@article {pmid42858690,
year = {2026},
author = {Guler Cekic, S and Vatansever, C and Akpinar, A and Belge, S and Shahrokhi, G and Unal, C and Altintas, A and Aydin, S and Can, F},
title = {Interactions between vaginal, periurethral and urinary microbiota in genitourinary syndrome of menopause and the effects of local estrogen therapy.},
journal = {Maturitas},
volume = {214},
number = {},
pages = {109146},
doi = {10.1016/j.maturitas.2026.109146},
pmid = {42858690},
issn = {1873-4111},
abstract = {OBJECTIVES: Alterations to the vaginal microbiota have been investigated in genitourinary syndrome of menopause but data regarding periurethral and urinary microbiota remain limited. We aimed to characterize vaginal, periurethral, and urinary microbiota in clinically stratified postmenopausal women and to evaluate the effects of estrogen therapy.

STUDY DESIGN: In this prospective study, postmenopausal women were categorized as controls without atrophy or symptoms, women with clinical atrophy without symptoms, symptomatic women, and symptomatic women receiving 12 weeks of vaginal estriol. Vaginal, periurethral, and bladder samples were collected.

MAIN OUTCOME MEASURES: Microbiota composition and diversity (alpha diversity - Shannon index; and beta diversity - Bray-Curtis dissimilarity) across urogenital niches and changes in these following estrogen therapy.

RESULTS: Vaginal and periurethral alpha diversity was higher in women with asymptomatic atrophy and symptomatic women at baseline than in controls and estrogen-treated women. Beta diversity analyses demonstrated separation of controls and estrogen-treated women from the atrophy groups at baseline. Controls exhibited Lactobacillus-enriched periurethral communities and Klebsiella-dominant urinary profiles. Women with asymptomatic atrophy and symptomatic women showed reduced Lactobacillus and increased anaerobic taxa in vaginal and periurethral niches, while urinary samples were characterized by Escherichia predominance. Notably, in women with asymptomatic atrophy, Lactobacillus abundance was higher in periurethral than vaginal samples. Estrogen therapy increased Lactobacillus abundance in vaginal and periurethral compartments and shifted urinary microbiota toward a control-like composition. Periurethral Streptococcus abundance correlated with sexual symptom scores.

CONCLUSIONS: Microbial alterations in genitourinary syndrome of menopause are compartment-specific and extend beyond the vagina. Periurethral microbiota may contribute to symptom expression, while local estrogen therapy promotes restoration of Lactobacillus-dominant urogenital microbiota.

CLINICALTRIALS: gov registration: NCT06633705.},
}

@article {pmid42858922,
year = {2026},
author = {Eftekharian, S and Rastkar, S},
title = {The Oral Microbiome in the Biological and Clinical Response to Photobiomodulation During Cancer Supportive Care: A Critical Mechanistic and Translational Review.},
journal = {Photodiagnosis and photodynamic therapy},
volume = {},
number = {},
pages = {105682},
doi = {10.1016/j.pdpdt.2026.105682},
pmid = {42858922},
issn = {1873-1597},
abstract = {Cancer therapy can disrupt the oral microbial ecosystem through mucosal injury, salivary dysfunction, immune suppression, antimicrobial exposure, dietary change, and altered oral hygiene. Photobiomodulation therapy (PBMT) is guideline-supported for prevention of oral mucositis in selected oncologic settings, but whether the oral microbiome contributes to PBMT response remains uncertain. This critical narrative review reframes the question from whether PBMT changes the oral microbiome to what role, if any, microbial ecology plays in the biological and clinical response to PBMT during cancer supportive care. Evidence is organized as direct clinical evidence, indirect clinical evidence, experimental microbial evidence, and mechanistic hypothesis. Direct clinical evidence is sparse and internally mixed: a four-patient uncontrolled pilot reported concurrent cytokine and microbiome shifts after PBMT, whereas a 2023 head-and-neck cancer case series reported clinical improvement in mucositis without significant pre-post changes in salivary bacterial community structure. The strongest current rationale therefore supports a host-first model in which PBMT modifies epithelial integrity, inflammatory and redox signaling, tissue repair, and possibly salivary physiology, thereby changing the ecological conditions experienced by oral microorganisms. Direct microbial photobiological effects remain plausible but are highly dependent on wavelength, irradiance, radiant exposure, oxygen availability, organism, and biofilm state, and should not be conflated with antimicrobial photodynamic therapy. We propose four non-equivalent roles for microbiome change: mediator, modifier, biomarker, or consequence of treatment response. Oral mucositis is the most informative clinical model, but causal interpretation requires longitudinal sampling, functional microbial assays, complete PBMT dosimetry, validated clinical and patient-reported outcomes, and rigorous control of antimicrobials, periodontal status, oral hygiene, diet, feeding support, and anticancer treatment. Microbiome modulation should currently be regarded as an emerging mechanistic hypothesis and research endpoint rather than an established mechanism of PBMT efficacy.},
}

@article {pmid42859003,
year = {2026},
author = {Dong, L and Luo, S and Misbahullah, SM and Xu, J and Wan, S and Gao, H and Qin, Z},
title = {Polymerization-dependent gut microbiome responses to curdlan β-1,3-glucan and its oligosaccharides.},
journal = {Food research international (Ottawa, Ont.)},
volume = {244},
number = {},
pages = {120524},
doi = {10.1016/j.foodres.2026.120524},
pmid = {42859003},
issn = {1873-7145},
mesh = {*beta-Glucans/metabolism/chemistry ; Humans ; *Gastrointestinal Microbiome/drug effects/physiology ; Feces/microbiology ; *Oligosaccharides/metabolism/chemistry ; Polymerization ; Fermentation ; Dietary Fiber/metabolism ; Fatty Acids, Volatile/metabolism ; Glucose/metabolism ; RNA, Ribosomal, 16S/genetics ; },
abstract = {β-1,3-Glucan is a dietary fiber with microbiome-modulating potential, yet the role of polymerization degree on microbial composition and metabolism remains unclear. Curdlan is an insoluble linear β-1,3-glucan widely used as a food hydrocolloid that provides a model to examine structure-dependent microbiome responses. We compared glucose, curdlan (CBG), and curdlan-derived β-1,3-glucan oligosaccharides (OBG) using anaerobic in vitro fermentation of pooled human feces. A multi-omics approach integrating 16S rRNA sequencing, shotgun metagenomics, short-chain fatty acid (SCFA) quantification, and untargeted metabolomics was applied to resolve taxonomic, functional, and metabolic shifts. Both CBG and OBG enriched Bacteroidota and enhanced carbohydrate metabolism relative to glucose, but through distinct pathways. CBG promoted polymer-associated carbohydrate processing, with enrichment of β-1,3-glucan-degrading enzymes such as GH16, Sus-like transport systems, and polysaccharide-specialized taxa (e.g., Prevotella and Bifidobacterium), and butyrate production. In contrast, OBG favored transporter-mediated substrate uptake, broader microbial participation (e.g. Parabacteroides and Enterobacteriaceae), and a metabolite profile enriched in amino acid-derived compounds and branched-chain SCFAs. These findings demonstrate that β-1,3-glucan polymerization degree governs microbiome functional routing and highlight polymerization degree as a tunable parameter for designing microbiome-directed carbohydrate ingredients with predictable metabolic outcomes.},
}

*beta-Glucans/metabolism/chemistry
Humans
*Gastrointestinal Microbiome/drug effects/physiology
Feces/microbiology
*Oligosaccharides/metabolism/chemistry
Polymerization
Fermentation
Dietary Fiber/metabolism
Fatty Acids, Volatile/metabolism
Glucose/metabolism
RNA, Ribosomal, 16S/genetics

@article {pmid42859016,
year = {2026},
author = {Ji, Q and Qu, H and Chen, D and Li, Q and Zong, L and Liu, Y and Huang, Y and Gu, R},
title = {Matrix-associated spatial structure contributes to compositional stability of a complex multispecies starter culture under microbial perturbation: Insights from kefir grains.},
journal = {Food research international (Ottawa, Ont.)},
volume = {244},
number = {},
pages = {120540},
doi = {10.1016/j.foodres.2026.120540},
pmid = {42859016},
issn = {1873-7145},
mesh = {*Kefir/microbiology ; Fermentation ; *Food Microbiology/methods ; *Microbiota ; Cultured Milk Products/microbiology ; },
abstract = {Complex multispecies starter cultures can enrich the metabolic and sensory diversity of fermented foods, but industrial use is limited by compositional drift, overgrowth of dominant taxa, and vulnerability to exogenous microbial contamination. Kefir grains (KG), a matrix-encapsulated complex starter culture with stable serial propagation, provide a model for how spatial structure contributes to starter stability. We compared matrix-associated KG with free kefir-fermented milk (FKFM), representing a grain-free liquid-phase kefir microbial community, under a large-scale microbial challenge. During the acute 24 h challenge, target-taxon drift estimated from PMA-qPCR data was lower in KG than in the liquid compartments. Ten-generation serial transfer caused stronger community restructuring and Shannon diversity loss in FKFM, whereas KG showed constrained compositional adjustment and remained relatively clustered in Bray-Curtis ordination space. Species-level metagenomic tracking showed broader expansion, retention, and cumulative drift of species-level signals corresponding to exogenous challenge strains in FKFM, while more of these signals in KG followed restricted/stable trajectories. Kefir cell-free supernatant inhibited multiple challenge strains beyond the effect of low pH, indicating a contribution of diffusible inhibitory factors. SEM and live/dead staining revealed rough matrix-associated surfaces and heterogeneous cell states in KG. Together, the results support a model in which spatial structure, prior niche occupancy, and diffusible inhibition jointly contribute to the compositional stability and anti-perturbation capacity of this complex starter culture, informing the design of spatially structured synthetic starter consortia for industrial fermentation.},
}

*Kefir/microbiology
Fermentation
*Food Microbiology/methods
*Microbiota
Cultured Milk Products/microbiology

@article {pmid42859175,
year = {2026},
author = {Khan, I and Khan, I and Noor, U and Irfan, M and Zhiqiang, L},
title = {Artificial intelligence in human microbiome research: from data integration to explainable translation.},
journal = {Archives of microbiology},
volume = {209},
number = {1},
pages = {},
pmid = {42859175},
issn = {1432-072X},
mesh = {Humans ; *Artificial Intelligence ; *Microbiota ; Multiomics ; Precision Medicine ; Translational Research, Biomedical ; Machine Learning ; Genomics ; },
abstract = {The human microbiome is integral to health, metabolism, immunity, and physical protection, with dysbiosis linked to metabolic disorders, autoimmune conditions, and cancer. High-throughput sequencing has generated massive datasets, but analyzing these complex, multidimensional data poses significant challenges. Artificial intelligence (AI), including machine learning, deep learning, and related approaches, offers powerful solutions for data integration, pattern recognition, functional annotation, and predictive modeling. AI applications in microbiome research include identifying microbial biomarkers, predicting disease susceptibility, elucidating microbial interactions, and optimizing personalized interventions. AI also enables integration of microbiome data with host genomics, transcriptomics, and clinical metadata, providing a holistic view of host-microbiome dynamics. Despite advances, challenges such as data heterogeneity, model interpretability, and limited sample sizes remain. This narrative review synthesizes literature from 2015 to 2025 without a formal systematic methodology. We conclude with three priority areas for AI-microbiome translation: improved interpretability, longitudinal modeling, and clinical integration. Leveraging AI in this field holds significant promise for accelerating precision medicine, improving diagnostics, and developing microbiome-targeted therapies, if interpretability and validation challenges are addressed.},
}

Humans
*Artificial Intelligence
*Microbiota
Multiomics
Precision Medicine
Translational Research, Biomedical
Machine Learning
Genomics

@article {pmid42859354,
year = {2026},
author = {Yu, S and Zheng, W and Pan, Y and Chen, L and Ma, J and Gao, M and Zou, W and Lu, Y and Zhao, Y},
title = {Cerebral cavernous malformations: epidemiology, molecular pathogenesis, diagnosis and therapy.},
journal = {Molecular biomedicine},
volume = {7},
number = {1},
pages = {},
pmid = {42859354},
issn = {2662-8651},
support = {82274233//National Natural Science Foundation of China/ ; BK20240146//Natural Science Foundation of Jiangsu Province/ ; 22KJA360007//Natural Science Research of Jiangsu Higher Education Institutions of China/ ; ZD202403//Jiangsu Province Traditional Chinese Medicine Science and Technology Development Plan Key Project/ ; },
mesh = {Humans ; *Hemangioma, Cavernous, Central Nervous System/therapy/epidemiology/diagnosis/genetics ; Animals ; Mutation ; },
abstract = {Cerebral cavernous malformations (CCMs) are cerebrovascular diseases characterized by vascular lesions of the central nervous system (CNS) that can result in epileptic seizures, headaches, focal neurologic deficits (FNDs), and hemorrhagic stroke. Germline and somatic loss-of-function (LOF) mutations in one of the three established CCM-associated genes, namely CCM1 (or krev interaction trapped protein 1, KRIT1), CCM2, and CCM3 (or programmed cell death 10, PDCD10), which have been validated as core drivers of CCM pathogenesis and progression. Over the past few decades, a substantially improved understanding of the hallmarks and molecular basis of CCMs has been achieved. Key pathological hallmarks include but are not limited to excessive angiogenesis, vascular leakage, endothelial-mesenchymal transition (EndMT), defective autophagy, inflammation and immune response, oxidative stress, influenced gut microbiome and altered brain vascular microenvironment. These hallmarks are orchestrated by dysregulated signaling cascades, notably MEKK3-KLF2/4, PI3K-mTOR, and RhoA-ROCK, which integrate genetic, inflammatory, and hemodynamic cues. Concurrently, sophisticated neuroimaging (MRI with SWI/QSM) and genetic testing now enable precise diagnosis and risk stratification. Although surgical resection remains the mainstay for accessible symptomatic lesions, a wave of mechanism‑based pharmacological candidates has shown promising efficacy in preclinical models, and several have advanced to early‑phase clinical trials. This review summarizes the current understanding of CCM epidemiology, molecular pathogenesis, diagnosis and therapy, highlighting how the evolving multi‑hit concept and the dissection of downstream signaling are paving the way towards personalized management of this complicated vascular disease.},
}

Humans
*Hemangioma, Cavernous, Central Nervous System/therapy/epidemiology/diagnosis/genetics
Animals
Mutation

@article {pmid42859437,
year = {2026},
author = {Saimee, Y and Okada, R and Inoue, D and Ike, M},
title = {Characterization of duckweed-associated bacteria from the Wolffia globosa microbiome: Strain-level effects on host growth and key determinants.},
journal = {AIMS microbiology},
volume = {12},
number = {3},
pages = {508-525},
pmid = {42859437},
issn = {2471-1888},
abstract = {Wolffia, a rootless duckweed in the family Lemnaceae, is increasingly recognized as a sustainable bioresource for food, animal feed, bioenergy, and biomaterials. Its productivity depends strongly on the associated microbiome, yet the functional roles of individual duckweed-associated bacteria (DAB) remain poorly understood. In this study, we evaluated the effects of DAB isolated from Wolffia globosa microbiomes on host plant growth and characterized their physiological traits. A total of 98 DAB strains were isolated from seven W. globosa microbiomes and individually co-cultivated with W. globosa, exhibiting diverse effects on host growth ranging from promotion to inhibition, with -14.6 to +12.9% of final effects on plant growth. Ten strains consistently promoted host growth and nine strains inhibited growth, which were identified as plant growth-promoting and growth-inhibiting bacteria, respectively. Of these, seven and four strains were identified within the core taxa of W. globosa microbiomes. At the community level, growth-promoting strains tended to be enriched in the growth-promoting microbiomes, whereas neutral or negative strains appeared to be enriched in the growth-inhibiting microbiomes. Taxonomic evaluation demonstrated that prominent promotive and inhibitory phenotypes occurred across six and five genera, respectively, with strain-level characteristics likely determining plant growth effects. Indole-related compound production by DAB emerged as a key physiological determinant associated with Wolffia growth. These findings provide a traceable strain set to advance our understanding of Wolffia-microbiome interactions and offer practical clues on microbiome engineering strategies to enhance Wolffia biomass productivity.},
}

@article {pmid42859514,
year = {2026},
author = {Khanday, S and Darmaki, AA and Malahifci, R and Alvavi, R and Ahmed, S and Nasr, DS},
title = {Gut microbiota and the gut-brain axis in autism spectrum disorder and attention-deficit/hyperactivity disorder: A scoping review of shared and disorder-specific mechanistic pathways.},
journal = {AIMS microbiology},
volume = {12},
number = {3},
pages = {548-563},
pmid = {42859514},
issn = {2471-1888},
abstract = {BACKGROUND: Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are among the most prevalent neurodevelopmental conditions worldwide, yet the biological mechanisms driving their onset and phenotypic variability remain incompletely understood. The gut-brain axis (GBA), a bidirectional network linking intestinal microbial communities to central nervous system function through endocrine, immune, neural, and metabolic pathways, has emerged as a candidate mechanism through which environmental factors interact with genetic susceptibility to shape neurodevelopmental outcomes.

OBJECTIVE: To systematically map the peer-reviewed evidence on gut microbiome-related mechanistic pathways in ASD and ADHD, we delineated features common to both disorders and identified areas of divergence and knowledge gaps requiring further investigation.

METHODS: A scoping review was performed following the PRISMA Extension for the Scoping Reviews (PRISMA-ScR) framework. PubMed, Scopus, and Google Scholar were searched for peer-reviewed studies published January 2018 through March 2025. Studies addressing gut microbiome composition, GBA signaling, or microbiome-directed interventions in ASD or ADHD were eligible for inclusion. Extracted data were synthesized using inductive thematic analysis via Covidence software.

RESULTS: Forty-five studies satisfied the eligibility criteria. Inductive analysis produced five mechanistic themes: Endocrine dysregulation and microbial metabolite signaling; neuronal signaling and neurotransmitter modulation; immune activation and neuroinflammation; gene-microbiota-environment interactions; and microbiota-targeted interventions. Studies on both disorders demonstrated modifications involving taxa with short-chain-fatty-acid-producing capacity; however, findings were varied and did not prove a common reduction in butyrate production. ASD was marked by pronounced dysregulation of the serotonergic system and tryptophan-kynurenine pathway and increased hypothalamic-pituitary-adrenal (HPA) axis responsiveness. On the other hand, the results in ADHD were majorly cross-sectional or preliminary, and the widely-m recognized dopaminergic dysfunction in ADHD has not been associated to specific microbiota alterations to date.

CONCLUSIONS: Evidence demonstrates the GBA as a useful research conceptual for investigating ASD and ADHD, although the strength of mechanistic evidence differs substantially between the two disorders. Translating these insights into therapeutic strategies will require longitudinal, multi-omic research designs capable of establishing causality and enabling patient stratification for precision microbiome-based interventions.},
}

@article {pmid42859518,
year = {2026},
author = {Wang, F and Zhang, S and Xu, L and Qian, J and Zou, B and Huo, S and Ma, A and Zhuang, G},
title = {Biocontrol of phytopathogenic fungi by Bacillus spp.: Strain screening, regulatory mechanisms, and field application.},
journal = {AIMS microbiology},
volume = {12},
number = {3},
pages = {564-594},
pmid = {42859518},
issn = {2471-1888},
abstract = {Bacillus species, which are among the most extensively studied and widely used rhizobacteria, have demonstrated potent antagonistic activity against a broad spectrum of phytopathogenic fungi, making them ideal microorganisms for biological control. Phytopathogenic fungi cause severe preharvest and postharvest losses in global crop production, significantly reducing yield and quality. The prolonged and heavy reliance on traditional chemical fungicides has resulted in environmental pollution and poses risks to human health. In this context, Bacillus-based biological control has emerged as an environmentally friendly, cost-effective, and sustainable alternative strategy. In this review, we provide a comprehensive overview of the screening of Bacillus strains for the biocontrol of phytopathogenic fungi. The possible mechanisms, including the production of a wide array of antifungal metabolites, the induction of systemic resistance in host plants, and indirect suppression through competition for nutrients and space, were also evaluated. Furthermore, the effects of multistrain synergistic consortia and the development of multifunctional Bacillus strains on biocontrol efficacy are discussed, and research advances in the application of Bacillus spp. in the control of soilborne diseases and phytopathogenic fungi are summarized. Finally, this review provides suggestions for the development of efficient Bacillus-based biocontrol agents, thereby promoting sustainable agricultural development.},
}

@article {pmid42859529,
year = {2026},
author = {Celeski, M and Marchetta, M and Sammartini, E and Sorropago, A and Basile, M and Morello, M and Salzillo, C and Bernardi, M and Mollo, P and Romeo, FJ and Cesaro, A and Golino, M},
title = {Inflammation After Transcatheter Aortic Valve Implantation: Mechanisms, Risk Stratification, and Therapeutic Implications.},
journal = {Reviews in cardiovascular medicine},
volume = {27},
number = {9},
pages = {52850},
pmid = {42859529},
issn = {2153-8174},
abstract = {Transcatheter aortic valve implantation (TAVI) elicits a sterile inflammatory response that is almost universal, yet highly heterogeneous in both magnitude and clinical impact. Initiated by endothelial injury, ischemia-reperfusion, and residual bioprosthetic immunogenicity, peri-procedural inflammation converges on activation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome and downstream interleukin-1β (IL-1β) and IL-6 signaling, leading to increased C-reactive protein levels. This response is further modulated by patient susceptibility, procedural complexity, and device-specific characteristics. While a controlled response promotes tissue repair and healing, exaggerated activation, which manifests as systemic inflammatory response syndrome in up to two-thirds of patients, has been consistently associated with higher mortality, conduction disturbances, new-onset atrial fibrillation, acute kidney injury (AKI), and subclinical leaflet thrombosis. Emerging evidence also implicates gut microbiome-derived metabolites and xenoantigen-driven adaptive immunity as additional contributors to the overall inflammatory burden. Serial biomarker assessment, including C-reactive protein trajectories, neutrophil-to-lymphocyte ratio, cancer antigen 125 (CA-125), and novel composite indices such as the neutrophil percentage-to-albumin ratio, combined with multimodality imaging, allows increasingly refined risk stratification. However, no anti-inflammatory therapy is currently established for routine use after TAVI. Colchicine has shown proof-of-concept signals, sodium-glucose cotransporter 2 inhibitors have demonstrated clinical benefit with pleiotropic anti-inflammatory properties, and lessons from IL-1 and IL-6 inhibition trials in ischemic heart disease provide a translational roadmap. This narrative review synthesizes the epidemiology, mechanisms, clinical consequences, and assessment of peri-TAVI inflammation. Moreover, this review proposes a pragmatic inflammatory subphenotyping framework that integrates baseline risk, procedural exposure, and biomarker kinetics. Such a framework may help bridge the gap between observational associations and precision-based therapeutic strategies, shifting peri-TAVI inflammation from a prognostic marker to a modifiable determinant of outcome.},
}

