally, 12 plasma metabolites were upregulated and 14 downregulated, including branched-chain amino acids (DL-leucine, DL-valine, D-isoleucine), organic acids (N-methyl-α-aminoisobutyric acid, guanidineacetic acid), and choline.

CONCLUSION: In db/db mice, the cohort receiving A. manihot (L.)-derived HKC had lower urinary albumin-to-creatinine ratio (UACR) and different intestinal microbiota and plasma metabolite profiles than the historical DN cohort, highlighting its therapeutic potential for DN.},
}

Animals
*Diabetic Nephropathies/drug therapy/microbiology/blood/metabolism
Mice
*Gastrointestinal Microbiome/drug effects
*Abelmoschus/chemistry
Male
Metabolomics
Metabolome/drug effects
Diabetes Mellitus, Experimental/drug therapy
*Plant Extracts/pharmacology
Diabetes Mellitus, Type 2/drug therapy
Disease Models, Animal
Mice, Inbred C57BL
*Drugs, Chinese Herbal/pharmacology

@article {pmid42845202,
year = {2026},
author = {Min, JH and Jo, YW and Her, Y and Kwon, JW},
title = {Gut-Skin Axis Revisited: A Nationwide Cohort Study on the Bi-directional Relationship Between Rosacea and Irritable Bowel Syndrome.},
journal = {Annals of dermatology},
volume = {38},
number = {5},
pages = {388-396},
doi = {10.5021/ad.25.210},
pmid = {42845202},
issn = {2005-3894},
support = {KNUH_2024-02-04//Institute of Medical Sciences, Kangwon National University/Korea ; RS-2025-24535069/KHIDI/Korea Health Industry Development Institute/Korea ; KNUH_2025-01-01//Kangwon National University Hospital/Korea ; },
abstract = {BACKGROUND: The gut-skin axis has emerged as a key concept linking cutaneous and gastrointestinal inflammation. Although prior studies have reported an increased risk of irritable bowel syndrome (IBS) among patients with rosacea, the reverse association remains unclear.

OBJECTIVE: To examine the bidirectional association between rosacea and IBS using a nationwide cohort database, clarifying whether IBS increases the risk of rosacea as well as the reverse relationship.

METHODS: We conducted a retrospective cohort study using the Korean National Health Insurance Service-National Sample Cohort (NHIS-NSC), including adults aged ≥20 years from 2002 to 2013. Incident cases of rosacea and IBS were identified using International Classification of Diseases, 10th Revision codes and matched to controls by age, sex, and index year. Cox proportional hazards models were applied to estimate adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs), controlling for sociodemographic and clinical covariates.

RESULTS: During follow-up, patients with rosacea showed a higher incidence of IBS than matched controls (56.3 vs. 36.9 per 1,000 person-years), with a significantly increased risk in the fully adjusted Cox model (aHR, 1.30; 95% CI, 1.11-1.52). Conversely, patients with IBS had a higher incidence of rosacea compared with matched controls (0.37 vs. 0.21 per 1,000 person-years), corresponding to an elevated adjusted risk (aHR, 1.61; 95% CI, 1.39-1.87). These bidirectional associations remained consistent across sensitivity and subgroup analyses.

CONCLUSION: This nationwide study demonstrates a reciprocal relationship between rosacea and IBS, underscoring shared inflammatory and neuroimmune mechanisms underlying the gut-skin axis.},
}

@article {pmid42845278,
year = {2026},
author = {Dhinakaran, AK and Voigt, AY and Szacik, A and Kang, SY and Giarratana, S and Oh, J and Jalili, S},
title = {Longitudinal microneedle sampling resolves tissue-restricted immune-microbiome dynamics in skin.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.04.24.26351513},
pmid = {42845278},
abstract = {The skin microbiome shapes local immunity, but the mechanisms of microbiome-immune crosstalk remain poorly understood. A major barrier to discovery is the lack of approaches that enable simultaneous, longitudinal measurement of microbes and immune cells from the same tissue without disrupting barrier integrity. Here we present a hydrogel-coated microneedle (MN) patch that enables minimally invasive co-sampling of viable microbes, immune cells, and interstitial fluid from skin. In humans, the patches were well tolerated and preserved inter-individual microbial signatures. Murine models colonized with commensal Staphylococcus epidermidis and the opportunistic pathogen Staphylococcus aureus , revealed distinct immune trajectories during commensal colonization, pathogen challenge, and commensal-pathogen co-colonization. Pathogen colonization drives progressive inflammatory amplification, whereas commensal exposure induces controlled immune activation that stabilizes over time. Notably, S. epidermidis reshapes pathogen-induced responses, producing a transient immune activation followed by attenuation of inflammation. These results establish MN sampling as a strategy to resolve immune-microbiome dynamics in barrier tissues and provide a framework for mechanistic studies of host-microbe interactions in health and disease.},
}

@article {pmid42845384,
year = {2026},
author = {Huang, Z and McGrath, PM and Ferdinand, DC and McCormick, BA and Ward, DV and Bucci, V and Haran, JP},
title = {Gut community-level analysis reveals an altered balance between Phocaeicola vulgatus and Bacteroides fragilis in Alzheimer's disease.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.12.743985},
pmid = {42845384},
issn = {2692-8205},
abstract = {Gut microbiome differences in Alzheimer's disease (AD) are typically cataloged taxon by taxon, yet bacterial competition and cross-feeding make species' roles dependent on the entire community. We analyzed 274 stool metagenomes from 119 older adults (18 with AD) as communities, retaining 22 recurring across 1,000 runs. Using our AI framework, we identified 15 species differing in abundance in AD, particularly the commensal Phocaeicola vulgatus (Cohen's d -0.91, 95% CI [-1.23, -0.59]), a finding robust to repeated sampling. It correlated negatively with its sister species, Phocaeicola dorei (r -0.57), suggesting possible niche competition; this replicated in an independent cohort (r -0.43). P. vulgatus was depleted in AD and the opportunistic pathogen Bacteroides fragilis enriched, shifting their balance toward B. fragilis (d -0.70), a modestly reproduced AD-associated pattern (d -0.24). Our findings suggest that AD-associated gut microbiome variation extends beyond taxon-specific abundance to the balance between specific species within a community matrix.},
}

@article {pmid42845408,
year = {2026},
author = {Glazier, J and Villegas, D and McClure, S and Ghali, J and Fuerte-Stone, J and Mimee, M},
title = {Mining Microbial Transcriptomes to Engineer Cell-Based Bacterial Biosensors in Gut-Resident Bacteroidaceae.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.10.744002},
pmid = {42845408},
issn = {2692-8205},
abstract = {The gastrointestinal tract is rich in metabolic, immune, and microbiome-derived signals that can inform the design of live biotherapeutics and diagnosis of intestinal disorders. Engineered cell-based biosensors can tap into this molecular information and report on their environment, yet their development in gut-resident symbionts has been limited by a lack of validated sensor systems. Here, we present a generalizable pipeline that leverages bacterial transcriptional profiling to identify environment-responsive systems for biosensor engineering. Candidate Sensors Systems (CSSs) mined from healthy, disease, and in vitro transcriptomes were assembled into a barcoded library in Bacteroidaceae chassis and screened in high-throughput in vivo to identify responsive promoters. A unique Bacteroidales ECF-type sigma factor operon with ties to sphingolipid metabolism and flux was highly responsive in chemically-induced colitis models. The biosensor responded robustly to disease and returned to baseline upon recovery, establishing an in vivo -driven strategy for discovering functional biosensors in non-model gut-resident bacteria.},
}

@article {pmid42845442,
year = {2026},
author = {Ragheb, M and Kiguchi, Y and Lin, JD and Hoffman, FT and Daigh, L and Chakraborty, M and Doyle, B and Grieshop, MP and Lin, A and Maghini, D and Spees, K and Bintu, L and Bassik, MC and Bhatt, AS},
title = {A microproteome screen identifies immunomodulatory bacterial microproteins encoded in expanded gene arrays in Leptotrichia.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.11.744246},
pmid = {42845442},
issn = {2692-8205},
abstract = {The human microbiome exerts broad influence in health and disease with associative studies implicating the microbiome in influencing immunity, cancer outcomes, and neurodegeneration. However, the molecular mediators of microbe-host communication remain poorly defined. Bacterial microproteins from the microbiome represent a largely uncharacterized class of potential regulators of host immunity. Here, we utilize functional genomics to interrogate 3,552 microproteins in order to identify novel microbial-immune interactions. We constructed a microproteome library from microbial metagenomic datasets, expressed it in macrophages and assayed for immunomodulatory activity. We identify several bacterial microproteins that drive macrophage M1 polarization. Among the strongest hits are a cluster of structurally related microproteins from Leptotrichia species, which are oral Gram-negative commensals associated with differential cancer outcomes. Genomic analysis reveals that Leptotrichia species encode these putative immunomodulatory microproteins in tandem arrays of up to 44 copies. These genes encode microproteins with varying sequences but conserved predicted structures. In an orthogonal approach, we demonstrate that bacterial expression of Leptotrichia microproteins influences macrophage cell state and function. As a whole, our findings identify novel microbial microproteins with immunomodulatory activity and provide a framework for future discovery of host-microbe interactions that influence human health.},
}

@article {pmid42845486,
year = {2026},
author = {De Santiago, A and Han, MK and Hargadon, SB and Marcellino Barros, M and Brito De Jesus, S and Pereira, TJ and Bik, HM},
title = {Marine nematodes exhibit widespread symbiosis, novel chemoautotrophy, and evolutionary conservation of holobiont taxa.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.12.744518},
pmid = {42845486},
issn = {2692-8205},
abstract = {Microbial symbioses drive the evolutionary and functional diversification of eukaryotic clades, from single-celled protists to large invertebrates. However, our knowledge of host-associated assemblages (the "holobiont") is limited in microscopic animal phyla with a body size <1mm, due to practical challenges such as low biomass and difficult taxonomy of host species. Marine nematodes represent an ideal case study for rapidly advancing our knowledge of bacterial-animal symbioses, representing a globally abundant invertebrate group with strong links to terrestrial and model organism species within the same phylum. Here, we sequenced the holobionts of 220 marine nematodes and generated 815 metagenome-assembled genomes (MAGs) of host-associated bacteria/archaea. Our data indicates that 20-34% of marine nematodes harbor an obligate intracellular symbiont, often with multiple endosymbionts co-occurring within the same host. Three bacterial phyla (Pseudomonadota Bacteroidota, and Verrucomicrobiota) account for three-quarters of all nematode-associated MAGs, and the majority of these holobiont MAGs represent deeply divergent lineages in the prokaryotic tree of life. The Flavobacteriaceae (a core microbiome taxon in C. elegans and other terrestrial nematodes), were consistently recovered across phylogenetically diverse marine nematode lineages, suggesting evolutionary conservation of holobiont taxa across marine and terrestrial environments. We also report a novel chemoautotroph family (Ca. Thionematobacter) recovered from nematode hosts in both deep-sea and shallow-water habitats, and report the first confirmed instance of Cardinium endosymbionts from marine invertebrates. Finally, ∼65% of nematode-associated MAGs are able to degrade chitin, via hexosaminidase, implying that benthic invertebrate holobionts make significant contributions to global carbon cycling. These results underline the importance of evaluating symbiosis in microscopic marine invertebrates, and accelerating our understanding of animal evolution and ecosystem dynamics in vast benthic habitats.},
}

@article {pmid42845678,
year = {2026},
author = {Birkner, T and Patricia Bartolomaeus, TU and McParland, V and Forslund-Startceva, SK and Löber, U},
title = {Systematic quantification and removal of host DNA contamination in 16S rRNA gene sequencing.},
journal = {Quantitative biology (Beijing, China)},
volume = {14},
number = {4},
pages = {e70055},
pmid = {42845678},
issn = {2095-4697},
abstract = {16S ribosomal RNA (rRNA) gene sequencing is a standard tool for microbial community analysis. Challenges can occur, particularly in low-biomass samples, when host DNA triggers off-target amplification. Low-biomass microbiome studies are particularly vulnerable to contamination from host DNA, which can obscure microbial signals and bias interpretation. This contamination presents a significant barrier to accurately characterizing microbial communities, especially in clinical or environmental samples with limited bacterial DNA. To systematically quantify and mitigate host DNA interference, we constructed a bacterial mock community dilution series spiked with controlled proportions of human DNA. Using 16S rRNA gene sequencing, we assessed how increasing host DNA affects microbial community profiles and evaluated several computational approaches for removing host-derived sequences, including pre-clustering filtering, post-clustering operational taxonomic unit (OTU) filtering, and the R package Decontam. We found that off-target amplification was more prevalent when the bacterial content was less than 10% relative to host DNA. Total DNA concentration induced minimal bias. Post-clustering OTU filtering and reference genome mapping effectively reduced host contamination. Among the tested correction strategies, post-clustering OTU filtering proved most effective and computationally sustainable, achieving nearly complete removal of host-derived reads with minimal effect on microbial diversity estimates. Although 16S rRNA gene sequencing remains a cost-effective and high-throughput technology, it requires rigorous methodological controls in low-biomass contexts. Our study offers a systematic evaluation of off-target amplification effects and practical mitigation strategies to improve the accuracy of microbial community analysis. The presented framework provides a robust and scalable approach for identifying and removing host contamination from low-biomass 16S rRNA sequencing data.},
}

@article {pmid42845732,
year = {2026},
author = {Meng, F and Zhang, J and Yuan, C and Li, R and Sun, Y and Jiang, H and Yang, S and Li, Y and Su, X},
title = {Precise assessment of facial skin based on multimodal data fusion of the microbiome.},
journal = {Quantitative biology (Beijing, China)},
volume = {14},
number = {3},
pages = {e70046},
pmid = {42845732},
issn = {2095-4697},
abstract = {The skin microecology plays a vital role in maintaining cutaneous health and is intricately linked to host skin phenotypes. However, there remains a lack of precise and quantitative biomarkers for evaluating skin health conditions, making it challenging to identify individuals at potential risk of microecological imbalance. In this study, we collected facial skin microbiomes from 242 female volunteers aged 16-50 years in Shanghai, China. Microbial communities were surveyed using 16S rRNA gene sequencing and integrated with high-resolution facial images and host skin phenotypes for comprehensive analysis. Our findings reveal that although the community complexity of the facial microbiome is comparable between individuals with "ideal" and "non-ideal" skin conditions, the composition and structure of key microbes varied significantly between the two groups. Differential abundance analysis further emphasized the role of interactions between the skin microbiome and host phenotypic traits in skin aging and status transitions. To enable a more holistic and quantitative assessment of facial skin status, we developed a novel multimodal skin index (MSI) that fuses multiple modal data from facial images, microbiome profiles, and host skin phenotype features through a deep learning-based framework. Importantly, MSI identified individuals with an outwardly healthy facial appearance but significant underlying microbial dysbiosis that conventional diagnostic approaches often overlook. This work enables the detection of such hidden risks, offering new avenues for individualized facial skin health assessment, precision dermatology, and microbiome-informed esthetic interventions.},
}

@article {pmid42845985,
year = {2026},
author = {Mehrotra, P and Vengadakrishnan, K and Mehrotra, P and Dan, S},
title = {Gut-brain axis dysfunction in Parkinson's disease: a meta-analysis of microbiome dysbiosis and intestinal barrier markers.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1909087},
pmid = {42845985},
issn = {2296-858X},
abstract = {BACKGROUND: Parkinson's disease (PD) has traditionally been conceptualized as a neurodegenerative disorder centered within the central nervous system. However, growing evidence suggests that gastrointestinal dysfunction, intestinal permeability abnormalities, and gut microbiome dysbiosis may contribute to disease initiation and progression in a subset of patients. While several studies have characterized microbial alterations in PD, the integration of dysbiosis with intestinal barrier dysfunction and emerging phenotype-oriented models remains incompletely synthesized.

METHODS: A systematic review and meta-analysis was conducted according to PRISMA 2020 guidelines. PubMed, Embase, Scopus, Web of Science, and Cochrane Library databases were searched from inception to January 2025 for studies evaluating gut microbiota composition and/or intestinal permeability markers in Parkinson's disease. Random-effects meta-analysis was performed using standardized mean differences (SMDs) with subgroup and sensitivity analyses exploring geographic variation, sequencing methodology, disease duration, and phenotype-specific findings.

RESULTS: Thirty-four studies were identified; one (an experimental fecal-microbiota-transfer study in mice) was reclassified as preclinical mechanistic evidence rather than a primary human dataset. The remaining 33 human studies comprised 1,588 PD patients and 1,449 healthy controls. Consistent microbial alterations were identified across studies, characterized by depletion of short-chain fatty acid-producing taxa including Prevotellaceae, Faecalibacterium, and Lachnospiraceae, alongside enrichment of Akkermansia, Bifidobacteriaceae, and Christensenellaceae. Elevated fecal calprotectin and zonulin levels suggested concomitant low-grade intestinal inflammation and impaired epithelial barrier integrity. In limited phenotype-stratified subgroup analyses, gut-first PD phenotypes showed potentially more pronounced dysbiosis patterns than brain-first phenotypes; this preliminary observation is based on very few phenotype-stratified studies and requires validation in larger, prospective cohorts. Functional interpretation of the included literature suggested potential alterations in butyrate metabolism, mucosal barrier maintenance, inflammatory signaling, and microbial-host immune interactions.

CONCLUSION: Parkinson's disease is associated with reproducible alterations in gut microbial composition together with evidence of intestinal barrier dysfunction. Although causality cannot be established from predominantly observational studies, the findings support a biologically plausible role for gut-related mechanisms in disease pathophysiology, with a preliminary signal for more pronounced involvement in gut-first PD phenotypes that remains to be confirmed. Future longitudinal and mechanistic studies integrating microbiome, metabolomic, and permeability data are required to clarify therapeutic and biomarker implications.

https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD420251078511, CRD420251078511.},
}

@article {pmid42846293,
year = {2026},
author = {Wang, Y and Guo, P and Shen, J},
title = {Gut microbiome diversity, genus-level variation, and associations with clinical features in critically ill patients.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1903736},
doi = {10.3389/fmed.2026.1903736},
pmid = {42846293},
issn = {2296-858X},
abstract = {BACKGROUND: Gut microbiota alterations are common in critical illness, but differences between critically ill patients with and without sepsis and their clinical relevance remain incompletely understood. We investigated gut microbial diversity, genus-level differences and their associations with inflammatory profiles and clinical outcomes in critically ill patients.

METHODS: This single-centre case-control study enrolled adult critically ill patients grouped by Sepsis-3 criteria. Gut microbiota was profiled by 16S rRNA sequencing. The primary M2 model, adjusted for age, intra-abdominal infection, pre-sampling anti-anaerobic antibiotic exposure, APACHE II score, and chronic kidney disease, was used for all adjusted analyses. Alpha diversity was analyzed with HC3-robust linear regression; beta diversity with PERMANOVA, PERMDISP, and dbRDA. Genus-level primary discovery used Wilcoxon rank-sum with Benjamini-Hochberg FDR and |log2 fold change| threshold. Complementary sensitivity analyses used fully adjusted MaAsLin2 and ANCOM-BC2 with pseudo-count sensitivity. Associations of the four Wilcoxon-identified genera with clinical variables were assessed via partial Spearman correlations, logistic regression, and longitudinal mixed-effects models.

RESULTS: Of 103 participants, 68 had sepsis and 35 did not. After M2 adjustment, Shannon, Simpson, and Pielou evenness were lower in sepsis (β = -0.60, -0.54, -0.60; all q = 0.025), whereas Chao1 richness and observed species did not differ. Bray-Curtis and Jaccard group effects did not meet FDR threshold. Wilcoxon identified higher Lactococcus_A and lower Ezakiella, Fenollaria, Peptoniphilus_B in sepsis. ANCOM-BC2 signals were not robust to pseudo-count sensitivity, and MaAsLin2 identified no significant genus (min q = 0.333), indicating genus-level findings inconsistent across methods. No cross-sectional clinical association met significance after FDR correction. Longitudinal analyses found time-by-genus interactions: Fenollaria with CRP (q = 0.010), Peptoniphilus_B with PCT (q = 0.042) and CRP (q = 0.010).