@article {pmid42859540,
year = {2026},
author = {Li, Y and Mo, C and Xie, Y and Huang, Z and Chen, L and Xie, X and Luo, J and Huang, S and Jiang, S and Zhang, T and Zhang, J and Wu, R and Wu, Q},
title = {The stone-degrading metabolic potential of the urinary microbiome: Sexual dimorphism and dysbiosis in urolithiasis.},
journal = {AIMS microbiology},
volume = {12},
number = {3},
pages = {595-609},
pmid = {42859540},
issn = {2471-1888},
abstract = {Urolithiasis is a prevalent global health burden characterized by high recurrence rates and marked sexual dimorphism. While the gut microbiome's role in oxalate degradation is established, the functional capacity of the local urinary microbiome remains largely unexplored. This study investigated the composition and function of the urinary microbiome in 40 healthy volunteers and 61 urolithiasis patients using 16S rRNA amplicon sequencing, alongside a retrospective analysis of stone composition in 2027 patients. We identified a diverse, ecologically structured microbiome in healthy urine dominated by genera such as Lactobacillus, Streptococcus, and Gardnerella. Significant sex-dependent differences were observed: While males exhibited higher microbial α-diversity, females demonstrated a distinct compositional structure with superior predicted functional capacity for stone degradation. Specifically, the female microbiome was enriched with enzymes including oxalyl-CoA decarboxylase, formyl-CoA transferase, urate oxidase, and purine nucleosidase. Correlation analysis identified Lactobacillus, Enterococcus, and Gardnerella as key contributors to this litholytic potential. Conversely, urolithiasis patients displayed significant dysbiosis, characterized by disrupted microbial networks and a marked reduction in these stone-degrading enzymes. Clinical data supported these findings, revealing a significantly higher prevalence of uric acid stones in males, consistent with their lower microbial degradation capacity. These findings suggest that the healthy urinary microbiome functions as a metabolically active defense system against stone formation. The observed sex-specific variations in microbial composition and enzymatic function provide a novel mechanistic explanation for the epidemiological sex disparities in urolithiasis, highlighting the urinary-kidney axis as a potential therapeutic target.},
}

@article {pmid42859560,
year = {2026},
author = {Dewan, A and Goulart, DB and Mascellino, MT},
title = {Gut microbiota dysbiosis: Pathogenic drivers and emerging phage-based therapeutics.},
journal = {AIMS microbiology},
volume = {12},
number = {3},
pages = {632-665},
pmid = {42859560},
issn = {2471-1888},
abstract = {Gut microbiota dysbiosis driven by pathogenic and opportunistic bacteria, including Clostridioides difficile, adherent-invasive Escherichia coli (AIEC), Salmonella enterica serovar Typhimurium, Fusobacterium nucleatum, Klebsiella pneumoniae, Enterococcus faecalis, and Campylobacter spp., disrupts colonization resistance, epithelial barrier integrity, and immune homeostasis, thereby contributing to the development of inflammatory and metabolic diseases. In this review, we summarize the mechanisms through which these microorganisms promote gut dysbiosis and critically evaluate current microbiome-targeted therapeutic strategies, including fecal microbiota transplantation (FMT), live biotherapeutic products (LBPs), probiotics, and bacteriophage (phage) therapy. We review the preclinical and emerging clinical evidence supporting phage-based targeting of major dysbiosis-associated pathogens and examine the principal challenges limiting clinical translation, including phage resistance, immune-mediated clearance, safety considerations related to temperate phages, manufacturing and delivery constraints, and regulatory barriers. Although evidence remains predominantly preclinical, advances in phage engineering, artificial intelligence-guided phage selection, and systems-level microbiome modeling are expanding the potential of personalized phage therapeutics. Collectively, these developments position bacteriophage therapy as a promising addition to future microbiome-directed strategies for restoring gut microbial homeostasis and managing dysbiosis-associated disease.},
}

@article {pmid42859703,
year = {2026},
author = {Bateman, A},
title = {Peer Bork (1963-2026): pioneer of computational biology, architect of bioinformatics resources, and visionary microbiome researcher.},
journal = {Bioinformatics advances},
volume = {6},
number = {1},
pages = {vbag227},
pmid = {42859703},
issn = {2635-0041},
}

@article {pmid42859978,
year = {2026},
author = {Gulyás-Oldal, V and Patay, G and Dézsi, C and Bezzegh, A and Szili, K},
title = {[The gut-muscle axis and the role of Roseburia inulinivorans in age-related muscle loss: a narrative review].},
journal = {Orvosi hetilap},
volume = {167},
number = {41},
pages = {1646-1654},
doi = {10.1556/650.2026.33641},
pmid = {42859978},
issn = {1788-6120},
mesh = {Humans ; *Sarcopenia/microbiology/physiopathology ; *Gastrointestinal Microbiome/physiology ; *Muscle, Skeletal ; Animals ; *Aging/physiology ; Muscle Strength/physiology ; Aged ; },
abstract = {Age-related muscle loss (sarcopenia) represents one of the most significant health burdens in a globally ageing population. The relationship between the gut microbiome and skeletal muscle, referred to as the gut-muscle axis, is the subject of increasing research, yet the identification of specific responsible microbial species and mechanisms has remained limited. This review aims to summarize the current evidence on the gut-muscle axis, with particular focus on the association between the intestinal bacterium Roseburia inulinivorans and muscle performance reported in a 2026 Gut publication, and to evaluate its clinical and therapeutic relevance. Narrative review based primarily on the study by Martinez-Tellez et al. (2026), supplemented by relevant literature on the gut-muscle axis, sarcopenia, and the ageing microbiome. The relative abundance of R. inulinivorans positively correlated with handgrip strength, leg press and bench press performance. Older adults with detectable R. inulinivorans showed 29% higher handgrip strength without a concomitant increase in cardiorespiratory capacity. In a murine model, oral supplementation produced approximately 30% increase in forelimb grip strength. The mechanism may operate not via butyrate but through activation of the purine and pentose phosphate pathways in muscle tissue. R. inulinivorans shows a species-specific association with muscle strength and represents a candidate target for nutraceutical interventions against sarcopenia and cachexia. Human randomized clinical trials and longitudinal studies accounting for sex differences are required to confirm these findings. Orv Hetil. 2026; 167(41): 1646-1654.},
}

Humans
*Sarcopenia/microbiology/physiopathology
*Gastrointestinal Microbiome/physiology
*Muscle, Skeletal
Animals
*Aging/physiology
Muscle Strength/physiology
Aged

@article {pmid42860030,
year = {2026},
author = {Mousa, AA and Zhang, H and Shen, J and Mao, S and Sun, X},
title = {Excessive Feed Sorting Is Associated With Altered Plasma Metabolism and Distinct Fermentation Responses of Pooled Rumen Microbiota in Dairy Cows.},
journal = {Journal of animal physiology and animal nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1111/jpn.70119},
pmid = {42860030},
issn = {1439-0396},
support = {32530100//Key Program of the National Natural Science Foundation of China/ ; ZJ26195012//Fundamental Research Funds for the Central Universities/ ; },
abstract = {Feed sorting behaviour in dairy cows alters dietary structure and has been associated with rumen dysfunction, but its systemic metabolic consequences and microbial acidogenic potential remain unclear. This study combined in vivo and in vitro approaches to investigate associations between feed sorting behaviour, host metabolism, and rumen microbial fermentation. Twenty-four mid-lactation Holstein cows were monitored for 28 days, from which 12 cows representing extreme feed-sorting phenotypes were selected: severe sorters for fine particles (SES; n = 6) and slight sorters (SLS; n = 6). Blood samples were collected for biochemical and metabolomic analyses, and pooled rumen fluid from selected cows within each sorting category was incubated in vitro with high-concentrate or high-forage substrates. Excessive sorting cows exhibited higher alanine aminotransferase, total cholesterol, and low-density lipoprotein cholesterol concentrations. Metabolomic analysis revealed alterations in carbohydrate, lipid, and amino acid metabolism, including changes in D-mannose, fumaric acid, mevalonic acid, oleic acid, glutamic acid, tryptophan, and gamma-aminobutyric acid concentrations. These changes were accompanied by increased concentrations of PGE2, histamine, and arachidonoyl ethanolamide, consistent with altered inflammatory and endocannabinoid signalling. In vitro incubation of pooled SES- and SLS-derived inocula with high-concentrate and high-forage substrates generated distinct fermentation profiles. Treatments containing SES-derived inocula were characterised by lower pH and greater total volatile fatty acid concentrations, particularly under high-concentrate conditions. These fermentation patterns were associated with higher relative abundances of Succinivibrionaceae UCG-002, Lachnobacterium, and Pseudobutyrivibrio. Overall, these findings suggest that feed sorting behaviour is associated with alterations in systemic metabolism and rumen microbial fermentation characteristics, providing new insight into the relationship between feeding behaviour and metabolic health in dairy cows.},
}

@article {pmid42860089,
year = {2026},
author = {Yan, Y and Zhang, W and Yu, F and Tang, Z and Ding, Y and Wang, D and Li, Y},
title = {Bistability of rhizosphere microbiomes shapes phosphorus partitioning in river networks under water diversion.},
journal = {Water research},
volume = {309},
number = {Pt A},
pages = {127113},
doi = {10.1016/j.watres.2026.127113},
pmid = {42860089},
issn = {1879-2448},
abstract = {Inter-basin water transfer projects are critical for mitigating water scarcity yet impose complex environmental disturbances, altering phosphorus (P) partitioning in recipient river networks. In these ecosystems, rhizosphere microbial communities (RMCs) act as biogeochemical engines regulating P partitioning among water, sediment, and biological phases. This regulatory capacity relies on structural and functional traits of RMC states. However, given their environmental sensitivity, RMCs are susceptible to water diversion disturbances. It remains unclear whether these disturbances drive state transitions and how these shifts reshape P partitioning. Here, we developed a stability landscape framework to characterize RMC states, identify their key environmental drivers, and examine effects on P partitioning in receiving river networks. Results revealed RMC bistability driven by the combination of the coefficient of variation of flow rate (CV_rate), turbidity, and temperature. One stable state maintained low water total P (WTP) and microbial biomass P (MBP), and high plant total P. This low-WTP state featured enrichment of Actinomycetota and Acidobacteriota, enhanced positive network cohesion, and abundant inorganic phosphorus solubilization genes (ppa, ppx). Conversely, the alternative state exhibited elevated WTP and MBP, enriching Cyanobacteriota and Bacteroidota, with simplified networks and enhanced organic phosphorus mineralization and transport genes (phoA, phnW, ugpAC, pstS). Furthermore, this stability landscape framework identified reference values for individual environmental drivers (temperature = 11.93°C, CV_rate = 5.93, turbidity = 21.92 NTU) to inform regulation favoring the low-WTP state. These findings provide a transferable quantitative framework, enabling water diversion operations to shift from reactive P pollution control toward proactive ecological regulation.},
}

@article {pmid42860111,
year = {2026},
author = {Tal, S},
title = {From dam to neonate: microbial, metabolic, and functional pathways shaping early-life development in dogs.},
journal = {Theriogenology},
volume = {268},
number = {},
pages = {118245},
doi = {10.1016/j.theriogenology.2026.118245},
pmid = {42860111},
issn = {1879-3231},
abstract = {Within minutes, the canine neonate transitions from placental support to respiration, thermoregulation, glucose homeostasis, feeding, and microbial colonization. These events are often considered separately, yet they form a connected developmental process that begins in the dam and continues through birth and lactation. This narrative review integrates evidence on maternal, microbial, metabolic, and functional determinants of early-life development in dogs. During gestation, maternal nutrition, metabolism, endocrine adaptation, and the maternal microbiota can influence fetal growth and maturation without requiring a viable fetal microbiota. At birth, loss of placental support coincides with physiological transition and rapid exposure to maternal and environmental microorganisms. Delivery mode, intrapartum care, antimicrobial exposure, and the interval to effective suckling can therefore affect several components of neonatal adaptation simultaneously. Colostrum and milk continue maternal support by supplying immunoglobulins, energy, growth-promoting factors, microorganisms, and a changing metabolite profile. The neonatal intestinal microbiota changes during the first weeks of life, in parallel with maturation of intestinal, immune, and metabolic functions. Low birth weight, inadequate early growth, hypothermia, hypoglycemia, impaired passive immune transfer, and altered intestinal microbial composition are associated with poor outcome, but their causal relationships remain incompletely resolved. Evidence supports careful management of the dam, prompt neonatal assessment, early colostrum intake, thermal and nutritional support, and longitudinal monitoring of weight and clinical activity. Microbiome-based risk prediction and targeted microbial interventions are plausible, but require prospective, multicenter validation before routine clinical use. An integrated dam-to-neonate framework may improve mechanistic research and early recognition of puppies at risk.},
}

@article {pmid42860129,
year = {2026},
author = {Dextro, RB and Rossmann, M and Freitas, AS and Domini, JA and Martins, GL and Shoichiro, U and Coutinho, LL and Cruz, AF and Ono, N and Tsai, SM},
title = {Management-Driven Effects in Soil Physicochemical Properties and Microbial Communities in Eastern Amazonian Agroforests.},
journal = {Environmental microbiology reports},
volume = {18},
number = {5},
pages = {e70432},
pmid = {42860129},
issn = {1758-2229},
support = {2022/13186-4//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2023/08974-6//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2024/03870-0//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2021/10626-0//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; 2024/06334-2//Fundação de Amparo à Pesquisa do Estado de São Paulo/ ; JK20231012//Japan Science and Technology Agency/ ; Finance Code 001//Coordenação de Aperfeiçoamento de Pessoal de Nível Superior/ ; 384253/2023-7//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; 130852/2023-6//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; 314806/2021-0//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; 300104/2025-1//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; 423437/2021-6//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; },
mesh = {*Soil Microbiology ; Brazil ; *Soil/chemistry ; Fungi/classification/genetics/isolation & purification ; *Microbiota ; Forests ; Bacteria/classification/genetics/isolation & purification ; Agriculture ; RNA, Ribosomal, 16S/genetics ; Agroecology ; Biodiversity ; Forestry ; },
abstract = {Agroforestry systems (AFS) are a promising bioeconomic strategy for sustainable land use and soil recovery in tropical regions. However, the potential effects of different management practices on soil microbial communities remain poorly understood. This study compared two neighbouring AFS in Tomé-Açu (PA, Brazil) with similar land-use, size, and productivity but contrasting management: organic inputs (AGF19) vs. chemical fertilization (AGF27), alongside a native forest reference area. Soil samples were evaluated through physicochemical properties, litter composition, and amplicon sequencing (16S rRNA and ITS) across three soil depths. Despite similar soil and litter characteristics, AGF19 showed a lower abundance of phytopathogenic fungi and associations with beneficial fungal taxa as biomarkers. In contrast, AGF27 exhibited signs of a microbiota shift towards a stress-related community. These findings could be partially associated with modest management changes like favouring organic inputs, influencing microbial diversity, functional guilds, and soil chemistry. Differences in management could be potentially linked with the identification of a phytopathogenic fungal taxon (e.g., Fusarium) as a biological marker of the community sampled in the AGF27 soil. Although different from the native forest, the results strengthen the role of AFS as a sustainable agroecological strategy. Regular soil monitoring and microbiome-informed practices are essential for sustainable management.},
}

*Soil Microbiology
Brazil
*Soil/chemistry
Fungi/classification/genetics/isolation & purification
*Microbiota
Forests
Bacteria/classification/genetics/isolation & purification
Agriculture
RNA, Ribosomal, 16S/genetics
Agroecology
Biodiversity
Forestry

@article {pmid42860166,
year = {2026},
author = {Omaima, HAAA and Saihood, SS and Burhan, AH and Aboomaima, WAA and Rostami, M and Raoufinia, R and Mahmoudi, A},
title = {Precision medicine in MASLD: Integrating genetics, multi-omics, and artificial intelligence for risk stratification and targeted therapy.},
journal = {Clinica chimica acta; international journal of clinical chemistry},
volume = {},
number = {},
pages = {122892},
doi = {10.1016/j.cca.2026.122892},
pmid = {42860166},
issn = {1873-3492},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly termed nonalcoholic fatty liver disease (NAFLD), encompasses a heterogeneous clinical spectrum ranging from isolated hepatic steatosis to metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, cirrhosis, and hepatocellular carcinoma. Differences in susceptibility to disease, progression and extrahepatic complications between individuals are due to many different variables, such as genetic, metabolic and environmental factors, sex, reproductive status and gut microbiota. Precision medicine offers a framework to navigate this complexity by combining clinical phenotyping with inherited genetic variation and large-scale multi-omics data including transcriptomics, epigenomics, proteomics, metabolomics, lipidomics, glycomics and microbiome analysis. Here we review the current evidence on important susceptibility genes, novel multi-omics biomarkers and polygenic risk scores, and discuss how these tools can improve risk prediction and sub-phenotyping. We also discuss artificial intelligence and machine learning algorithms that integrate clinical, imaging and molecular information to allow for non-invasive diagnosis and staging. Finally, we highlight precision-based therapeutic approaches such as oligonucleotide-based agents, genotype-stratified lifestyle and pharmacological interventions, and digitally supported personalized lifestyle programs. We outline the remaining challenges and research priorities needed to integrate precision hepatology into routine care, highlighting the identification of clinically actionable MASLD subtypes and the equitable translation of findings into improved long-term outcomes.},
}

@article {pmid42860290,
year = {2026},
author = {Liang, C and Chen, D and Sun, S and Yang, A and Qiao, J and Wu, S},
title = {Relay Architectures and Ecological Strategies of Quorum Sensing Effects on Microbial Interactions.},
journal = {Environmental microbiology},
volume = {28},
number = {10},
pages = {e70440},
doi = {10.1111/1462-2920.70440},
pmid = {42860290},
issn = {1462-2920},
support = {2024YFA0920200//National Key Research and Development Program of China/ ; 32300022//National Natural Science Foundation of China/ ; },
mesh = {*Quorum Sensing ; *Microbial Interactions ; Ecosystem ; Bacteria/metabolism ; *Bacterial Physiological Phenomena ; },
abstract = {Microbial communities assemble in heterogeneous habitats, where quorum sensing (QS) influences interactions beyond signalling populations. Yet QS studies are commonly organized by signal type, circuit, or phenotype, obscuring the routes by which a QS event reaches neighbouring populations and why they prevail in particular settings. This Review synthesizes evidence from host-associated, terrestrial, marine, and aquatic systems to develop a two-dimensional framework for QS-mediated ecological effects. The framework distinguishes three relay architectures by which QS activity in one population affects another: direct perception of the source signal, exposure to a QS-regulated chemical effector, or response to a QS-associated change in a shared host or environment. It then identifies the ecological strategies that these architectures can support, including shared signal accessibility, reciprocal coordination, asymmetric cue responsiveness, resource monopolization, and competitive or community restructuring. Across habitats, spatial structure, resource accessibility, host-associated conditions, and temporal variability shape which relay architectures are feasible and the ecological consequences they generate. The framework positions QS as a context-dependent process through which population-state sensing is translated into neighbour responses, changes in habitat conditions, and community assembly. It establishes testable expectations for predicting which QS-mediated interactions arise in a habitat and for designing interventions that steer microbiome function.},
}

*Quorum Sensing
*Microbial Interactions
Ecosystem
Bacteria/metabolism
*Bacterial Physiological Phenomena

@article {pmid42860401,
year = {2026},
author = {Xu, Z and Jiang, H and Huang, W and Chan, A and Lin, Y and Chan, T and Lui, RN and Wong, MTL and Mak, JWY and Chan, FKL and Chevarin, C and Colombel, JF and Buisson, A and Ng, SC},
title = {Fecal microbiota transplantation for the decolonization of mucosal adherent-invasive Escherichia coli in Crohn's disease: an open-label pilot study.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42860401},
issn = {2041-1723},
mesh = {Humans ; *Crohn Disease/therapy/microbiology ; Pilot Projects ; *Fecal Microbiota Transplantation/methods/adverse effects ; Female ; *Escherichia coli/genetics/physiology ; Male ; Feces/microbiology ; Adult ; *Intestinal Mucosa/microbiology ; Middle Aged ; RNA, Ribosomal, 16S/genetics ; *Escherichia coli Infections/therapy/microbiology ; Young Adult ; Gastrointestinal Microbiome ; Treatment Outcome ; },
abstract = {Adherent-invasive Escherichia coli (AIEC) is implicated in Crohn's disease (CD) pathogenesis, but whether fecal microbiota transplantation (FMT) clears mucosal AIEC and alters fecal and mucosal microbiomes has not been studied. In this open-label pilot study, thirty adults with CD and seropositivity for serum anti-E.coli antibody (AEcAb) received a single colonoscopic FMT from one of two donors (ClinicalTrials.gov identifier NCT05611866). The primary outcome was adverse events (AEs) within 12 weeks after FMT; secondary outcomes included changes in mucosal AIEC, clinical measures, and fecal and mucosal microbiome profiles. Shotgun metagenomic sequencing for fecal samples and 16S rRNA sequencing for ileal mucosal samples were performed at baseline and after FMT. Baseline AEcAb levels were higher in patients with mucosal AIEC colonization (p = 0.019) and remained elevated after FMT. No FMT-related serious adverse events were reported. FMT was associated with mucosal AIEC decolonization in all 8 evaluable baseline-positive patients. Mucosal alpha diversity increased after FMT (p = 0.023), which correlated with reduced fecal calprotectin (p = 0.034). Microbial pathway profiles in CD patients resembled those of their respective donors with reduced donor-recipient dissimilarity post-FMT (p = 0.030), particularly among recipients with mucosal AIEC decolonization (p = 0.039). In conclusion, this open-label pilot study demonstrates the feasibility of FMT for modulating mucosal AIEC colonization in CD and highlights the importance of capturing microbial changes at the disease site that may be undetectable in fecal samples.},
}

Humans
*Crohn Disease/therapy/microbiology
Pilot Projects
*Fecal Microbiota Transplantation/methods/adverse effects
Female
*Escherichia coli/genetics/physiology
Male
Feces/microbiology
Adult
*Intestinal Mucosa/microbiology
Middle Aged
RNA, Ribosomal, 16S/genetics
*Escherichia coli Infections/therapy/microbiology
Young Adult
Gastrointestinal Microbiome
Treatment Outcome

@article {pmid42860412,
year = {2026},
author = {Barno, AR and Villela, HDM and Cardoso, PM and García, FC and Cui, G and Delgadillo-Ordoñez, N and Rosado, AS and Thomas, T and Aranda, M and Voolstra, CR and Peixoto, RS},
title = {Bacterial inoculation elicits changes to the coral epigenome.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42860412},
issn = {2041-1723},
mesh = {Animals ; *Anthozoa/microbiology/genetics ; DNA Methylation ; *Vibrio/physiology ; *Epigenome ; *Epigenesis, Genetic ; Probiotics ; Heat-Shock Response/genetics ; },
abstract = {Environmental shifts can cause epigenetic modifications in corals associated with changes in gene expression and physiology, although it remains unclear if associated bacteria can also induce such changes. Here, we inoculate nubbins of the coral Pocillopora verrucosa with an opportunistic pathogen, Vibrio coralliilyticus, and/or a coral probiotic, Cobetia sp., and subject the nubbins to heat stress. We show that pathogen exposure leads to distinct DNA methylation changes compared to the control, probiotic, and co-inoculation groups. We also confirm that DNA methylation broadly correlates with coral gene expression; however, individual correlations are restricted to a subset of genes. We then highlight genes altered by pathogen inoculation that show similar responses in their expression and methylation. Notably, coral probiotic exposure mitigates specific epigenetic changes caused by pathogen inoculation, which correlates with increased stress resilience and higher coral survival rates. Although many aspects remain to be resolved, evidence that bacteria alter coral epigenomes may help clarify the role of microbiome interactions in coral resilience.},
}

Animals
*Anthozoa/microbiology/genetics
DNA Methylation
*Vibrio/physiology
*Epigenome
*Epigenesis, Genetic
Probiotics
Heat-Shock Response/genetics

@article {pmid42860477,
year = {2026},
author = {Li, K and Xie, L and Li, Y and Xiong, Y and Ai, Y},
title = {Gastric Intestinal Metaplasia After Helicobacter pylori Eradication: Reframing the Reversibility Controversy.},
journal = {Digestive diseases and sciences},
volume = {},
number = {},
pages = {},
pmid = {42860477},
issn = {1573-2568},
abstract = {PURPOSE: To critically examine the evidence for and against reversibility of gastric intestinal metaplasia (GIM) after Helicobacter pylori eradication, reframe the two-decade controversy, and propose a hypothesis-generating framework for risk-stratified management.

METHODS: Narrative synthesis of meta-analyses, cohort studies, randomized controlled trials, and mechanistic studies (2007-2026) identified through PubMed and Web of Science.

RESULTS: The evidence has swung from early meta-analyses (2007-2011) concluding against IM reversibility to recent syntheses (2023-2025) demonstrating regression with prolonged follow-up. In early 2026, two reviews reached opposing conclusions: Song and Yu proposed an oncogenic memory model of persistent mucosal injury, epigenetic and immune alterations, and microbiome dysbiosis, while Chen et al. maintained that part of GIM exhibits meaningful reversibility. Extending this framework, we propose a fourth, largely irreversible dimension-histological memory-encompassing spasmolytic polypeptide-expressing metaplasia (SPEM) progression and stem cell niche alteration, which deepens the mucosal injury component of oncogenic memory. Known predictive factors (OLGA/OLGIM stage, subtype, age, eradication timing, and oncogenic memory burden) are organized into a unified reversibility gradient that reframes the binary question in risk-stratified terms, from which a hypothesis-generating three-tier surveillance framework is derived.

CONCLUSION: GIM reversibility is a continuous function of lesion characteristics, host factors, time since eradication, intervention intensity, and oncogenic memory burden rather than a binary property. The clinically relevant question is whose GIM, under what conditions, over what time frame, and with what residual risk reduction. The frameworks are hypothesis-generating, not validated clinical recommendations; prospective validation of risk-stratified surveillance represents the most urgent research priority.},
}

@article {pmid42860521,
year = {2026},
author = {Zhou, Q and Wang, K and Chen, J and Wang, H and Tan, X and Huang, X and Lin, Z and Xu, X and Jin, X and Zhang, S and Xiao, L and Zou, Y and Zhang, T and Liu, X},
title = {Structural Variants in the Human Genome Associated With Gut Microbiome and Blood Metabolic Traits With Potential Causal Links.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e78201},
doi = {10.1002/advs.78201},
pmid = {42860521},
issn = {2198-3844},
support = {32670077//National Natural Science Foundation of China/ ; 32200548//National Natural Science Foundation of China/ ; 2023YFC2509400//National Key R&D Program of China/ ; //Youth S&T Talent Support Programme of Guangdong Provincial Association for Science and Technology/ ; },
abstract = {Research on genetic variants affecting the gut microbiome and blood metabolites has mainly focused on single nucleotide variants (SNPs), leaving structural variants (SVs) largely unexplored. Here, we analyzed high-coverage (∼42×) whole-genome sequencing data from 2002 individuals and constructed a catalog of 138 859 high-confidence SVs, including 44.3% variants not represented in public SV resources. Genome-wide association analyses of 22 519 common SVs identified 30 microbiome-associated and 48 metabolite-associated SV loci, including 19 study-wide significant associations. Notable signals included an Asian-specific 6.5k deletion at TENT2 associated with Coprobacillus sp. 29_1 abundance (β = 0.158, p = 2.5 × 10[-9]) and a deletion covering HBA1/HBA2/HBM/HBQ1 linked to nine blood metabolic traits (strongest for MCV; β = -0.570, p = 1.22 × 10[-91]). Conditional and variance-partitioning analyses indicated that SVs capture complementary genetic information beyond tested SNP signals. SV-based Mendelian randomization delineated putative directional relationships, including Clostridium ramosum with serum uric acid and hyperuricemia. In vitro experiments further supported three predicted metabolite-microbe interactions, showing that vitamin K1 inhibited Coprococcus comes, hydroxyproline inhibited Veillonella parvula, and cysteine promoted Fusobacterium mortiferum growth. Together, our study provides a comprehensive SVs resource and highlights SVs as overlooked genetic determinants of host-microbiome-metabolome interactions relevant to human physiology and disease.},
}

@article {pmid42860590,
year = {2026},
author = {Lee, MJ and Kim, IS and Ahn, SH and Chung, W and Kang, YE and Jeon, SM and An, JH and Pyo, CH and Jeong, J and Kim, YE and Yoon, J and Choi, KY and Lee, SE and Kim, HS and Lee, S and O'Keeffe, S and Park, JO and Lee, JY and Bae, JW and Kim, DE and Lee, H and Kim, SH and Yeo, WH and Yeo, MK and Oh, E and Jo, EK and Heo, JY},
title = {Vagal sensing of altered gut microbiota links to externalizing behaviors.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2743919},
doi = {10.1080/19490976.2026.2743919},
pmid = {42860590},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Vagus Nerve/physiology/metabolism ; Mice ; Mice, Knockout ; Male ; Solitary Nucleus/metabolism ; Amygdala/metabolism ; Mice, Inbred C57BL ; *Behavior, Animal ; },
abstract = {Interoceptive brain responses triggered by intestinal microbiota influence mood-related behaviors such as anxiety and depression. Although genetic mutations can alter the gut microbiome, how alterations in the gut microbiome associated with host genetic variations relate to behavioral outcomes is not fully understood. We investigated how Sirtuin 3 (Sirt3) deficiency is linked to altered gut-brain interactions and mood-related behaviors. Gut microbiota composition and behavior were compared between Sirt3-knockout (KO) and wild-type (WT) mice. Cohousing and heterozygous littermate controls were used to assess microbiome-related contributions to behavioral differences. Transcriptomic profiling assessed region-specific gene expression in the limbic system. Metabolites in the nucleus of the solitary tract (NTS), potentially related to gut-brain vagal signaling, were analyzed. The role of the vagus nerve was further tested using subdiaphragmatic vagotomy in the Sirt3-KO mouse model, along with measurements of plasma choline levels in mice. Sirt3-KO mice displayed mood-related neurobehavioral changes and alterations in synaptic plasticity-related genes in the amygdala and the bed nucleus of the stria terminalis (BNST), accompanied by alterations in gut microbiome composition. Elevated plasma choline levels in Sirt3-KO mice, together with reduced neurotransmitter-related metabolites (e.g., γ-aminobutyric acid [GABA] in the NTS), suggest that externalizing behaviors in Sirt3-KO mice involve vagus nerve-dependent gut-brain axis signaling. Consistent with the involvement of vagal signaling, vagotomized Sirt3-KO mice were similar to WT mice in these measures, including GABA levels in the NTS and synaptic plasticity-related changes in the amygdala and BNST. Our findings support a model in which host genetic variation-associated microbiome alterations are sensed through sustained gut-vagal signaling under non-stressed conditions, correlating with NTS neurotransmitter alterations and externalizing behavioral phenotypes.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Vagus Nerve/physiology/metabolism
Mice
Mice, Knockout
Male
Solitary Nucleus/metabolism
Amygdala/metabolism
Mice, Inbred C57BL
*Behavior, Animal

@article {pmid42860688,
year = {2026},
author = {Liu, Y and Hu, Y and Xu, M and Ma, Z and Li, J and Liu, H and Wei, X},
title = {Integrated Quantitative and Relative Microbiome Profiling Reveals a Bacterial Group Associated With Primary Apical Periodontitis Severity and Sharing a Predicted Virulence-Associated Functional Signature.},
journal = {International endodontic journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/iej.70289},
pmid = {42860688},
issn = {1365-2591},
support = {SHH-2022-YJ-B03//Shanghai Stomatological Hospital Institutional Project/ ; 23Y11910100//Shanghai Science and Technology Innovation Action Medical Innovation Research Project/ ; },
abstract = {AIM: To overcome the confounding effects of taxonomic heterogeneity in primary apical periodontitis (AP), this study aimed to characterize the quantitative and compositional profiles of the root canal microbiota associated with severe clinical features (percussion tenderness, large periapical lesions, and sinus tracts) using integrated relative (RMP) and quantitative microbiome profiling (QMP).

METHODOLOGY: Root canal samples from 52 patients (out of 62 initially enrolled) with primary AP were analysed using spike-in-based 16S rRNA sequencing. Microbial load, diversity, and taxonomic composition were evaluated across these three predefined clinical features (with large lesions defined as ≥ 5 mm). Spearman correlation analysis was applied to assess the associations between differentially abundant genera and clinical severity. Furthermore, PICRUSt2 was used to infer functional profiles and calculate taxonomic contributions to enriched pathways under both RMP and QMP frameworks.

RESULTS: Samples with percussion tenderness exhibited significantly elevated microbial loads, with similar trends observed for large periapical lesions and sinus tracts. Percussion-positive samples also showed significantly higher Inverse Simpson index and Pielou's evenness index, whereas no significant differences in alpha diversity were observed for large periapical lesions or sinus tracts. Beta diversity did not differ significantly across any of the three clinical features under either QMP or RMP. Spearman correlation analysis identified a core bacterial group-Porphyromonas, Treponema, Tannerella, Peptostreptococcus, Selenomonas, Fusobacterium, and Fretibacterium-whose members showed broadly positive associations with all three clinical features in both relative and absolute abundance. Functional inference revealed these taxa collectively accounted for a shared set of virulence-associated pathways (e.g., lipopolysaccharide/peptidoglycan biosynthesis and protein export) consistently enriched in severe cases.

CONCLUSIONS: Despite taxonomic heterogeneity in the root canal microbiota, severe clinical features of primary AP were associated with elevated microbial load and with increased relative and absolute abundances of a candidate bacterial group, whose members converged on a shared set of virulence-associated pathways, suggesting that compositionally diverse communities may nevertheless converge on common virulence-related functions.},
}

@article {pmid42860924,
year = {2026},
author = {},
title = {Correction to "Deciphering Gut Microbiome Dynamics in Irritable Bowel Syndrome Using Deep Learning".},
journal = {Neurogastroenterology and motility},
volume = {38},
number = {10},
pages = {e70445},
doi = {10.1111/nmo.70445},
pmid = {42860924},
issn = {1365-2982},
}

@article {pmid42860978,
year = {2026},
author = {Eleutério Junior, J and Eleutério, RMN and Gonçalves, AK and Giraldo, PC},
title = {Bacterial vaginosis: a narrative review of concepts and best practices.},
journal = {Gynecology and pelvic medicine},
volume = {9},
number = {},
pages = {37},
pmid = {42860978},
issn = {2617-4499},
abstract = {BACKGROUND AND OBJECTIVE: Bacterial vaginosis (BV) is a multifaceted condition characterized by an imbalance of the vaginal microbiota. This disruption includes not only Gardnerella vaginalis but also a range of anaerobic bacteria, with clinical outcomes varying according to the specific bacterial composition. This review aims to provide an updated overview of the concepts, diagnosis, and management of BV.

METHODS: We conducted a search on MEDLINE (Medical Literature Analysis and Retrieval System Online), Google Scholar, and Scopus for publications in English, prior to September 2025, using the keywords [vaginal microbiota] OR [vaginal microbiome] OR [vaginosis] OR [bacterial vaginosis] OR [dysbiosis] AND [vagina] AND [diagnosis] AND [treatment]. We also reviewed the references of the articles obtained through our literature searches.

KEY CONTENT AND FINDINGS: BV is characterized by a shift from aerobic to anaerobic microbiota. Anaerobic bacteria and their metabolites can significantly impact the local immune response, resulting in various complications in women's reproductive health. Although most affected individuals remain asymptomatic, dysbiosis may negatively influence pregnancy outcomes and elevate the risk of sexually transmitted infections. Diagnosis is traditionally based on the Amsel criteria and Nugent Score. More recently, nucleic acid amplification tests, particularly those utilizing multiplex platforms, have been implemented to identify bacterial species such as Gardnerella, Fannyhessea, and Sneathia. Bacterial composition and the presence of biofilm are critical factors influencing treatment outcomes. Alternatives to conventional antibiotic therapy, including biofilm-disrupting agents and probiotics, are essential for addressing persistent and recurrent BV.

CONCLUSIONS: BV has long been recognized, and diagnosis has traditionally been based on Amsel's criteria and Nugent's score. While new diagnostic tools have offered valuable insights, they have also introduced new questions about this complex condition. Metronidazole remains the primary treatment, although adjuvant therapies, such as biofilm disruption and probiotics, are often required. Further large-scale, in-depth studies are needed to address ongoing uncertainties.},
}

@article {pmid42861078,
year = {2026},
author = {Aguilera-Garrido, A and Lemée, A and Claudel, J and Alem, H},
title = {Strategies for modelling the intestinal mucus interface: Focus on drug transport and host-microbiota interactions.},
journal = {International journal of pharmaceutics: X},
volume = {12},
number = {},
pages = {100672},
pmid = {42861078},
issn = {2590-1567},
abstract = {The intestinal mucus barrier is a complex, dynamic hydrogel that plays a central role in host-microbiota interactions, nutrient transport, and protection against pathogens. Understanding its physicochemical properties has become essential for developing predictive in vitro and in silico models for drug delivery, microbiome research, and disease modelling. Over the past decade, advances in polymer chemistry, glycoscience, and microfluidics have enabled the development of increasingly sophisticated mucus models that mimic structural, rheological, and biochemical features of native intestinal mucus. This review provides a comprehensive overview of recent progress in gut-mucus chemical model development, focusing on mucin biochemistry, hydrogel-based synthetic systems, microphysiological platforms, and an introduction on computational modelling approaches. Special emphasis is placed on emerging strategies to reproduce mucus heterogeneity, viscoelasticity, and microbial interactions. We critically assess the strengths and limitations of current models and highlight future directions for improving physiological relevance, including multi-scale integration and personalized mucus modelling. This review aims to provide a framework for researchers developing next-generation mucus models for biomedical and pharmaceutical applications.},
}

@article {pmid42861307,
year = {2026},
author = {Cheung, SM and Cheng, CY and Ponnusamy, VK and Tsai, KF and Kung, CT and Huang, WT and You, HL and Li, SH and Lee, WC and Cheng, FJ and Chaithanya, V},
title = {Endocrine Disruptors, Gut Microbiota, and Type 2 Diabetes: Bridging Mechanisms to Probiotic-Based Therapeutic Approaches.},
journal = {Diabetes, metabolic syndrome and obesity : targets and therapy},
volume = {19},
number = {},
pages = {636877},
pmid = {42861307},
issn = {1178-7007},
abstract = {Genetic and lifestyle factors alone cannot explain the rising global burden of type 2 diabetes mellitus (T2DM). Growing evidence implicates endocrine-disrupting chemicals (EDCs) found in plastics, pesticides, food packaging, industrial products, and contaminated water as significant environmental contributors to metabolic dysfunction. EDCs, including bisphenol A (BPA), phthalates, per- and polyfluoroalkyl substances (PFAS), persistent organic pollutants (POPs), and heavy metals, have been associated with insulin resistance, pancreatic β-cell dysfunction, oxidative stress, mitochondrial impairment, chronic inflammation, and epigenetic modifications that collectively promote T2DM pathogenesis. The gut microbiota has emerged as a potential mediator of EDC-associated metabolic disruption, whereby chemical exposures may alter microbial diversity, disturb the Firmicutes/Bacteroidetes ratio, impair short-chain fatty acid production, decrease intestinal barrier integrity, driving metabolic endotoxemia and systemic inflammation. This narrative review examines the major EDCs associated with diabetes, their molecular and metabolic mechanisms of action, and their interactions with the gut microbiota, drawing on current experimental and epidemiological evidence. Special emphasis is placed on probiotic supplementation as an emerging therapeutic strategy targeting the EDC-gut microbiota-metabolic axis. Current evidence for probiotics in EDC-associated metabolic dysfunction is predominantly preclinical, with studies suggesting improvements in microbial homeostasis, pancreatic oxidative damage, and glucose metabolism. However, available evidence remains heterogeneous and human clinical trials specifically examining probiotic intervention in EDC-exposed populations at risk of T2DM remain absent, representing a fundamental translational gap that future research must urgently address. Advancing precision medicine approaches, integrating microbiome profiling, metabolomics, epigenetic analysis, and coordinated efforts across toxicology, clinical medicine, and public health, will be essential to reducing the growing global burden of environmentally driven type 2 diabetes.},
}

@article {pmid42861577,
year = {2026},
author = {Samra, NA and Suliman, SGI and Al-Hadad, M and Boomsma, DI and Alhantoobi, F and Alsamahi, M and Abufarajallah, H and Al Tikriti, A and Aung, Z and Richards, S and Sajini, A and Mousa, M and Sulaiman, F and Osman, W},
title = {Toward "Obesityomics": Domain-Specific Omics in Precision Obesity Medicine with a Brief AI Perspective.},
journal = {Obesity reviews : an official journal of the International Association for the Study of Obesity},
volume = {},
number = {},
pages = {e70226},
doi = {10.1111/obr.70226},
pmid = {42861577},
issn = {1467-789X},
support = {RIG-2024-017//Khalifa University of Science, Technology and Research/ ; },
abstract = {BACKGROUND: Obesity's global rise has outpaced the effectiveness of "one-size-fits-all" prevention and treatment strategies. The promise of precision medicine lies in addressing the etiological and biological diversity of obesity and transforming it into actionable endotypes.

OBJECTIVES: In a narrative review, we analyze "obesityomics," looking at the contributions each omics layer makes to understanding and managing obesity. The areas we evaluate are genomics (heritability, polygenic risk, and monogenic forms), epigenomics (development and environment imprinting), transcriptomics (tissue-specific programs of adipose, liver, muscle, and hypothalamus), proteomics (signaling networks and adipokines), metabolomics and lipidomics (fuel partitioning, lipotoxicity, and metabolic inflection points), and microbiome science (metabolites, host-microbe interactions, and microbial ecology). Our domain-by-domain (single-omics) approach demonstrates how disease taxonomy, causal pathways, and biomarkers can be refined and targeted therapeutically.

DISCUSSION: We argue that "obesityomics" is a pragmatic approach to aligning omics modalities to the right questions at the right time, not a wholesale merger of datasets. Artificial intelligence (AI)-including machine learning and deep learning-should be used in conjunction with quality control, feature selection, modest data integration, and obesity intervention prediction. Among the key challenges in managing sensitive multilayer data are harmonization, standardization, reproducibility, equitable representation, and governance. The translation priorities include prospective studies related to patient-centered outcomes, biomarker panels that are clinic-ready, interoperability standards, and cost-effectiveness evaluations.

CONCLUSION: The review maps concrete steps to assist people with obesity in making better choices by identifying what each omics domain excels at and introducing a brief AI perspective.},
}

@article {pmid42861589,
year = {2026},
author = {Xie, YZ and Sun, CX and Fu, TT and Jin, Z and Nalinratana, N and Rojsitthisak, P and Zhao, K and Hua, JS and Pei, FY and Wang, XH},
title = {Nanoformulated Curcumin Ameliorates Ulcerative Colitis via Gut Microbiota Modulation and Barrier Function Restoration.},
journal = {The American journal of Chinese medicine},
volume = {},
number = {},
pages = {1-26},
doi = {10.1142/S0192415X26500837},
pmid = {42861589},
issn = {1793-6853},
abstract = {The gut microbiota is increasingly recognized as a key mediator of the anticolitis effects of curcumin (CUR). However, the clinical translation of this promising activity is severely hampered by CUR's low solubility and poor bioavailability. Although nanoencapsulation represents a promising strategy to address these limitations, the preventive effect of nanocurcumin (nano-CUR) against colitis remains largely unexplored. The present study aimed to elucidate the preventive effects of nano-CUR on intestinal barrier function, gut microbiota composition, and metabolic profiles in a murine model of dextran sulfate sodium (DSS)-induced colitis. The results demonstrated that pre-supplementation of nano-CUR significantly ameliorated disease severity, attenuated intestinal barrier disruption, and suppressed colonic inflammation in mice with DSS-induced colitis. Mechanistically, integrated 16S rRNA sequencing and untargeted metabolomics demonstrated that nano-CUR-restored microbial homeostasis and enhanced the production of short-chain fatty acids, linking microbial shifts to anti-inflammatory outcomes. Fecal microbiota transplantation (FMT) further validated the causal role of the nano-CUR-remodeled microbiota in conferring protection. Collectively, these findings decipher the mechanism by which nano-CUR interacts with the gut microbiota, confirming that dietary nano-CUR consumption protects against ulcerative colitis by modulating the gut microbiome and its metabolic output.},
}

@article {pmid42861590,
year = {2026},
author = {Deng, LR and Zhong, YM and Zhu, SF and Wu, ZY and Chen, FJ and Huang, CY and Wu, QY and Tomlinson, B and Tan, HE and Li, YH},
title = {Anemoside B4 from Pulsatilla chinensis Ameliorates Ulcerative Colitis by Inhibiting Inflammatory Responses via the Modulation of the Gut Microbiota-Immune Interplay.},
journal = {The American journal of Chinese medicine},
volume = {},
number = {},
pages = {1-29},
doi = {10.1142/S0192415X26500849},
pmid = {42861590},
issn = {1793-6853},
abstract = {We previously demonstrated that anemoside B4 (AB4) exerts a beneficial effect in a dextran sulfate sodium (DSS)-induced murine model of ulcerative colitis (UC). In this study, we further explored the mechanism of AB4 against UC from the perspective of gut microbiota-immune interplay. The gut microbiota was depleted in two DSS-induced colitis models to investigate the modulatory effects of the gut microbiome on immune responses and the activity of AB4. In parallel, adoptive transfer of CD4[Formula: see text]CD62L[Formula: see text] T cells into Rag1-deficient (Rag1[-/-]) mice was used to elucidate the alterations in the gut microbiota associated with immune-mediated colitis as well as the modulation by AB4. qPCR, ELISA and western blotting were used to determine the inflammatory responses of mice with colitis, while immunohistochemistry and flow cytometry were employed to determine the CD4[Formula: see text] T cell function and the underlying mechanism. Metagenomic sequencing analysis was used to detect changes in the intestinal microbiota. The depletion of the gut microbiota attenuated disease severity and immune responses in mice with DSS-induced acute and chronic colitis. Notably, the inhibitory effects of orally administered AB4 on colitis progression and immune responses were abrogated. In addition, colitis induced by adoptive transfer of CD4[Formula: see text]CD62L[Formula: see text] T cells into Rag1[-/-] mice was accompanied by CD4[Formula: see text] T cell engraftment and alterations in gut microbiota. Remarkably, all these pathological changes were significantly attenuated by AB4. Crucially, we found that AB4 suppresses the proliferation, migration, and differentiation of CD4[Formula: see text] T cells, which provides a mechanistic basis for its immunosuppressive effects. Collectively, these findings indicate that the gut microbiota and the immune system, particularly CD4[Formula: see text] T cells, interact with each other in the initiation of colitis. We show that, by targeting this gut microbiota-immune interplay, AB4 is a promising therapeutic strategy for UC.},
}

@article {pmid42861600,
year = {2026},
author = {Liu, Y and Ning, X and Liu, Y and Yu, Z and Liu, J and Xu, X and Zhao, J and Sun, S},
title = {Potential Roles of Escherichia coli in IgA Nephropathy: Evidence, Mechanistic Hypotheses and Microbiota-Targeted Strategies.},
journal = {Microbial biotechnology},
volume = {19},
number = {10},
pages = {e70455},
doi = {10.1111/1751-7915.70455},
pmid = {42861600},
issn = {1751-7915},
support = {82470735//National Natural Science Foundation of China/ ; 2023TD-02//Shaanxi Provincial Health Commission/ ; 2023-ZDLSF-15//Key Research and Development Program of Shaanxi Province/ ; 2022ZDLSF03-12//Key Research and Development Projects of Shaanxi Province/ ; },
mesh = {Humans ; *Glomerulonephritis, IGA/microbiology/therapy/pathology ; *Escherichia coli/pathogenicity ; Animals ; *Gastrointestinal Microbiome ; Immunoglobulin A/metabolism ; },
abstract = {IgA nephropathy (IgAN), the most common primary glomerular disease, involves mucosa-kidney axis dysregulation, with gut dysbiosis increasingly implicated in its pathogenesis. Certain Escherichia coli (E. coli) strains harbour virulence-associated features that promote intestinal colonization, barrier disruption and immune activation. Recent microbiome and metagenomic studies have reported an enrichment of E. coli in patients with IgAN, suggesting a potential link to the mucosa-kidney axis. Nevertheless, E. coli may contribute to IgAN through two major pathways. First, sustained LPS exposure may induce aberrant production of galactose-deficient IgA1 (Gd-IgA1) by stimulating B cells and activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome in macrophages, thereby amplifying systemic and renal inflammation. Second, metabolic reprogramming is associated with increased circulating sphingosine-1-phosphate (S1P) and altered production of indole and trimethylamine (TMA); S1P may promote mesangial proliferation and fibrosis, whereas indole- and TMA-related pathways may contribute to tubulointerstitial injury and chronic kidney disease (CKD) progression. Beyond conventional gut microbiota-targeted interventions, emerging precision therapeutic strategies offer promising new directions for the etiological treatment of IgAN. This review summarizes E. coli virulence factors, pathogenesis, and host, environmental, and ecological factors driving its gut expansion in IgAN patients and outlines corresponding therapeutic strategies.},
}