CONCLUSIONS: Sepsis was associated with lower values for selected alpha-diversity measures, whereas differences in overall community composition were modest. Four genera met the primary FDR- and effect-size-adjusted Wilcoxon criteria, but genus-level differences were not consistently supported across Wilcoxon, ANCOM-BC2 and MaAsLin2, indicating these are exploratory signals rather than confirmed candidates. Associations with clinical features and inflammatory markers were limited; therefore, these findings should be considered exploratory and validated using multiple analytical approaches in independent cohorts.},
}

@article {pmid42846506,
year = {2026},
author = {Zhang, X and Zhang, X and Ban, Z and White, JC and Xu, Y and Yang, J and Hou, X and Wu, F and Xing, B and Zhao, Q},
title = {Understanding the regulatory mechanisms of nanomaterials on carbon metabolism in plants.},
journal = {Fundamental research},
volume = {6},
number = {5},
pages = {2974-2985},
doi = {10.1016/j.fmre.2026.04.023},
pmid = {42846506},
issn = {2667-3258},
abstract = {Agricultural nanotechnology offers innovative strategies to enhance crop productivity by modulating fundamental physiological processes in plants. Despite growing evidence that nanomaterials (NMs) can significantly promote crop growth, a standardized theoretical framework explaining the underlying mechanisms remains elusive. This review proposes a systematic framework to elucidate how NMs positively regulate plant carbon assimilation and partitioning to ultimately enhance crop yield. We categorize internal carbon flow into three interconnected modules:(1) inorganic-organic carbon inter-conversion (photosynthesis and respiration), (2) organic carbon intra-conversion (sucrose and starch metabolism, alongside amino acid and fatty acid metabolism), and (3) supporting metabolic processes (nitrogen and secondary metabolism) that supply essential substrates and energy. To enhance carbon assimilation, NMs must be strategically selected to improve photosynthetic light conversion efficiency, electron transport, and enzyme activities, promote fatty acid metabolism, and bolster the glutamine synthetase-glutamate synthase (GS-GOGAT) cycle in nitrogen metabolism. Furthermore, NMs can modulate root exudates and reshape the structure and function of the rhizosphere microbiome, which in turn establishes a feedback loop that influences plant carbon assimilation and partitioning. This review also addresses the critical trade-offs between the economic potential and environmental risks of NMs, providing essential insights for their sustainable implementation in agriculture. Collectively, it provides a mechanistic framework for understanding NMs-plant interactions, paving the way for the rational design of nano-agricultural tools for sustainable yield improvement.},
}

@article {pmid42846579,
year = {2026},
author = {Chulenbayeva, L and Rakhmankulova, A and Kamzayeva, N and Kozhakhmetov, S and Kovenskiy, A and Nurgaziyev, M and Ukybassova, T and Kushugulova, A},
title = {Immune remodeling in HPV-associated cervical disease.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1918480},
doi = {10.3389/fcimb.2026.1918480},
pmid = {42846579},
issn = {2235-2988},
mesh = {Humans ; Female ; *Papillomavirus Infections/immunology/virology/pathology ; Cytokines/metabolism ; *Human Papillomavirus Viruses/immunology ; Vagina/immunology/microbiology/virology ; Cervix Uteri/immunology/virology/pathology ; Microbiota ; *Uterine Cervical Dysplasia/immunology/virology/pathology ; *Uterine Cervical Diseases/immunology/virology/pathology ; },
abstract = {INTRODUCTION: Persistent high-risk HPV infection is the principal cause of cervical dysplasia, but variation in disease phenotype may also be associated with differences in the local immune and microbial environment.

METHODS: We characterized the cervicovaginal immune microenvironment in relation to HPV status, vaginal community state type (CST), and cytological grade.

RESULTS: HPV-positive samples showed reduced IL-4 and IL-17E/IL-25, while IFN-α2 and IL-3 varied across community state types in a non-monotonic, CST-specific manner: IFN-α2 was relatively elevated in the Lactobacillus gasseri-dominant CST II, and IL-3 was specifically reduced in the Lactobacillus jensenii-dominant CST V. Cytological category was associated with non-monotonic, marker-specific immune variation, with LSIL showing lower IL-4, IFN-γ, IL-17F, PDGF-AB/BB, IL-17E/IL-25, and PDGF-AA levels relative to NILM, while ASC-H showed a distinct rather than uniformly progressive immune profile. CLR-based multi-kingdom analyses identified a restricted set of taxon-cytokine associations after correction of the relative-abundance scale, prespecified prevalence and abundance filtering, and multiple-testing correction. Significant bacterial associations were confined to the genus level, whereas viral associations were observed at the family, genus, and species levels and fungal associations at the family level. Phocaeicola-IL-10 and Rountreeviridae-MIP-1β were the only associations that additionally remained significant after global BH-FDR correction across all taxon-immune-marker tests. Viral and fungal findings were interpreted as exploratory because of substantially lower non-bacterial sequencing depth.

DISCUSSION: These microbial associations provide additional context for the observed immune-marker differences. These findings support further investigation of multi-kingdom host-microbiome immune relationships in HPV-associated cervical abnormalities.},
}

Humans
Female
*Papillomavirus Infections/immunology/virology/pathology
Cytokines/metabolism
*Human Papillomavirus Viruses/immunology
Vagina/immunology/microbiology/virology
Cervix Uteri/immunology/virology/pathology
Microbiota
*Uterine Cervical Dysplasia/immunology/virology/pathology
*Uterine Cervical Diseases/immunology/virology/pathology

@article {pmid42846758,
year = {2026},
author = {Zhang, W},
title = {Restoring NAD[+] pathways in brain aging and neurodegenerative diseases: roles of vitamin B3 metabolites, gut microbiota, and exercise in cognitive health.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1865556},
doi = {10.3389/fnut.2026.1865556},
pmid = {42846758},
issn = {2296-861X},
abstract = {Aging and neurodegenerative disorders (NDDs) are intricately linked to a gradual deterioration in nicotinamide adenine dinucleotide (NAD[+]) metabolism, compromised mitochondrial functionality, persistent inflammation, and modified gut-brain interactions. Derivatives of vitamin B3, such as niacin, nicotinamide, nicotinamide riboside, and nicotinamide mononucleotide, have been identified as pivotal NAD[+] precursors that possess the potential to support cellular bioenergetic processes and modulate pathways associated with brain aging. Evidence from preclinical studies and emerging clinical investigations suggests that NAD[+]-enhancing interventions may improve mitochondrial function and modulate neuroinflammatory pathways, thereby supporting cellular processes involved in synaptic plasticity and cognitive function; however, their long-term efficacy and clinical relevance in NDDs remain to be fully established. Concurrently, physical exercise serves as a robust physiological stimulus that augments NAD[+] biosynthesis, modulates hypoxia-inducible factor-1α-dependent adaptive responses, fosters neurotrophic signaling, and enhances both vascular and metabolic health of the brain. Furthermore, emerging evidence suggests that the gut microbiota directly contributes to NAD[+] homeostasis by regulating vitamin B3 precursor availability, tryptophan metabolism, and host metabolic signaling, while also influencing the efficacy of NAD[+]-enhancing interventions, thereby affecting systemic inflammation, metabolic equilibrium, and the production of neuroactive metabolites. Collectively, the interaction among vitamin B3 supplementation, physical activity, and gut microbiota may represent a promising framework for investigating strategies aimed at supporting cognitive health and brain resilience during aging, although definitive therapeutic applications require further validation. This review integrates current molecular, preclinical, and clinical evidence to establish mechanistic links between NAD[+] metabolism, brain aging, cognitive dysfunction, and neurodegeneration, while emphasizing current limitations and future translational challenges associated with combining vitamin B3 metabolites, exercise, and microbiome-targeted approaches.},
}

@article {pmid42846765,
year = {2026},
author = {Yang, Y and Zhang, D and Liu, W},
title = {Gut microbiome-driven mechanisms in inflammatory bowel disease-associated interstitial lung disease: from dysbiosis to therapeutic implications.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1967125},
doi = {10.3389/fcimb.2026.1967125},
pmid = {42846765},
issn = {2235-2988},
mesh = {Humans ; *Inflammatory Bowel Diseases/complications/microbiology/therapy ; *Dysbiosis/complications ; *Lung Diseases, Interstitial/therapy/etiology/microbiology ; *Gastrointestinal Microbiome ; Animals ; Intestinal Barrier Function ; },
abstract = {Inflammatory bowel disease (IBD) is a chronic, relapsing immune-mediated disorder of the gastrointestinal tract. Interstitial lung disease (ILD) associated with inflammatory bowel disease has been receiving increasing attention. With advances in the gut-lung axis theory, accumulating epidemiological and mechanistic evidence indicates that the association between IBD and ILD is not coincidental or merely driven by drug toxicity, but rather reflects a systemic disease spectrum involving microbiome dysbiosis and cross-organ immune dialogue. This article presents a critical narrative review that systematically summarizes the mechanisms underlying IBD-related ILD, focusing on causal evidence from large cohort and Mendelian randomization studies. It also looks at how gut microbial metabolites remotely regulate lung immune homeostasis, the inflammatory cascades triggered by gut barrier disruption and bacterial translocation, and the therapeutic potential of microbiome-based interventions. This article examines the main limitations and controversies, including the limited accuracy of animal models, the unclear causal link between microbial changes and disease onset, and the challenges in selecting clinical trial endpoints. It also outlines future research directions, focusing on integrating multi-omics, non-invasive diagnostic models, and strategies to distinguish drug-induced lung injury from primary disease involvement. This review aims to elucidate the pathogenesis of this cross-organ disease spectrum and to provide a theoretical foundation for both basic research and clinical translation.},
}

Humans
*Inflammatory Bowel Diseases/complications/microbiology/therapy
*Dysbiosis/complications
*Lung Diseases, Interstitial/therapy/etiology/microbiology
*Gastrointestinal Microbiome
Animals
Intestinal Barrier Function

@article {pmid42846826,
year = {2026},
author = {Tang, M and Li, J and Zhang, C and Tu, R and Wang, S},
title = {Gut-brain immune dysregulation in Parkinson's disease: a hypothesis-forming narrative review of trained immunity.},
journal = {Frontiers in aging neuroscience},
volume = {18},
number = {},
pages = {1973833},
doi = {10.3389/fnagi.2026.1973833},
pmid = {42846826},
issn = {1663-4365},
abstract = {Parkinson's disease (PD) is increasingly understood as a multisystem disorder in which gastrointestinal dysfunction, immune remodeling, protein aggregation, and central neurodegeneration interact across the disease course. Although gut microbiota alterations are repeatedly reported in PD, taxonomic differences alone do not explain how peripheral ecological signals acquire neurological relevance. This review therefore focuses on immune translation: the processes through which dysbiosis, microbial metabolites, intestinal barrier stress, and mucosal inflammation may reshape peripheral immunity and lower the threshold for central neuroinflammatory responses. Particular attention is given to trained immunity as a mechanistic framework that may connect repeated low-grade gut-derived stimulation with persistent innate immune reprogramming. Direct evidence that trained immunity drives PD remains limited; the concept is presented as a testable bridge rather than an established causal pathway. We integrate this framework with age-related immunosenescence and inflammaging, enteric nervous system vulnerability, vagal communication, alpha-synuclein pathology, blood-brain barrier signaling, and microglial priming. Human microbiome studies, Parkinsonian animal models, LPS-based innate immune-memory paradigms, and emerging intervention trials are considered according to their evidentiary level and major confounders, including constipation, diet, medication exposure, geography, and disease stage. The resulting model accommodates body-first, brain-first, and mixed trajectories rather than assigning a universal gut origin to PD. Therapeutically, the evidence supports a shift from nonspecific microbiome normalization toward mechanism-matched strategies that combine ecological, immune, metabolic, and clinical biomarkers. Longitudinal prodromal cohorts and integrated multi-omics with immune phenotyping will be essential to determine whether gut-brain immune signatures identify causal pathways, progression markers, or treatment-responsive subgroups.},
}

@article {pmid42846861,
year = {2026},
author = {Kumar, M and Singh, P and Almohannadi, N and Al Khodor, S},
title = {Translational approaches in microbiome research: from functional mechanisms to next-generation therapeutics.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1943873},
doi = {10.3389/fmicb.2026.1943873},
pmid = {42846861},
issn = {1664-302X},
abstract = {Microbiome research has made substantial progress toward clinical translation over the past 2 decades, moving from associative observations toward mechanistic investigation, validation, and therapeutic intervention. This narrative review examines recent advances in the clinical application of microbiome research over the past 5 years, focusing on non-invasive microbiome-derived biomarkers and therapeutic strategies, including personalized probiotics and prebiotics, fecal microbiota transplantation (FMT), and engineered microbial therapeutics, while evaluating the strength of the supporting evidence. Microbiota-based treatments for recurrent Clostridium difficile infection are currently at the forefront of clinical translation, whereas applications in inflammatory, metabolic, neurological, and oncological disorders remain largely investigational. We further examine these translational barriers while highlighting opportunities to integrate microbiome data with systems biology and advanced analytics to improve clinical outcomes and advance precision medicine. By linking mechanistic discoveries with their current level of clinical development, this narrative review critically evaluates the available translational microbiome evidence, identifies key bottlenecks and unresolved knowledge gaps, and outlines priorities for the responsible integration of microbiome-based diagnostics and therapeutics into clinical practice.},
}

@article {pmid42846992,
year = {2026},
author = {Wang, L and Wang, J and Zhang, Y and Wang, B and Sun, X and Li, Y and Yan, J and Yun, K and Su, H},
title = {Longitudinal dynamics of the gut microbiome during methamphetamine addiction and abstinence.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1911776},
doi = {10.3389/fmicb.2026.1911776},
pmid = {42846992},
issn = {1664-302X},
abstract = {INTRODUCTION: Methamphetamine (METH) addiction is a chronic neuropsychiatric disorder characterized by severe abstinence symptoms and high relapse rates, yet the temporal dynamics of gut microbiota alterations across addiction and abstinence phases remain poorly understood.

METHODS: In this study, we performed a longitudinal microbiome analysis to characterize differences between phases and time-dependent remodeling of the gut microbiota in a mouse model. Fecal samples were collected at defined time points across a 60-day addiction phase followed by a 60-day abstinence phase and analyzed using 16S rRNA gene sequencing.

RESULTS: Distinct microbial compositions, diversity and community structure differences were observed between addiction and abstinence phases. Microbial communities during the addiction phase exhibited greater dispersion, whereas progressive stabilization was observed during abstinence. Time-series analyses revealed characteristic alterations in Verrucomicrobia and Actinobacteria during prolonged addiction and early abstinence. At the genus level, Butyricimonas, Candidatus Arthromitus, Enterococcus, and Turicibacter exhibited reproducible phase- and temporal-dependent dynamic patterns. Based on these microbial signatures, random forest models were constructed for phase classification and temporal prediction. The classification model achieved higher model performance during the addiction phase, whereas performance declined during abstinence, reflected by reduced variance explained and increased heterogeneity in gut microbiota composition. Temporal prediction models further demonstrated differential predictive performance between phases.

DISCUSSION: These findings identify reproducible temporal changes in gut microbiota across addiction and abstinence and highlight candidate microbial signatures for understanding addiction progression and distinguishing different phases.},
}

@article {pmid42847684,
year = {2026},
author = {Xiao, S and Zhuang, Q and Cui, G and Li, Y},
title = {Lung microbiome community state types are associated with ventilator-associated pneumonia risk: a secondary analysis of the MicroNAV cohort.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0126326},
doi = {10.1128/spectrum.01263-26},
pmid = {42847684},
issn = {2165-0497},
abstract = {UNLABELLED: In the publicly available MicroNAV cohort, baseline diversity analyses did not distinguish patients who developed ventilator-associated pneumonia (VAP) from non-VAP patients, leaving it unresolved whether community-state structure contains risk information. In an independent secondary analysis, we reprocessed raw 16S rRNA gene sequencing data from bronchoalveolar lavage samples using DADA2 exact amplicon sequence variant inference and decontam quality control, and analyzed 75 at-risk mechanically ventilated patients with paired longitudinal sampling (40 VAP and 35 non-VAP). No baseline genus distinguished future VAP from non-VAP by DESeq2 or MaAsLin3 after adjustment for sex and Glasgow Coma Scale (all adjusted P > 0.05). Dirichlet multinomial mixture modeling identified three community state types (CSTs) with distinct ecological profiles. In cause-specific Cox regression, CST1, a high-burden, oral-associated state, was associated with higher VAP hazard than CST2, a low-burden, diverse state (hazard ratio, 2.85; 95% CI, 1.15-7.02, P = 0.023; Gray's test, P = 0.042). Adding CST to a burden-only model improved fit (likelihood-ratio test, P = 0.041), whereas pathogen species cultured at VAP onset did not differ by baseline CST (simulated Fisher's exact test, P = 0.98). During ventilation, 12 oral-associated genera declined while total bacterial burden remained stable (linear mixed model, P = 0.66), but the association between commensal loss and subsequent VAP was not consistent across abundance scales. Baseline IL-1β and TNF-α concentrations were explained primarily by bacterial burden rather than community composition. These findings suggest that baseline lower-airway ecological states capture VAP susceptibility information not resolved by single-taxon, diversity, or burden-only analyses.