Humans
*Glomerulonephritis, IGA/microbiology/therapy/pathology
*Escherichia coli/pathogenicity
Animals
*Gastrointestinal Microbiome
Immunoglobulin A/metabolism

@article {pmid42861948,
year = {2026},
author = {Wojtkowiak, A and Shinfuku, MS and Lewin, GR},
title = {No strain, no gain: within-host bacterial microdiversity and human health.},
journal = {Infection and immunity},
volume = {},
number = {},
pages = {e0006226},
doi = {10.1128/iai.00062-26},
pmid = {42861948},
issn = {1098-5522},
abstract = {It is well established that within a bacterial species, genotypic and phenotypic variation leads to differences in virulence, antibiotic susceptibility, and metabolism. However, there is also increasing evidence that often multiple variants of the same species co-inhabit the same site in the human body, both during health and disease. This within-host microdiversity can develop over time for pathogens in chronic infections and has been observed for many members of the microbiota, for instance in the gut and on the skin. Research is just beginning to uncover how this within-host intra-species diversity develops and why it matters. Intra-species diversity is largely stable over time, with occasional selective sweeps of new genotypes, and the overall level of diversity is modulated by both microbe-microbe and microbe-host interactions. Furthermore, data indicate that within-host microdiversity can impact the stability of bacterial communities, their antimicrobial resistance, and the efficacy of probiotics and microbiota transplants. Here, we describe the evolutionary and ecological processes that promote high or low within-host microdiversity and the extent of this diversity in the human microbiota and in infections. In addition, we consider how microdiversity within individuals shapes the functional role of the human microbiota and the progression of disease. Together, within-host microdiversity is a newly developing way to think about the diversity of human-associated microbes, with implications in how we treat chronic infections and manipulate our microbiota to promote health.},
}

@article {pmid42861952,
year = {2026},
author = {Alvarez-Aponte, ZI and Anagu, HI and Mok, KC and Nguyen, ST and Trotter, VV and Taga, ME},
title = {Cobamide-based interactions between soil bacteria can be predicted based on monoculture growth.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0130026},
doi = {10.1128/aem.01300-26},
pmid = {42861952},
issn = {1098-5336},
abstract = {Interactions between microbes shape the structure and function of microbial communities. While studying interactions is key to understanding microbial communities as a whole, gaining a detailed mechanistic view is challenging due to the number of co-occurring interactions. Here, we focus on a single class of shared nutrients, the cobalamin (vitamin B12) family of enzyme cofactors known as cobamides, to study nutrient interactions in laboratory consortia of increasing complexity. Measuring cobamide-dependent growth of two soil Caulobacter isolates in monoculture revealed that each grows faster within a distinct range of cobamide concentrations. Co-culturing the two isolates demonstrated that the cobamide concentration predictably determines which isolate predominates. These results suggest that, although the two organisms appear functionally redundant, with identical metabolic capabilities predicted in their genomes, they may occupy distinct niches in their environment based on cobamide concentration. We further examined the ability of cobamide-producing Mesorhizobium and Priestia isolates to share cobamides and found that both support the cobamide-dependent growth of the two Caulobacter isolates. The Caulobacter isolates could coexist in tri-cultures with each producer following serial passaging, indicating the producers can support the growth of multiple cobamide-dependent organisms. We analyzed the metabolic capacity encoded in the genomes of the four isolates and found that cobamides are likely the main shared nutrient in our co- and tri-cultures. These results highlight the utility of cobamides as a model nutrient to characterize and predict interactions in bacterial consortia of increasing complexity.IMPORTANCEInteractions between microbes shape their communities and the world around them. Because microbial communities are physically and chemically complex, predicting microbial interactions is often difficult. Using a set of four bacteria isolated from the same soil environment, we generated and tested predictions about the interactions involving a family of model nutrients related to cobalamin (vitamin B12). Understanding and predicting interactions can lead to greater insights into microbiome function.},
}

@article {pmid42818378,
year = {2026},
author = {Ghezzi, H and Wolff, R and Jain, A and Burckhardt, JC and Hunter, M and Ng, KM and Carasso, S and Geva-Zatorsky, N and Garud, N and Tropini, C},
title = {Growth capacity and mortality burden shape microbial persistence under osmotic stress in Bacteroides thetaiotaomicron.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42818378},
issn = {2692-8205},
support = {R35 GM151023/GM/NIGMS NIH HHS/United States ; },
abstract = {Microbial persistence in the gut is central to sustaining beneficial host-microbiota interactions; however, characterizing determinants of persistence in vivo can be challenging due to the complexity of native microbial communities interacting with the host. Here, we used a defined microbial consortium to demonstrate that intrinsic in vitro growth capacity becomes increasingly predictive of in vivo relative abundance as intestinal osmolality increases. In Bacteroides thetaiotaomicron, in vivo abundance was higher than predicted from growth capacity alone, indicating that additional physiological factors contribute to persistence. We identify mortality as one such determinant: adaptation to prolonged osmotic stress markedly reduced cell loss without enhancing growth capacity. This adaptive phenotype was associated with rapid and reversible phase variation in cell surface-associated PUL78/80 rather than fixed de novo mutations, with the PUL78/80-OFF state becoming progressively enriched among surviving cells as mortality increased. Our findings demonstrate that in addition to growth capacity, reduced cell loss can provide a distinct route to microbial persistence during environmental perturbation.},
}

@article {pmid42853402,
year = {2026},
author = {Sonji, G and Sonji, N and El Katerji, A},
title = {Beyond gastric acid: pharmacologic modulation of the tumor microenvironment by vonoprazan and its drug-interaction implications for chemotherapy and immunotherapy.},
journal = {Cancer chemotherapy and pharmacology},
volume = {96},
number = {1},
pages = {},
pmid = {42853402},
issn = {1432-0843},
mesh = {*Pyrroles/pharmacology/administration & dosage ; Humans ; *Sulfonamides/pharmacology/administration & dosage ; *Tumor Microenvironment/drug effects ; Animals ; *Antineoplastic Agents/pharmacology ; Drug Interactions ; Gastric Acid/metabolism ; Immunotherapy/methods ; *Neoplasms/drug therapy/pathology ; Proton Pump Inhibitors/pharmacology ; },
abstract = {PURPOSE: Vonoprazan, a potassium-competitive acid blocker, possesses distinct pharmacokinetic and pharmacodynamic properties, including a high pKa , prolonged systemic exposure, and sustained hypochlorhydria, that may have implications beyond gastric acid suppression for anticancer drug interactions and the tumor microenvironment.

METHODS: We critically reviewed preclinical and clinical literature to evaluate vonoprazan's potential effects across two proposed biological axes: the intracellular/organelle axis, involving potential lysosomal drug sequestration, pH regulation, autophagy, and apoptotic signaling, and the systemic microbiome axis, involving acid-suppression-associated microbial alterations and potential consequences for antitumor immunity.

RESULTS: Vonoprazan enhanced cisplatin cytotoxicity in MCF-7 breast cancer cells and attenuated cisplatin-associated nephrotoxicity in rats, while altering autophagy-related markers. Separate cancer-cell studies found no increase in VEGF expression under the tested conditions, in contrast to several proton pump inhibitors. Conversely, a retrospective NSCLC cohort associated vonoprazan exposure with higher hazards of progression and death during immune checkpoint inhibitor therapy, although causality was not established. A 2026 pharmacovigilance analysis also identified increased cholangitis reporting among immune checkpoint inhibitor-exposed reports with co-reported vonoprazan, although causality was not established. Clinical evidence for microbiome alterations is emerging, but their relevance to anticancer treatment outcomes remains uncertain.

CONCLUSION: Available evidence supports a context-dependent pharmacologic framework rather than a uniform oncologic effect. Direct evidence for tumor-cell accumulation and vonoprazan-specific effects on V-ATPase activity in tumors remains limited. Prospective clinical and translational studies are needed to determine the clinical relevance of these potential interactions and to define appropriate use alongside anticancer therapies.},
}

*Pyrroles/pharmacology/administration & dosage
Humans
*Sulfonamides/pharmacology/administration & dosage
*Tumor Microenvironment/drug effects
Animals
*Antineoplastic Agents/pharmacology
Drug Interactions
Gastric Acid/metabolism
Immunotherapy/methods
*Neoplasms/drug therapy/pathology
Proton Pump Inhibitors/pharmacology

@article {pmid42853772,
year = {2026},
author = {Khan, MD and Ali, MA and Chaudhry, AS and Ahsan, A and Ahmad, I},
title = {Fusobacterium nucleatum mediated crosstalk drives cisplatin resistance in head and neck cancer.},
journal = {Oncology},
volume = {},
number = {},
pages = {1},
doi = {10.1159/ocl/aebag021},
pmid = {42853772},
issn = {1423-0232},
abstract = {Cisplatin remains a cornerstone of head and neck cancer (HNC) treatment, yet resistance frequently undermines therapeutic efficacy. Emerging evidence implicates Fusobacterium nucleatum, enriched in the tumour microbiome, in promoting chemoresistance via molecular and microenvironmental mechanisms. This review synthesises evidence from PubMed, Scopus, and Web of Science (January 2015-September 2025) examining F. nucleatum's contribution to cisplatin resistance in HNC. Cisplatin resistance involves tumour-intrinsic pathways, such as nucleotide excision repair, homologous recombination, and ATP7B-mediated drug efflux. F. nucleatum indirectly enhances resistance via Wnt5a/Ca[2+]-NFATc3 signalling, downregulation of p53 and E-cadherin, and activation of the NLRP3 inflammasome, which recruits myeloid-derived suppressor cells. It also amplifies inflammation and chemoresistance by escalating the senescence-associated secretory phenotype, promoting a tumour-supportive microenvironment. These findings highlight microbiome host crosstalk as a therapeutic target, suggesting that microbiota-directed strategies alongside cisplatin may improve outcomes in resistant HNC.},
}

@article {pmid42853809,
year = {2026},
author = {Woodyear, S and Binti, NN and Caddy, SL},
title = {Why does rotavirus vaccine effectiveness vary around the globe?.},
journal = {PLoS pathogens},
volume = {22},
number = {10},
pages = {e1014670},
pmid = {42853809},
issn = {1553-7374},
mesh = {Humans ; *Rotavirus Vaccines/immunology ; *Rotavirus Infections/prevention & control/immunology ; *Vaccine Efficacy ; *Rotavirus/immunology ; },
abstract = {Rotavirus vaccines have transformed the prevention of severe childhood diarrhea globally, yet their effectiveness remains markedly lower in low- and middle-income countries (LMICs), where rotavirus mortality is greatest. Understanding the biological and environmental determinants of this disparity is critical for optimizing existing vaccination strategies and informing next-generation vaccine development. This review examines the factors contributing to variable rotavirus vaccine effectiveness across different settings, with a focus on maternal antibodies, infant gut health, co-infections, co-vaccinations and human genetic polymorphisms. Maternal antibodies, transferred transplacentally and through breast milk, can inhibit vaccine replication in the infant gut. Maternal antibody interference may be exacerbated in LMICs due to higher maternal antibody levels, driven by increased rates of natural rotavirus exposure and prolonged breastfeeding. Malnutrition, disruption of the gut microbiome, and environmental enteric dysfunction collectively impair intestinal immune responses, with their relative contributions also varying by geography. Co-administration of the oral poliovirus vaccine and concurrent enteric infections represent additional sources of interference that are more prevalent in resource-limited settings. Host genetic factors, particularly polymorphisms in fucosyltransferase genes governing histo-blood group antigen expression, further modulate vaccine immunogenicity across populations. These factors do not act in isolation; rather, they interact to shape the gut environment and collectively limit oral vaccine replication. Addressing rotavirus vaccine inequity will require context-specific strategies that combine optimized vaccine scheduling, nutritional and microbiome-targeted interventions, and the development of novel vaccine platforms capable of overcoming the unique immunological challenges of LMICs.},
}

Humans
*Rotavirus Vaccines/immunology
*Rotavirus Infections/prevention & control/immunology
*Vaccine Efficacy
*Rotavirus/immunology

@article {pmid42853928,
year = {2026},
author = {Liu, J and Zhang, N and Lei, Y and Wang, X and Zhang, X and Huang, W and Ding, C and Xie, D and Yu, J and Tuan, RS and Li, ZA},
title = {Effects of probiotics on joint homeostasis and osteoarthritis: Development of microbe-gut-cartilage axis-on-a-chip.},
journal = {Science advances},
volume = {12},
number = {41},
pages = {eaeg8557},
pmid = {42853928},
issn = {2375-2548},
mesh = {*Probiotics/pharmacology ; *Osteoarthritis/metabolism/microbiology/pathology/drug therapy ; Humans ; *Homeostasis/drug effects ; *Lab-On-A-Chip Devices ; *Joints/metabolism/drug effects ; *Cartilage/metabolism/drug effects ; Microphysiological Systems ; Microbiota ; Organoids/metabolism ; Animals ; Chondrocytes/metabolism ; Multiomics ; },
abstract = {Although emerging evidence implicates gut microbiome-cartilage cross-talk in the pathogenesis of osteoarthritis (OA), the most common joint disease, studying this microbe-gut-joint axis remains challenging due to limitations of animal models and conventional in vitro systems. Here, we report a microbe-gut-cartilage axis-on-a-chip (MGCAoC) that recreates tissue-specific microenvironments with oxygen gradients and physiological fluid shear. The computer simulation-optimized chip design generates an anoxic-oxic interface for the gut module and enables perfusion of probiotic metabolites to human cartilage organoids without cross-contamination. Multiomics profiling suggested that probiotic metabolites may promote cartilage anabolism, potentially involving PI3K and MAPK pathway, and this effect was associated with up-regulated collagen type II and aggrecan expression while suppressing metalloproteinases. In inflamed cartilage organoids, these metabolites were associated with reduced proinflammatory signaling while preserving matrix integrity. The chondroprotective effects were confirmed using cartilage organoids derived from patients with OA treated with identified metabolites. This MGCAoC enables mechanistic investigation of gut-joint axis physiology and provides a versatile preclinical tool for screening probiotic-based OA therapeutics.},
}

*Probiotics/pharmacology
*Osteoarthritis/metabolism/microbiology/pathology/drug therapy
Humans
*Homeostasis/drug effects
*Lab-On-A-Chip Devices
*Joints/metabolism/drug effects
*Cartilage/metabolism/drug effects
Microphysiological Systems
Microbiota
Organoids/metabolism
Animals
Chondrocytes/metabolism
Multiomics

@article {pmid42854067,
year = {2026},
author = {Tu, H and Chen, M and Zhu, P and Hong, J and He, L},
title = {Mapping mitochondria-associated research in inflammatory bowel disease: A bibliometric and network analysis.},
journal = {Medicine},
volume = {105},
number = {41},
pages = {e51103},
doi = {10.1097/MD.0000000000051103},
pmid = {42854067},
issn = {1536-5964},
mesh = {*Inflammatory Bowel Diseases ; *Bibliometrics ; Humans ; *Mitochondria/metabolism ; *Biomedical Research ; },
abstract = {BACKGROUND: Mitochondria-associated research has become increasingly prominent in inflammatory bowel disease (IBD), but its publication growth, collaboration structure, knowledge base, and thematic evolution have not been comprehensively quantified.

METHODS: Web of Science Core Collection records published from 2010 through 2025 were retrieved on September 19, 2025. Of 215 candidate records, 112 met prespecified eligibility criteria. The 111 records with complete Full Record and Cited References metadata were used for primary analyses; 1 additional eligible record was included only in an annual-output sensitivity analysis. Bibliometrix/Biblioshiny, VOSviewer 1.6.20, and R were used for descriptive, network, temporal, and robustness analyses.

RESULTS: Annual output increased significantly (Kendall τ = 0.638, P = .0009; Sen slope = 1.20 publications/year, 95% confidence interval 0.50-1.71), whereas annualized citation impact showed no significant monotonic trend after exclusion of 2025 (Spearman ρ = 0.093, P = .742). China led corresponding-author output (39 articles), while the United States had the highest aggregate citation count (985). Multi-country publications accounted for 35 of 111 articles (31.5%). The largest institutional collaboration component contained 53 organizations in 8 clusters, and the author component contained 15 authors in 2 clusters. The primary author-keyword network included 22 terms, 6 clusters, 90 links, and a total link strength of 181. Mitophagy, mitochondrial dynamics, and machine learning were positioned toward the recent end of the temporal spectrum. Cited-source and cited-reference networks were densely interconnected, indicating a shared multidisciplinary knowledge base.

CONCLUSION: Mitochondria-associated IBD research expanded substantially during 2010 to 2025, with concentrated geographic leadership, recurrent but uneven international collaboration, and overlapping themes spanning inflammation, epithelial biology, metabolism, mitochondrial quality control, and host-microbiome interactions. The findings provide a reproducible map of the literature but should not be interpreted as evidence of biological causality or discrete mechanistic pathways.},
}

*Inflammatory Bowel Diseases
*Bibliometrics
Humans
*Mitochondria/metabolism
*Biomedical Research

@article {pmid42854346,
year = {2026},
author = {Londoño, E and Dieudonné, RJ and Savulionyte, G and Lucas Poggio, J and Philp, M and Vu, JV},
title = {Antibiotic resistance is associated with anastomotic leak after surgery for diverticular disease.},
journal = {American journal of surgery},
volume = {262},
number = {},
pages = {117256},
doi = {10.1016/j.amjsurg.2026.117256},
pmid = {42854346},
issn = {1879-1883},
abstract = {INTRODUCTION: Patients with diverticulitis frequently receive multiple courses of antibiotics before surgery, which may promote antibiotic resistance. We hypothesized that antibiotic resistance is associated with anastomotic leak after surgery for diverticular disease.

METHODS: We retrospectively reviewed patients undergoing surgery for diverticular disease and linked microbiology data to our institution's National Surgical Quality Improvement Program database.

RESULTS: From 2016 to 2024, 159 patients underwent surgery for diverticular disease. The rates of anastomotic leak, infectious complications, and mortality were 9%, 29%, and 4%, respectively. Of the 101 (64%) patients with microbiology data, 40% had one or more organisms with antibiotic resistance. After logistic regression, antibiotic resistance was associated with a higher likelihood of anastomotic leak (OR 9.8, 95% CI 1.4-66.1, p = 0.019) and overall infectious complications (OR 3.3, 95% CI 1.3-8.6, p = 0.015).

CONCLUSIONS: Among patients undergoing surgery for diverticular disease, having bacteria with clinically significant antibiotic resistance was associated with a higher likelihood of anastomotic leak and infectious complications.},
}

@article {pmid42854450,
year = {2026},
author = {Zaongo, SD and Bado, I},
title = {Pathophysiological contributions of P-selectin glycoprotein ligand-1 to early- and late-onset colorectal cancer.},
journal = {Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie},
volume = {204},
number = {},
pages = {119978},
doi = {10.1016/j.biopha.2026.119978},
pmid = {42854450},
issn = {1950-6007},
abstract = {The incidence of early-onset colorectal cancer (CRC) is rising steadily alongside traditional late-onset disease, yet the pathophysiological mechanisms distinguishing these two entities remain largely elusive. Herein, we address this knowledge gap by examining the distinctive properties of P-selectin glycoprotein ligand (PSGL)-1 within the CRC landscape. Given that both early- and late-onset CRC are underpinned by chronic gut inflammation, the potential role of PSGL-1 in this context warrants close investigation. First, we synthesize current evidence on the contributions of PSGL-1 to CRC pathogenesis and propose its function as a molecular bridge between early- and late-onset disease forms. Second, we explore the mechanistic links connecting PSGL-1 to established protumorigenic pathways and to the gut microbiome, reinforcing its emerging significance in CRC development. Finally, by offering deeper insights into the putative roles of PSGL-1 in promoting CRC, we inform new directions for clinical and therapeutic strategies centered on PSGL-1-directed investigation.},
}

@article {pmid42854469,
year = {2026},
author = {Fan, Z and Chen, Y and Li, Y and Dong, Y and An, X and Li, J and Su, L and Wu, D},
title = {The gut-pancreas axis in chronic pancreatitis: Microbiota-endogenous GLP-1 interactions and candidate repair pathways.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128749},
doi = {10.1016/j.micres.2026.128749},
pmid = {42854469},
issn = {1618-0623},
abstract = {Chronic pancreatitis (CP) is a progressive fibroinflammatory disorder with limited disease-modifying options. Human CP studies report gut microbial and intestinal-barrier alterations, predominantly in cross-sectional cohorts. This review integrates CP-specific clinical and experimental observations with mechanistic evidence from cell, rodent, and non-CP human studies. Barrier disruption can increase lipopolysaccharide exposure and engage Toll-like receptor 4-associated inflammatory and fibrogenic signaling, whereas microbial and host-derived metabolites regulate enteroendocrine L-cell secretion through defined receptor-mediated and metabolic pathways. Human glucagon-like peptide-1 (GLP-1) studies in CP show heterogeneous responses, while CP trials have not yet connected microbiota-driven GLP-1 changes to disease progression. Evidence for direct pancreatic GLP-1 receptor (GLP-1R) signaling is strongest in β cells; reported immune, stellate-cell, and exocrine effects derive largely from preclinical or pharmacological studies and should not be equated with physiological endogenous GLP-1 exposure. CP-specific animal studies reported attenuated fibrosis or improved barrier and immune endpoints after microbiota-directed interventions, whereas limited human synbiotic trials reported improvements in selected gastrointestinal or perioperative outcomes but did not assess endogenous GLP-1, microbiome engraftment, pancreatic fibrosis, or disease progression. Together, these findings support a biologically coherent and testable microbiota-metabolite-endogenous GLP-1 framework for CP, with causal direction and clinical relevance requiring longitudinal validation. Translation requires microbiome-stratified CP trials incorporating functional microbiome and metabolite profiling; basal and meal-stimulated measurements of active and total GLP-1, together with peptide YY; prespecified clinical outcomes; mediation and treatment-by-biomarker analyses; and long-term safety assessment.},
}

@article {pmid42854479,
year = {2026},
author = {Wang, XL and He, Y and Yu, N and Ma, YX and Pan, W and Gong, JX and Wang, C and Zhou, HR and Yang, L and Tan, QG and Lu, Q and Wei, S and Ji, R and Miao, AJ},
title = {Environmental aging alters the toxicity profiles of nanoplastics and generates biologically active soluble products.},
journal = {Journal of hazardous materials},
volume = {517},
number = {},
pages = {143805},
doi = {10.1016/j.jhazmat.2026.143805},
pmid = {42854479},
issn = {1873-3336},
abstract = {Nanoplastics (NPs) health risks are widely recognized, yet assessments largely regard particles as the principal toxic entity and overlook soluble aging products generated during environmental exposure. Here, we examine how environmental aging alters NP toxicity profiles and generates biologically active soluble products. Polystyrene (PS) and polymethyl methacrylate (PMMA) NPs were subjected to long-term (365 days) solar-relevant UV aging (315-400 nm) to provide an environmentally realistic framework for evaluating transformation-driven effects. By physically separating aged particles from low-molecular-weight aging products, we found that aging attenuated particle-associated toxicity while generating products that retained substantial biological activity. Integrated histological, transcriptomic, and metabolomic analyses of blood, gut, liver, and brain revealed distinct patterns of tissue injury and metabolic disruption across aged particle and aging product exposures. Aged particles induced fewer and weaker hepatic transcriptional changes than pristine particles, whereas soluble fractions mainly affected circulating metabolism, with 70 and 30 differential serum metabolites for PMMA and PS, respectively. Multi-omics integration and targeted manipulation of gut bacteria linked both components to microbiome-dependent modulation of host metabolism. Environmental aging therefore altered NP toxicity profiles and generated biologically active soluble fractions, highlighting the importance of evaluating residual particles and soluble aging-associated fractions separately.},
}

@article {pmid42854551,
year = {2026},
author = {Li, Z and Zhang, N and Dai, L and Meng, X and Huang, J and Hei, Q and Mei, Z and Xiong, H},
title = {Bairesi Pills ameliorates vitiligo-like depigmentation by reducing hippuric acid accumulation and regulating MAPK14/β-catenin mediated melanogenesis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {162},
number = {},
pages = {158822},
doi = {10.1016/j.phymed.2026.158822},
pmid = {42854551},
issn = {1618-095X},
abstract = {BACKGROUND: Bairesi Pills is a traditional Uyghur medicinal formula prescribed for vitiligo. However, its bioactive constituents and specific pharmacological mechanisms remain to be fully elucidated.