IMPORTANCE: In mechanically ventilated ICU patients without pulmonary infection at baseline, the early lower-airway ecosystem may contain information about subsequent ventilator-associated pneumonia (VAP) susceptibility. In this independent reanalysis of the public MicroNAV cohort, baseline lower-airway communities classified by Dirichlet multinomial mixture modeling resolved into ecological states with different subsequent VAP risk, while individual genera, bacterial burden alone, and the eventual cultured pathogen did not explain the signal. Mechanical ventilation produced shared community restructuring: oral-associated genera declined and other taxa expanded, yet total bacterial burden remained stable, indicating ecological replacement rather than bacterial clearance. This restructuring was not consistently VAP-specific, and apparent community state type-dependent differences in declining-genus loss partly reflected different starting proportions. Together, these findings extend the original cohort by separating starting state heterogeneity from ventilation-associated restructuring. They suggest that initially noninfected ventilated airways represent distinct host-microbial terrains that may differ in vulnerability to pneumonia.},
}

@article {pmid42847686,
year = {2026},
author = {Lane, KR and Meyer-Kaiser, KS and Collens, AB and Leal, CV and Collins, AG and Herrera, S and Hansel, CM},
title = {Deep-sea siliceous sponges harbor distinct and functionally diverse microbiomes.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0174726},
doi = {10.1128/aem.01747-26},
pmid = {42847686},
issn = {1098-5336},
abstract = {Sponges, phylum Porifera, are long-lived and basal-branching metazoans that play important roles in ocean biogeochemistry and host diverse microbial communities. Siliceous sponges form a major clade of the Porifera; however, their microbiome is not well characterized, particularly in the deep ocean. Here, we used shotgun metagenomics to investigate the composition of the microbial communities of 13 siliceous sponges collected from four sites near Puerto Rico from depths ranging from 400 to 1,900 meters. Nine of the sponges in this study are from five sponge families that have not previously been sequenced using shotgun metagenomics. We assembled a total of 176 metagenome-assembled genomes from 20 bacterial phyla and 1 archaeal phylum. Ammonia-oxidizing archaea (AOA) Nitrosopumilaceae dominated most siliceous sponge microbial communities and was strikingly the sole symbiont associated with one sponge (Farrea). Overall, microbiome diversity was relatively low across siliceous sponges, except for a Phloeodictyidae, which is likely a high microbial abundance (HMA) sponge. Our results suggest that host sponge phylogeny may shape microbial community structure, with limited evidence for an environmental role. The sponge-associated microbial communities contained genetic capabilities for diverse metabolic functions, particularly contributing to the carbon, nitrogen, and sulfur cycles. In addition to the AOA, evidence of potential for microbial autotrophy was found through the presence of genes for RuBisCO, methanotrophy, and ATP citrate lyase. These results reveal both conserved relationships and metabolic flexibility across siliceous sponge lineages, suggesting unique evolutionary dynamics and demonstrating the importance of microbial metabolism to sponge host health and nutrient cycling in the oligotrophic deep ocean.IMPORTANCEMarine sponges, emerging ~600 million years ago, have close relationships with microorganisms, but the microbiome of deep-sea siliceous sponges is not well understood. Siliceous sponges play essential roles in deep-sea ecosystems by providing habitats for other metazoans and mediating carbon, nitrogen, and sulfur cycling; however, they remain some of the least-studied sponges. By shotgun sequencing DNA from 13 siliceous sponges collected near Puerto Rico, this study found that host sponge phylogeny is linked to microbial community composition and structure. Ammonia-oxidizing archaea dominated the microbial communities associated with marine sponges, likely playing key roles in utilizing metabolic byproducts and supporting host health. Other microbes also contributed to nutrient cycling and contained the potential to fix carbon, suggesting metabolic flexibility, which may benefit sponge hosts in low-resource environments. These findings emphasize the ecological importance of siliceous sponge-microbe symbioses and contribute to our understanding of the drivers shaping their structure and function.},
}

@article {pmid42847700,
year = {2026},
author = {Singh, VY and Gadekar, VP and Sasikumar, S and Lokshanan, RMR and Senthamizhan, V and Prithiviraj, B and Sinha, H and Raman, K},
title = {Microbial communities on station and train surfaces in Chennai Metro: insights into urban transit microbiome.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0043326},
doi = {10.1128/msphere.00433-26},
pmid = {42847700},
issn = {2379-5042},
abstract = {UNLABELLED: Urban public transport systems, particularly metro networks, serve as key hubs for microbial transmission, yet the urban microbiome in densely populated regions like India remains poorly characterized. Understanding these environments is crucial for public health, especially in light of the COVID-19 pandemic and growing concerns about antimicrobial resistance (AMR). This study is the first of its kind to investigate the microbial communities and the presence of AMR genes in the Chennai Metro system. We collected 96 surface swabs from 12 metro stations across two lines, focusing on surfaces that people frequently touch, such as handrails, kiosks, banisters, and ticket counters. Of the collected samples, 47 met quality control standards and were subjected to shotgun metagenomic sequencing, and 41 samples with more than 1 million reads were included in our analysis. Our findings indicate that surface type significantly influences microbial community structure, with kiosks exhibiting the highest microbial diversity. Comparative analysis with global urban data sets revealed unique microbial patterns specific to Chennai, including nine species that were notably more prevalent in our samples than in other urban transit systems worldwide. Furthermore, through pangenome analysis, we generated high-quality metagenome-assembled genomes that elucidated the adaptive strategies of dominant microbial species in this urban environment. Despite their relatively low abundance, several AMR families were widely distributed across the data set, with over 80% of samples containing at least one associated AMR gene, including families linked to rifamycins, multidrug resistance, and sulfonamides. This study lays a foundation for understanding the urban microbiome in India, emphasizing distinct regional characteristics and underscoring the need for sustained monitoring to mitigate disease transmission risks in high-density transit settings.

IMPORTANCE: Densely populated urban transit systems are critical hubs for microbial exchange, yet the mass transit microbiomes of Indian cities remain largely uncharacterized, representing a significant gap in global surveillance. Our study provides the first comprehensive metagenomic analysis of the Chennai Metro, a high-traffic transit network serving millions. Our findings highlight the unique environmental drivers shaping urban microbiota in India. Chennai, with over 12 million residents and a metro system serving over 105 million passengers annually, is an ideal yet uncharacterized environment for studying microbial dynamics, surface-microbe interactions, and environmental antimicrobial resistance reservoirs.},
}

@article {pmid42847788,
year = {2026},
author = {Mikhail, A and Bhullar, H and Dalal, R and Goyal, P and Shah, N and Pan, B and Fredericks-Younger, J and Feldman, CA and Subramanian, G},
title = {Making a case for dental clinical practice guidelines for elective antibiotic use: an institutional retrospective study.},
journal = {Quintessence international (Berlin, Germany : 1985)},
volume = {0},
number = {0},
pages = {0},
doi = {10.3290/j.qi.b7121933},
pmid = {42847788},
issn = {1936-7163},
abstract = {BACKGROUND: Antibiotic overuse disrupts host-microbiome equilibrium, and increases risks of diarrhea, drug allergies, and multi-drug resistance. Dentists are the third largest prescribers of oral antibiotics in the US. Investigating antibiotic prescribing patterns alongside dental procedures may identify opportunities to reduce antibiotic overuse.

METHOD: Institutional antibiotic prescriptions (Abx-Rx) dispensed with dental procedures were retrospectively reviewed from 2017-2022. Augmentin® (USAntibiotics, TN) and clindamycin prescriptions were investigated for nonindicated vs. well-reasoned use, comparing implant-related and extraction-related procedures.

RESULTS: Over 7,158 Abx-Rx, dispensed with 3,320 (56% of) implant-related, 4,084 (14% of) extraction-related, and 256 overlapping visits, included amoxicillin (79.75%), clindamycin (7.23%), Augmentin® (6.3%), azithromycin (4.2%), and penicillin VK (1.53%). Implant-related procedures were 7.8-fold more likely than extraction-related to involve Abx-Rx [95% CI: 7.392-8.373, p<0.05]. Use of Augmentin® and clindamycin (the two most dispensed broad-spectrum antibiotics) in dental procedures was evaluated further. Over 60% of Augmentin® prescriptions (n=352) were implant-related, of which 88% were nonindicated, versus 48% of dental extractions-related. Implant-related Augmentin® prescriptions were 8-fold more likely to be pre-emptive [95% CI 4.676, 14.47, p<0.05)]. Of 460 clindamycin prescriptions, implant-related prescriptions (30%) were 1.5-fold more likely nonindicated than were extraction-related [95%CI 1.019, 2.443, p<0.05]; 76% occurred in patients reporting penicillin allergy.

CONCLUSION: Implant-related procedures more frequently involved nonindicated, broad-spectrum antibiotic use, highlighting the need for evidence-based guidelines to reduce antibiotic overuse. Clindamycin use can further be reduced with the justified use of alternative safer antibiotics and minimizing mislabeling of penicillin allergy. Clinical Practice Guidelines for antibiotic use following dental procedures can promote judicious antibiotic use.},
}

@article {pmid42847914,
year = {2026},
author = {Wu, D and Quzong, C and Jia, Z and Schwalb, A and Guggenberger, G and Wang, S and Dorji, T and Pester, M},
title = {Nitrogen fertilization outweighs plant species loss in shaping bacterial belowground diversity in an alpine meadow on the central Tibetan Plateau.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag110},
pmid = {42847914},
issn = {1574-6941},
abstract = {Plant species loss and nitrogen fertilization affect grassland biodiversity. However, their interactive effects on plant communities, soil properties, and the soil microbiome remain insufficiently understood. We analyzed how the removal of plant species, with and without urea addition, influenced plant diversity, soil properties, and soil bacterial communities in a Tibetan Plateau grassland. Continuous plant species removal and urea addition over seven years modified plant beta-diversity equally strong, while urea exerted a stronger negative effect on plant alpha-diversity. Both, plant species removal and urea addition caused soil acidification and an increase in NO2[-]/NO3[-], while dynamics in TOC and TON were mainly driven by the growing season. Structural equation modeling identified soil acidification via urea addition as the most important indirect driver that negatively affected bacterial alpha-diversity and shifted bacterial beta-diversity. Urea addition also exerted direct negative effects on bacterial alpha- and beta-diversity, causing repression of oligotrophic (Acidobacteriota, Chloroflexota, Planctomycetota, Gemmatimonadota) and stimulation of copiotrophic (Bacillota, Bacteroidota, Pseudomonadota) bacterial taxa. Plant species removal caused slight increases in bacterial alpha-diversity, paralleled by less diverse but more even plant communities. We show that soil acidification by urea fertilization outweighs plant species loss in its negative effect on bacterial soil biodiversity in Tibetan grasslands.},
}

@article {pmid42848148,
year = {2026},
author = {Li, Y},
title = {The gut-pancreas axis: microbial dysbiosis as a pathogenic driver of diabetes and pancreatic cancer.},
journal = {Medical oncology (Northwood, London, England)},
volume = {43},
number = {11},
pages = {},
pmid = {42848148},
issn = {1559-131X},
mesh = {Humans ; *Pancreatic Neoplasms/microbiology/metabolism/pathology ; *Dysbiosis/complications/microbiology ; *Gastrointestinal Microbiome/physiology ; *Diabetes Mellitus, Type 2/microbiology ; Animals ; *Pancreas/metabolism/microbiology/pathology ; Signal Transduction ; },
abstract = {The gut microbiome dysbiosis is a potential contributing mediator for the gut and pancreas link. The gut microbiome contributes to the development of both diabetes and pancreatic cancer. There are approximately two distinct ways through which the gut microbiome leads to cell damage and then systemic inflammatory responses. The gut microbiome generates a unique set of metabolic products, activating diverse pathways and cytokines. The bottom line for this process leads to the generation of systemic inflammation. In type 2 diabetes, inflammatory signaling predominantly disrupts IRS-1/PI3K/AKT signaling, impairing insulin receptor pathways and glucose absorption, triggering β-cell malfunction and insulin resistance. Dysbiosis-associated inflammatory signaling in pancreatic cancer stimulates the growth of the tumour via activating oncogenic pathways, immune evasion, and epithelial-mesenchymal transition (EMT). The bacterial metabolites can cause. DNA mutations and affect the signaling pathways of cancer cells. In addition, this review offers an integrated microbiome-driven inflammatory-metabolic paradigm utilizing the gut-pancreas axis to associate pancreatic cancer and diabetes. A realistic and in-depth understanding of the above-described processes could result in the development of new techniques for the targeted modification of the gut microbiome for the prevention and management of such diseases.},
}

Humans
*Pancreatic Neoplasms/microbiology/metabolism/pathology
*Dysbiosis/complications/microbiology
*Gastrointestinal Microbiome/physiology
*Diabetes Mellitus, Type 2/microbiology
Animals
*Pancreas/metabolism/microbiology/pathology
Signal Transduction

@article {pmid42848192,
year = {2026},
author = {Giardino, M and Pasquini, V},
title = {Converging etiopathogenetic pathways and early prevention opportunities for autism and neurodevelopmental disorders in the first 1000 days of life: a brief narrative review.},
journal = {Neuropsychiatrie : Klinik, Diagnostik, Therapie und Rehabilitation : Organ der Gesellschaft Osterreichischer Nervenarzte und Psychiater},
volume = {},
number = {},
pages = {},
pmid = {42848192},
issn = {2194-1327},
abstract = {Neurodevelopmental disorders, including autism spectrum disorder, result from complex interactions between genetic susceptibility and early-life environmental exposures that shape brain development. Their increasing prevalence represents a major public health challenge, highlighting the need for effective preventive strategies. This brief narrative review synthesizes current evidence on the converging etiopathogenetic pathways-including genetic vulnerability, environmental risk factors, epigenetic regulation, neuroinflammation, and gut microbiome alterations-that operate during the first 1000 days of life and collectively influence neurodevelopmental trajectories. We also discuss early prevention opportunities targeting modifiable risk factors during this critical developmental window, when heightened neuroplasticity may maximize the effectiveness of preventive interventions. Viewing autism spectrum disorder and related neurodevelopmental disorders through the lens of shared biological mechanisms, provides a framework for precision prevention, facilitates earlier identification of at-risk individuals, and supports the development of multidisciplinary strategies aimed at improving lifelong neurodevelopmental health and reducing the long-term burden on affected individuals, families, and healthcare systems.},
}

@article {pmid42848247,
year = {2026},
author = {Sagawa, T and Hirakawa, M and Nagashima, H and Fujikawa, K},
title = {Tumor microenvironment and gut microbiome in immunotherapy resistance in gastric cancer: clinical questions, biological mechanisms, and evidence-based therapeutic perspectives.},
journal = {Medical oncology (Northwood, London, England)},
volume = {43},
number = {11},
pages = {},
pmid = {42848247},
issn = {1559-131X},
mesh = {Humans ; *Stomach Neoplasms/immunology/microbiology/drug therapy/therapy/pathology ; *Tumor Microenvironment/immunology ; *Drug Resistance, Neoplasm/immunology ; *Gastrointestinal Microbiome/immunology/drug effects ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; *Immunotherapy/methods ; },
abstract = {Immune checkpoint inhibitors (ICIs) have improved systemic therapy for advanced gastric and gastroesophageal junction cancer, yet primary and acquired resistance remain common and are incompletely explained by established tumor biomarkers. This narrative review evaluates the connected roles of the tumor microenvironment (TME), host immunity, and the gut microbiome in shaping ICI resistance in gastric cancer. We performed a structured PubMed search through 28 August 2026 and prioritized gastric cancer-specific clinical and translational evidence, supplemented by systematic reviews, meta-analyses, and mechanistically relevant studies from other tumor types when necessary. Within the gastric cancer TME, cancer-associated fibroblasts, myeloid cells, regulatory T cells, extracellular matrix remodeling, hypoxia, angiogenesis, and T-cell exhaustion can promote immune exclusion or dysfunction. Microbial diversity, microbial metabolites, antibiotics, proton pump inhibitors, defined live biotherapeutics, fecal microbiota transplantation, and diet may influence systemic antitumor immunity, but most human evidence is retrospective, cross-sectional, or derived from non-gastric cancers. Clinically, antibiotic stewardship, reassessment of unnecessary acid suppression, and nutritional optimization are reasonable supportive measures, whereas routine probiotic supplementation, Clostridium butyricum MIYAIRI 588 for ICI sensitization, and fecal microbiota transplantation remain investigational in gastric cancer. Future studies should integrate longitudinal exposures, serial TME profiling, stool metagenomics, medication use, nutritional status, and clinical outcomes. The TME-gut microbiome axis is therefore a biologically plausible framework for biomarker-guided research, but current evidence does not justify empiric microbiome-directed anticancer therapy in gastric cancer.},
}

Humans
*Stomach Neoplasms/immunology/microbiology/drug therapy/therapy/pathology
*Tumor Microenvironment/immunology
*Drug Resistance, Neoplasm/immunology
*Gastrointestinal Microbiome/immunology/drug effects
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
*Immunotherapy/methods

@article {pmid42848321,
year = {2026},
author = {Sanz-Puente, I and Abdelfattah, A and Robledo, M},
title = {The Wheat Seed Microbiome as a Model for Understanding the Transmission of Beneficial Plant-Associated Bacteria.},
journal = {Journal of experimental botany},
volume = {},
number = {},
pages = {},
doi = {10.1093/jxb/erag499},
pmid = {42848321},
issn = {1460-2431},
abstract = {Beneficial plant-microbe interactions are fundamental to plant nutrition, growth, stress tolerance and disease resistance. However, because microorganisms are not encoded by the plant genome, the mechanisms by which microbial associations persist across generations remain unresolved. In this review, we examine the emerging evidence that seeds function not only as reproductive structures but also as reservoirs of microorganisms that may facilitate the maintenance and transmission of selected microbial partners. We synthesize current knowledge of seed microbiome diversity, ecological functions and assembly processes, highlighting the roles of maternal, floral, pollen-mediated and environmental transmission, together with host selection and microbial interactions. We then evaluate evidence that seed-borne microorganisms contribute to plant microbiome assembly and may support the multigenerational persistence of beneficial taxa. Using wheat as a model system, we explore how domestication and host genetic control have shaped microbial communities, assess evidence for recurrent the seed-borne presence of specific bacterial taxa, propose a candidate wheat seed bacterial meta-core based on taxa repeatedly detected across independent studies, and highlight Pantoea as a candidate lineage showing evidence of within-generation persistence and multigenerational transmission across generations. Finally, we discuss the conceptual and methodological challenges that currently limit our understanding of microbiome inheritance as a general biological principle and explore how this knowledge may guide future microbiome-assisted crop improvement. Together, these findings position seeds as key ecological and evolutionary hubs through which beneficial plant-microbe interactions may persist and potentially be inherited across generations.},
}

@article {pmid42848445,
year = {2026},
author = {Cromb, S and Mayboca-Padilla, D and Bedi, R and Narvaez-Bravo, C},
title = {Evaluating packaged ice safety using culture-based and metagenomic methods.},
journal = {Microbiology (Reading, England)},
volume = {172},
number = {10},
pages = {},
pmid = {42848445},
issn = {1465-2080},
mesh = {*Metagenomics/methods ; *Ice/analysis ; *Bacteria/isolation & purification/genetics/classification/drug effects ; *Food Microbiology ; Food Safety ; Drug Resistance, Bacterial/genetics ; Pseudomonas/isolation & purification/genetics ; },
abstract = {Ice can serve as a vector for microbial contamination, presenting potential risks to public health. This study aimed to evaluate the microbial quality and safety of commercially available ice in Manitoba as well as to characterize the microbiome of ice cubes and assess the presence of antimicrobial resistance (AMR) genes. Samples from five different brands, four non-International Packaged Ice Association (IPIA)-accredited and one IPIA-accredited brand, were collected from retail stores between May and August 2024. Ice samples were tested using membrane filtration for total plate count, Escherichia coli, coliforms, Pseudomonas, yeasts, moulds and Enterococcus and screened for Listeria monocytogenes and Salmonella. Separate filtration samples were collected for metagenomic analysis. Membrane filtration results showed that 12.8% of samples from non-IPIA-accredited brands failed to meet IPIA standards for total coliforms, whereas 100% of samples from the IPIA-accredited brand complied. All samples tested negative for foodborne pathogens when conventional culture-based methods were used. However, metagenomic sequencing revealed the presence of pathogen-associated DNA. A diverse resistome was identified across all brands, including the IPIA-accredited sample, with genes conferring resistance to β-lactams, aminoglycosides and biocides. Recovered Pseudomonas isolates were identified as Pseudomonas lactis, a psychrotrophic species capable of growth at refrigeration temperatures. Biofilm assays demonstrated that recovered P. lactis formed biofilms at both 4 and 10 °C, with significantly greater biofilm formation observed at 4 °C. Our findings demonstrate consistent compliance among the IPIA-accredited brand, while variability and failures occurred among non-accredited producers. The detection of cold-adapted, biofilm-forming bacteria such as Pseudomonas spp., which can reduce sanitizer efficacy and protect co-existing micro-organisms, including potential pathogens harbouring AMR genes, highlights the need for targeted environmental monitoring using key indicator organisms such as Pseudomonas spp. Broader adoption of IPIA standards could strengthen microbial control practices and enhance consumer protection within the Canadian packaged ice industry.},
}

*Metagenomics/methods
*Ice/analysis
*Bacteria/isolation & purification/genetics/classification/drug effects
*Food Microbiology
Food Safety
Drug Resistance, Bacterial/genetics
Pseudomonas/isolation & purification/genetics