PURPOSE: This study aims to elucidate the underlying mechanisms and identify the active constituents of Bairesi Pills in the treatment of vitiligo.

METHODS: A hydroquinone-induced vitiligo mouse model was established to evaluate the effects of Bairesi in vivo. Serum untargeted metabolomics and gut microbiome analyses were integrated to identify key differential metabolites and explore the association between gut dysbiosis and skin depigmentation. In vitro, melanocyte oxidative injury models were established using H₂O₂ or hippuric acid. Transcriptome sequencing was performed to screen differentially expressed genes and related signaling pathways. MAPK14 overexpression and pharmacological inhibition were further used to verify the effects and mechanisms of Bairesi and its active constituents in alleviating hippuric acid-induced oxidative stress.

RESULTS: In vivo, Bairesi ameliorated oxidative stress and promoted pigment deposition in vitiligo-like mice, which was associated with enhanced intestinal mucosal barrier integrity, reshaped gut microbiota, and reduced hippuric acid accumulation. In vitro, H₂O₂ or hippuric acid induced oxidative injury and MAPK activation in melanocytes, whereas Bairesi, piperine, and quercitrin suppressed MAPK14 activation, alleviated oxidative stress, and restored melanin synthesis, but these protective effects were attenuated by MAPK14 overexpression.

CONCLUSION: Bairesi Pills ameliorates vitiligo-like depigmentation by reshaping the gut microbiota-metabolite profile, reducing hippuric acid accumulation, and reversing HA-induced oxidative stress through inhibition of MAPK14 phosphorylation.},
}

@article {pmid42854696,
year = {2026},
author = {Cabello-Yeves, E and Samarra, A and Summers, K and Comas, I and Wellington, E and Millard, A and Collado, MC and Marina, A},
title = {Breastfeeding and maternal microbial reservoirs are associated with infant gut phageome development during the first year of life.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {103107},
doi = {10.1016/j.xcrm.2026.103107},
pmid = {42854696},
issn = {2666-3791},
abstract = {The early-life assembly of the gut microbiome is a critical determinant of long-term health, yet the role of bacteriophages in this process remains poorly understood. Here we longitudinally profile the gut phageome of 34 mother-infant dyads during the first year of life with metagenomics and a phage-centered computational workflow. Phage diversity increases with age, paralleling bacterial diversification but following distinct ecological trajectories. Shared viral populations across maternal and infant samples are consistent with potential maternal contribution, although not indicative of direct transmission. Feeding-related variables are consistently associated with phageome composition at specific developmental stages. No single factor fully explains phageome variation, supporting a multifactorial model involving maternal, environmental, and dietary inputs. Together, these findings provide a framework for understanding early-life phage ecology, positioning phages as active participants in early microbiome assembly and supporting the inclusion of viral components in microbiome-based strategies aimed at promoting healthy ecosystem development in infancy.},
}

@article {pmid42854767,
year = {2026},
author = {Burman, A and Bell, PT and Chambers, D and Martinu, T},
title = {CLAD: translating basic science to clinical practice.},
journal = {The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.healun.2026.10.005},
pmid = {42854767},
issn = {1557-3117},
abstract = {Chronic lung allograft dysfunction (CLAD), a fibrotic manifestation of chronic rejection, remains the major barrier to long-term survival after lung transplantation. CLAD is increasingly recognised as the final common pathway of diverse alloimmune injuries, augmented by non-alloimmune insults, that culminate in irreversible airway and parenchymal remodelling. Recent advances in molecular profiling, single-cell technologies, and biomarker discovery, with corroboration by novel animal and in vitro models, are redefining CLAD pathogenesis. Emerging data implicate distinct pathways involving cytotoxic and senescent T cells, humoral alloimmunity, innate immune activation, epithelial dysfunction, aspiration, and microbial dysbiosis. These observations support a shift from clinical phenotypes such as bronchiolitis obliterans and restrictive allograft syndromes toward biologically defined endotypes that may better predict disease progression and therapeutic responsiveness. Furthermore, the recent recognition of acute lung allograft dysfunction (ALAD) as a heterogeneous syndrome highlights an opportunity to identify and characterise graft injury before irreversible fibrosis develops. Biomarkers such as donor-derived cell-free DNA, airway transcriptomic signatures, autoantibodies, epithelial injury markers and microbiome-derived signals may facilitate risk stratification, patient enrichment and endotype-guided clinical trials. This review highlights recent mechanistic and translational advances in CLAD and discusses how molecular endotyping may enable earlier diagnosis, targeted intervention and more efficient therapeutic development. We hope that these highlights will generate enthusiasm for even greater collaboration between basic and translational researchers, and optimism regarding strategies for earlier detection and treatment of CLAD.},
}

@article {pmid42854825,
year = {2026},
author = {Zhang, Y and Lu, R},
title = {Characteristics of metagenome and metabolomics of biliary flora in biliary acute pancreatitis for severity prediction.},
journal = {Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract},
volume = {},
number = {},
pages = {102625},
doi = {10.1016/j.gassur.2026.102625},
pmid = {42854825},
issn = {1873-4626},
abstract = {OBJECTIVE: To investigate the characteristics of the metagenome and metabolomics of biliary flora in patients with acute biliary pancreatitis and its predictive value for the severity of the disease.

METHODS: This study included 80 ABP patients (Jan 2022 - Dec 2024) and 30 healthy controls. ABP patients were divided into mild (n = 50) and moderate-severe (n = 30) groups using the revised Atlanta criteria. Chao1 index, Shannon index, relative abundances of Klebsiella, Enterococcus, and Escherichia coli, serum amylase, and C-reactive protein (CRP) were compared. ROC analysis assessed predictive value of Shannon index, Klebsiella abundance, and CRP for severity. Correlations between these parameters and severity were examined.

RESULTS: Significant differences were observed among the three groups in Chao1 and Shannon indices, relative abundances of the three bacterial genera, and serum amylase and CRP levels (all P < 0.05). ROC analysis showed that Shannon index, Klebsiella relative abundance, and CRP level predicted disease severity with AUCs of 0.804, 0.804, and 0.850, respectively (P < 0.05). Shannon index was negatively correlated with ABP severity, while Klebsiella abundance and CRP level were positively correlated with severity (P < 0.05).

CONCLUSION: In this cohort, biliary microbiome characteristics and serum inflammatory markers were associated with the severity of biliary acute pancreatitis. The Shannon index, Klebsiella relative abundance, and CRP showed exploratory discriminatory performance. These findings provide a basis for further prospective validation; they do not establish a causal driving factor, a clinically validated early-warning system, or an individualized treatment strategy.},
}

@article {pmid42854928,
year = {2026},
author = {Rezende, LG and Dos Santos, WT and de Freitas, A and Vilela, FMP and Midlej, V and Húngaro, HM and de Paula, ACC and Maltarollo, VG and Jaeger, LH},
title = {Evaluation of antitrichomonal activity of coffeewaste compounds against different Trichomonas vaginalis strains: An in vitro and in silico study.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {108860},
doi = {10.1016/j.micpath.2026.108860},
pmid = {42854928},
issn = {1096-1208},
abstract = {Trichomoniasis is a Sexually Transmitted Infection (STI) caused by the protozoan Trichomonas vaginalis, closely related to secondary viral infections that have a high impact in the public health costs. Nitroimidazole drugs are the only available treatment options. Thus, refractory cases have emerged in recent years, leading to the necessity of therapeutic alternatives. The use of coffee by-products such as pulp, husks and leaves may represent a sustainable alternative for treatment. The aim of the study was to evaluate the trichomonacidal activity in vitro and in silico of compounds commonly isolated from coffee waste. For this, caffeine, chlorogenic acid, quinic acid, caffeic acid, and mangiferin were tested in vitro for their anti-T. vaginalis activities against strains CDC085 and JT. Transmission electron microscopy (TEM) and molecular docking were performed to unravel a possible mechanism of action. Cytotoxicity in vitro was performed against HeLa cells and vaginal microbiome bacterial isolate, Lactobacillus jensenii. Caffeine, chlorogenic acid, and quinic acid presented potent activity against CDC085 strain of T. vaginalis, with IC50 of 4.83 μM, 10.01 μM, and 12.73 μM, respectively. TEM showed alterations in trophozoites hydrogenosomes for both organic acids treatments and autophagy process when treated with caffeine. The compounds had no inhibitory effect against the JT strain. Quinic acid revealed promising interactions with parasite's lactate dehydrogenase (LDH) through in silico molecular docking. The three promising compounds did not show cytotoxicity against HeLa cells (selectivity index > 10) nor against bacteria from the vaginal microbiota (MIC>400 μM). Our findings have pointed caffeine and quinic acid as potent anti-T. vaginalis agents, with impactful IC50 values and primarily safe against HeLa and L. jensenii cells. Their exact mechanism of action still remains unclear, although TEM and molecular docking results may orientate next steps regarding autophagy alterations and LDH interaction, respectively. We highlight that coffee-derived compounds should be considered as drug candidates for trichomoniasis, presenting promising agents with potential for further preclinical evaluation.},
}

@article {pmid42854947,
year = {2026},
author = {Yang, Y and Yu, H and Wang, J and Yang, S and Han, J and Jin, W and Luo, D and Zhou, S and Ma, C},
title = {Species-associated toxicological trajectories in social bees exposed to sublethal metribuzin: A multi-omics perspective on host-microbiome interactions.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {411},
number = {Pt A},
pages = {129320},
doi = {10.1016/j.envpol.2026.129320},
pmid = {42854947},
issn = {1873-6424},
abstract = {The divergent sensitivities of honeybees (Apis mellifera) and bumblebees (Bombus terrestris) to agrochemicals challenge the one-species-fits-all framework of ecological risk assessment, yet the mechanistic basis for this variation remains underexplored. Here, we used an integrated multi-omic approach, combining transcriptomics, metabolomics, and gut metagenomics, to map the species-associated responses of these pollinators under sublethal metribuzin (MET) exposure (30 mg/kg). Honeybees, exhibited broad transcriptional activation accompanied by suppressed P450 and glutathione S-transferase (GST) activities, metabolically associated with a disruption in cellular cofactor (NADPH/FAD) biosynthesis pathways, coincided with midgut tissue pathology and microbial structural dysbiosis. Conversely, bumblebees showed targeted cytochrome P450 (CYP) induction and elevated P450/GST activities, linked to an energy-intensive rewiring of carbohydrate metabolism that supported both xenobiotic clearance and antioxidant defense. While the bumblebee gut microbiota remained structurally stable, it displayed functional shifts toward xenobiotic efflux and cellular cytoprotection. Collectively, our multi-omic landscapes delineate two divergent correlative models: metabolic impairment coupled with microbial dysbiosis in honeybees, versus physiological resilience associated with microbiome functional plasticity in bumblebees. These findings propose a testable framework wherein baseline metabolic capacity shapes species-associated trajectories of host-microbiome interactions under herbicide stress, highlighting the critical need to incorporate mechanistic insights from multi-species comparisons into future ecological risk assessments.},
}

@article {pmid42855483,
year = {2026},
author = {Heinzinger, LR and Segal, LN and Dickson, RP},
title = {The role of the respiratory microbiome in acute and chronic respiratory diseases.},
journal = {Nature reviews. Microbiology},
volume = {},
number = {},
pages = {},
pmid = {42855483},
issn = {1740-1534},
abstract = {The lungs, once considered sterile, are now known to contain diverse, dynamic microbial communities that are metabolically active and immunologically consequential even in health. In respiratory disease, these communities undergo quantitative and compositional changes that predict clinical trajectories and may contribute to pathogenesis. The past decade of research has advanced our understanding of the complex bidirectional relationship between the respiratory tract and the microbial communities it encounters. In health, the lungs are nutrient poor and defended by robust host defences, limiting local microbial growth and keeping bacterial populations sparse and transient. Yet, in respiratory disease, the ecological conditions of the lungs permit and promote the outgrowth of select microorganisms. Recent in vivo and ex vivo discoveries explain how this respiratory dysbiosis is both a cause and a consequence of airway and alveolar injury. To leverage the respiratory microbiome for therapeutic benefit, we must interrogate both how disease-altered microbial communities shape immune responses, treatment efficacy and outcomes, and how host and environmental factors, in turn, shape the respiratory microbiome. In this Review, we synthesize current insights into how the respiratory microbiome contributes to chronic and acute lung diseases and explore its clinical implications for diagnosis, prognosis and therapy.},
}

@article {pmid42855692,
year = {2026},
author = {Alshinnawy, AS and Rashwan, EA and Swelam, MS and Mohamed, MR and Sayed, AA},
title = {Toward regionally equitable precision medicine: microbiota‑associated mechanisms and emerging personalized strategies in multiple sclerosis.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
pmid = {42855692},
issn = {1479-5876},
mesh = {Humans ; *Multiple Sclerosis/microbiology/therapy/immunology ; *Precision Medicine ; Animals ; *Microbiota ; Gastrointestinal Microbiome ; },
abstract = {Multiple sclerosis (MS) is a chronic immune-mediated disorder of the central nervous system in which dysregulated immune signalling and barrier dysfunction play central pathogenic roles. Increasing evidence implicates the gut microbiota as a key modulator of host immune homeostasis; however, current understanding is largely derived from Western cohorts and remains fragmented at the mechanistic level. This review synthesizes global evidence alongside emerging data from underrepresented regions, including Egypt, Iran, and India, to delineate molecular pathways linking MS-associated dysbiosis to immune dysregulation. Across studies, dysbiosis is consistently associated with impaired short-chain fatty acid-mediated immunoregulation, skewing toward proinflammatory Th1/Th17 responses, and disruption of intestinal and blood-brain barrier integrity, with region-dependent functional signatures involving oxidative stress and neurotransmitter and tryptophan metabolism. Several regional signatures reported here derive from a single pilot-scale cohort and should be regarded as hypothesis-generating pending independent validation, and current microbiota-targeted interventions remain investigational rather than established disease-modifying therapies for MS. We critically examine microbiota-derived signals, including short-chain fatty acids, lipopolysaccharide, and polysaccharide A, that modulate dendritic cell programming, regulatory T-cell differentiation, and neuroinflammatory cascades. We further evaluate microbiome-targeted therapeutic strategies and discuss how sex, regional context, and sequencing methodology influence functional interpretation and therapeutic responsiveness. Finally, we propose a roadmap for regionally equitable precision medicine, advocating for standardized multi-omics and culturally inclusive longitudinal designs to move beyond empiric interventions toward personalized, strain-defined biotherapeutics tailored to the unique microbial and environmental landscapes of MS patients worldwide.},
}

Humans
*Multiple Sclerosis/microbiology/therapy/immunology
*Precision Medicine
Animals
*Microbiota
Gastrointestinal Microbiome

@article {pmid42855914,
year = {2026},
author = {Lansac, C and De la Riva, I and Miñarro, M and Plewnia, A and Longo, AV and Burrowes, PA},
title = {Host and Environmental Factors Outweigh Pathogen in Shaping Skin Microbiome of a Threatened Andean Amphibian Community.},
journal = {Molecular ecology},
volume = {35},
number = {19},
pages = {e70586},
pmid = {42855914},
issn = {1365-294X},
support = {PGC2018-097421-B-I00//Ministerio de Ciencia e Innovación/ ; NSF-IOS-2011278//National Science Foundation/ ; NSF-IOS-2011281//National Science Foundation/ ; 1104226N//Research Foundation Flanders/ ; },
mesh = {Animals ; *Skin Microbiome ; *Batrachochytrium/pathogenicity ; RNA, Ribosomal, 16S/genetics ; Seasons ; Phylogeny ; Bacteria/classification/genetics ; *Amphibians/microbiology ; *Skin/microbiology ; Ecosystem ; Endangered Species ; Host-Pathogen Interactions ; *Microbiota ; *Anura/microbiology ; },
abstract = {The fungal pathogen Batrachochytrium dendrobatidis (Bd) has driven severe amphibian declines across the Neotropics, yet some species persist under enzootic pathogen conditions following epizootics. We investigated whether skin bacterial communities and host mucosome activity contributed to the persistence of seven amphibian species in a once megadiverse Chocó-Andean community that experienced drastic Bd-associated declines. Across dry and wet seasons, we characterized skin bacterial communities using 16S rRNA metabarcoding and assessed mucosome-mediated inhibition of a local Bd lineage using in vitro challenge assays. Host species identity was the strongest predictor of bacterial community composition, while season and reproductive mode, which were strongly associated with habitat use, also contributed to microbiome structure. Host phylogeny was associated with broad-scale bacterial community patterns, whereas Bd infection status and intensity explained little variation. Putative Bd-inhibitory bacteria were detected in all host species and occurred at greater relative abundance during the dry season and in species with aquatic larvae, but neither their richness nor abundance was associated with Bd infection or load. Mucosome assays showed little to no inhibition of Bd growth in most species; only Pristimantis laticlavius, one of the few species whose abundance increased following the historical Bd epizootic, exhibited slight inhibition. Overall, host identity, seasonality, and habitat-associated reproductive mode, rather than current Bd infection, were the principal drivers of amphibian skin bacterial community composition. The widespread occurrence of putative Bd-inhibitory bacteria and their enrichment in some persistent hosts are consistent with a potential microbiome-mediated response, but limited mucosome activity indicates that the microbiome alone is unlikely to explain host persistence. Integrating host immune traits, pathogen characteristics, and environmental conditions will be necessary to understand long-term host-pathogen coexistence in this threatened amphibian community.},
}

Animals
*Skin Microbiome
*Batrachochytrium/pathogenicity
RNA, Ribosomal, 16S/genetics
Seasons
Phylogeny
Bacteria/classification/genetics
*Amphibians/microbiology
*Skin/microbiology
Ecosystem
Endangered Species
Host-Pathogen Interactions
*Microbiota
*Anura/microbiology

@article {pmid42855925,
year = {2026},
author = {Abreu, MDS and Morais, RPL and Pereira, TF and Sales, PHDH and Leão, JC and Carvalho, AAT},
title = {Oral Microbiota Associated With Parkinson'S Disease: A Systematic Review.},
journal = {Special care in dentistry : official publication of the American Association of Hospital Dentists, the Academy of Dentistry for the Handicapped, and the American Society for Geriatric Dentistry},
volume = {46},
number = {5},
pages = {e70272},
pmid = {42855925},
issn = {1754-4505},
mesh = {Humans ; *Parkinson Disease/microbiology ; *Microbiota ; *Mouth/microbiology ; },
abstract = {AIMS: To evaluate the available evidence on the association between oral microbiota composition and Parkinson's disease (PD), including its relationship with disease severity and clinical features.

METHODS AND RESULTS: This systematic review was registered in PROSPERO (CRD42024560059) and conducted according to the PRISMA 2020 statement. Searches were performed in PubMed, Embase, Web of Science, LILACS, Scopus, and SciELO. Observational studies evaluating the oral microbiota of adults with PD were included. Eleven studies, predominantly case-control, were analyzed, with 16S rRNA sequencing used in 90.9% of them. The genera most frequently associated with PD were Lactobacillus (45.45%), Prevotella (36.7%), and Streptococcus (36.7%). Most studies reported differences in beta diversity, indicating a distinct oral microbial profile in patients with PD. Higher Lactobacillus abundance and lower Neisseria abundance were associated with greater disease severity and poorer cognitive performance in some studies. According to the GRADE approach, the certainty of the evidence was very low.

CONCLUSION: The available evidence suggests that PD is associated with alterations in oral microbiota composition. However, because the evidence is derived predominantly from observational studies, causal relationships cannot be established. Longitudinal studies using standardized microbiome methodologies are needed to validate these microbial signatures as candidate biomarkers.},
}

Humans
*Parkinson Disease/microbiology
*Microbiota
*Mouth/microbiology

@article {pmid42856070,
year = {2026},
author = {Zvi, E and Chi, C and Tang, TS and Bobba, S and Neely, M and Chatzis, R and Kern, JS and Akbarzadeh, S and Pattaroni, C},
title = {The Early Burn Wound Microbiome, Not Donor-Site Transfer, Marks Graft Healing Outcome.},
journal = {Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society},
volume = {34},
number = {5},
pages = {e70217},
pmid = {42856070},
issn = {1524-475X},
mesh = {Humans ; *Burns/microbiology/surgery ; *Wound Healing/physiology ; Skin Microbiome ; *Skin Transplantation/methods ; Female ; Male ; Adult ; Middle Aged ; *Microbiota ; *Transplant Donor Site/microbiology ; },
abstract = {Healing after split-skin grafting remains difficult to anticipate in small-area burns, particularly when wounds show no clinically diagnosed infection. We tested whether the burn wound microbiome before grafting captures early wound states linked to subsequent healing. Twenty-six adults with mid-dermal to full-thickness burns involving < 10% total body surface area underwent longitudinal sampling at surgery, graft check and clinic review. At surgery, swabs were collected from the burn wound before grafting, the split-skin donor site and anatomically matched uninjured control skin. Across 170 infection-free samples, microbiome profiling showed that pre-grafting burn wounds already had reduced microbial diversity and distinct community structure compared with matched control skin. This baseline dysbiosis included depletion of commensal-associated anaerobes, including Finegoldia and Anaerococcus and enrichment of opportunistic burn-associated taxa, including Pseudomonas and Acinetobacter. Donor sites acquired a related wound-like microbiome and remodelled in parallel with burn wounds during healing, but post-grafting burn microbiota were not preferentially similar to matched donor sites, arguing against a donor-to-burn microbial transfer. The clearest clinical signal was present before grafting: lower burn wound diversity at surgery was associated with delayed healing, and baseline community structure differed in wounds that later required regrafting. These findings suggest that the pre-grafting burn wound microbiome may provide an early, infection-independent marker of healing trajectory and should be tested as a predictive biomarker in larger prospective cohorts.},
}

Humans
*Burns/microbiology/surgery
*Wound Healing/physiology
Skin Microbiome
*Skin Transplantation/methods
Female
Male
Adult
Middle Aged
*Microbiota
*Transplant Donor Site/microbiology

@article {pmid42856123,
year = {2026},
author = {Ma, J and Kundu, P and Randolph, T and Navarro, S and Hullar, M},
title = {Mediation Analysis with Compositional Exposures.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.09.24.754147},
pmid = {42856123},
issn = {2692-8205},
abstract = {Understanding the causal pathways linking the gut microbiome to downstream biomarkers and clinical outcomes is central to microbiome research. When the microbiome acts as the exposure, the high dimensionality and compositional structure of the data introduce unique methodological challenges for mediation analysis. To address these challenges, we propose a latent variable mediation framework that captures variation in microbial composition through a microbial balance, defined as the log-ratio between two unknown subsets of taxa. This balance serves as a latent scalar exposure and simplifies the estimation of the overall indirect effect at the community level, while simultaneously identifying specific taxa that contribute to the overall direct and indirect effects. We describe the model's estimation and inference, and illustrate the method using data from the Multiethnic Cohort-Adiposity Phenotype Study, where we examine the mediation pathway from the gut microbiome through lipopolysaccharide-binding protein, a marker of metabolic endotoxemia, to percent liver fat.},
}

@article {pmid42856217,
year = {2026},
author = {Shreshta, R and Rajczewski, AT and Ogurtsov, A and Do, KT and Alves, G and Yu, YK and Willets, M and Kleiner, M and Griffin, TJ and Jagtap, PD},
title = {Evaluation of Parallel Accumulation-Serial Fragmentation methods for metaproteomics using a model microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.08.13.670166},
pmid = {42856217},
issn = {2692-8205},
abstract = {We present a multi-organism, ground-truth metaproteomic dataset generated using data-dependent acquisition Parallel Accumulation-Serial Fragmentation (ddaPASEF) and data-independent acquisition (diaPASEF) on a trapped ion mobility mass spectrometer. The dataset comprises 28 species (30 strains) spanning Archaea, Bacteria, Eukarya, and bacteriophages, assembled into an uneven mock community with a 400-fold dynamic range of organismal abundance. Four biological replicates were processed using a standardized sample preparation workflow and analyzed using described LC-MS conditions. Raw data, search outputs, protein coverage metrics, quantitative abundance estimates, and strain-specific peptide evidence are provided. The dataset enables evaluation of proteome depth, proteome coverage, quantitative reproducibility, and strain-level resolution across acquisition strategies. diaPASEF yielded broader peptide and protein detection and deeper sequence coverage, while both methods accurately quantified high-abundance organisms. Detection evidence for low-abundance bacteriophages and single-amino-acid-variant peptides is included to support benchmarking of taxonomic and strain-resolved analyses. This dataset provides a comprehensive reference for developing and validating metaproteomic workflows, protein inference strategies, and ion mobility-aware computational tools.},
}

@article {pmid42856223,
year = {2026},
author = {Li, L and Hussein, M and Falkner, KL and Genco, RJ and Sun, Y and Wactawski-Wende, J and Buck, MJ and Hatzikirou, H and Diaz, PI},
title = {A population-scale landscape of the subgingival microbiome reveals divergent routes to periodontal dysbiosis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.09.24.754177},
pmid = {42856223},
issn = {2692-8205},
abstract = {Periodontitis is an archetypical mucosal inflammatory disease in which microbiome dysbiosis at the tooth-epithelial interface interacts with host genetic and behavioral risk factors to drive immune-mediated tissue destruction. Although subgingival microbiome compositional shifts are thought to parallel disease severity, microbiome variation at the population-level and its relationship to periodontal clinical phenotypes and disease-modifying factors remain poorly defined. Here, we use unsupervised manifold learning to map the compositional landscape of the subgingival microbiome in 1,355 adults spanning periodontal health to severe periodontitis. We identified eight latent microbiome states organized along a branching continuum from eubiosis to dysbiosis. An intermediate microbial configuration marked ecological destabilization and bifurcation into two distinct periodontitis-associated dysbiotic trajectories, distinguished by links to gingival inflammation and smoking. Although the microbiome trajectories broadly tracked periodontal destruction, a minority of individuals showed discordant microbiome-clinical phenotypes, with some individuals with periodontitis retaining otherwise eubiotic microbiomes enriched for low-abundance pathobionts, while some cases of health or mild disease had highly dysbiotic communities, suggesting distinct host susceptibility. Together, these findings define a population-scale ecological landscape of the subgingival microbiome, reveal divergent trajectories to periodontal dysbiosis, and highlight heterogeneity in the relationship between microbial community structure and clinical disease expression.},
}

@article {pmid42856254,
year = {2026},
author = {Akhi, R and Williams, DW and Greenwell-Wild, T and Burns, AS and Mistry, S and Brenchley, L and Bouladoux, N and Vujkovic-Cvijin, I and Belkaid, Y and Emiola, A and Moutsopoulos, NM},
title = {IgG sequencing maps systemic antibody binding to oral commensals and pathobionts in health and periodontitis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.09.28.753837},
pmid = {42856254},
issn = {2692-8205},
abstract = {The oral cavity harbors one of the body's most diverse microbial communities, which continuously seeds the bloodstream and gastrointestinal tract, particularly in periodontitis, a disease in which both barrier permeability and microbial burden increase. Despite this constant systemic exposure, overt bacteremia from oral organisms is rare, suggesting an active surveillance system that contains this reservoir. Here, we apply IgG-sequencing to comprehensively map mucosal and systemic antibody recognition of the oral microbiome across paired oral fluid and serum from healthy individuals and patients with periodontitis. We find that IgG-binding is only weakly predicted by microbial abundance, suggesting taxon-specific and largely conserved IgG-binding of commensals, many of them streptococci which dominate antibody recognition irrespective of disease state. Periodontitis broadens the repertoire of IgG-bound taxa to include particular disease-associated pathobionts while preserving robust targeting of health-associated symbionts. Comparison of salivary and serum antibody profiles further uncovers a subset of commensal streptococci, including species implicated in infective endocarditis, that acquire disproportionate systemic IgG binding in periodontitis. Together, these findings establish a taxon-level atlas of humoral immunosurveillance at a major mucosal-microbial interface and reveal how periodontal disease reshapes systemic antibody recognition of both pathobionts and commensals.},
}

@article {pmid42856459,
year = {2026},
author = {Takeuchi, T and Reddy, A and Robinson, EK and Kotaka, KM and Higginbottom, SK and Sonnenburg, ED and Sonnenburg, JL},
title = {Functional Divergence in Gut Clostridia from Hadza Hunter-Gatherers Reveals Diet-Adapted Metabolic Machinery That Shapes Gut Ecology.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.09.29.755216},
pmid = {42856459},
issn = {2692-8205},
abstract = {Lifestyle changes associated with industrialization, including shifts in diet, are linked to extensive remodeling of the human gut microbiome. Investigating the gut microbiomes of traditional populations living non-industrialized lifestyles, such as the Hadza hunter-gatherers of Tanzania, therefore offers insight into bacterial taxa and functions depleted in industrialized microbiomes. Despite pronounced compositional differences that correspond to lifestyle, many commensal gut species are shared between industrialized and non-industrialized populations, raising a fundamental question of whether and how their functional repertoires diverge across contrasting gut environments. Here, by integrating strain-resolved metagenomics with culturomics and in vivo models, we identify phylogenetic and functional divergence within prevalent gut species shared between Hadza and industrialized populations, particularly among members of the Clostridia class. Dorea longicatena , prevalent across diverse human populations independent of lifestyle, is a poorly characterized member of Clostridia. Using strains of this D. longicatena isolated from either Hadza or industrialized human stool samples, we uncover metabolic pathways selectively enriched in Hadza strains, including machinery for utilizing plant-derived pectic polysaccharides. We further demonstrate that this Hadza-enriched polysaccharide-utilization machinery can be leveraged with its cognate dietary substrate to promote D. longicatena colonization within a model industrialized microbiota, reshaping intestinal and portal-vein metabolite profiles. Together, our findings reveal substantial functional divergence within gut bacterial species shared across lifestyles, providing a framework for identifying diet-responsive strains and pathways that may complement ecological and metabolic functions underrepresented in industrialized microbiotas.},
}

@article {pmid42856478,
year = {2026},
author = {Sedeek, M and Ayoub, A and Hany, E and Bahaa, A and Bahr, A and Saher, O and Ahmed, S},
title = {Microbiome-aware oral drug delivery: excipient-microbiome interactions and nanocarrier design rules for predictable formulation performance.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1942291},
pmid = {42856478},
issn = {1663-9812},
abstract = {Oral drug delivery remains the predominant administration route, but formulation strategies rarely account systematically for the gut microbiome. The microbiome can alter drug metabolism, excipient behavior, nanocarrier interactions, and interpatient variability. This review integrates evidence on microbial drug metabolism, excipient-microbiome interactions, nanocarrier engineering, microbiota-responsive delivery, and experimental models. Clinically relevant examples include digoxin inactivation by Eggerthella lenta, bacterial levodopa metabolism, and microbial beta-glucuronidase-mediated irinotecan toxicity. Microbiota-degradable polysaccharides may serve as colon-targeted release triggers, whereas some surfactants and polymers may create context-dependent microbiome or barrier risks. Nanocarrier size, charge, coating, mucoadhesion, mucus penetration, biodegradability, enzyme responsiveness, and surfactant burden are treated as microbiome-interface variables. We propose an authors' evidence-informed framework comprising an excipient classification, nanocarrier design rules, microbiota-responsive decision logic, and a tiered testing roadmap. These proposals are not established regulatory classifications; they are intended to support more predictable and patient-relevant oral formulation development.},
}

@article {pmid42856507,
year = {2026},
author = {Din, MO and Brennan, C and Zhao, J and Oles, R and Patel, L and Birmingham, A and Sevilir, DM and Hansen, L and Wright, GM and Ambre, M and Tomita, M and Boyer, T and Gonzalez, A and Ackermann, G and McDonald, D and Kralicek, S and Hecht, G and Hasty, J and Smarr, L and Knight, R},
title = {Genome-resolved ecology and evolution of the microbiome enabled by quantitative long-read metagenomics.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.09.28.754546},
pmid = {42856507},
issn = {2692-8205},
abstract = {Standard metagenomics resolves microbial communities only in relative terms and at coarse taxonomic resolution, obscuring how individual strains change in absolute abundance and evolve within a host. We present long-read quantiomics (LRQ), a quantitative metagenomics platform coupling long-read sequencing with plasmid-based internal standards to recover high-quality genomes, including from degraded or low-input stool, and measure absolute, genome-resolved strain abundances. We validate LRQ using large plasmid standards and bacterial spike-ins, then apply it to eight years of dense sampling from an individual with colonic Crohn's disease. LRQ resolves co-resident strains of the same species following opposing trajectories with inflammation. Escherichia coli, long treated as a single pathobiont, separates into two sub-populations with opposing inflammation responses; the inflammation-associated lineage carries an immune-evasion module of virulence-associated metal-acquisition, biofilm, capsule and toxin genes. We observe genome-wide adaptive sweeps on timescales matched to disease incidence. LRQ therefore converts long-read metagenomics from a genome-recovery tool into a quantitative framework providing absolute, strain-level measurement of microbial ecology and evolution.},
}

@article {pmid42856639,
year = {2026},
author = {Strength, RE and Angelova, A and Robbins, E and Levy, S and McCauley, KE and Lloyd, KM and Margolis, EB and Burns, AS and Mistry, S and Subramanian, P and Dassner, A and Zerbe, C and Band, VI and Namasivayam, S and Chen, Q and Esadah, E and Rees, K and Bacorn, M and Prasad, R and LaPoint, P and Romero-Soto, HN and Dekker, JP and Sears, CL and Shapiro, C and Hamdy, RF and Campos, JM and Hourigan, SK},
title = {Coming Into Resistance: Clinically Important Antibiotic Resistance Genes in NICU vs. Healthy Infants.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.09.23.26363796},
pmid = {42856639},
abstract = {IMPORTANCE: Antibiotic-resistant infections in neonates often arise from the infant's own colonizing bacteria harboring antibiotic resistance genes (ARG). This study evaluates ARG that impact antibiotic selection and drive resistance-related mortality, termed clinically important antibiotic resistance genes (CI-ARG).

OBJECTIVE: To determine differences in gut CI-ARG abundance in children from birth through 3 years old, stratified by neonatal intensive care unit (NICU) admission and antibiotic (abx) exposure in the first two months.

DESIGN: Cohort study (sequencing, analysis completed 2025-2026) using shotgun metagenomic sequencing of stool samples from infants in two studies: "Neonatal Intestinal Microbiome" (+NICU groups, 2015-2022), "The First 1000 Days of Life and Beyond" (-NICU groups, 2018-2021). Infants grouped into four cohorts: +NICU/+abx, +NICU/-abx, -NICU/-abx, and -NICU/+abx. Prespecified CI-ARG abundance compared longitudinally among groups.

SETTING: NICU, well-baby nursery, Inova Fairfax Hospital, Virginia.

PARTICIPANTS: +NICU criteria: admission to the NICU, anticipated length of stay (LOS) of at least five days, maternal age ≥18 years. -NICU: parents with good general health and age ≥18 years enrolled prior to infant birth. Stool samples: adequate stool processing volume, at least one stool sample from before one month and after one year of age, 7-day minimum between serial samples.

EXPOSURES: NICU versus well-baby nursery; antibiotics versus none in first two months of corrected age.

MAIN OUTCOMES AND MEASURES: Predefined primary outcome-longitudinal CI-ARG abundance by group, compared using linear mixed effects models with adjustment for multiple comparisons (Benjamini-Hochberg procedure). Predefined secondary outcomes-differences in overall microbiota and resistome composition.

RESULTS: 1000 serial stool samples, 179 infants (birth-39 months). Longitudinal abundance significantly differed among cohorts for 11 CI-ARG (p<0.05); often higher in the +NICU groups in early life, with or without antibiotic exposure. Abundance of ARG conferring resistance to aminoglycosides, macrolides, and fluoroquinolones later decreased below -NICU levels. mecA , which often drives methicillin resistance in Staphylococcus , was detected only in +NICU infants during premature period.

CONCLUSIONS: This longitudinal study demonstrates significant longitudinal CI-ARG differences in children grouped by early-life NICU status and/or antibiotic exposure. Future studies should explore the mechanisms driving these CI-ARG changes and evaluate their impact on infection risk and community spread.

KEY POINTS: Question: How do clinically important antibiotic resistance genes (CI-ARG) differ longitudinally among infants up to 3 years old based on NICU admission and antibiotic exposure in the first two months of life?Findings: In this cohort study of 179 infants through 39 months of age, longitudinal abundance was significantly different for 11 prespecified CI-ARG, often higher in the NICU groups in early life, with or without antibiotic exposure.Meaning: Children with a history of NICU hospitalization, whether due to the NICU environment itself, prematurity, or other factors, may have increased CI-ARG burden early in life, irrespective of direct antibiotic exposure.},
}

@article {pmid42856976,
year = {2026},
author = {Sharma, S and Pachauri, A and Nagar, H and Thakkar, V and Patel, K},
title = {Targeting gut dysbiosis: a new frontier in MASLD management.},
journal = {Frontiers in systems biology},
volume = {6},
number = {},
pages = {1937809},
pmid = {42856976},
issn = {2674-0702},
abstract = {Globally, Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prominent leading cause of CLD, which is intricately linked with obesity, T2D, and metabolic syndrome. Recent insights in pathophysiologically of MASLD have shifted from the traditional "two-hit" model to a "multiple-hit" paradigm, demonstrating the importance of understanding the gut-liver axis and gut dysbiosis as central drivers of disease progression. Hence, this narrative review explores the mechanistic pathways through which an altered gut microbiome contributes to MASLD, by specifically emphasizing intestinal barrier disruption, endotoxemia, altered bile acid metabolism, and SCFA imbalance. These dysregulations trigger oxidative stress, leading to systemic inflammation and insulin resistance, propelling simple steatosis toward steatohepatitis and fibrosis at last. Furthermore, we also highlighted the diagnostic utility of microbial signatures and multi-omics approaches in identifying disease-specific microbial shifts, such as the depletion of beneficial SCFA-producing bacteria like Faecalibacterium and Akkermansia. Eventually, to address the growing hepatic-associated health burden, microbiome-targeted therapeutics can emerge as one of the promising contributors. In this review, we synthesise and demonstrate the current and prospective interventions, including dietary modifications, biotics (probiotics, prebiotics, synbiotics), and FMT. Additionally, we also show the transition of care toward precision microbiome therapies utilizing engineered bacteria, bacteriophages, and AI-guided patient stratification. While current microbiome-centric treatments demonstrate promise in modulating hepatic inflammation and restoring mucosal integrity, their clinical translation remains hindered by patient heterogeneity and a lack of standardized protocols. Ultimately, managing MASLD effectively will require moving beyond broad ecosystem resets toward highly tailored, multi-omics-driven precision medicine to accurately target individualized microbial deficits.},
}

@article {pmid42857043,
year = {2026},
author = {Fang, C and Wang, C and Wang, R and Lu, YF and Ma, L},
title = {Gut microbial characteristics and kynurenine-related metabolism across sarcopenia groups: associations with neuromuscular and physical function.},
journal = {Frontiers in aging neuroscience},
volume = {18},
number = {},
pages = {1883616},
pmid = {42857043},
issn = {1663-4365},
abstract = {BACKGROUND: Sarcopenia is characterized by heterogeneous alterations in muscle mass, strength, and physical performance and may involve interactions among the gut microbiota, tryptophan metabolism, and neuromuscular function. However, these biological characteristics across different sarcopenia stages remain incompletely understood. This study investigated gut microbial characteristics, kynurenine-related metabolism, circulating biomarkers, and physical function in older adults with different sarcopenia status.

METHODS: In this cross-sectional study, 67 older adults were classified according to the Asian Working Group for Sarcopenia 2019 criteria as non-sarcopenia (NSG, n = 17), possible sarcopenia (PSG, n = 20), or sarcopenia (SG, n = 30). Muscle mass, handgrip strength, and multidimensional physical performance were assessed. Serum C-terminal agrin fragment (CAF), tumor necrosis factor-α (TNF-α), amino acids, kynurenine (KYN), and tryptophan (Trp) were measured, and the KYN/Trp ratio was calculated. Gut microbiome composition was characterized by shotgun metagenomic sequencing. Differential abundance was evaluated using MaAsLin2 with adjustment for age and body mass index (BMI), and exploratory correlations among microbial genera, metabolites, circulating biomarkers, and physical function were examined with false discovery rate correction.

RESULTS: ASMI was significantly lower in the SG group than in the NSG and PSG groups, whereas several measures of physical performance differed among groups without a uniform stepwise pattern. No significant differences were observed in alpha diversity, beta diversity, or the Firmicutes/Bacteroidetes ratio, and sarcopenia group explained only 3% of the variation in overall microbial community composition (PERMANOVA, R [2] = 0.03, p = 0.226). Several genus-level associations were nominally significant after adjustment for age and BMI, but none remained significant after BH-FDR correction. After adjustment for age and BMI, serum KYN concentrations and the KYN/Trp ratio were significantly higher in the SG group than in the NSG group (p = 0.011 and p = 0.043, respectively), whereas Trp and the measured amino acids showed no significant pairwise differences. The unadjusted increase in CAF across sarcopenia groups was attenuated after covariate adjustment, and TNF-α did not differ significantly among groups. Exploratory correlation analyses identified several FDR-significant associations across microbial, metabolic, and functional domains, including negative associations of KYN and KYN/Trp with handgrip strength and a positive association between CAF and 6-m gait speed(GS).

CONCLUSION: Established sarcopenia was associated with altered circulating kynurenine-related metabolism despite the absence of pronounced differences in overall gut microbial community structure. Exploratory cross-domain associations further suggest potential interactions among gut microbial characteristics, tryptophan metabolism, and neuromuscular and physical function. These findings support further investigation of host-microbial tryptophan metabolism in sarcopenia but do not establish a causal microbiota-kynurenine-NMJ pathway.},
}

@article {pmid42857052,
year = {2026},
author = {Xue, K and Ji, M and Zou, L},
title = {Functional heterogeneity and health impacts of oral bacterial ectopic colonization.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1915341},
pmid = {42857052},
issn = {1664-302X},
abstract = {The oral cavity is the second most colonized anatomical site after the intestinal tract, and due to its unique and diverse microbial community, it constitutes a distinct biome. The oral microbiota is an integral part of the human microbiome ecosystem, maintaining the balance of the oral microecology. However, when this balance of the oral microecology is disrupted, oral bacteria not only cause oral diseases but also spread to other parts of the body through various pathways. These oral bacteria colonizing outside the oral cavity may exhibit different functional roles from those in the oral cavity, thereby contributing to or exacerbating pathological processes in distant organs, such as experimental colitis, hepatic steatosis, and opportunistic bacteremia. By analyzing compositional changes in the oral and gut microbiota, the risk of certain diseases can be predicted at an early stage, and timely interventions can be implemented. This review summarizes the colonization and disease-causing effects of several major oral bacteria (Streptococcus, Veillonella, Prevotella, Lactobacillus, Helicobacter pylori, Fusobacterium nucleatum, Porphyromonas gingivalis, Tannerella forsythia) in the oral cavity and other sites. To provide conceptual rigor, we explicitly distinguish among passive ectopic detection, stable ectopic colonization, and functionally active pathogenicity. Furthermore, we highlight how ectopic oral bacteria undergo context-dependent metabolic adaptations in new niches, rather than simply replicating their oral profiles.},
}

@article {pmid42857184,
year = {2026},
author = {Zhang, C and Chen, Z and Cai, Y and Yuan, J and Wang, G and Li, G},
title = {Ruminant versus non-ruminant manure composting: carbon-to-nitrogen ratio and associated physicochemical traits impact divergent pollutant emissions.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1890442},
pmid = {42857184},
issn = {1664-302X},
abstract = {Composting can convert livestock manure into valuable fertilizer, but the relationships between manure type, which essentially reflects differences in carbon-to-nitrogen ratio (C/N) and other associated physical properties, and pollutant gas emissions remain poorly quantified. We monitored temperature, pH, carbon, nitrogen, sulphur contents, bacterial succession, and emissions of methane (CH4), nitrous oxide (N2O), ammonia (NH3) and hydrogen sulfide (H2S) during aerobic composting of non-ruminant manure (chicken and pig) and ruminant manure (sheep and cattle). Sheep and cattle manure (characterized by higher C/N) reached maturity earlier and emitted 30-93% less greenhouse gases and odor than chicken and pig manure (characterized by lower C/N), although cattle manure produced slightly more CH4. High emissions from chicken and pig manure coincided with dominance of Bacillus and Defluviitalea, which declined as readily available carbon was depleted. In contrast, sheep and cattle manure was associated with Actinomadura and Corynebacterium, genera that correlated with the immobilization of nitrogen and sulphur into stable forms during the degradation of recalcitrant carbon. Ammonium concentration was strongly correlated with the overall emission rate, yet the microbial taxa associated with the process shifted predictably with animal diet. The observed associations provide a basis for future hypothesis-driven experiments. The findings provide a microbiome-based guide for controlling and minimizing atmospheric pollution during composting.},
}

@article {pmid42857238,
year = {2026},
author = {Ma, J and Hou, Z},
title = {Gut Microbiota-Immune-Inflammation Axis as a Putative Pathogenic Axis in Chronic Insomnia: Mechanistic Dissection of NLRP3 Inflammasome and NF-κB Signaling.},
journal = {International journal of general medicine},
volume = {19},
number = {},
pages = {645057},
pmid = {42857238},
issn = {1178-7074},
abstract = {Chronic insomnia represents one of the most prevalent sleep disorders worldwide, yet current symptomatic treatments largely fail to target its root pathophysiology. Moving beyond conventional neurocentric frameworks, converging evidence positions gut microbiota dysbiosis as a potential upstream contributor to insomnia via the microbiota-gut-brain axis, with immune-inflammatory cascades serving as proposed mediating pathway. Mechanistically, disrupted gut microbial communities compromise intestinal mucosal barrier integrity, enabling lipopolysaccharide translocation that activates TLR4-mediated NF-κB signaling. This triggers systemic low-grade inflammation, marked by elevated pro-inflammatory cytokines IL-1β, IL-6, IL-17 and TNF-α, reduced anti-inflammatory IL-4 and IL-10, and Th17/Treg immune imbalance. Centrally, circulating inflammatory signals activate the NLRP3 inflammasome, driving caspase‑1‑dependent pyroptosis and a pro‑inflammatory microglial activation state (conventionally described as "M1‑like" polarization), which disrupts sleep-wake neural circuitry and hypothalamic-pituitary-adrenal axis homeostasis. Dysregulated PI3K/Akt signaling and aberrant microbial metabolites-including depleted short-chain fatty acids and a pathological shift in tryptophan metabolism toward the neurotoxic kynurenine pathway-further amplify the vicious cycle between sleep disturbance and neuroinflammation. This review systematically maps the full pathological cascade from intestinal dysbiosis to central insomnia phenotypes, and compares translational strategies including psychobiotic strains, fecal microbiota transplantation, dietary intervention and traditional Chinese medicine formulas targeting this axis. Collectively, this work proposes an integrated microbiota-immune-sleep regulatory framework, offering novel mechanistic insights and microbiome-based therapeutic avenues for precision insomnia management.},
}

@article {pmid42857378,
year = {2026},
author = {Zhang, Y and Cidan, Y and Xu, J and Li, B},
title = {CRC-TrustBench: benchmarking cross-study and cross-country generalization in gut metagenomic colorectal cancer prediction.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1971707},
pmid = {42857378},
issn = {1664-302X},
abstract = {BACKGROUND: Gut metagenomic classifiers for colorectal cancer (CRC) are often evaluated with random splits that place samples from the same studies, countries, or processing workflows in both training and test sets, potentially inflating apparent performance. We developed CRC-TrustBench, a leakage-aware framework for evaluating cross-study and cross-country generalization and probability reliability.