@article {pmid40873226,
year = {2026},
author = {Singh, V and Yadav, A and Taj, T and Islam, A and Mantry, S and Debnath, B and Kumar, B and Ashique, S},
title = {Decoding the Gut-Brain Axis in Alzheimer's Disease: Emerging Perspectives.},
journal = {CNS & neurological disorders drug targets},
volume = {25},
number = {8},
pages = {621-644},
pmid = {40873226},
issn = {1996-3181},
mesh = {Humans ; *Alzheimer Disease/metabolism/microbiology ; *Gastrointestinal Microbiome/physiology ; Animals ; *Dysbiosis/metabolism ; *Brain/metabolism ; *Brain-Gut Axis/physiology ; Blood-Brain Barrier/metabolism ; Intestinal Barrier Function ; },
abstract = {Alzheimer's disease (AD) is a leading source of dementia, evidenced by cognitive debility, tau neurofibrillary tangles, and amyloid-β plaques. Recent studies emphasize the gut-brain axis as a vital element in the pathogenesis of Alzheimer's disease, involving microbial, neuronal, immunological, and hormonal mechanisms. The composition of gut microbiota dysbiosis is determined by growth in intestinal barrier permeability and activation of immune cells, which causes impaired function of the blood-brain barrier that stimulates neural injury, neuronal loss, neuroinflammation, and eventually AD. Various studies have reported that the gut microbiota plays a crucial role in brain function and changes in individual behavior, as well as in bacterial amyloid formation. Growing experimental and clinical data specify the conspicuous role of intestinal dysbiosis and microbiota- host interactions in AD. The importance of this paper is the focus on the potential association of AD and gut microbiota and also a discussion of the therapeutic modalities of inhibiting gut dysbiosis.},
}

Humans
*Alzheimer Disease/metabolism/microbiology
*Gastrointestinal Microbiome/physiology
Animals
*Dysbiosis/metabolism
*Brain/metabolism
*Brain-Gut Axis/physiology
Blood-Brain Barrier/metabolism
Intestinal Barrier Function

@article {pmid42836733,
year = {2026},
author = {Li, D and Qu, Z and Feng, W and Zhou, X and Cai, L},
title = {Network-guided synthesis of antagonistic microbiota for suppressing maize stalk rot disease.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag243},
pmid = {42836733},
issn = {1751-7370},
abstract = {Plant-associated microbiomes play a crucial role in sustaining host health and fitness, but how pathogen invasion reshapes microbial interaction networks and how to leverage this for developing effective biocontrol strategies remain poorly understood. This study investigated the maize microbiome under Fusarium stalk rot stress by integrating large-scale amplicon sequencing, network refinement, and experimental validation. To distinguish biological interactions from spurious associations driven by environmental and geographic factors, we applied a refined analytical framework to filter out abiotic correlations. The resulting interaction networks revealed that pathogen infection significantly increased network complexity and the proportion of potential negative interactions across all maize compartments except seeds. Specifically, potential negative interactions with Fusarium were significantly enriched in the rhizosphere microbiome, encompassing numerous uncultured taxa and known biocontrol genera (e.g., Epicoccum, Burkholderia, and Nocardioides). Representative strains from these taxa were subsequently isolated and assembled into a synthetic microbial community (SynCom). This refined network-derived SynCom significantly suppressed maize stalk rot caused by Fusarium verticillioides and F. graminearum. In non-sterilized soil, this SynCom exhibited significantly stronger disease-suppressive effects than either the randomly assembled SynCom or the SynCom derived from the unrefined network. Integrated transcriptomic and metabolomic analyses suggested that the SynCom confers resistance through the production of antifungal metabolites, including azelaic acid, and potentially through the induction of host defense responses. Collectively, our study provides meaningful insights into plant-microbe interaction under pathogen stress and suggests an analytical-experimental workflow that integrates computational ecology with experimental validation for developing biocontrol strategies against maize stalk rot.},
}

@article {pmid42836844,
year = {2026},
author = {Dobrila, HA and Licha, H and Hryckowian, AJ},
title = {EndD mediates butyrate-dependent toxin release and sporulation in Clostridioides difficile.},
journal = {Journal of bacteriology},
volume = {},
number = {},
pages = {e0034126},
doi = {10.1128/jb.00341-26},
pmid = {42836844},
issn = {1098-5530},
abstract = {Clostridioides difficile is an urgent threat to human health. Current treatments for C. difficile infections (CDIs) are antibiotics and microbiome restoration therapy (MRT) for recurrent cases. However, antibiotics contribute to antibiotic resistance and recurrent CDIs, and the long-term sustainability and accessibility of MRTs remain to be determined. Since a dysbiotic gut microbiome is the primary risk factor for CDI, a better understanding of the interactions between C. difficile, the microbiome, and the host will aid development of treatments with improved precision. Emerging evidence supports that butyrate, a prominent end product of gut microbiome metabolism, is a key determinant of C. difficile pathogenesis. Notably, C. difficile releases more of its toxins (TcdA and TcdB) in butyrate-rich environments. Here, we demonstrate that butyrate-dependent toxin release is not driven by two previously characterized modes of toxin release (e.g., TcdE-dependent secretion or Cwp19-dependent autolysis). Instead, butyrate enhances the expression of a broadly conserved endolysin (EndD), which is responsible for butyrate-dependent toxin release. We additionally demonstrate that endD-dependent toxin release does not universally occur under all growth conditions, that its expression is dependent on the late-stage sporulation sigma factor SigK, and that endD enhances butyrate-dependent sporulation. Overall, our findings provide deeper insight into butyrate-dependent effects on C. difficile pathogenesis and set the stage for future work to better understand the molecular and genetic underpinnings of endD regulation.IMPORTANCEClostridioides difficile is a leading cause of infectious diarrhea. The gut microbiome-derived short-chain fatty acid butyrate triggers C. difficile to release its major virulence factors, toxins TcdA and TcdB. Here, we show that butyrate-dependent toxin release is independent of classical secretion or autolytic pathways and is instead mediated by EndD, an endolysin broadly conserved among C. difficile clinical isolates. We also demonstrate that endD expression is governed by the sporulation factor SigK and enhances sporulation, directly linking transmission and virulence. Uncovering how C. difficile couples metabolic sensing to EndD-mediated toxin release and sporulation advances our understanding of pathogen-microbiome interactions and highlights potential targets for non-antibiotic therapeutics.},
}

@article {pmid42836883,
year = {2026},
author = {Wnuk, M and Szczęch, J and Żuk, G and Szmatoła, T and Oklejewicz, B and Samotij, D and Lewińska, A and Reich, A},
title = {Characterization of oral microbiome in atopic dermatitis patients treated with dupilumab or upadacitinib.},
journal = {Clinical oral investigations},
volume = {30},
number = {11},
pages = {},
pmid = {42836883},
issn = {1436-3771},
mesh = {Humans ; *Dermatitis, Atopic/drug therapy/microbiology ; Male ; *Microbiota/drug effects ; Female ; *Antibodies, Monoclonal, Humanized/therapeutic use ; Adult ; Treatment Outcome ; RNA, Ribosomal, 16S ; *Mouth/microbiology ; },
abstract = {OBJECTIVES: Dysbiosis, an imbalanced state of microbial communities in the human body, may contribute to autoimmune diseases such as atopic dermatitis (AD). While the role of affected skin-gut microbiome axis in AD is well established, still little is known about the relationship between oral microflora-based dysbiosis and AD progression and treatment.

MATERIALS AND METHODS: 16S rRNA gene amplicon sequencing of the V3-V4 hypervariable region was used to characterize the bacterial profiles of saliva samples from fifteen AD patients treated with dupilumab, an antibody against interleukin-4 receptor, or upadacitinib, an inhibitor of JAK1 kinase, for sixteen weeks. Oral microbiome data were compared with the Eczema Area and Severity Index (EASI).

RESULTS: Analysis revealed that at phylum level, Actinomycetota decreased significantly upon treatment (from a median of 11.87% to 6.15%; q = 0.0094), with a reciprocal increase in Bacteroidota (from 19.78% to 28.39%; q = 0.0185).

CONCLUSIONS: Although all patients showed clinical improvement, the cohort did not permit assessment of a dose-response relationship between EASI score and Actinomycetota abundance. Thus, larger, more heterogeneous cohorts and mechanistic data (e.g., metabolomics-based identification of microbiome-derived metabolites) are needed to validate these findings and clarify their relevance as a potential therapeutic marker in AD.

CLINICAL RELEVANCE: The parallel decline in oral Actinomycetota abundance and EASI score highlights a potential link between the oral microbiome and treatment response in AD, warranting further investigation. In the absence of non-responders, this association does not yet support Actinomycetota as a potential biomarker of treatment efficacy.},
}

Humans
*Dermatitis, Atopic/drug therapy/microbiology
Male
*Microbiota/drug effects
Female
*Antibodies, Monoclonal, Humanized/therapeutic use
Adult
Treatment Outcome
RNA, Ribosomal, 16S
*Mouth/microbiology

@article {pmid42836953,
year = {2026},
author = {Saxena, A and Javed, M and Trehanpati, N},
title = {Gut microbiome-enteric virus interactions: mechanisms, clinical implications, and translational directions.},
journal = {Journal of gastroenterology},
volume = {},
number = {},
pages = {},
pmid = {42836953},
issn = {1435-5922},
abstract = {The gut microbiome influences epithelial barrier integrity, metabolite availability, mucosal immune tone, and vaccine responsiveness, all of which are relevant to enterically transmitted viral infection. Norovirus and rotavirus primarily replicate in the intestinal mucosa and cause acute gastroenteritis, whereas poliovirus replicates in the gut and may disseminate systemically. Hepatitis A virus and hepatitis E virus are acquired through the intestine and shed fecally, but their dominant clinical manifestation is hepatitis. This review synthesizes evidence linking the bacteriome, phageome/virome, and mycobiome with these viruses, while explicitly distinguishing direct enteric virus mechanisms from broader microbiome-immune or metabolite pathways and from cross-kingdom evidence extrapolated from intestinal inflammation or pathobiont studies. The strongest evidence supports selected virus-bacterium and virus-metabolite mechanisms, including bacterial glycan interactions in norovirus, bacterial LPS-mediated poliovirus stabilization, bile acid-dependent human norovirus replication in enteroids, and rotavirus-associated barrier disruption. Human studies remain dominated by stool-based associations that are difficult to separate from inflammation, diet, antibiotic exposure, diarrhea, and sampling time. We therefore rank evidence across experimental, organoid, animal, human observational, and clinical-translational levels, and highlight concrete applications for severe gastroenteritis risk prediction, prolonged shedding, impaired barrier recovery, and oral vaccine nonresponse. Future progress will require longitudinal, spatially resolved, multi-kingdom, and multi-omics studies linked to human-relevant experimental systems.},
}

@article {pmid42837023,
year = {2026},
author = {Rahim, M and G, G},
title = {Effects of an endophytic bacterial consortium derived from Zingiberaceae on growth, yield, and curcuminoid biosynthesis in Curcuma longa L.},
journal = {World journal of microbiology & biotechnology},
volume = {42},
number = {10},
pages = {},
pmid = {42837023},
issn = {1573-0972},
mesh = {*Curcuma/microbiology/growth & development/metabolism ; *Endophytes/isolation & purification/classification/metabolism/genetics ; *Zingiberaceae/microbiology ; *Bacteria/isolation & purification/classification/metabolism/genetics ; Indoleacetic Acids/metabolism ; *Microbial Consortia/physiology ; Rhizome/microbiology ; RNA, Ribosomal, 16S/genetics ; Diarylheptanoids ; *Curcumin/metabolism ; Phylogeny ; Ammonia/metabolism ; Siderophores/metabolism ; },
abstract = {Endophytic bacteria, integral to the plant microbiome, possess considerable potential for improving the cultivation and sustainability of medicinal plants. These bacteria are essential for various plant functions, including growth enhancement, nutrient uptake, and resistance to biotic and abiotic stressors. This study recovered 29 endophytic bacterial isolates from the rhizomes of five Zingiberaceae species: Zingiber officinale, Curcuma longa, Kaempferia galanga, Alpinia purpurata, and Hedychium coronarium. These isolates were evaluated for plant growth-promoting (PGP) traits, including mineral solubilization, indole-3-acetic acid (IAA) production, siderophore production, ammonia production, and hydrogen cyanide (HCN) production. From these, superior isolates were chosen to create five distinct compatible consortia, whose plant growth-promoting (PGP) activities were further assessed to ultimately identify the most effective consortium, C4, which included Bacillus sp. and Lysinibacillus sp., and exhibited the highest overall PGP activity among the consortia tested. In vivo assessment utilizing mung bean determined 10[8] CFU mL[-1] as the optimal inoculum concentration, demonstrating the greatest improvement in vegetative development. The subsequent field application in turmeric markedly enhanced plant height (36.5%), leaf area (28.8%), tiller production (82.1%), and rhizome yield (69.6%) relative to the control. The re-isolation of the inoculated bacteria from harvested rhizomes supported their persistence within plant tissues under field conditions. Consortium-treated plants exhibited enhanced biochemical quality, evidenced by estimated increases in curcumin (29.7%), demethoxycurcumin (26.0%), bisdemethoxycurcumin (40.7%), total curcuminoids (30.2%), and volatile oil content (5.4%). Quantitative real-time PCR demonstrated a 1.51-fold upregulation of the curcumin synthase gene (CURS2), which was associated with increased curcuminoid accumulation, suggesting a potential influence on curcuminoid biosynthesis. These findings demonstrate that consortium C4 represents a promising eco-friendly microbial bioinoculant for sustainable turmeric cultivation and quality improvement.},
}

*Curcuma/microbiology/growth & development/metabolism
*Endophytes/isolation & purification/classification/metabolism/genetics
*Zingiberaceae/microbiology
*Bacteria/isolation & purification/classification/metabolism/genetics
Indoleacetic Acids/metabolism
*Microbial Consortia/physiology
Rhizome/microbiology
RNA, Ribosomal, 16S/genetics
Diarylheptanoids
*Curcumin/metabolism
Phylogeny
Ammonia/metabolism
Siderophores/metabolism

@article {pmid42837107,
year = {2026},
author = {Elhady, A and Ashrafi, S and Wennrich, JP and Stadler, M and Hirt, H and Heuer, H},
title = {Rhizosphere Microbiomes Respond to Plant-Parasitic Nematode Cues and Contribute to Host Defence.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70964},
pmid = {42837107},
issn = {1365-3040},
support = {EL 1038/2-1//Deutsche Forschungsgemeinschaft/ ; },
abstract = {Plant-parasitic nematodes (PPNs) cause major crop losses, while current nematicides face increasing regulatory restrictions and often show inconsistent efficacy. We tested whether nematode-associated cues activate rhizosphere microbiomes and cuticle-associated fungi to produce suppressive metabolites that impair nematodes and stimulate host defence. Maize rhizosphere microbiomes from different soils and fungal isolates recovered from nematode cuticles were exposed to Meloidogyne hapla, after which cell-free filtrates were assessed for juvenile mortality, root invasion, gall formation, egg production and reactive oxygen species (ROS) accumulation in tomato. Nematode-conditioned microbiome filtrates increased M. hapla juvenile mortality relative to nonconditioned controls across soils, although the magnitude of this effect varied with soil origin. Several fungal isolates also showed suppressive activity against Pratylenchus penetrans in maize and M. hapla in tomato, with distinct outcomes across biological assays. Among them, Akanthomyces sp. F20/JKI73389 was selected for mechanistic follow-up: stimulation by M. hapla, or by nematode-derived molecules, induced F20 to release a filtrate that reduced nematode root invasion and triggered a strong ROS response in host tissue. UHPLC-MS analysis further revealed a distinct nematode-induced metabolite profile in F20, including six candidate features that were absent from non-stimulated controls and were provisionally associated with enhanced nematode mortality. These results support a model in which nematode-derived cues alter the metabolite output of indigenous rhizosphere microbes and associated fungi in ways linked to nematode suppression and host defence, highlighting their potential as environmentally compatible tools for PPN management.},
}

@article {pmid42837186,
year = {2026},
author = {Jamil, R and Huibner, S and Yang, P and Nnamutete, J and White, JL and Sokoll, L and Pollock, J and Nakalanzi, M and Bukenya, SP and Kiboneka, SD and Agaba, M and Nalubowa, MJ and Anok, A and Kigozi, G and Galiwango, RM and Coburn, B and Liu, CM and Prodger, JL and Tobian, AA and Kaul, R},
title = {Impact of sexual debut on urethral immunology and microbiome in adolescent males from Rakai, Uganda.},
journal = {The Journal of clinical investigation},
volume = {},
number = {},
pages = {},
doi = {10.1172/JCI208629},
pmid = {42837186},
issn = {1558-8238},
abstract = {BACKGROUND: The penile urethra is a primary site of HIV acquisition in males, although little is known about the urethral determinants of HIV susceptibility. Inflammation at other genital sites enhances HIV risk, and studies suggest that some inflammatory urethral bacteria may be vaginally acquired. Here, we characterize the impact of sexual debut on the microbiome and immune milieu of the penile urethra in adolescent males from Rakai, Uganda.

METHODS: A cohort of 185 self-reported sexually naïve adolescent males from Rakai, Uganda were followed longitudinally for 3 years, with questionnaires administered every 3 months and urethral swabs collected annually. Urethral soluble immune factors were quantified by chemiluminescent multiplex immunoassay and bacterial 16S rRNA sequencing was performed. Unsupervised clustering and mixed-effects models were used to assess associations between sexual debut and the urethral microbiome and immune milieu.

RESULTS: Unsupervised clustering at 36 months identified two distinct urethral Community State Types (CSTs): CST-1 was dominated by Streptococcus mitis and CST-2 by bacteria associated with bacterial vaginosis (BV), particularly Sneathia amnii and Gardnerella vaginalis. CST-2 was greatly enriched at 36 months compared to baseline and was associated strongly with sexual debut. Individual bacterial taxa enriched in CST-2 were associated with both sexual debut and elevated urethral inflammatory cytokines, independent of serum testosterone and penile circumcision status.