METHODS: From 2,340 MetaGenoPolis V16 source samples, we curated 1,953 CRC or healthy samples from 15 studies and 10 countries; 185 adenoma samples were retained outside binary model development as a challenge population. Subject-aware random, leave-one-study-out (LOSO), and leave-one-country-out (LOCO) protocols were applied to taxonomic profiles with 2,543 features and functional profiles with 378 features. We compared Elastic Net, LightGBM, cohort-balanced Elastic Net, and pre-specified neural domain-robust methods using fold-specific pre-processing. The Microbiome Leakage and Confounding Audit (MiLCA) quantified study and country shortcuts, while Platt calibration, conformal-style sets, and selective abstention were evaluated without outer-test labels.

RESULTS: For taxonomic profiles, LightGBM achieved an area under the receiver operating characteristic curve (AUROC) of 0.874 under random splitting, 0.827 under LOSO, and 0.821 under LOCO; the single pre-specified RANDOM estimate was numerically higher than the held-out-domain summaries. Microbiome profiles predicted study and country identity, and a descriptive feature-level audit indicated pervasive study-associated structure. Cohort balancing yielded limited gains, and neural domain-robust methods did not consistently outperform LightGBM. Platt scaling reduced the mean LOCO Brier score from 0.180 to 0.169 and log loss from 0.630 to 0.521. LightGBM conformal-style coverage fell below the pre-specified 90 and 95% targets, while uncertainty-based abstention reduced error relative to matched-random rejection in most recorded repeats. Functional profiles were less predictive, although more functional features met the pre-specified high-stability tiers.

DISCUSSION: The tiered features remain stable candidate hypotheses, and raw counts are not directly comparable across the differently sized feature spaces. Adenoma predictions were heterogeneous, and no reviewed external resource met all criteria for formal independent evaluation. CRC-TrustBench separates in-distribution discrimination from cohort generalization and probability reliability without implying clinical deployment or independent external validation.},
}

@article {pmid42857515,
year = {2026},
author = {Karthick, V and Thamarai, R and Amalraj, S and Narayanasamy, K},
title = {Cytopathology of the microbiome-immune interface: Emerging applications of cytology in infectious, inflammatory, and neoplastic conditions.},
journal = {CytoJournal},
volume = {23},
number = {},
pages = {57},
pmid = {42857515},
issn = {0974-5963},
abstract = {OBJECTIVES: The objective of the study is to synthesize current evidence on the microbiome-immune interface as reflected in cytopathologic specimens and to explore the emerging diagnostic, prognostic, and translational applications of cytology in infectious, inflammatory, and neoplastic diseases.

MATERIAL AND METHODS: This narrative review integrates published literature on cytopathology, microbiome research, and immune profiling. Relevant studies examining cytologic specimens, including fine-needle aspiration, effusion cytology, liquid-based cytology, and lavage samples, were evaluated for their contributions to understanding host-microbe interactions. Emphasis was placed on studies incorporating molecular microbiome analysis (16S ribosomal ribonucleic acid sequencing, metagenomics), immunocytochemistry, cytokine profiling, and digital image analysis.

RESULTS: Cytologic specimens provide a minimally invasive platform that captures dynamic interactions between epithelial cells, immune infiltrates, and microbial communities. In infectious diseases, cytology enables direct pathogen visualization while reflecting immune activation patterns such as granuloma formation and neutrophilic inflammation. In chronic inflammatory disorders, cytologic features including lymphoid infiltrates and macrophage activation may correspond with microbiome-driven immune dysregulation. In oncology, tumor-associated microbiota detectable in cytology samples influence immune checkpoint expression, macrophage polarization, and tumor microenvironment remodeling. Integration of molecular assays, single-cell technologies, and artificial intelligence further enhances the ability of cytology to characterize microbiome-immune signatures within limited specimens.

CONCLUSION: Cytopathology is evolving from a purely morphologic discipline into an integrative platform that bridges microbial ecology and immune dynamics. Incorporating microbiome profiling and immune phenotyping into routine cytologic evaluation holds promise for improved disease stratification, early detection, and personalized therapeutic decision-making. Recognizing cytology as a window into the microbiome-immune interface may redefine its role in precision medicine across infectious, inflammatory, and neoplastic conditions.},
}

@article {pmid42857532,
year = {2026},
author = {Agoni, L and Martinelli, C and Cortellino, S and Giordano, A and De Seta, F},
title = {Feeding the estrobolome with sweet prebiotics?.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1957439},
pmid = {42857532},
issn = {2296-861X},
abstract = {BACKGROUND: Sweeteners are widely consumed, yet their effects on the gut microbiota remain incompletely characterized, while their potential influence on the estrobolome has received little direct investigation. Although many sweeteners are absorbed in the small intestine, a variable fraction reaches the colon, where it interacts with the gut microbiota. Some sweeteners may also meet the definition of a prebiotic when they are selectively utilized by host microorganisms and such utilization confers a demonstrated health benefit. Because the estrobolome encompasses microbial genes encoding estrogen-metabolizing enzymes, including β-glucuronidases and sulfatases, sweetener-induced changes in gut microbial composition or function could plausibly influence enterohepatic estrogen metabolism and systemic estrogen availability.

METHODS: This narrative review synthesizes current evidence on the effects of different sweeteners on the gut microbiota and examines their potential implications for the estrobolome. We summarize the consensus definition of prebiotics, the classification, metabolism, and colonic availability of major sweeteners, and review the biological basis of the estrobolome, with particular emphasis on microbial estrogen metabolism.

RESULTS: Experimental and human studies indicate that individual sweeteners can modify gut microbial composition and metabolic activity, but the direction and magnitude of these effects vary substantially according to the compound, dose, study model, and host context. However, direct studies evaluating the impact of sweeteners on estrobolome function are lacking, and potential effects currently remain inferential, based largely on reported changes in microbial taxa known or presumed to harbor genes encoding estrogen-metabolizing enzymes rather than on direct measurements of gene expression or enzymatic activity.

CONCLUSION: Current evidence provides a biological basis for considering sweeteners as potential modulators of the estrobolome, although evidence directly linking individual sweeteners to changes in estrobolome function remains lacking. Well-designed multi-omic clinical studies integrating dietary exposure, gut microbiota composition, estrobolome function, estrogen metabolism, and clinically relevant outcomes are needed to establish the physiological and clinical relevance of this relationship and determine whether it can ultimately inform personalized nutritional strategies.},
}

@article {pmid42857638,
year = {2026},
author = {Chen, J and Jiang, J and Zhou, X and Fan, L and Wu, F and Liang, P and Song, H and Wang, J and Luo, J and Zhu, G},
title = {Characteristics of Microbiota in Different Segments of the Digestive Tract of Orange-Collared Keelback (Rhabdophis himalayanus).},
journal = {Ecology and evolution},
volume = {16},
number = {10},
pages = {e74508},
pmid = {42857638},
issn = {2045-7758},
abstract = {The gastrointestinal tract of animals plays an essential role in digestion and nutrient absorption. The diversity of gut microbiota is critical for maintaining the physiological functions of animals. However, current research has focused primarily on mammals; research on the gut microbiota of reptiles, particularly snakes, remains limited. This study utilized metagenomic sequencing and untargeted metabolomics to investigate the microbial community composition and functional potential in the stomach, large intestine, and small intestine of the Orange-collared Keelback (Rhabdophis himalayanus). The results demonstrate that the three most dominant phyla in the R. himalayanus gut microbiota are Pseudomonadota, Actinomycetota, and Bacillota. Moreover, analysis of microbial communities across the stomach, small intestine, and large intestine shows no significant differences in α-diversity and β-diversity among the three regions. Linear Discriminant Analysis Effect Size (LEfSe) reveals significant differences in the gut microbiota abundance. MetaStats analysis further reveals significant differences in the abundance of both microbial taxa and CAZymes. Although overall metabolite profiles did not differ significantly among gastrointestinal regions, pairwise analyses identified differentially abundant metabolites associated with amino acid, lipid, nucleotide, and cofactor metabolism. Gut microbiota from different parts of the digestive tract may reveal a unique characteristic of the gut microbiome of R. himalayanus and the impact of microbial community structure on function. Collectively, these findings expand our understanding of gastrointestinal microbial communities and associated functional potential in an understudied snake species.},
}

@article {pmid42857718,
year = {2027},
author = {Frenquelli, M and Farinello, D and Sisti, S and Rovida, A and Lenti, E and Ferrarese, R and Bordini, J and Scarfò, L and Clementi, N and Canducci, F and Brendolan, A and Ghia, P},
title = {Influence of gut microbiota on chronic lymphocytic leukemia development and aggressiveness.},
journal = {Gut microbes reports},
volume = {4},
number = {1},
pages = {2717015},
pmid = {42857718},
issn = {2993-3935},
abstract = {Chronic lymphocytic leukemia (CLL) is highly heterogeneous both clinically and biologically. Although genetic factors have been identified, several lines of evidence suggest a role for environmental factors in disease onset and progression. Diet is a recognized risk factor for various diseases, including cancer, with an established relationship to the composition of the gut microbiome. Taking advantage of the widely used Eμ-TCL1 transgenic model, we investigated the relationship between diet, the gut microbiota, and CLL development. We randomized a cohort of Eμ-TCL1 mice to receive a normal standard diet (N) (n = 15) or an experimental diet rich in low-complexity carbohydrates and lower in proteins and fibers (HC/LPF) (n = 16) and observed a progressive shift in microbiome composition in animals fed with the HC/LPF diet, accompanied by an acceleration of disease progression and shortened survival. These effects were associated with an increase in Firmicutes and Proteobacteria and a decrease in Bacteroidetes in mice fed with the HC/LPF diet. Our data suggest a close link between the HC/LPF diet and Oscillospira, Ruminococcus, Mucispirillum, AF12, and Rikenella genera, possibly affecting CLL development. The present work paves the way for detailed studies to be conducted in controlled cohorts of patients with CLL to elucidate the role of diet in disease incidence and evolution.},
}

@article {pmid42857747,
year = {2026},
author = {Villoch-Rosado, R and Acosta, D and Morales-Santiago, L and González-Tardí, IM and Medina-Rodríguez, O and Ríos-Rodríguez, K and Agront-Medina, I and Alvarado-Andino, AE and Báez-Rodríguez, LA and Calderón-Nuñez, A and Cátala-Cátala, AG and Delgado-Negrón, N and Figueroa-Reyes, TL and Mojica-Pérez, L and Rosa-López, H and Santos-Bermúdez, A and Rodríguez-Zayas, J and Tosado-Rodríguez, EL},
title = {Role of the Gut Microbiome in Natural and Synthetic Drug Efficacy and Safety: A Narrative Review.},
journal = {Applied microbiology (Basel, Switzerland)},
volume = {6},
number = {10},
pages = {113},
pmid = {42857747},
issn = {2673-8007},
abstract = {The gut microbiome has emerged as an important determinant of the metabolism, efficacy, and safety of many therapeutic agents, expanding the traditional host-centered view of pharmacology. Direct microbial biotransformation is particularly relevant to orally administered compounds, whereas the gut microbiome can also influence systemically administered therapies indirectly through immune, inflammatory, barrier, and hepatic pathways. Beyond its established roles in nutrient metabolism, immune regulation, and maintenance of epithelial homeostasis, the microbiome functions as a metabolically active organ capable of transforming endogenous molecules, dietary compounds, xenobiotics, and therapeutic agents through an extensive repertoire of microbial enzymes and metabolites. These interactions influence virtually every stage of drug disposition by modifying pharmacokinetics, pharmacodynamics, bioavailability, therapeutic efficacy, and toxicity. This narrative review summarizes current knowledge of the composition and functional diversity of the gut microbiome and examines the molecular mechanisms underlying host-microbe-drug interactions, including direct microbial biotransformation, regulation of intestinal barrier integrity, immune modulation, bile acid metabolism, and microbial control of hepatic drug-metabolizing pathways. We further discuss the impact of these mechanisms across multiple therapeutic areas, including oncology, neurological and psychiatric disorders, cardiovascular medicine, diabetes, metabolic diseases, and microbiome-dependent activation of natural products. Emphasis is placed on recent advances in cancer therapy, where the microbiome has emerged as a key determinant of responses to chemotherapy, immune checkpoint inhibitors, oncolytic viruses, and other immunotherapies. The review also highlights the bidirectional relationship between drugs and microbial communities, illustrating how pharmaceuticals reshape the microbiome while microbial ecosystems simultaneously influence therapeutic outcomes. Finally, we discuss emerging technologies, including multi-omics approaches, artificial intelligence, organ-on-chip models, and microbiome-targeted interventions, that are accelerating the integration of pharmacomicrobiomics into drug discovery and precision medicine. Collectively, current evidence supports recognizing the microbiome as an integral component of human pharmacology and a promising source of predictive biomarkers and therapeutic targets for the development of safer, more effective, and personalized treatment strategies.},
}

@article {pmid42857755,
year = {2026},
author = {Jeong, YS and Kim, PS and Tak, EJ and Sung, H and Lee, JY and Kim, HS and Bae, JW},
title = {Gut microbiome shifts during frog development parallel host-association patterns across vertebrate lineages.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1931668},
pmid = {42857755},
issn = {1664-302X},
abstract = {The developmental habitat transitions between aquatic and terrestrial environments in frogs offer a compelling model to investigate how environmental shifts shape gut microbiota. However, our understanding of how these transitions influence gut microbial communities across frog development remains limited. Here, we investigated how habitat changes during frog development affect gut microbiota composition and compared these patterns with host-microbiome interactions across vertebrates. Frog gut microbiota composition changed across developmental stages, and the proportion attributable to the surrounding environmental communities was highest at the egg stage and declined thereafter. Functional analysis of gut microbiota revealed that oxygen-related microbial phenotypes shifted from aerobic to anaerobic during development. Habitat preference analysis further demonstrated that mammals have higher proportions of animal-associated microbes in their guts than non-mammals (Actinopterygii, Amphibia, Aves, and Reptilia). These findings indicate that the aquatic-to-terrestrial transition is accompanied by a reduction in the environmental contribution to the gut community rather than by an increase in host selection, providing an ecological framework for interpreting host-association patterns across vertebrate lineages.},
}

@article {pmid42858106,
year = {2026},
author = {Gangopadhayya, A and Dovih, PD and Garg, KM and Chattopadhyay, B},
title = {Oxford Nanopore Long-Read Sequencing of Bat Guano and Urine for Microbiome Characterization and Pathogen Detection.},
journal = {Journal of visualized experiments : JoVE},
volume = {},
number = {236},
pages = {},
doi = {10.3791/70544},
pmid = {42858106},
issn = {1940-087X},
mesh = {Animals ; *Chiroptera/microbiology/urine ; *Microbiota/genetics ; RNA, Ribosomal, 16S/genetics ; *Sequence Analysis, DNA/methods ; *Nanopore Sequencing/methods ; DNA, Bacterial/genetics/urine ; Polymerase Chain Reaction/methods ; },
abstract = {Deoxyribonucleic acid (DNA) sequencing has made possible the study of genetic sequences for taxonomic assignment, mutational analyses, and novel organism discovery. Long-read sequencing methods offer advantages over short-read methods because they can sequence entire DNA molecules without requiring fragmentation. This protocol describes a workflow for microbiome characterization and pathogen detection through the extraction, sequencing, and analysis of DNA from bat environmental samples, including guano and urine, using tailored approaches for each sample type. Pre-processing of guano and urine is performed prior to DNA extraction using a spin-column-based method to disrupt sample matrices and lyse microorganisms that may be present. This protocol further describes the preparation of sequencing libraries using either extracted DNA directly or polymerase chain reaction (PCR) products targeting the full-length 16S ribosomal RNA gene for prokaryotic and archaeal taxa and a partial 18S ribosomal RNA gene for eukaryotic taxa. PCR amplification of the full-length 16S ribosomal RNA gene is achieved using universal primers. Magnetic bead-based DNA purification is employed at multiple stages, including following PCR amplification of the 16S or 18S ribosomal RNA genes. Library preparation includes end repair, barcode ligation, pooling of barcoded DNA, and adapter ligation. Libraries are sequenced on a nanopore sequencing platform and analyzed using the EPI2ME bioinformatics workflow. Sequencing runs are performed on MinION flow cells, with run settings adjusted using the MinKNOW sequencing software. Runs are configured for 72 h with basecalling enabled for the raw data collected, generating the sequence-read files that are sorted according to barcode assignment. This workflow enables high-throughput sequencing of multiple samples in a single run, and the resulting sequence data are used for taxonomic classification of prokaryotic, archaeal, and eukaryotic organisms present in each sample, supporting wildlife microbiome characterization, environmental surveillance, and pathogen detection.},
}

Animals
*Chiroptera/microbiology/urine
*Microbiota/genetics
RNA, Ribosomal, 16S/genetics
*Sequence Analysis, DNA/methods
*Nanopore Sequencing/methods
DNA, Bacterial/genetics/urine
Polymerase Chain Reaction/methods

@article {pmid42858216,
year = {2026},
author = {Khan, A and Ullah, Z and Siraj, M and Younas, S and Wahab, S and Waris, A and Hong, ST},
title = {The Gut Microbiota-Epilepsy Axis: Bibliometric Trends, Mechanistic Insights, and Microbiota-Targeted Next-Generation Therapeutic Opportunities.},
journal = {Molecular neurobiology},
volume = {63},
number = {1},
pages = {},
pmid = {42858216},
issn = {1559-1182},
mesh = {Humans ; *Epilepsy/therapy/microbiology ; Animals ; *Gastrointestinal Microbiome/physiology ; Dysbiosis ; Brain ; },
abstract = {Epilepsy is a complex neurological disorder with diverse underlying causes. Growing evidence suggests that gut dysbiosis may promote epileptogenesis by disrupting short-chain fatty acids, tryptophan-kynurenine metabolism, immune signaling, and neuronal excitability. In this review, we combine findings from human and animal studies to explain how gut dysbiosis may influence seizures through the gut-brain axis. We highlight emerging and less-discussed mechanisms, including vagus nerve signaling, microbial amyloids, bacterial extracellular vesicles (BEVs), the queuosine salvage pathway, and multi-kingdom microbiota interactions. We also summarize microbiota profiling studies and describe dysbiosis patterns linked to seizure. To support translation, we propose a peri-ictal multi-omics strategy for biomarker discovery. This includes standardized sampling and integration of metagenomics, metabolomics, and host transcriptomics. In addition, our bibliometric analysis further shows rapidly growing global interest in this topic. Recent studies increasingly focus on the gut-brain axis, ketogenic diet, and inflammation-driven mechanisms. Finally, we outline both established approaches and emerging next-generation microbiome-based therapeutic strategies, including SCFA-restoring synbiotics, engineered psychobiotics, bacteriophage therapy, and AI-guided personalization. These advances highlight the microbiota as modifiable target for adjunctive epilepsy management and provide a translational roadmap for future mechanistically informed research and clinical interventions.},
}

Humans
*Epilepsy/therapy/microbiology
Animals
*Gastrointestinal Microbiome/physiology
Dysbiosis
Brain

@article {pmid42858415,
year = {2026},
author = {Trovato, F and Chello, C and Amato, S and Di Guardo, A and Amore, E and Bennardo, L and Richetta, AG and Grieco, T and Nisticò, SP and Pellacani, G and Dattola, A},
title = {Shared Pathways between Psoriasis and Atopic Dermatitis.},
journal = {Dermatology practical & conceptual},
volume = {16},
number = {3},
pages = {},
doi = {10.5826/dpc.1603a6662},
pmid = {42858415},
issn = {2160-9381},
abstract = {INTRODUCTION: Psoriasis and atopic dermatitis are leading examples of chronic inflammatory dermatoses with distinct clinical manifestations, pathogenesis, and demographic patterns. However, recent research has revealed overlapping immunological pathways that could serve as promising therapeutic targets.

OBJECTIVES: To synthesize the principal immunological, epidermal barrier, and microbiome pathways shared by psoriasis and atopic dermatitis and to discuss their potential translational and therapeutic implications.

METHODS: We conducted a narrative review of the literature on PubMed from January 2000 to June 2024, using keywords such as "psoriasis," "atopic dermatitis," "cytokine pathways," "T cells," and "environmental triggers." Studies were selected based on their relevance to shared mechanisms between these diseases, focusing on cytokine profiles, immune cell activity, and skin barrier dysfunction.

RESULTS: Our review identified significant overlaps in cytokine-mediated pathways, particularly the IL-17/IL-22 axis, which mediates keratinocyte hyperproliferation and inflammation in both diseases. T cell dysregulation, including Th17 and Th22 activity, plays a pivotal role in maintaining chronic inflammation. Both conditions also exhibit impaired skin barrier function, linked to filaggrin loss-of-function mutations in atopic dermatitis and abnormal keratinocyte differentiation in psoriasis.

CONCLUSION: These findings suggest that targeting shared mechanisms, such as the Th17 and Th22 pathways, along with barrier repair strategies may enable dual therapeutic benefits. This review underscores the potential for integrative treatment approaches and personalized medicine in managing chronic inflammatory skin disorders.},
}

@article {pmid42858484,
year = {2026},
author = {Suo, J and Wang, Y and Ma, M and Liu, X and Li, C and Hu, Y and Feng, Z and Ma, Y and Cheng, S and Li, F and Zhu, J and Nian, H},
title = {Polypharmacological targeting of atopic dermatitis by natural products: A mechanism-driven systematic review.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {162},
number = {},
pages = {158850},
doi = {10.1016/j.phymed.2026.158850},
pmid = {42858484},
issn = {1618-095X},
abstract = {BACKGROUND: Atopic dermatitis (AD) involves interconnected disturbances in epidermal barrier function, immune regulation, microbial homeostasis, and neuroimmune itch. Natural products influence several of these processes, but their mechanistic and clinical evidence remains fragmented.

PURPOSE: To assess natural product-based interventions for AD within a polypharmacological framework and identify priorities for clinical translation.

STUDY DESIGN: Mechanism-driven systematic review with qualitative narrative synthesis.

METHODS: PubMed and the Web of Science Core Collection were searched from inception to March 2026. Eligible studies evaluated isolated natural compounds, characterized extracts or formulations, natural lipids, or microbe-derived interventions in patients with AD or validated experimental models. Evidence was synthesized by chemotype, pathological axis, molecular target or pathway, study design, and translational relevance.

RESULTS: A total of 156 original studies were retained. Reported effects clustered around epidermal differentiation and lipid homeostasis, inflammatory signaling, host-microbial interactions, and pruriceptive pathways. Preclinical studies provided mechanistic evidence for barrier-restorative, immunomodulatory, microbiome-related, and antipruritic effects involving multiple pathways. Clinical studies reported improvements in disease severity, barrier-related measures, pruritus, and quality of life, although findings varied across interventions and study designs. Direct target engagement, exposure-response relationships, and contributions of individual constituents in multicomponent preparations remained incompletely resolved.