CONCLUSION: The penile urethra is colonized by BV-associated bacteria after penile-vaginal sex debut. Their presence in the urethra induces local inflammation and may serve as a reservoir for subsequent reintroduction into the vagina of female sexual partners.},
}

@article {pmid42837295,
year = {2026},
author = {Kiefer, ZE and Anderson, CJ and Rahic-Seggerman, FM and Schmitz-Esser, S and Ross, JW},
title = {Metagenome shotgun sequencing allows insights into the functional potential of the vaginal microbiome associated with pelvic organ prolapse in sows†.},
journal = {Biology of reproduction},
volume = {},
number = {},
pages = {},
doi = {10.1093/biolre/ioag222},
pmid = {42837295},
issn = {1529-7268},
abstract = {Pelvic organ prolapse (POP) is a leading cause for sow mortality in the United States. Recent work has evaluated biological factors associated with POP, and differences have been observed within the vaginal microbiota of sows at high risk using 16S rRNA gene amplicon sequencing. Additional functional studies are needed to better understand the relationship of dysbiosis of the vaginal microbiome with POP risk in sows. The current study's objective was to provide information about the functional potential of the sow vaginal microbiome, and to identify candidate genes and organisms that may be associated with POP. For this, metagenome shotgun sequencing was conducted on DNA extracted from 16 vaginal swab samples from late gestation sows. Of the 16 samples, 8 were from sows at high risk and 8 from sows at low risk for POP. Of the 8 samples from sows at high risk for POP four subsequently experienced POP. Subsequent contigs were annotated to generate a gene catalog of the vaginal microbiome of sows. The contigs were binned into metagenome assembled genomes (MAGs), resulting in 10 high-quality MAGs identified as Mannheimia varigena, Corynebacterium maris, Turicibacter bilis, Staphylococcus hyicus, Streptococcus dysgalactiae, Anaerococcus prevotii, Actinobacillus rossii, Prevotellaceae, Methanobrevibacter, and Veillonella caviae. MAGs classified as Streptococcus dysgalactiae and Staphylococcus hyicus contained potential virulence factors that are linked to the weakening of the connective tissue of the reproductive tract. This work provides initial insights into the functional potential of the vaginal microbial communities in late gestation sows in relation to POP and reproductive health.},
}

@article {pmid42837719,
year = {2026},
author = {Pant, B and Khan, M and Kabir, AH},
title = {Localized co-inoculation of compatible Bacillus subtilis and Trichoderma afroharzianum is associated with shifts in the root microbiome and improves plant performance in sorghum.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128751},
doi = {10.1016/j.micres.2026.128751},
pmid = {42837719},
issn = {1618-0623},
abstract = {Although bacterial-fungal consortia have been investigated for plant growth promotion, their effects on sorghum performance and associated root microbial taxa remain less characterized. Here, we investigated how individual and combined inoculation with Bacillus subtilis and Trichoderma afroharzianum influenced sorghum performance and root microbiome assembly. The in vitro co-culture assay demonstrated the compatibility of B. subtilis and T. afroharzianum as a microbial consortium. The B. subtilis-T. afroharzianum consortium demonstrated the highest CPPI (composite plant performance index) and shoot fresh weight in sorghum, while all inoculation treatments improved multiple growth and physiological traits. Split-root analysis showed that bilateral root co-inoculation generally produced the greatest whole-plant growth response. Also, B. subtilis-T. afroharzianum co-inoculation increased carbon levels in both roots and leaves, accompanied by enhanced rhizosphere siderophore production consistent with improved nutrient status. In microbial community analysis, neither bacterial nor fungal alpha or beta diversity differed significantly among treatments, although exploratory taxon-level analyses identified selective treatment-associated shifts in microbial taxa. The B. subtilis-T. afroharzianum consortium showed significant enrichment in plant growth-promoting Actinoplanes, siderophore-producing Enterobacter, and the plant-beneficial fungal genus Podospora. Interestingly, neither inoculant significantly improved sorghum growth in sterile soil, suggesting their potential dependence on the enriched microbes. Co-occurrence network analysis identified Rhodoplanes, Serendipita, and Zopfiella among hub taxa associated with B. subtilis-T. afroharzianum co-inoculation, suggesting potential roles in microbial community connectivity and organization. Furthermore, the persistence of Streptomyces and Serendipita, particularly the latter, suggests the presence of a beneficial microbial core that may contribute to sustained rhizosphere functioning. In addition, Bacillus and Serendipita were identified as indicator taxa associated with the inoculated treatment combinations. Devosia was associated with chlorophyll content, siderophore production, and shoot height, whereas Serendipita correlated with shoot biomass under the B. subtilis-T. afroharzianum co-inoculation. Taken together, these findings demonstrate improved sorghum performance following B. subtilis-T. afroharzianum co-inoculation and identify associated microbial taxa that warrant further functional validation in the field settings.},
}

@article {pmid42838033,
year = {2026},
author = {van Renterghem, AWJ and Voest, EE},
title = {Diet-microbiome interactions enhance cancer immunotherapy in obesity.},
journal = {Cell metabolism},
volume = {38},
number = {10},
pages = {1946-1948},
doi = {10.1016/j.cmet.2026.08.021},
pmid = {42838033},
issn = {1932-7420},
mesh = {*Obesity/immunology/microbiology/complications ; *Immunotherapy/methods ; Humans ; *Neoplasms/therapy/immunology/complications/microbiology ; Animals ; *Gastrointestinal Microbiome/immunology ; *Diet ; },
abstract = {In a recent issue of Nature, Desharnais and colleagues show that diet-dependent remodeling of the gut microbiome promotes anti-tumor immunity and may explain the enhanced efficacy of immune checkpoint blockade observed in obesity. Their study identifies dietary intervention as a promising strategy to optimize the host for cancer immunotherapy.},
}

*Obesity/immunology/microbiology/complications
*Immunotherapy/methods
Humans
*Neoplasms/therapy/immunology/complications/microbiology
Animals
*Gastrointestinal Microbiome/immunology
*Diet

@article {pmid42838119,
year = {2026},
author = {Messina, C},
title = {Gut microbiota and neuromuscular disorders: a comprehensive review.},
journal = {Arquivos de neuro-psiquiatria},
volume = {84},
number = {9},
pages = {1-13},
pmid = {42838119},
issn = {1678-4227},
mesh = {Humans ; *Neuromuscular Diseases/microbiology/physiopathology ; *Gastrointestinal Microbiome/physiology ; Probiotics/therapeutic use ; },
abstract = {Emerging evidence highlights a bidirectional interaction between the gut microbiota (GM) and the neuromuscular system, suggesting that microbial composition and metabolic activity may play a pivotal role in the pathophysiology of several neuromuscular diseases (NMDs). This comprehensive review synthesizes current evidence on GM alterations across a broad spectrum of NMDs, emphasizing their potential implications for disease mechanisms and management. Gut microbial shifts have been consistently associated with immune dysregulation, systemic inflammation, and metabolic disturbances that may contribute to neuromuscular dysfunction. Beyond their pathogenetic relevance, these alterations hold diagnostic and therapeutic promise. Probiotic supplementation, dietary modulation, and other microbiota-targeted strategies have shown preliminary benefits in alleviating symptoms and improving metabolic balance in selected NMDs, although existing studies remain limited and heterogeneous. This review offers an integrative perspective, positioning the GM not only as a potential biomarker for diagnosis and disease monitoring but also as a novel therapeutic target. A deeper understanding of the gut-muscle-nerve axis could pave the way for more personalized and mechanism-based approaches in neuromuscular medicine, particularly for disorders where disease-modifying treatments are still lacking. Further well-designed, longitudinal, and mechanistic studies are warranted to elucidate causal relationships and translate microbiome research into clinical application.},
}

Humans
*Neuromuscular Diseases/microbiology/physiopathology
*Gastrointestinal Microbiome/physiology
Probiotics/therapeutic use

@article {pmid42838172,
year = {2026},
author = {Cobuccio, L and Moser, K and Jacot, D and Kapel, N and Tsaousis, AD and Galperine, T},
title = {Clinical significance of Dientamoeba fragilis and Blastocystis: Lessons from clinical trials, cohort studies, and faecal microbiota transplantation - a narrative review.},
journal = {Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmi.2026.09.031},
pmid = {42838172},
issn = {1469-0691},
abstract = {BACKGROUND: The adoption of highly sensitive syndromic multiplex PCR panels led to an increase in Blastocystis and Dientamoeba fragilis detection, two of the most commonly identified intestinal protists worldwide. With positivity rates of 15-25% on syndromic gastrointestinal panels, a positive result frequently triggers antimicrobial treatment despite uncertain clinical significance.

OBJECTIVES: To synthesise multi-dimensional evidence on the pathogenicity of Blastocystis and D. fragilis from multiple lines of investigation and to propose a pragmatic clinical decision framework for interpreting positive test results.

SOURCES: A systematic search of PubMed/MEDLINE (inception to January 2026) was conducted using structured queries for Blastocystis and D. fragilis across thematic blocks: epidemiology, molecular diagnosis, pathogenicity mechanisms, clinical trials, faecal microbiota transplantation (FMT), and microbiome associations. No language restriction was applied. Study selection prioritised randomised controlled trials, prospective FMT cohorts, large-scale metagenomic analyses, and systematic reviews. Reference lists of retrieved articles were manually screened.

CONTENT: Current evidence suggests asymptomatic carriage is the biological norm for both organisms, and no specific subtypes, genotypes, or parasite load thresholds have been consistently linked to disease. Three placebo-controlled randomised controlled trials (RCTs) showed no treatment benefit: two conducted in paediatric populations and one an adult pilot study. FMT cohort studies demonstrate safe transmission without adverse events. Metagenomic analyses of nearly 57,000 individuals have identified an association between Blastocystis carriage, greater microbial diversity, and more favourable cardiometabolic profiles, although the direction and causality of these relationships remain unclear.

IMPLICATIONS: In immunocompetent hosts, detection of Blastocystis or D. fragilis does not indicate disease; for Blastocystis in particular, carriage should be regarded as an ecological marker of the intestinal microbiota. A clinical decision algorithm is proposed in which reassurance is the default, treatment is reserved for exceptional circumstances (severe immunosuppression or chronic unexplained symptoms after thorough exclusion of alternative diagnoses), and clinical response, not PCR clearance, serves as the only meaningful endpoint.},
}

@article {pmid42838218,
year = {2026},
author = {Lin, MY and Zhang, T and Wang, L and Wang, Q and Wang, SY and Jiang, N and Wang, YF and Zheng, LL and Wang, R and Yang, CZ and Zhao, ZH and Yan, XY and Shan, SQ and Yang, DL and Liu, J and Jin, S and Dong, JH},
title = {Deciphering the Metastatic Nexus: Molecular Drivers and Therapeutic Frontiers in Cholangiocarcinoma Lymph Node Dissemination.},
journal = {Cancer letters},
volume = {},
number = {},
pages = {218881},
doi = {10.1016/j.canlet.2026.218881},
pmid = {42838218},
issn = {1872-7980},
abstract = {Lymph node metastasis (LNM) is a major determinant of staging and outcome in cholangiocarcinoma (CCA), yet its mechanisms, biomarkers, anatomical heterogeneity, and treatment evidence remain insufficiently integrated. This review develops an LNM-centered framework in which lymphatic invasion, lymphangiogenesis, genomic alterations and metabolic reprogramming, and reciprocal tumor microenvironment remodeling interact to shape CCA LNM by enabling lymphatic entry, dissemination, immune evasion, tumor-cell survival, and nodal colonization. A subtype-aware synthesis distinguishes small-duct-type and large-duct-type intrahepatic CCA, positions the latter as a biological bridge to perihilar and distal CCA, and maps subtype-associated lymphangiogenic, matrix-remodeling, metabolic, stromal, and immune programs. Translationally, serum ANGPTL4 and exosomal TTN-AS1 are prioritized as candidate adjuncts to preoperative radiologic nodal assessment and CA19-9, whereas tissue ITGB6 represents a comparatively well-characterized candidate for postoperative or biopsy-integrated LNM risk assessment. For node-positive CCA requiring systemic therapy, PD-1/PD-L1 blockade plus gemcitabine-cisplatin provides the first-line backbone. Additional opportunities include intensified chemoimmunotherapy and antiangiogenic combinations, postoperative and locoregional multimodal treatment, genotype-directed or cellular therapies, and mechanism-informed targeting of chemoresistance, oncogenic and lymphangiogenic signaling, stromal and immune niches, and metabolic adaptation. Epigenetic circuitry and post-transcriptional regulation represent emerging regulatory layers, while microbiome-immune interactions provide testable hypotheses for LNM. We propose spatial multi-omics across paired primary tumors, pathologically negative tumor-draining nodes, and metastatic nodes, integrated with pathology-validated liquid biopsy, to identify where metastatic competence emerges and how nodal niches are conditioned. Together, this mechanism-to-clinic synthesis provides a subtype-aware roadmap for biomarker validation, LNM-specific endpoints, and rational therapeutic intervention.},
}

@article {pmid42838366,
year = {2026},
author = {Zhang, W and Matuszek, G and Dolnikowski, GG and Lamon-Fava, S and Ausman, LM and Lichtenstein, AH and Matthan, NR},
title = {Differential effects of stearic, palmitic and oleic acid enriched diets on gut microbiome, bile acid and cholesterol metabolism in mildly hypercholesterolemic post-menopausal females: A secondary analysis of a randomized controlled trial.},
journal = {The American journal of clinical nutrition},
volume = {},
number = {},
pages = {101561},
doi = {10.1016/j.ajcnut.2026.101561},
pmid = {42838366},
issn = {1938-3207},
abstract = {BACKGROUND: Stearic acid (18:0), a saturated fatty acid (SFA), does not raise plasma LDL cholesterol concentrations compared with palmitic acid (16:0), and has similar effects to oleic acid (18:1), but underlying mechanisms remain unclear.

OBJECTIVES: To determine if the hypocholesterolemic effects of dietary 18:0 and 18:1 relative to 16:0 are mediated by alterations in gut microbiome, bile acid (BA), and cholesterol metabolism.

METHODS: Secondary analysis of a randomized controlled crossover trial in mildly hypercholesterolemic postmenopausal females (n=17) who consumed isocaloric diets enriched in 18:0, 16:0 or 18:1 for 5-weeks each with 2-week washouts. Gut microbiome composition, plasma and fecal BA profiles, cholesterol absorption and synthesis markers, and related gene expression were assessed at the end of each dietary phase. Diet effects and multi-omics associations were evaluated using mixed-effects and multivariate models, accounting for repeated measures.

RESULTS: Fecal microbiome diversity was stable across diets, with modest species-level differences. Both 18:0 and 18:1 diets resulted in lower fasting total primary BAs (-159.1 (-313.0,-5.7), and -200.2 (-353.0,-47.7), mean difference (95% CI), respectively) and higher non-fasting unconjugated PBA concentrations (2.7 (1.1,6.4) and 2.4 (1.1,5.6), geometric mean ratio (95% CI), respectively) compared to the 16:0 diet. The 18:0 diet resulted in lower fecal secondary BAs compared to the 18:1 diet (-15.2 (-27.8, -2.6), mean difference (95% CI)) and higher non-fasting conjugated BAs compared to the 16:0 diet (1.4 (0.8,2.3) geometric mean ratio (95% CI)). FXR and SHP expression were 3-4 fold higher (p<0.01), and cholesterol synthesis:absorption ratio 22-24% lower, after both 18:0 and 18:1 compared to the 16:0 diet (p <0.05). Multi-omics analyses identified moderate-to-strong correlations (r = 0.43 to 0.72) among microbes, BAs, gene expression, cholesterol metabolism markers, and lipid profiles.

CONCLUSIONS: The cholesterol-lowering effects of 18:0 and 18:1 relative to 16:0 involved shared hepatic regulation of BA and cholesterol metabolism, while 18:0 uniquely modulated specific microbial taxa and BAs, suggestive of altered enterohepatic BA recycling.

CLINICAL TRIAL REGISTRY: https://clinicaltrials.gov/study/ NCT02145936.},
}

@article {pmid42838398,
year = {2026},
author = {Tang, X and Chao, H and Li, C and Sun, J and Li, W and Sun, Y and Lan, T and Ma, J},
title = {Multiomics reveals alterations in the gut microbiome, host proteins, and host metabolites correlating with SADS-CoV pathogenicity and the immune response in piglets.},
journal = {Virologica Sinica},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.virs.2026.10.001},
pmid = {42838398},
issn = {1995-820X},
abstract = {Swine acute diarrhea syndrome coronavirus (SADS-CoV) infection causes severe acute diarrhea, vomiting, and lethality in piglets. To explore the molecular mechanisms by which intestinal flora regulate viral infection, we conducted multi-omics analysis [proteomics, metabolomics, short-chain fatty acids (SCFA) quantification] and 16S rRNA sequencing on intestinal mucosal and fecal samples from piglets infected with highly pathogenic SADS-CoV P7 stain or low-pathogenic SADS-CoV P83 strain. In both ileal mucosa and fecal samples, the abundance of Enterobacteriaceae was markedly higher in the highly pathogenic strain infection group than in either the control group or the low-pathogenic strain infection group. The concentration of SCFAs was significantly lower in the highly pathogenic SADS-CoV infected pigs than the low-pathogenic strain infected pigs, and SCFA levels were negatively correlated with the abundance of Enterobacteriaceae and Escherichia coli in the ileal mucosa. Compared with the low-pathogenic group, differentially expressed proteins in the highly pathogenic group were mainly associated with extracellular matrix-receptor interaction and focal adhesion pathways. SADS-CoV P7 infection increased both the adhesion capacity and the number of adherent Escherichia coli O157 on IPEC-J2 cells. This study demonstrates that the highly pathogenic SADS-CoV P7 strain remodels gut microbiota to exacerbate intestinal inflammation and tissue damage via activating integrin alpha5-mediated extracellular matrix-pathogen interactions. In contrast, the low-pathogenic SADS-CoV P83 strain exhibits attenuated virulence due to a lack of these regulatory pathways. This study elucidates the distinct pathogenic mechanisms of highly pathogenic and low-pathogenic SADS-CoV strains and provides critical insights for the development of broad-spectrum anti-coronavirus therapeutics and rational vaccine design.},
}

@article {pmid42838406,
year = {2026},
author = {Nasiri, V and Jameie, F},
title = {The Parasite Paradox: Therapeutic Insights from Parasite-Host Interactions - A Focus on Beneficial Physiological Modulations.},
journal = {Acta tropica},
volume = {},
number = {},
pages = {108362},
doi = {10.1016/j.actatropica.2026.108362},
pmid = {42838406},
issn = {1873-6254},
abstract = {A compelling and paradoxical body of evidence challenges the traditional view of parasites solely as pathogens. This narrative review synthesizes a growing literature suggesting that specific, chronic parasitic infections-particularly by helminths, but also certain protozoa-can, under precise ecological conditions, confer a spectrum of protective and ameliorative effects on the host. We comprehensively detail these effects across two interconnected domains. First, we examine organ-specific immunomodulation, focusing on the attenuation of inflammatory and autoimmune pathologies within the cardiovascular, neuroinflammatory, renal, hepatic, and pulmonary systems. Second, we explore systemic physiological modulations that extend beyond classic immunology, including enhanced tissue repair, improved metabolic homeostasis, neuroprotection, anti-tumor activity, and the engineering of a health-promoting gut microbiome. Underpinning these benefits are shared mechanistic pillars: the induction of regulatory T cells (Tregs) and anti-inflammatory cytokines (IL-10, TGF-β), polarization of macrophages toward an M2 reparative phenotype, and profound remodeling of the gut microbiota. Crucially, we emphasize that these "benefits" are incidental by-products of host-parasite co-evolution, observed only in contexts of low-burden, chronic infection with particular species, and are vastly outweighed by the direct morbidity of active parasitosis. The true translational promise lies in parasite-inspired pharmacology: the identification, synthesis, and therapeutic application of discrete parasite-derived molecules to treat inflammatory, metabolic, degenerative, and neoplastic diseases, offering a novel paradigm for drug discovery inspired by nature's most adept manipulators of host biology.},
}

@article {pmid42838456,
year = {2026},
author = {Lee, B and Yoo, J and Jeon, HJ and Kim, YJ and Cheng, X and Kim, SE and Moon, JJ and Lee, Y},
title = {Barrier-reinforcing hyaluronic acid-bilirubin nanodelivery of methylprednisolone for synergistic modulation of the intestinal barrier, immune system, and gut microbiome in colitis.},
journal = {Journal of controlled release : official journal of the Controlled Release Society},
volume = {},
number = {},
pages = {115439},
doi = {10.1016/j.jconrel.2026.115439},
pmid = {42838456},
issn = {1873-4995},
abstract = {Inflammatory bowel disease (IBD) is characterized by a self-reinforcing cycle of intestinal barrier dysfunction, gut microbiome dysbiosis, and aberrant mucosal immune responses. Methylprednisolone (MPS) is a potent immunosuppressant used for IBD and may beneficially modulate the gut microbiome, but its systemic adverse effects and potential impairment of epithelial repair limit its therapeutic use. To overcome these limitations, we developed MPS-loaded hyaluronic acid-bilirubin nanoparticles (MPS@HABN), an oral nanomedicine designed to protect the intestinal epithelium from MPS-associated injury while enhancing the otherwise limited immune and microbiome modulation achieved by low-dose HABN. MPS@HABN limited premature drug release, increased MPS accumulation in the inflamed colon, and reduced systemic exposure and thymic involution. It also protected intestinal epithelial cells from MPS-associated and oxidative injury. In contrast, low-dose HABN alone showed limited immune and microbiome modulation, whereas free MPS caused intestinal barrier damage and systemic toxicity such as thymic involution. In a DSS-induced colitis model, MPS@HABN improved intestinal barrier function while enhancing immune and microbiome modulation, resulting in robust therapeutic efficacy beyond that of either component alone at a low HABN dose and a clinically relevant MPS dose. These findings support combining the complementary activities of MPS and HABN to overcome corticosteroid-associated epithelial injury and the limited efficacy of low-dose HABN, thereby helping to disrupt the pathological barrier-immune-microbiome cycle in colitis.},
}

@article {pmid42838463,
year = {2026},
author = {Pan, ZY and Wu, MT and Lau, CI and Yang, FY},
title = {Spleen-targeted ultrasound restores gut-brain homeostasis in colitis via vagal neuroimmune modulation.},
journal = {Brain, behavior, and immunity},
volume = {139},
number = {},
pages = {107045},
doi = {10.1016/j.bbi.2026.107045},
pmid = {42838463},
issn = {1090-2139},
abstract = {Inflammatory bowel disease (IBD) is increasingly recognized as a systemic disorder involving gut-brain axis dysfunction and neuropsychiatric comorbidities, yet safe and mechanistically defined neuromodulatory strategies remain limited. This study aimed to investigate whether non-invasive spleen-targeted ultrasound regulates gut-brain communication through peripheral neuroimmune signaling in colitis. Male C57BL/6J mice with dextran sulfate sodium (DSS)-induced acute colitis were treated with focused ultrasound stimulation of the spleen (sFUS) at intensities of 0.5 or 1.0 W/cm[2]. Subdiaphragmatic vagotomy (SDV) or sham surgery was performed before DSS induction and subsequent sFUS treatment to examine the involvement of vagal signaling. Therapeutic outcomes were evaluated using histological, molecular, microbiome, transcriptomic, and behavioral analyses. sFUS attenuated intestinal and neuroinflammation by reducing the mRNA levels of the pro-inflammatory cytokines IL-1β, IL-6, and TNF-α, together with modulation of splenic cholinergic signaling and attenuation of systemic inflammatory responses. Furthermore, sFUS restored intestinal barrier integrity by increasing the expression of the tight junction proteins ZO-1 and Occludin, with significant restoration of ZO-1 only at 0.5 W/cm[2], ameliorating histopathological damage and re-establishing gut microbiota homeostasis. These protective effects were associated with improvements in anxiety-like behavior and cognitive performance. Importantly, the therapeutic benefits of sFUS were abolished by SDV, demonstrating their dependence on intact vagal signaling, and were accompanied by activation of the nucleus tractus solitarius-locus coeruleus circuit and adrenergic-cAMP-MAPK-CREB/BDNF signaling in the prefrontal cortex. Our findings establish the spleen as an accessible peripheral neuroimmune hub and identify sFUS as a promising non-invasive strategy for IBD-associated dysfunction of the gut-brain axis.},
}

@article {pmid42838538,
year = {2026},
author = {Mesnage, R},
title = {Effects of Glyphosate and Glyphosate-Based Herbicides on the Mammalian Gut Microbiome: A Critical Review.},
journal = {Journal of applied toxicology : JAT},
volume = {},
number = {},
pages = {},
doi = {10.1002/jat.70475},
pmid = {42838538},
issn = {1099-1263},
abstract = {Glyphosate has long been considered to pose negligible direct risk to mammals on the grounds that its molecular target, 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS), of the shikimate pathway, is absent from animal cells. This rationale is inaccurate as a complete toxicological argument, because the shikimate pathway is present in some commensal bacteria in the mammalian gut. This review appraises the evidence that glyphosate and glyphosate-based herbicides (GBHs) perturb the gut microbiome of mammals. Controlled rodent studies provide the most consistent evidence, with several reporting shifts in community composition, including a depletion of lactobacilli, sometimes accompanied by intestinal inflammation, altered microbial metabolism and increased intestinal permeability. Experimental evidence indicates that luminal aromatic amino acid availability attenuates the antibacterial effect. Formulated products are frequently more disruptive than the active ingredient alone. Some studies suggest that the gut mycobiome is also affected. Neurobehavioural and reproductive outcomes have also been reported, although microbiome-mediated causality is not established in most studies. Glyphosate-induced effects are strongly influenced by dose, by whether the active ingredient or a formulated product is tested, by sex and by a developmental window of exposure. Available human data, confined to in vitro systems and small biomonitoring cohorts, are limited. In conclusion, glyphosate and some GBHs can perturb the rodent gut microbiome under defined experimental conditions. These animal findings are relevant to hazard assessment and support inclusion of microbiome endpoints in regulatory toxicology, although the magnitude and health relevance of comparable effects at realistic human exposures remain uncertain.},
}

@article {pmid42838722,
year = {2026},
author = {Ware, K and Ollberding, N and Duan, Q and Haslam, D and Phipatanakul, W and Glazman, M and Bernstein, JA},
title = {Ultraviolet irradiation and the home microbiome in childhood asthma: An exploratory environmental analysis.},
journal = {Allergy and asthma proceedings},
volume = {},
number = {},
pages = {},
doi = {10.2500/aap.2026.47.260079},
pmid = {42838722},
issn = {1539-6304},
abstract = {BACKGROUND: Ultraviolet (UV) filtration units installed into central heating, ventilation, and air conditioning systemshave been shown to modify indoor environmental microbiomes (EM), but it remains unclear whether central UV air filtrationsystems as a targeted intervention alters the EM sufficiently to modify asthma outcomes.

OBJECTIVE: The objective was to investigate changes in the microbiome from dust samples collected before and after installation of a central UV filtration system in homes of children with mild-moderate persistent asthma.

METHODS: Enrolled pediatric subjects with asthma were randomized to receive UV filtration or sham devices in their heating,ventilation, and air conditioning units. Dust samples were collected from the furnace filters and each child's bedroominflow air ducts from the first 20 homes randomized at the two largest recruiting sites at the time of device placement and atstudy completion (12 months), along with periodic measurements of asthma outcomes markers by using the Composite Asthma Severity Index. Microbial DNA from each paired dust sample underwent shotgun metagenomic sequencing, and taxonomic profiles were generated with MetaPhlAn 4. Associations between changes in bacterial species abundance and changes in asthma severity were assessed with Microbiome Multivariable Associations with Linear Models in R.

RESULTS: A total of 14 paired dust samples (7 from the UV homes and 7 from the sham homes) from inflow air ducts with sufficient quantity of dust were included for EM analysis. Within the UV filtration homes, false discovery rate adjusted q-values< 0.05 identified associations between worsening asthma severity and reduced relative abundance of common gastrointestinalcommensals, such as Bacteroides and Bifidobacterium, previously linked to a reduced risk of allergic disease and asthma; no associations at this threshold were observed in the sham homes.

CONCLUSION: An exploratory study of UV air filtration units installed in homes of children with asthma identified hypothesis-generating associations between bacterial species changes and asthma severity; because the study was underpowered forbetween-arm comparisons, these findings do not establish that UV air filtration caused the microbiome changes and should not be interpreted as confirmatory of a UV-specific effect.Clinical trial NCT02715375, www.

CLINICALTRIALS: gov.},
}

@article {pmid42838993,
year = {2026},
author = {Torfs, JRR and Kreyer, M and Wittouck, S and Ahannach, S and Lebeer, S and Eens, M and Fruth, B and Staes, N},
title = {Ageing processes in the bonobo gut microbiome mirror human patterns.},
journal = {NPJ biofilms and microbiomes},
volume = {12},
number = {1},
pages = {},
pmid = {42838993},
issn = {2055-5008},
support = {1124921N//Fonds Wetenschappelijk Onderzoek/ ; 12AZ624N//Fonds Wetenschappelijk Onderzoek/ ; S006424N//Fonds Wetenschappelijk Onderzoek/ ; 1249124N//Fonds Wetenschappelijk Onderzoek/ ; DOCPRO37054//Universiteit Antwerpen/ ; Lacto-Be 852600//HORIZON EUROPE European Research Council/ ; },
mesh = {Animals ; *Pan paniscus/microbiology ; *Aging ; Humans ; *Gastrointestinal Microbiome ; *Bacteria/classification/genetics/isolation & purification ; RNA, Ribosomal, 16S/genetics ; Animals, Zoo/microbiology ; Biodiversity ; Feces/microbiology ; Aged ; },
abstract = {Ageing is associated with changes in the human gut bacterial microbiome: with age, it becomes more diverse, intra- and interindividual variability increases and it shows a decline in core bacterial genera and an expansion of rarer genera. While recent evidence in model organisms suggests these patterns may arise through stochastic processes rather than host-driven selection, the role of life-time exposures, or the exposome, remains poorly understood. Here, we characterise age-related gut microbiome dynamics in 165 bonobos (Pan paniscus) from wild and zoo-housed populations, aged 2 to 71 years, providing a comparative framework to disentangle conserved from context-dependent ageing trajectories in the gut microbiome in hominids. Across both environments, ageing was associated with increased microbial diversity and reduced core microbiome abundance, paralleled by a rise in low-abundance taxa, recapitulating patterns seen in humans. Notably, instability and uniqueness increased with age in zoo-housed, but not wild bonobos, mirroring patterns restricted to industrialised human populations. Moreover, cumulative exposure to distinct environments over an individual's lifetime substantially contributes to microbiome uniqueness. Our findings suggest that while gut microbiome ageing is broadly conserved across hominids, its expression is modulated by environmental context, offering insight into the evolutionary and ecological drivers of microbial ageing in humans.},
}

Animals
*Pan paniscus/microbiology
*Aging
Humans
*Gastrointestinal Microbiome
*Bacteria/classification/genetics/isolation & purification
RNA, Ribosomal, 16S/genetics
Animals, Zoo/microbiology
Biodiversity
Feces/microbiology
Aged

@article {pmid42839257,
year = {2026},
author = {Wirth, U and Vilchez-Vargas, R and Fuchs, F and Schardey, J and Koch, N and Kühn, F and Renz, BW and Werner, J and Schulz, C and Andrassy, J},
title = {The biliary microbiome in symptomatic cholelithiasis: a prospective comparison across distinct bacterial niches.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {42839257},
issn = {1471-2180},
support = {CS-076//Munich Clinician Scientist Program/ ; },
mesh = {Humans ; Prospective Studies ; Female ; *Cholelithiasis/microbiology ; *Bacteria/classification/genetics/isolation & purification ; RNA, Ribosomal, 16S/genetics ; Feces/microbiology ; Bile/microbiology ; Saliva/microbiology ; *Microbiota ; Male ; Aged ; Middle Aged ; DNA, Bacterial/genetics/chemistry ; Sequence Analysis, DNA ; *Biliary Tract/microbiology ; Adult ; DNA, Ribosomal/genetics/chemistry ; },
abstract = {BACKGROUND: Cholelithiasis is highly prevalent in the Western world and frequently requires surgical or endoscopic intervention. However, the composition and role of the biliary microbiome remain poorly understood. This study aimed to characterize and compare bacterial communities of the biliary niche with saliva and faeces in patients with cholelithiasis.

METHODS: In this prospective observational study, patients with symptomatic cholecystolithiasis, chronic or acute cholecystitis, and choledocholithiasis were included. Bacterial community composition was characterized across bile, gallstone, saliva, and faecal samples using 16 S rRNA-based sequencing. Community-level and genus-level differences were assessed according to anatomical niche and clinical diagnosis, complemented by compositional sensitivity analyses and predicted functional profiling.

RESULTS: A total of 227 samples from 81 patients were analyzed. Bacterial community composition was strongly determined by anatomical niche (PERMANOVA, R² = 0.273, P < 0.001), with bile and gallstone communities being most closely related but remaining significantly distinct (R² = 0.146, q < 0.001). Diagnosis-associated differences were predominantly confined to the biliary compartments and remained significant after adjustment for age, explaining 7.9% of variation in bile and 14.1% in gallstones, whereas no significant associations were observed in saliva or faeces. Compositionally aware analysis with continuous age adjustment identified robust diagnosis-associated signals in bile, including Escherichia/Shigella, Leptotrichia, Serratia, and Pseudomonas. Biliary communities were characterized by taxa including Enterococcus, Escherichia/Shigella, Serratia, and Pseudomonas. In bile, Escherichia/Shigella increased with inflammatory disease, while Pseudomonas decreased; compositionally aware analysis confirmed diagnosis-associated differences for Escherichia/Shigella, Leptotrichia, and Serratia. Predicted bacterial functions showed even stronger anatomical compartmentalization (R² = 0.507, P = 0.001), whereas diagnosis-associated functional differences were limited to two MetaCyc pathways in gallstones. Sensitivity analyses provided no evidence that prolonged antibiotic exposure significantly affected biliary bacterial diversity or community composition.

CONCLUSION: This comprehensive multi-niche analysis demonstrates pronounced taxonomic and predicted functional compartmentalization of bacterial communities across saliva, bile, gallstones, and faeces in patients with cholelithiasis. Diagnosis-associated alterations were predominantly observed within biliary niches, with Escherichia/Shigella emerging as a consistent taxon associated with inflammatory biliary disease. These findings identify anatomical niche as a major determinant of bacterial community structure and support disease-associated alterations within the biliary microbiome.

TRIAL REGISTRATION: German Clinical Trials Register (Deutsches Register Klinische Studien) DRKS00030566 (retrospectively registered 20250818).},
}

Humans
Prospective Studies
Female
*Cholelithiasis/microbiology
*Bacteria/classification/genetics/isolation & purification
RNA, Ribosomal, 16S/genetics
Feces/microbiology
Bile/microbiology
Saliva/microbiology
*Microbiota
Male
Aged
Middle Aged
DNA, Bacterial/genetics/chemistry
Sequence Analysis, DNA
*Biliary Tract/microbiology
Adult
DNA, Ribosomal/genetics/chemistry

@article {pmid42839368,
year = {2026},
author = {Li, L and Wu, S and Cui, Y and Wang, L and Zhang, X and Yan, Z},
title = {Salivary Microbiome Profiles in Burning Mouth Syndrome With Gastroesophageal Reflux Disease Comorbidity: A Comparative Analysis.},
journal = {Oral diseases},
volume = {},
number = {},
pages = {},
doi = {10.1111/odi.70526},
pmid = {42839368},
issn = {1601-0825},
support = {82170967//National Natural Science Foundation of China/ ; },
abstract = {OBJECTIVES: Gastroesophageal reflux disease (GERD) has been recognized as a common comorbidity of burning mouth syndrome (BMS), suggesting potential interactions within the oral-gastrointestinal axis. This study aimed to test whether GERD comorbidity is associated with salivary microbiome profiles among patients with BMS.

MATERIALS AND METHODS: Saliva samples from primary BMS patients without GERD (PBMS), BMS patients with GERD (GBMS), and healthy controls were analyzed using 16S rRNA gene sequencing. Microbial diversity, community structure, and differential taxa were assessed, and taxa were evaluated using receiver operating characteristic analysis.

RESULTS: Significant differences in salivary microbiome profiles were observed among GBMS, PBMS, and controls (p = 0.009). Both GBMS and PBMS showed higher abundances of Actinobacteriota and Rothia compared with controls, indicating shared BMS-associated microbial features. However, GBMS exhibited reduced microbial richness and enrichment of Porphyromonas and Parvimonas.

CONCLUSIONS: BMS patients exhibit shared oral microbiome alterations, while GERD comorbidity is associated with a distinct salivary microbial profile characterized by reduced microbial richness and enrichment of Porphyromonas and Parvimonas. These findings suggest that GERD status may represent a potential clinical stratification factor for identifying biologically distinct subgroups of BMS, providing insight into disease heterogeneity and supporting future investigations of symptom variability and treatment response.},
}

@article {pmid42839672,
year = {2026},
author = {Zhu, L and Xiong, X and Zhang, Q and Cai, W and Wang, Y},
title = {Single-Microbe Transcriptomics Reveal Functional Heterogeneity in Sediment Microbiomes.},
journal = {Small methods},
volume = {},
number = {},
pages = {e71082},
doi = {10.1002/smtd.71082},
pmid = {42839672},
issn = {2366-9608},
support = {2024C03005//Pioneer R&D Programs of Zhejiang Province/ ; 2024SSYS0022//Key R&D Program of Zhejiang/ ; },
abstract = {Sediment microbiomes drive global biogeochemical cycling, but their functional heterogeneity and transcriptional activity are hardly resolved at single-cell resolution. We optimized a scalable single-microbe RNA sequencing workflow for environmental muddy sediment samples, achieving high-throughput single cell sequencing across environmental gradients. The method integrates iohexol-based microbial enrichment, optimized enzymatic digestion step, droplet-based single-cell barcoding, and RNA sequencing, then generating a transcriptomic atlas of 55 859 high-quality microbial cells from 8 composite samples covering freshwater, estuarine and nearshore marine habitats. Comparison with metagenomic data showed a high consistency in species composition, supporting the reliability of single-microbe RNA sequencing in community profiling. Taxonomic analysis revealed site-specific microbial communities associated with methane oxidation, sulfur cycling and anaerobic nitrogen metabolism. 15 distinct functional clusters were identified transcriptionally, showing functional heterogeneity within sedimentary microbiome. Co-expression network analysis further resolved coordinated gene modules, with module activities varying across samples. Overall, this work establishes a practical framework for single-microbe transcriptomics in sediment systems and demonstrates the potential of single-cell resolution to uncover functional heterogeneity within complex microbial communities.},
}

@article {pmid42839749,
year = {2026},
author = {Williams, JN and Barker, DA and Millet, AJ and Carcache, JM and Francis, JS},
title = {Petal infrared transmission warms flowers and reduces microbial abundance.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.71608},
pmid = {42839749},
issn = {1469-8137},
support = {//Florida Atlantic University/ ; },
abstract = {Flowers create distinct internal microclimates, yet how these conditions filter microbial abundance remains poorly understood. We tested whether petal light transmission and internal floral temperature influence microbial abundance in two co-occurring species, Lyonia lucida and Lyonia fruticosa (Ericaceae), which have translucent petal 'windows' that modify internal light environments. We measured internal and external floral temperatures, quantified culturable microbial abundance (yeasts, molds, bacteria), and assessed ultraviolet (UV) and infrared (IR) petal transmission using spectrometry. We then experimentally tested the UV resistance of microbial communities across 108 flowers from 18 plants. Additionally, we used manipulative light experiments to test whether IR radiation drove differences in floral warming between these two species. Petal windows transmitted more UV and IR radiation than pigmented tissue. Internal floral temperature predicted microbial abundance, with warmer flowers harboring fewer microbes. A spectral filter experiment confirmed that IR radiation warms L. lucida flowers but not L. fruticosa, while natural variation in UV transmission did not predict microbial abundance or UV resistance. Petal spectral traits shape floral microclimate and microbial abundance primarily through temperature-mediated filtering linked to IR-driven warming rather than passive UV sterilization. These results position flowers as microhabitats where petal traits constrain microbial communities.},
}

@article {pmid42839869,
year = {2026},
author = {Liang, J and Wei, X and Shang, C and Shao, S and Hao, W and Ren, Y},
title = {Integrated Analysis of Gut Microbiota and Fecal Metabolites in Chinese Patients With Rheumatoid Arthritis: Associations With Disease Activity.},
journal = {International journal of rheumatic diseases},
volume = {29},
number = {10},
pages = {e70905},
doi = {10.1111/1756-185x.70905},
pmid = {42839869},
issn = {1756-185X},
support = {KC22064//Xuzhou Science and Technology Program/ ; //The Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University Green Seedling Project Reserve Talent Project/ ; },
mesh = {Humans ; *Arthritis, Rheumatoid/microbiology/diagnosis/metabolism ; *Feces/microbiology/chemistry ; Female ; *Gastrointestinal Microbiome ; Cross-Sectional Studies ; Male ; *Metabolomics/methods ; Middle Aged ; *Bacteria/metabolism/classification/genetics ; Ribotyping ; Case-Control Studies ; China/epidemiology ; Adult ; Biomarkers ; Severity of Illness Index ; Dysbiosis ; East Asian People ; },
abstract = {AIM: Rheumatoid arthritis (RA) is a chronic autoimmune disease with intestinal dysbiosis implicated through the gut-joint axis. This study aimed to delineate fecal microbiome and metabolomic signatures in RA and identify biomarkers associated with disease activity.

METHOD: Twenty-eight RA patients and 19 healthy controls were included in this cross-sectional study. Gut microbiota was characterized by 16S rRNA sequencing with operational taxonomic unit (OTU) and amplicon sequence variant (ASV) analysis. Fecal metabolites were profiled using untargeted metabolomics. Correlations between microbiota, metabolites, and disease activity indices were assessed.

RESULTS: RA patients showed altered alpha diversity and distinct microbial composition versus healthy controls. Eight differential genera and three species were identified based on the combined OTU and ASV analyses. Allisonella was enriched in RA and positively correlated with disease activity, whereas Bifidobacterium adolescentis showed a negative correlation trend with autoantibody/inflammatory markers. Metabolomic analysis revealed 31 and 36 altered metabolites in both ion modes. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment indicated dysregulation of unsaturated fatty acid biosynthesis and tryptophan metabolism. Microbiota-metabolite pairs correlated with disease activity.

CONCLUSION: RA is characterized by distinct gut microbiota and fecal metabolite alterations associated with disease activity. Specific microbial taxa and metabolic pathways may serve as biomarkers, lending further support to the gut-joint axis in RA pathogenesis.},
}

Humans
*Arthritis, Rheumatoid/microbiology/diagnosis/metabolism
*Feces/microbiology/chemistry
Female
*Gastrointestinal Microbiome
Cross-Sectional Studies
Male
*Metabolomics/methods
Middle Aged
*Bacteria/metabolism/classification/genetics
Ribotyping
Case-Control Studies
China/epidemiology
Adult
Biomarkers
Severity of Illness Index
Dysbiosis
East Asian People

@article {pmid42839967,
year = {2026},
author = {Tian, L and Bai, Y and Wang, S and Wang, C and Gao, J and Zhou, J and Xiang, W},
title = {Codonopsis pilosula inulin-type fructan CPA ameliorates diarrhea-predominant irritable bowel syndrome via regulation of ER stress-induced autophagy and modulation of gut microbiota.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1715972},
pmid = {42839967},
issn = {1663-9812},
abstract = {Diarrhea-predominant irritable bowel syndrome (IBS-D) is characterized by diarrhea, abdominal pain, and recurrent symptoms, posing significant clinical challenges. This study utilized the GSE36701 dataset from the Gene Expression Omnibus (GEO) and applied weighted gene co-expression network analysis (WGCNA) to identify IBS-D-associated genes, with a specific focus on endoplasmic reticulum (ER) stress. Codonopsis pilosula, a traditional Chinese medicinal herb, and its active inulin-type fructan monomer CPA, exhibit potential gastrointestinal protective effects. This study evaluated the therapeutic effects of CPA both in vivo, using an IBS-D model induced by senna leaf combined with chronic unpredictable stimuli, and in vitro, using a lipopolysaccharide (LPS)-induced IBS-D model in NCM460 cells. Hematoxylin-Eosin Staining (H&E), Alcian Blue-Periodic Acid-Schiff Staining (AB-PAS), immunohistochemistry (IHC), Immunofluorescence (IF), Elisa, qRT-PCR and Western blots were used to detect relative indices in this research. Our results indicated that CPA treatment improved IBS-D symptoms, including increased body weight, reduced abdominal withdrawal reflex, and normalized stool consistency. Histological analysis revealed improved colonic crypt and gland morphology, reduced inflammatory cell infiltration, and increased goblet cell numbers. CPA also upregulated tight junction protein expression, anti-inflammatory cytokines, and neuroeffector neuropeptide Y (NP-Y) levels. In addition, CPA downregulated ER-stress and autophagy markers, including p-eIF2α/eIF2α, ATF4, Bip, CHOP, Beclin-1, Atg5, P62, and LC3B. Additionally, CPA influenced gut microbiota composition, increasing microbial diversity and restoring microbial balance in IBS-D rats. Linear discriminant analysis Effect Size (LEfSe) identified CPA-responsive taxa, further supporting CPA's role in promoting a balanced and diverse gut microbiome. These experimental results suggested that CPA alleviates IBS-D by modulating the gut microbiota, regulating autophagy through the ER stress signaling pathway, and reinforcing colonic barrier integrity. This study highlights CPA as a promising therapeutic candidate for IBS-D.},
}

@article {pmid42839976,
year = {2026},
author = {Kapoor, A and Kumar, R and Gupta, A and Sansar, B and Mishra, BK and Chaudhary, M and Rungta, A and Kallapura, G and Prabhash, K},
title = {The microbiome and its impact on the epigenome in cancer.},
journal = {Frontiers in epigenetics and epigenomics},
volume = {4},
number = {},
pages = {1857307},
pmid = {42839976},
issn = {2813-706X},
abstract = {The complex interplay between the human microbiome and epigenetic regulation represents one of the most rapidly evolving frontiers in cancer biology. The trillions of microorganisms residing in and on the human body collectively termed the microbiota may influence the host gene expression through epigenetic mechanisms, including DNA methylation, histone modification, and non-coding RNA regulation. In cancer patients, is associated with disruption of the normal epigenetic landscape, contributing to oncogenesis, tumor progression, immune evasion, and therapeutic resistance. This review synthesizes current evidence on how specific microbial metabolites such as short-chain fatty acids, secondary bile acids, and folate derivatives modulate epigenetic marks in tumor cells and the tumor microenvironment. We further discuss the emerging concept of the "oncobiome" and examine how microbiome-epigenome crosstalk influences cancer risk, progression, and response to therapy including chemotherapy, immunotherapy, and epigenetic drugs. Finally, we explore the translational potential of microbiome modulation as an adjunct strategy in cancer epigenomics, highlighting key research gaps and future directions.},
}

@article {pmid42840007,
year = {2026},
author = {Wang, Y and Zheng, H and Yue, C and Liang, J and He, X and Mo, L and Huang, J and Yu, X},
title = {A systematic analysis of gut microbiome characteristics in Chinese patients with gestational diabetes mellitus.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1902356},
pmid = {42840007},
issn = {2296-861X},
abstract = {OBJECTIVE: To systematically analyze the change pattern of core gut microbiota in Chinese gestational diabetes mellitus (GDM) patients and provide basis for GDM early microecological screening and probiotic intervention.

METHODS: Databases including PubMed, web of science, CNKI, and Wanfang were searched to identify reports on the association between gut microbiota and GDM. A quantitative system evaluation was conducted to assess the changes in core gut microbiota levels (such as Bifidobacterium, Lactobacillus, etc.) in GDM.

RESULTS: Totally, 31 studies involving 6,157 subjects were included. Systematic analysis revealed that levels of Bifidobacterium (SMD = -2.47, 95%CI: -2.86 to -2.09) and Lactobacillus (SMD = -1.82, 95% CI: -2.04 to -1.60) in the GDM were significantly lower than those in controls; while Enterobacteriaceae (SMD = 1.75, 95% CI: 1.53 to 1.98) and Enterococcus (SMD = 1.18, 95%CI: 1.03 to 1.32) were significantly higher than those in non-GDM. Sensitivity analysis shows that the above findings are relatively robust.

CONCLUSION: GDM exhibit significant gut microbiota dysbiosis. The reduction in Bifidobacterium and Lactobacillus and the increase in Enterobacteriaceae and Enterococcus may be important micro biological features for the onset and progression of GDM.},
}

@article {pmid42840110,
year = {2026},
author = {Le, CT and Fujiwara, F and Nguyen, TT and Dinh, HA and Tran, PT and Tran, TT and Nguyen, NT and Shiba, H and Tsubo, M and Watanabe, KN and Ichihashi, Y},
title = {Rhizosphere and fruit microbiome variation across Coffea canephora farms representing conventional, transitional, and organic management.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1899736},
pmid = {42840110},
issn = {1664-302X},
abstract = {Robusta coffee (Coffea canephora Pierre ex A. Froehner) is a major global cash crop, and an increasing number of coffee farms are transitioning from conventional to organic management. To investigate how coffee-associated microbiomes vary across different management histories, bacterial communities from the rhizosphere and fruits of three farms representing conventional, transitional organic, and organic management were profiled using 16S rRNA gene amplicon sequencing, differential abundance analysis, and functional prediction. Differential abundance analysis of rhizosphere and fruit bacterial communities identified the largest number of differentially abundant taxa between the conventional and organic farms, fewer between the transitional organic and organic farms, and relatively few between the conventional and transitional organic farms. In the rhizosphere, these differences included taxa related to nitrogen cycling and contrasting soil resource conditions. Approximately 30% of bacterial taxa were shared between rhizosphere and fruit microbiomes, including lactic acid bacteria (Lactobacillus plantarum, Leuconostoc mesenteroides) and acetic acid bacteria (Kozakia baliensis, Gluconobacter) that are known to influence coffee fermentation. Shared genera accounted for more than 85% of the bacterial relative abundance detected in fruits, indicating a close correspondence between rhizosphere and fruit-associated bacterial communities. Although each management category was represented by only one farm, preventing the separation of management effects from farm-specific environmental and historical factors, these findings provide exploratory insights into microbiome variation among coffee farms with contrasting management histories and identify candidate microbial patterns for further validation in independently replicated studies.},
}

@article {pmid42840187,
year = {2026},
author = {Anand, L and Corbin, KR},
title = {Global in silico analysis reveals a core gut microbiota in fall armyworm (Spodoptera frugiperda) shaped by geography and diet.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag233},
pmid = {42840187},
issn = {2730-6151},
abstract = {Fall armyworms (Spodoptera frugiperda) are an invasive agricultural pest whose adaptability and resilience are increasingly linked to their gut microbiota. In this study, we performed a global-scale in-silico meta-analysis of publicly available 16S rRNA datasets to identify a conserved core gut microbiota and assess how geography and diet shape microbial community structure and function. Using both prevalence-based and unsupervised clustering approaches, we defined a robust global core microbiota composed of 88 high-confidence ASVs, including genera such as Enterococcus, Pseudomonas, and Acinetobacter, which were consistently present regardless of geographical region or diet. These taxa are important in nutrient metabolism, detoxification, and stress tolerance, contributing to host fitness and ecological success. Geographic origin significantly influenced gut microbiota diversity and composition, with continent- and country-level differences supported by alpha/beta diversity metrics and supervised machine learning classification (AUC = 1.0). Diet also influenced microbial community structure, although its effect was weaker than that of geography, explaining 11.9% of the variation compared to 13.5%. Functional predictions using PICRUSt2 revealed region-specific enrichment of pathways related to xenobiotic degradation, amino acid metabolism, and vitamin biosynthesis, suggesting specific microbial taxa may contribute to host adaptation and resilience through these metabolic functions. This is the first global synthesis of the S. frugiperda gut microbiota that integrates geographic and dietary factors. The identification of a global-level conserved core microbiota provides a foundation for developing synthetic microbial communities and microbiome-informed pest management strategies aimed at enhancing control efficacy.},
}

@article {pmid42840223,
year = {2026},
author = {Lu, J and Yang, Y},
title = {Omics-based biomarkers of immune-related organ toxicities associated with immune checkpoint inhibitors: a scoping review and evidence map.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1945286},
pmid = {42840223},
issn = {1664-3224},
mesh = {Humans ; *Immune Checkpoint Inhibitors/adverse effects ; Multiomics ; Biomarkers ; Genomics/methods ; Metabolomics ; Proteomics ; *Drug-Related Side Effects and Adverse Reactions/diagnosis/etiology ; Animals ; },
abstract = {BACKGROUND: Immune checkpoint inhibitors (ICIs) can cause immune-related adverse events (irAEs) across multiple organs. High-throughput omics approaches may help characterize susceptibility, molecular mechanisms, diagnostic features, and monitoring markers related to irAEs; however, evidence remains dispersed across platforms, clinical applications, and toxicity phenotypes.

OBJECTIVE: To map original human evidence in which high-throughput omics approaches were directly linked to irAE susceptibility, occurrence, severity, diagnosis, longitudinal monitoring, clinical course, recovery, response to irAE-directed treatment, or mechanistic characterization. Methods: This scoping review and evidence map followed a registered protocol and was informed by PRISMA-ScR and JBI guidance. PubMed/MEDLINE, Scopus, Web of Science Core Collection, and Embase were searched from January 1, 2014, with the final database search completed on July 9, 2026. Eligible studies involved ICI-exposed patients or human biospecimens, implemented high-throughput genomics/statistical genetics, transcriptomics, proteomics, metabolomics/lipidomics, microbiome/metagenomics, single-cell or spatial omics, immune-repertoire sequencing, or integrated multi-omics approaches, and directly evaluated an irAE outcome. Genome-wide statistical-genetic studies were retained as a conditional evidence category. Targeted single-marker studies, routine laboratory biomarkers, efficacy-only omics analyses, non-ICI populations, non-original reports, case reports, and preclinical-only omics studies were excluded.

RESULTS: The searches identified 4,669 records. After removal of 1,151 duplicates, 3,518 unique records were screened and 433 reports were sought for retrieval. Thirty-two reports could not be retrieved for full-text assessment. Of 401 reports assessed in full text, 315 were excluded and 86 studies were included. Omics domains were non-mutually exclusive: transcriptomics was used in 50 studies, single-cell/spatial omics in 31, proteomics in 20, microbiome/metagenomics in 20, immune-repertoire sequencing in 16, genomics/statistical genetics in 14, and metabolomics/lipidomics in 6. Forty-seven studies contributed to two or more omics domains in the platform audit; after accounting for overlapping analytical modalities, 35 studies met the predefined criteria for true multi-omics integration involving independent molecular layers. Forty-five studies addressed mixed or general irAEs; among organ-specific studies, myocarditis/cardiovascular toxicity (n=10), pneumonitis/lung toxicity (n=9), and gastrointestinal/colitis toxicity (n=8) were most frequent.

CONCLUSIONS: The high-throughput omics literature directly evaluating irAEs is substantially smaller than the broader biomarker literature and is dominated by transcriptomic and single-cell approaches. Most evidence remains exploratory, with limited independent assessment of predefined models or signatures, incomplete coverage of endocrine, renal, neurologic, hematologic, pancreatic, and musculoskeletal toxicities, and substantial gaps between molecular discovery and clinical implementation. Prospective multicenter cohorts, standardized irAE phenotyping, longitudinal sampling, and independent validation are required to support clinical implementation. Future studies integrating multiple molecular layers with advanced computational approaches may improve biomarker discovery and individualized risk stratification but require transparent development and rigorous validation.

https://osf.io/g79cv, identifier g79cv.},
}

Humans
*Immune Checkpoint Inhibitors/adverse effects
Multiomics
Biomarkers
Genomics/methods
Metabolomics
Proteomics
*Drug-Related Side Effects and Adverse Reactions/diagnosis/etiology
Animals

@article {pmid42840254,
year = {2026},
author = {Rodriguez-Perera, D and Yoshimura, K and Fahrmann, J and Dou, R},
title = {Correction: Editorial: Cancer cell metabolism and tumor microenvironment remodel.},
journal = {Frontiers in genetics},
volume = {17},
number = {},
pages = {1995063},
doi = {10.3389/fgene.2026.1995063},
pmid = {42840254},
issn = {1664-8021},
abstract = {[This corrects the article DOI: 10.3389/fgene.2026.1921001.].},
}

@article {pmid42840285,
year = {2026},
author = {Ruan, XF and Xue, XM and Deng, GP and Wu, HM and Chen, S and Hu, XD and Zhu, FF and Luo, YY and Wen, DT},
title = {Inflammatory landscape of Gardnerella vaginalis-associated bacterial vaginosis in rats: an integrated multi-omics analysis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1914434},
pmid = {42840285},
issn = {1664-3224},
mesh = {Animals ; Female ; *Vaginosis, Bacterial/microbiology/metabolism/immunology/pathology ; Multiomics ; *Gardnerella vaginalis/immunology ; Rats ; Rats, Sprague-Dawley ; Disease Models, Animal ; Cytokines/blood ; RNA, Ribosomal, 16S/genetics ; Vagina/microbiology/metabolism/immunology/pathology ; Inflammation/microbiology ; Metabolome ; Metabolomics ; Microbiota ; NF-kappa B/metabolism ; },
abstract = {BACKGROUND: Bacterial vaginosis (BV) is a prevalent vaginal dysbiosis primarily associated with Gardnerella vaginalis (G. vaginalis). However, its pathogenic mechanisms remain incompletely understood, particularly the interplay between microbial dysbiosis and host metabolic perturbations. In this study, a G. vaginalis-associated BV-like rat model was established, and integrated multi-omics analysis was performed to characterize its inflammatory landscape.

METHODS: Female Sprague-Dawley rats received antibiotic pretreatment followed by intravaginal inoculation with G. vaginalis to establish a BV-like model. Gram staining, histological examination, and serum cytokine enzyme-linked immunosorbent assay (ELISA) evaluated the model phenotype. 16S rRNA gene sequencing characterized the vaginal microbiota, and UHPLC-MS/MS profiled the vaginal metabolome. ELISA quantified serum metabolites. Western blotting (WB) assessed proteins related to Toll-like receptor (TLR)/nuclear factor-kappa B (NF-κB) signaling in uterine tissues.

RESULTS: The BV-like phenotype was characterized by clue cell-like epithelial cells, histopathological injury, and an altered serum cytokine profile. 16S sequencing revealed nonsignificant trends toward increased diversity and reduced evenness in the model group. Although overall microbial community composition did not differ significantly between groups, within-group dispersion was significantly lower in the model group. The genera Gardnerella, Staphylococcus, Bacteroides, and Aerococcus were overrepresented, whereas Collinsella was underrepresented; among these genera only Aerococcus remained significant after FDR correction. Untargeted vaginal metabolomics and targeted serum measurements indicated enhanced arachidonic acid (AA)-related metabolism and compartment-specific remodeling of tryptophan (TRP) metabolism. Group-adjusted partial correlation analysis identified nominal positive correlations of Gardnerella with AA and Collinsella with 5-hydroxyindole-3-acetic acid (5-HIAA), as well as a nominal negative correlation of Blastococcus with thromboxane B2 (TXB2); however, none remained significant after FDR correction. WB revealed increased abundance of uterine proteins associated with TLR2/4-NF-κB-COX-2 inflammatory signaling in the model group.

CONCLUSIONS: These findings suggest that the G. vaginalis-associated BV-like phenotype is linked to vaginal microbial alterations, enhanced AA-related metabolism, compartment-specific remodeling of TRP metabolism, and upregulation of proteins related to uterine TLR/NF-κB inflammatory signaling. This microbiome-metabolome-immune network may help explain how G. vaginalis-associated vaginal dysbiosis contributes to BV-like inflammatory changes and may be related to endometrial inflammation.},
}

Animals
Female
*Vaginosis, Bacterial/microbiology/metabolism/immunology/pathology
Multiomics
*Gardnerella vaginalis/immunology
Rats
Rats, Sprague-Dawley
Disease Models, Animal
Cytokines/blood
RNA, Ribosomal, 16S/genetics
Vagina/microbiology/metabolism/immunology/pathology
Inflammation/microbiology
Metabolome
Metabolomics
Microbiota
NF-kappa B/metabolism

@article {pmid42840357,
year = {2026},
author = {Huang, Q and Xiang, H and Liu, Q and Zhang, Y and Zou, J and Gao, Z and Yang, L and Zeng, H and Liu, J},
title = {Fecal microbiota transplantation and peri-stoma microbiome management in patients with intestinal stomas: from mechanisms to clinical translation.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1913974},
pmid = {42840357},
issn = {2234-943X},
abstract = {BACKGROUND: Fecal diversion-induced dysbiosis in the defunctioned intestinal segment represents a common pathogenic basis for diversion colitis, anastomotic leakage, and long-term metabolic sequelae in patients with permanent stomas. This review proposes the novel concept of "Peri-stoma Microbiome Management (PSMM)" and critically evaluates the clinical evidence for fecal microbiota transplantation (FMT), defined microbial consortia, bacteriophages, and postbiotics. It is important to emphasize that PSMM is a proposed conceptual framework; most of its components have not been prospectively validated in stoma patients.

MAIN BODY: The core pathological process involves a dramatic reduction in butyrate-producing obligate anaerobes, depriving colonocytes of their primary energy substrate. In experimental models, butyrate depletion impairs mitochondrial function and autophagic flux, with subsequent NLRP3 inflammasome activation; whether this pathway operates identically in the defunctioned human colon remains to be directly investigated. Collagenolytic pathobionts such as Enterococcus faecalis may expand under antibiotic pressure and secrete matrix metalloproteinase-9 that degrades anastomotic extracellular matrix. However, anastomotic leakage is a multifactorial complication, involving tissue ischemia, tension, patient comorbidities, and microbial factors. The PSMM framework encompasses four phases: (I) pre-stoma creation microbial pre-habilitation and risk prediction; (II) microbiota monitoring and intervention during stoma maintenance; (III) pre-reversal targeted decolonization using bacteriophages and engineered microbiota reconstruction; and (IV) long-term metabolic maintenance for permanent stoma carriers. Bacteriophages show promise for precision decolonization but face significant challenges, including bacterial resistance, narrow host range, manufacturing complexity, and regulatory barriers. Multi-omics monitoring remains aspirational due to high costs, long turnaround times, and lack of clinical integration.

CONCLUSION: The PSMM framework provides a structured conceptual approach for integrating microbiome-targeted strategies into the care of patients with intestinal stomas. However, most interventions remain investigational and require validation in adequately powered randomized trials.},
}

@article {pmid42840393,
year = {2026},
author = {Liu, W and Yu, Q and Xue, X},
title = {Beyond cervicovaginal limitations: potential bidirectional interactions between HPV infection and mucosal microbiota from oral, anorectal and penile sites - a mini-review.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1962165},
pmid = {42840393},
issn = {2235-2988},
mesh = {Humans ; *Papillomavirus Infections/virology/microbiology/epidemiology ; *Microbiota ; Male ; *Human Papillomavirus Viruses ; Female ; *Penis/microbiology/virology ; Vagina/microbiology/virology ; *Mouth/microbiology/virology ; *Mucous Membrane/microbiology/virology ; *Anal Canal/microbiology/virology ; Dysbiosis ; Papillomaviridae ; },
abstract = {Most existing studies focusing on human papillomavirus (HPV)-microbiota interactions are confined to the cervicovaginal tract, while mucosal microecological crosstalk at oral, anorectal and penile sites remains insufficiently summarized. This mini-review provides a narrative synthesis of current sequencing and epidemiological evidence regarding potential bidirectional interactions between HPV infection and site-specific mucosal microbiota across extra-cervicovaginal niches in both males and females. Oral HPV reshapes microbial composition in a sex-, race- and population-dependent manner; periodontal dysbiosis, high-risk HPV and Candida albicans jointly form a tripartite oncogenic axis that may contribute to oral squamous cell carcinoma, and periodontal inflammation independently elevates oral HPV susceptibility. Among men who have sex with men, pro-inflammatory anaerobes such as Bacteroides fragilis and Sneathia accumulate in anorectal HPV-related lesions, and concurrent HIV or sexually transmitted bacterial co-infections worsen mucosal dysbiosis and viral persistence. On penile skin, Corynebacterium is associated with a lower prevalence of HPV, whereas anaerobe-dominant community state types increase high-risk HPV risk, with HIV-induced baseline dysbiosis masking HPV-specific penile microbial signatures. Collectively, tissue-specific mucosal dysbiosis may represent an important co-factor linked to persistent HPV infection and subsequent malignant transformation. This review offsets long-standing sex-related and anatomical research bias, clarifies multi-site host-virus-microbe mechanisms, and provides theoretical support for developing microbiota-based biomarkers and microecological interventions to prevent non-cervical HPV-associated malignancies.},
}

Humans
*Papillomavirus Infections/virology/microbiology/epidemiology
*Microbiota
Male
*Human Papillomavirus Viruses
Female
*Penis/microbiology/virology
Vagina/microbiology/virology
*Mouth/microbiology/virology
*Mucous Membrane/microbiology/virology
*Anal Canal/microbiology/virology
Dysbiosis
Papillomaviridae

@article {pmid42840421,
year = {2026},
author = {Chai, Z and Wang, M and Zheng, J and Yu, J},
title = {Gut dysbiosis in difficult-to-treat rheumatoid arthritis: hypothesized microbial endotypes, persistent inflammation, and pharmacological treatment resistance.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1939732},
pmid = {42840421},
issn = {1663-9812},
abstract = {Difficult-to-treat rheumatoid arthritis (D2T RA) remains a major clinical problem despite treat-to-target care and an expanding range of disease-modifying antirheumatic drugs (DMARDs). D2T RA includes biologically distinct states, particularly persistent inflammatory refractory rheumatoid arthritis (PIRRA) and non-inflammatory refractory rheumatoid arthritis (NIRRA). Direct microbiome evidence in D2T RA is sparse, but studies in established RA, at-risk populations, and treatment-response cohorts suggest that intestinal ecological disruption may sustain inflammation through barrier failure, persistent microbial-product sensing, and impaired metabolite-mediated immune regulation. Gut microorganisms may also influence drug response, especially to methotrexate, while antirheumatic therapy can remodel the microbial ecosystem. We therefore synthesize the literature into three hypothesis-generating functional states, provisionally termed inflammation-amplifying, immune-tolerance-deficient, and poor-drug-response-associated microbial endotypes. These states are not validated patient classes and may overlap or evolve over time. We also propose a microbiota-treatment resistance feedback loop, explicitly as an inferential model rather than an established causal pathway. Microbiota-directed adjuncts are evaluated according to evidence maturity, mechanistic fit, and safety. Overall, the gut microbiota is best considered a potential upstream modifier linking mucosal immunity, persistent inflammation, and pharmacological response, with the most coherent mechanistic relevance to PIRRA. Prospective D2T RA cohorts with objective inflammatory phenotyping, longitudinal multi-omics, and detailed drug-exposure data are needed before these concepts can inform clinical stratification or treatment.},
}

@article {pmid42840453,
year = {2026},
author = {Xiao, R and Hao, Y and Gong, Y and She, A and Ma, Q and Lin, M and Guo, Y and Jiang, T},
title = {Phage therapy for multidrug-resistant pulmonary infections: bridging precision matching, lung delivery, host immunity, and clinical translation.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1968526},
pmid = {42840453},
issn = {2235-2988},
mesh = {Humans ; *Phage Therapy/methods ; *Drug Resistance, Multiple, Bacterial ; Lung/microbiology/immunology ; Animals ; *Bacteriophages/physiology ; Bacteria/drug effects/virology ; Microbiota ; *Respiratory Tract Infections/therapy/microbiology/immunology ; Anti-Bacterial Agents/therapeutic use ; },
abstract = {Chronic pulmonary infections caused by multidrug-resistant (MDR) bacteria are a growing global health problem, and the declining effectiveness of conventional antibiotics increases the need for alternative antimicrobial strategies. Unlike broad-spectrum antibiotics, bacteriophages are highly specific, and their use therefore offers not only antibacterial activity but also the possibility of reshaping the airway microbial ecosystem in a targeted manner. In this review, we reframe phage therapy as a precision microbiome-modulating strategy for chronic pulmonary infections. We first review precision pathogen identification and phage-host matching, then discuss formulation engineering for pulmonary delivery, and then examine the interactions between phages and host immune barriers. We further analyze how phage therapy may selectively deplete MDR pathogens while sparing the commensal microbiota and how it may remodel the airway microbial ecosystem, and we critically evaluate the clinical evidence, distinguishing preclinical data, case-based evidence, observational studies, and controlled trials. By integrating these dimensions, we identify the main scientific and technical challenges and evidence gaps that currently limit clinical implementation, and we discuss strategies that could support the development of safe, effective, and clinically applicable phage-based therapies for chronic pulmonary infections.},
}

Humans
*Phage Therapy/methods
*Drug Resistance, Multiple, Bacterial
Lung/microbiology/immunology
Animals
*Bacteriophages/physiology
Bacteria/drug effects/virology
Microbiota
*Respiratory Tract Infections/therapy/microbiology/immunology
Anti-Bacterial Agents/therapeutic use

@article {pmid42840456,
year = {2026},
author = {Zhang, B and Brown, R and Bayer, A and Waring, J and Morgan, BP and Marchesi, JR and Zhou, Y},
title = {Profiling Gut Microbiome and Metabolites Aids Diagnosis and Prediction of Progression in Mild Cognitive Impairment.},
journal = {MedComm},
volume = {7},
number = {10},
pages = {e71045},
pmid = {42840456},
issn = {2688-2663},
abstract = {Accumulating evidence suggests a link between the gut microbiota and metabolome and mild cognitive impairment (MCI); however, it remains largely unknown whether these parameters can aid MCI diagnosis and predict disease progression. We comprehensively characterized gut microbiota and metabolomic profiles in fecal samples from 35 individuals, including 16 spousal pairs in which one partner had MCI. Compared with controls, MCI cases exhibited significantly elevated levels of Izemoplasmatales spp. in the fecal microbiome and proline in the metabolome, along with decreased levels of Ruminococcus spp., Lachnospira spp., and fumaric acid. Among MCI cases, rapid progressors showed significantly increased Bilophila spp. in the microbiome, accompanied by higher arginine, aspartic acid, and hypoxanthine in the metabolome, and reduced Coprococcus spp., compared with slow progressors. Machine learning models integrating microbiota and metabolite features identified marker sets that accurately distinguished MCI cases from matched cognitively healthy controls (AUC: 0.944) and predicted rapid disease progression, with the integrated model outperforming single-modality models for diagnosis. These findings identify distinct gut microbiota and metabolite signatures associated with MCI, highlighting their potential as candidate biomarkers for early diagnosis and risk stratification, thereby addressing the unmet need for simple tests for early detection.},
}

@article {pmid42840472,
year = {2026},
author = {Fang, S and Yang, X and Liu, F},
title = {From microbiome to outcome: the cascading effects of combining acid suppressants with anti-tuberculosis therapy.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1959574},
pmid = {42840472},
issn = {2296-858X},
abstract = {Gastrointestinal adverse reactions occur in up to 71.8% of patients receiving anti-tuberculosis drugs (ATDs), and acid-suppressing agents are frequently co-prescribed to alleviate these symptoms. Direct evidence from human studies demonstrates that ATDs alone reduce gut microbial diversity, deplete short-chain fatty acid (SCFA)-producing bacteria, and promote opportunistic pathogen overgrowth. Concurrently, acid suppressants, particularly proton pump inhibitors (PPIs), raise intragastric pH and facilitate oral-to-gut translocation of bacteria, independently disrupting microbiota composition and metabolic pathways. In this review, we systematically examine the distinct effects of ATDs and acid suppressants on the gut microbiota, the role of the gut-lung axis in tuberculosis immunity, and, on the basis of mechanistic evidence, propose a theoretical cascade under dual exposure: synergistic microbiota depletion, dual metabolic pathway inhibition, immune homeostasis imbalance, and potentially worsened clinical outcomes. This cascade represents a hypothesis-generating framework derived from preclinical and mechanistic studies, rather than an established clinical pathway, and the critical links from dysbiosis to delayed sputum conversion, poor lesion resolution, or increased drug-induced liver injury currently lack direct human confirmation. On the basis of the available evidence, we recommend that clinicians strictly follow indications for acid suppressants, prefer H2 receptor antagonists(H2RAs) over PPIs, and limit treatment to the shortest effective duration. Probiotics and other microbiota-targeted interventions show promise as adjunctive strategies, but their long-term efficacy remains to be validated. Large-scale prospective studies are urgently needed to test the hypothesized cascade, confirm the direct impact of combined therapy on treatment outcomes, and establish microbiota-based biomarkers for predicting therapeutic response.},
}

@article {pmid42840477,
year = {2026},
author = {Seo, JH and Park, JS and Park, JJ and Hah, YS},
title = {The oral-gastric microbial axis in children: salivary signatures as non-invasive biomarkers for pediatric gastritis and Helicobacter pylori infection.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1934250},
pmid = {42840477},
issn = {2235-2988},
mesh = {Humans ; *Helicobacter Infections/microbiology/diagnosis ; *Biomarkers/analysis ; *Helicobacter pylori/genetics/isolation & purification ; *Gastritis/microbiology/diagnosis ; Child ; *Saliva/microbiology ; *Mouth/microbiology ; Gastric Mucosa/microbiology ; Child, Preschool ; *Stomach/microbiology ; *Gastrointestinal Microbiome ; },
abstract = {Helicobacter pylori is commonly acquired in childhood, with the mouth a presumed portal of entry, although the relative contributions of oral-oral, gastro-oral, and fecal-oral transmission remain unresolved. It is a principal cause of pediatric gastritis, yet most infected children are asymptomatic, and the pediatric mucosa mounts a tolerogenic response rather than the aggressive inflammation seen in adults. In the pathway defined by pediatric guidelines, diagnosis depends on endoscopy with multiple gastric biopsies, an invasive reference standard not suitable for serial assessment; non-invasive tests are reserved largely for confirming eradication and have age-specific limitations in young children. This narrative review, supported by a structured literature search, develops the oral-gastric microbial axis as an organizing framework for non-invasive pediatric assessment, on the premise-not yet demonstrated longitudinally-that early oral colonization shapes later gastric disease: the two compartments are ecologically continuous, and acid-tolerant oral bacteria that survive gastric transit provide a pro-inflammatory metabolic input to the mucosa. We evaluate candidate salivary and oral signatures-taxonomic, H. pylori-specific, and metabolic-and grade each on two axes: the population generating the evidence (pediatric, adult, or non-human) and the stage of biomarker development reached, each tied to a stated target condition. The picture is asymmetric: the connectivity argument is well supported and the mechanistic account coherent, but the model has not been demonstrated end-to-end in children. A few signatures have genuine pediatric support, and salivary assays targeting the H. pylori 23S rRNA gene reach the clinical-assay stage on pediatric evidence, with sensitivity of 87-94% but specificity ranging from 80% to 100% in the two cohorts with recoverable two-by-two data; no candidate has been independently validated in children, most evidence is adult-derived, and whether the oral cavity is a true H. pylori reservoir remains unresolved. Because a single, unreplicated comparative study indicates that H. pylori remodels the gastric microbiota differently in children than in adults, adult signatures cannot be assumed transferable. We conclude that oral-gastric signatures currently suit research stratification rather than clinical decision-making, and specify the longitudinal, multi-omics, viability-resolved studies needed to advance them toward clinical validity.},
}

Humans
*Helicobacter Infections/microbiology/diagnosis
*Biomarkers/analysis
*Helicobacter pylori/genetics/isolation & purification
*Gastritis/microbiology/diagnosis
Child
*Saliva/microbiology
*Mouth/microbiology
Gastric Mucosa/microbiology
Child, Preschool
*Stomach/microbiology
*Gastrointestinal Microbiome

@article {pmid42840492,
year = {2026},
author = {Li, H and Zheng, J and Zhang, G and Dong, X and Zhang, Z and Lu, S and Gao, F},
title = {Microbiota-mediated gut-brain communication following whey protein supplementation and resistance training: current evidence linking gastrointestinal function and cognitive health.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1918695},
pmid = {42840492},
issn = {2235-2988},
mesh = {Humans ; *Whey Proteins/administration & dosage ; *Cognition/physiology/drug effects ; *Gastrointestinal Microbiome/drug effects/physiology ; *Dietary Supplements ; *Gastrointestinal Tract/physiology/microbiology ; *Brain/physiology ; *Resistance Training ; Animals ; Brain-Gut Axis ; },
abstract = {Whey protein supplementation in conjunction with resistance training (RT) has emerged as a promising strategy that may modulate microbiota-mediated gut-brain communication, with potential implications for gastrointestinal (GI) function and cognitive health. Evidence from both preclinical and clinical studies suggests that whey protein supplementation and exercise, including RT, may influence gut microbial composition and function through changes in substrate availability, intestinal physiology, and host-microbe interactions. Whey protein supplementation has been associated with source-dependent changes in gut microbial communities, including alterations in the abundance of Bacteroidetes, Bifidobacterium, and butyrate-producing taxa, whereas exercise particularly aerobic exercise, with more limited evidence for RT-has been associated with greater microbial diversity and an increased abundance of short-chain fatty acids (SCFAs)-producing bacteria. Although direct evidence evaluating the combined effects of whey protein supplementation and RT remains limited, available findings suggest that their combination may influence microbial metabolic activity in addition to microbial composition. Microbiota-derived metabolites, particularly SCFAs, together with exercise- and whey protein-induced changes in gut hormone secretion, including glucagon-like peptide-1, peptide YY, and cholecystokinin, may represent plausible mechanistic links between the GI tract and the central nervous system. These pathways may contribute to the regulation of intestinal barrier integrity, neuroendocrine communication, immune responses, and neuroplasticity. Experimental evidence further suggests that whey protein supplementation combined with exercise, including RT, may contribute to reduced oxidative stress and neuroinflammation and may support brain-derived neurotrophic factor signaling; however, direct evidence linking microbiota-mediated changes to cognitive outcomes in combined intervention studies remains scarce. Nevertheless, findings remain heterogeneous because of differences in protein dosage, exercise protocols, intervention duration, study populations, and individual microbiome variability. Overall, current evidence supports the biological plausibility of microbiota-mediated gut-brain communication as a potential mechanism underlying the effects of whey protein supplementation and RT; however, well-designed human studies directly evaluating gut microbiota, gut-brain signaling, and cognitive outcomes are needed to confirm these proposed relationships.},
}

Humans
*Whey Proteins/administration & dosage
*Cognition/physiology/drug effects
*Gastrointestinal Microbiome/drug effects/physiology
*Dietary Supplements
*Gastrointestinal Tract/physiology/microbiology
*Brain/physiology
*Resistance Training
Animals
Brain-Gut Axis

@article {pmid42840576,
year = {2026},
author = {Attieh, P and Nassif, M and Maghzal, M and Bedran, A and Kassas, J and Othman, M and Sahyoun, F and Harb, F and Azar, S and Ghadieh, HE},
title = {MASLD beyond the liver: decoding the gut-genetic-metabolic nexus.},
journal = {Frontiers in gastroenterology (Lausanne, Switzerland)},
volume = {5},
number = {},
pages = {1824548},
pmid = {42840576},
issn = {2813-1169},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly non-alcoholic fatty liver disease, is the most prevalent chronic liver disorder globally and is tightly linked to obesity, diabetes, dyslipidemia, and metabolic syndrome. MASLD spans a continuum from simple steatosis to metabolic dysfunction-associated steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Its pathogenesis is driven by complex interactions among host genetics, metabolic stress, dietary factors, gut microbiota dysbiosis, immune dysregulation, and oxidative injury. The gut-liver axis plays a central role, with microbial metabolites and altered intestinal permeability driving hepatic inflammation and fibrogenesis. Genetic variants, including PNPLA3, TM6SF2, and MBOAT7, modulate disease susceptibility and metabolic pathways. Emerging therapies target interconnected mechanisms through lifestyle interventions, microbiome-directed strategies, bile acid signaling, incretin-based treatments, and antifibrotic approaches. Advances in omics technologies and biomarkers support precision medicine frameworks. Despite major advances in mechanistic understanding, resmetirom has recently become the first FDA-approved therapy for adults with non-cirrhotic MASH and moderate-to-advanced fibrosis. Nevertheless, effective treatment options remain limited, emphasizing the need for additional mechanism-based and personalized therapeutic strategies.},
}