CONCLUSION: Natural products provide a pharmacologically diverse basis for intervention across interconnected AD pathways. Current evidence supports therapeutic potential and multitarget activity, although polypharmacological synergy, comparative efficacy, and long-term safety require further validation. Clinical translation requires reproducible product characterization, direct mechanistic validation, pharmacokinetic assessment, human-relevant models, and well-designed clinical studies.},
}

@article {pmid42858636,
year = {2026},
author = {Lewis, N and Levenstein, JM and Villani, A},
title = {Gut microbiota composition in adolescents with ADHD: associations with fatty acid and micronutrient intakes.},
journal = {Journal of psychiatric research},
volume = {204},
number = {},
pages = {76-87},
doi = {10.1016/j.jpsychires.2026.10.006},
pmid = {42858636},
issn = {1879-1379},
abstract = {INTRODUCTION: Gut microbiome alterations have been reported in attention-deficit/hyperactivity disorder (ADHD), yet evidence in adolescents and links to diet and symptoms are limited. This study investigated gut microbiota composition and associations with ADHD symptoms and nutrient intakes in Australian adolescents.

METHODS: This case-control study involved 39 adolescents aged 13-18 years with clinician-confirmed ADHD (n = 18) and healthy controls (n = 21). Gut microbiota were profiled using full-length 16S rRNA sequencing (PacBio HiFi). Alpha and beta diversity, the Firmicutes/Bacteroidota ratio, and relative abundances were compared between controls and ADHD. ADHD subtype (combined and inattentive) differences were also explored. Associations between taxa, selected energy-adjusted nutrient intakes, and ADHD symptom severity were assessed.

RESULTS: No group differences were observed in alpha or beta diversity or the Firmicutes/Bacteroidota ratio. Nominal relative abundance differences in ADHD included enrichment of Peptostreptococcales (p = .039), Coriobacteriaceae (p = .039), Collinsella (p = .045), Gemmiger (p = .038), and an unclassified Subdoligranulum species (p = .039), and reduction of Eubacterium F/Eubacterium xylanophilum (p = .040). Compared to inattentive ADHD, combined ADHD had lower abundance of Bacteroides and Parabacteroides species. The strongest associations were found between Peptostreptococcales and omega-3s (positive). Folate, beta-carotene, vitamin D, magnesium, added sugars, and monounsaturated fat were also nominally associated with taxa. No taxa-symptom correlations were significant.

CONCLUSION: Adolescents with ADHD exhibited several nominal relative abundance differences in gut microbiota. Associations between taxa and specific nutrient intakes highlight potential relevance of nutrition-microbiome interactions in ADHD, and warrant additional research.},
}

@article {pmid42858661,
year = {2026},
author = {Feng, H and Zhou, X and Miao, Y and Jin, X and Wang, J and Yang, P and Zhang, X and Yang, Y and Chen, H and Cai, P and Ding, X},
title = {Solar-photoaged maize leaf residues reshape soil physicochemical-biological processes and Fe-Cd biogeochemistry.},
journal = {Journal of hazardous materials},
volume = {517},
number = {},
pages = {143873},
doi = {10.1016/j.jhazmat.2026.143873},
pmid = {42858661},
issn = {1873-3336},
abstract = {Solar photoaging endows maize leaf residues with persistent redox activity through the spontaneous generation of oxygen-centered environmentally persistent free radicals (EPFRs). Upon soil incorporation, these long-lived radicals and their derived dissolved organic matter (DOM) act as electron donors that promote Fe(III) reduction to Fe(II), followed by Fe(II) reoxidation and reprecipitation, thereby promoting reduction-initiated Fe(III)/Fe(II) redox cycling. This process profoundly shapes soil properties by expanding the organic carbon pool, yet it accelerates soil acidification and triggers root-localized oxidative stress, which induces lipid peroxidation and partially offsets the growth-promoting effect of biomass amendment. Concurrently, the persistent oxidative pressure and oxygen consumption reshape the indigenous soil microbiome, shifting it toward iron-reducing consortia (e.g., Gammaproteobacteria and Bacillus circulans). Crucially, this radical-Fe process is associated with the conversion of labile ion-exchangeable Cd into more stable Fe/Mn oxide-bound fractions. Consequently, heavy metal translocation in the soil-plant system is effectively blocked, mitigating root and shoot Cd accumulation in Ipomoea aquatica by up to 50%. This study demonstrates a novel nature-based strategy coupling organic waste recycling with sustainable in-situ heavy metal remediation.},
}

@article {pmid42852618,
year = {2026},
author = {Eke, AC},
title = {Obstetric Pharmacomicrobiomics.},
journal = {Clinical pharmacology and therapeutics},
volume = {},
number = {},
pages = {},
pmid = {42852618},
issn = {1532-6535},
abstract = {Pregnancy is characterized by physiologic, metabolic, immunologic, and microbial adaptation. Medication use during pregnancy is common. Yet, therapeutic response often remains unpredictable because obstetric pharmacology has historically focused on pharmacokinetic changes while paying little attention to host-microbiome-drug interactions. Pharmacomicrobiomics, the study of bidirectional interactions between the microbiome and therapeutic agents, has emerged as an important frontier in precision medicine. Increasing evidence demonstrates that the maternal microbiome may influence drug bioavailability, metabolism, efficacy, toxicity, immune response, and placental signaling during pregnancy. Conversely, medications used in obstetric practice, including antibiotics, antiretrovirals, metformin, iron supplementation, and proton pump inhibitors, may reshape maternal microbial ecosystems with downstream implications for maternal-fetal health. Pregnancy introduces pharmacomicrobiomic complexity because the maternal gut, vaginal, and oral microbial communities evolve across gestation, while the placenta and fetus are exposed to microbial metabolites and microbe-associated signals without convincing evidence of stable resident microbiomes. Emerging data suggest that microbial composition may influence preterm birth, hypertensive disorders of pregnancy, gestational diabetes mellitus, obesity, fetal growth, immune development, and therapeutic responsiveness. This mini-review examines recent advances in obstetric pharmacomicrobiomics with emphasis on microbial regulation of drug metabolism, pregnancy-associated microbial remodeling, microbiome-mediated therapeutic variability, placental and fetal implications, and future translational applications. We propose that obstetric pharmacology is entering a systems biology era in which the maternal microbiome should be investigated as a potentially important determinant of therapeutic response rather than treated solely as a background physiologic variable. Integrating microbiome science into maternal-fetal therapeutics may ultimately improve individualized treatment strategies, drug development, and precision obstetric pharmacology.},
}

@article {pmid42852882,
year = {2026},
author = {Gómez-Garzón, C and O'Brien, VP and Chen, Q and Garman, KS and Salama, NR},
title = {Metaplasia creates a permissive niche for select Fusobacterium species in the stomach.},
journal = {mBio},
volume = {},
number = {},
pages = {e0174726},
doi = {10.1128/mbio.01747-26},
pmid = {42852882},
issn = {2150-7511},
abstract = {Infection with Helicobacter pylori is the major risk factor for gastric cancer worldwide; yet the exact mechanisms behind this link remain unclear. H. pylori-associated tissue changes often disrupt the gastric microbiome, enabling secondary gastric colonization by oral bacteria. Among these secondary colonizers, Fusobacterium species have documented associations with several gastrointestinal cancers. We found that both F. animalis and F. nucleatum invade cultured human gastric adenocarcinoma cells, but F. animalis exhibited higher adherence and invasion, and hypoxic conditions promoted higher bacterial survival. Both adherence and invasion were inhibited by exogenous GalNAc, a glycan commonly observed in membrane glycoproteins of adenocarcinoma cells and a target of the fusobacterial adhesin Fap2. Using a mouse model of stomach metaplasia, we found that F. animalis colonized gastric tissue only after metaplasia onset, growing in multispecies biofilms in the mucus layer, while F. nucleatum colonized neither healthy nor metaplastic gastric tissue. Metaplasia led to upregulation of Gal-GalNAc in the stomach, and reduced gastric acidity allowed higher F. animalis loads in this model. By contrast, inflammation and the presence of H. pylori did not significantly influence stomach colonization by F. animalis. Further assessment of additional Fusobacterium species and strains revealed that whereas all tested species can invade gastric cancer cells in vitro, only F. animalis and F. polymorphum robustly colonize the metaplastic gastric tissue of the mouse model similar to F. animalis. Overall, our data support a model in which H. pylori-induced metaplasia makes the stomach susceptible to secondary infection by other cancer-associated microbes, including some Fusobacterium species.IMPORTANCEHelicobacter pylori infection is the primary risk factor for gastric cancer worldwide, yet the underlying cancer-promoting mechanisms are not fully defined. Our study shows that metaplasia, a precancerous condition typically triggered by H. pylori and characterized by specific changes in gene expression and tissue remodeling, can enable secondary infection by other cancer-associated bacteria. Specifically, we found that certain species of the genus Fusobacterium, linked to several gastrointestinal cancers, colonize the stomach only after the onset of metaplasia. Metaplasia-associated changes in the stomach include altered surface sugars and reduced acidity, which together may create a more permissive environment for bacterial growth. Our findings support a model in which disruptions of gastric tissue architecture induced by chronic H. pylori infection facilitate colonization by other cancer-related bacteria, contributing to the growing body of evidence highlighting the role of bacteria in cancer development.},
}

@article {pmid42852886,
year = {2026},
author = {Rolando, JL and Carnes, AL and Hodges, M and Joesting, H and Kostka, JE},
title = {Leaf damage is associated with alteration of microbiome composition and abundance in the Spartina alterniflora phyllosphere.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0159726},
doi = {10.1128/spectrum.01597-26},
pmid = {42852886},
issn = {2165-0497},
abstract = {UNLABELLED: Spartina alterniflora, the dominant plant species in salt marshes along the Atlantic and Gulf of Mexico coastlines of the Americas, is affected by disease and sudden vegetation dieback. Despite the foundational role of S. alterniflora in low-elevation salt marshes, the response of the native leaf-associated microbiome (i.e., phyllosphere microbiome) to leaf damage resulting from disease and environmental stress has not been explored. We hypothesized that healthy and damaged plants would show differentiation in their phyllosphere microbiomes following primary infection or exposure to environmental stressors. Here, we analyzed changes in prokaryotic and fungal relative abundance, diversity, and community composition in the S. alterniflora phyllosphere microbiome. We compared natural marsh and greenhouse plants in Georgia and South Carolina, USA, and collected leaves from healthy and damaged natural plants across two contrasting Spartina phenotypes that differ in their exposure to environmental stress. Our results show that plant origin (i.e., greenhouse vs natural marsh), plant health status (i.e., healthy vs damaged), and plant phenotype (i.e., short vs tall Spartina) affect microbial relative abundance, alpha diversity, and community composition in the S. alterniflora phyllosphere. Damaged leaves presented higher microbial abundance and alpha diversity than healthy leaves, suggesting microbial proliferation following leaf damage. Plants raised from seeds in the greenhouse presented the lowest microbial abundance and Shannon diversity for both prokaryotic and fungal communities, indicating that in natural ecosystems the phyllosphere microbiota is acquired predominantly through horizontal transmission from the environment. Overall, this study provides novel insights into the assembly of the S. alterniflora phyllosphere microbiome.

IMPORTANCE: Salt marshes are tidally influenced coastal wetlands that provide a range of ecosystem services to global and local communities, including protection from storm surge, water purification, and carbon sequestration. Spartina alterniflora is the dominant plant species in Atlantic and Gulf of Mexico marshes in the Americas. Fungal disease and exposure to environmental stressors have previously been described in marsh ecosystems and linked to extensive and sudden vegetation dieback in the southeastern USA. In this study, we propose that microbial proliferation follows plant damage caused by either fungal disease or environmental stress, leading to profound changes in native leaf-associated microbiota abundance, diversity, and composition. Using greenhouse plants as a control, we also demonstrate that microbes colonizing marsh leaves are acquired predominantly from the environment. Overall, this study advances the ecological understanding of the S. alterniflora leaf microbiome assembly, establishing a baseline to inform future work harnessing plant-associated microbes for ecosystem restoration.},
}

@article {pmid42852908,
year = {2026},
author = {Zhao, J and Lu, Z and Liu, Q and Liu, J and Wang, L and Huang, J and Yang, F and Yu, H},
title = {Multi-omics elucidate octapeptin mechanisms in alleviating intestinal injury in mice challenged with ETEC K88 via modulated microbial and host pathways.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0103226},
doi = {10.1128/msystems.01032-26},
pmid = {42852908},
issn = {2379-5077},
abstract = {The mechanisms whereby antimicrobial peptides (AMPs) confer intestinal protection during enteric bacterial infection remain unclear. Here, we examined the protective effects and underlying mechanisms of the AMP, octapeptin, against intestinal infection induced by enterotoxigenic Escherichia coli K88 (ETEC K88) in mice. Octapeptin ameliorated intestinal injury by modulating gut microbiome-host interactions. When compared with ETEC K88 mice, octapeptin significantly attenuated growth retardation, systemic oxidative stress, pro-inflammatory cytokine elevation, and ileal morphological damage. Integrated cecal microbiome, metabolome, and ileal transcriptome analyses revealed that octapeptin reversed ETEC K88-induced dysbiosis, notably increasing beneficial genera abundance. Concomitantly, octapeptin altered microbial metabolite profiles and significantly influenced ileal gene expression in circadian rhythm regulation. Correlation analysis and variance partitioning further identified a coherent "microbiota-metabolite-transcriptome" axis underlying these phenotypic improvements. Thus, octapeptin alleviates ETEC K88-induced intestinal injury via multi-level interactions that restore microbial ecology and regulate host circadian and immune pathways, thereby highlighting host-directed AMP mechanisms.IMPORTANCEAntimicrobial peptides are promising alternatives to antibiotics, but how they work inside the body remains poorly understood. Using a multi-omics approach, this study shows that octapeptin, a natural cyclic lipopeptide, protects mice against intestinal infection by reshaping the gut microbiota, reprogramming gut metabolites, and stabilizing host circadian clock genes that are disrupted by infection. These findings reveal a previously unrecognized link between gut microbes and the intestinal circadian clock. This mechanistic framework could guide the development of peptide-based strategies to prevent enteric infections in animals.},
}

@article {pmid42853339,
year = {2026},
author = {Pachiou, A and Damanaki, M and Paqué, PN and Rahiotis, C and Pappa, E},
title = {Oral microbiome alterations in individuals with type 1 diabetes: a systematic review.},
journal = {Clinical oral investigations},
volume = {30},
number = {11},
pages = {},
pmid = {42853339},
issn = {1436-3771},
mesh = {Humans ; *Diabetes Mellitus, Type 1/microbiology ; *Microbiota ; *Mouth/microbiology ; Glycemic Control ; Glycated Hemoglobin/analysis ; },
abstract = {OBJECTIVES: To systematically evaluate associations between glycemic control and oral microbial findings in individuals with type 1 diabetes mellitus (T1DM), distinguishing targeted detection of selected taxa from comprehensive oral microbiome profiling.

MATERIALS AND METHODS: A systematic search of PubMed, Embase, and Scopus was conducted from database inception to June 2025 in accordance with the PRISMA statement. The protocol was prospectively registered in PROSPERO. Human studies investigating the relationship between glycemic control and the oral microbiome in individuals with T1DM were eligible for inclusion. Two reviewers independently performed study selection, data extraction, and risk of bias assessment. Due to substantial methodological heterogeneity, findings were synthesized qualitatively.

RESULTS: Forty-two studies met the eligibility criteria. Most were cross-sectional and assessed glycemic control using glycated hemoglobin (HbA1c), with heterogeneous thresholds. Saliva and subgingival plaque were the most frequently sampled oral sites. Targeted studies commonly reported associations between poorer glycemic control and selected periodontal pathogens or oral Candida carriage, whereas findings for cariogenic microorganisms were inconsistent. Only four studies used comprehensive culture-independent community profiling; these studies reported differences in community composition and/or diversity, but the small number and methodological heterogeneity preclude a uniform conclusion regarding the direction of diversity change.

CONCLUSIONS: Poorer glycemic control is associated with selected oral microbial alterations in individuals with T1DM, particularly in periodontal and Candida-focused studies. However, the predominance of targeted assays, cross-sectional designs, and substantial methodological heterogeneity limits conclusions about whole-community oral microbiome dysbiosis or causality. Well-designed longitudinal studies using standardized clinical phenotyping and comprehensive microbiome profiling are needed.

CLINICAL RELEVANCE: Poor glycemic control may coexist with adverse oral microbial and clinical findings in individuals with T1DM. These associations support attention to established preventive dental care and periodontal assessment as part of multidisciplinary diabetes care; however, oral microbiome monitoring is not yet validated as a clinical biomarker of glycemic status or oral disease risk.},
}

Humans
*Diabetes Mellitus, Type 1/microbiology
*Microbiota
*Mouth/microbiology
Glycemic Control
Glycated Hemoglobin/analysis

@article {pmid42848816,
year = {2026},
author = {Flores Iglesias, JC and Méndez López, LF},
title = {Gut Microbiota-Mediated Biotransformation of Coumarins.},
journal = {Xenobiotica; the fate of foreign compounds in biological systems},
volume = {},
number = {},
pages = {1-22},
doi = {10.1080/00498254.2026.2747088},
pmid = {42848816},
issn = {1366-5928},
abstract = {1. Coumarins are plant-derived secondary metabolites widely present in foods, spices, and medicinal plants. Their limited intestinal absorption and extensive host metabolism allow a variable fraction to reach the colon, where gut microorganisms can transform them into metabolites with distinct physicochemical and biological properties.2. This review synthesizes current evidence on gut microbiota-mediated coumarin biotransformation, focusing on microbial taxa, metabolic reactions, structural determinants, and consequences for biological activity. Reported transformations include deglycosylation, reduction, O-demethylation, hydroxylation, deprenylation, and lactone ring opening. Recent studies have identified multiple human gut bacteria capable of coumarin reduction and implicated the NADPH-dependent reductase NemA in this process. Gut bacteria may also generate simple coumarins from dietary phenolic precursors. These transformations can modify biological activity, while coumarins and their metabolites may reciprocally influence microbial composition and metabolism.3. Current evidence supports gut microbiota as an important determinant of coumarin metabolism, but its physiological relevance in humans remains uncertain. Key gaps include interindividual variability, specific microbial enzymes and taxa, enterohepatic recycling, and the contribution of the gut mycobiome. Integrated microbiome, metabolomic, and pharmacokinetic approaches are needed to establish the contribution of microbiota-derived metabolites to coumarin bioactivity and safety.},
}

@article {pmid42848888,
year = {2026},
author = {Huus, KE and , and Abo, H and Tan, YH and Atay, E and Rytter, H and Keller, R and Dauser, S and Vu, DL and Azad, MB and Knight, R and Ke, A and Lotoski, L and Langlois, MA and Liu, R and Tyakht, AV and Youngblut, N and Kang, SM and Parsonnet, J and Maier, L and Chassaing, B and Kremsner, PG and Gewirtz, AT and Esen, M and Ley, RE and Gabor, JJ and Gaile, JM and Fleischmann, WA and Siebner, AS and Smeenk, G and Flügge, J and De Moraes, RA and Jakob, D and Prokipchuk, A and Wilhelm, C},
title = {The human gut microbiome primes fever after vaccination.},
journal = {Science (New York, N.Y.)},
volume = {394},
number = {6820},
pages = {eaea7733},
doi = {10.1126/science.aea7733},
pmid = {42848888},
issn = {1095-9203},
mesh = {Adult ; Animals ; Female ; Humans ; Male ; Mice ; Diet ; Feces/microbiology ; *Fever/etiology/immunology/microbiology ; Flagellin/immunology/metabolism/genetics ; *Gastrointestinal Microbiome/immunology ; Germ-Free Life ; Inflammation ; SARS-CoV-2/immunology ; *Vaccination/adverse effects ; *Viral Vaccines/adverse effects ; Organoids ; *Eubacteriales/immunology ; *BNT162 Vaccine/adverse effects/immunology ; Mice, Inbred C57BL ; Mice, Knockout ; Toll-Like Receptor 5/genetics ; Calcium-Binding Proteins/genetics ; Apoptosis Regulatory Proteins/genetics ; },
abstract = {Fever is a common adverse reaction to vaccination, contributing to vaccine hesitancy and reduced uptake. To understand variation in fever risk, we longitudinally profiled fecal microbiota, oral temperature, and serological markers in 171 healthy adults receiving Severe acute respiratory syndrome coronavirus 2 mRNA vaccines. Fever risk correlated with low-grade intestinal inflammation, increased abundance of flagellated Lachnospiraceae bacteria, and increased flagellin expression prevaccine. Microbiomes from fever-high donors triggered stronger inflammation in human intestinal organoids and drove flagellin-dependent vaccine reactions in gnotobiotic mice. Moreover, microbiome flagellin phenotypes and murine vaccine reactions were modifiable by diet. Consistent with this, human fever risk was associated with self-reported diet and metabolic markers. These findings identify the gut microbiome as a driver of vaccine-induced fever, suggesting that microbiome-targeting strategies could modulate immune tone and improve vaccine side effects.},
}

Adult
Animals
Female
Humans
Male
Mice
Diet
Feces/microbiology
*Fever/etiology/immunology/microbiology
Flagellin/immunology/metabolism/genetics
*Gastrointestinal Microbiome/immunology
Germ-Free Life
Inflammation
SARS-CoV-2/immunology
*Vaccination/adverse effects
*Viral Vaccines/adverse effects
Organoids
*Eubacteriales/immunology
*BNT162 Vaccine/adverse effects/immunology
Mice, Inbred C57BL
Mice, Knockout
Toll-Like Receptor 5/genetics
Calcium-Binding Proteins/genetics
Apoptosis Regulatory Proteins/genetics

@article {pmid42848904,
year = {2026},
author = {Pulendran, B},
title = {Before the immunological Big Bang.},
journal = {Science (New York, N.Y.)},
volume = {394},
number = {6820},
pages = {170-171},
doi = {10.1126/science.ael7318},
pmid = {42848904},
issn = {1095-9203},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Vaccination/adverse effects ; Fever/immunology ; Inflammation/immunology ; Animals ; },
abstract = {The nature of the gut microbiome before vaccination influences later inflammatory reactions and fever.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Vaccination/adverse effects
Fever/immunology
Inflammation/immunology
Animals

@article {pmid42848938,
year = {2026},
author = {Dailey-Chwalibóg, T and Mertens, A and Fehr, K and Shu, CH and Jauhal, A and Manus, MB and Deng, L and Toe, LC and Muhammed, A and Pasha, A and Shafiq, Y and Iqbal, N and Khan, W and Nisar, MI and Baxter, JB and Beggs, MR and Sundararaman, N and Van Eyk, JE and Bode, L and Hubbard, A and Lagerborg, KA and Jain, M and Hampel, D and Shahab-Ferdows, S and Allen, LH and Lachat, C and DeBoer, MD and Jehan, F and Aghaeepour, N and Shenhav, L and McDermid, JM and Azad, MB},
title = {Nutritional interventions' impacts on human milk: Three trials in low-resource settings.},
journal = {Science (New York, N.Y.)},
volume = {},
number = {},
pages = {},
doi = {10.1126/science.aee9284},
pmid = {42848938},
issn = {1095-9203},
abstract = {Human milk (HM) composition is variable to support changing infant needs and is influenced by maternal diet and health. We harmonized HM data from three randomized trials in Burkina Faso (MISAME-III), Pakistan (Mumta-LW), and Tanzania (ELICIT) within the International Milk Composition (IMiC) Consortium to test how maternal nutrition affects HM composition. Balanced energy-protein (BEP) supplements or nicotinamide given to lactating mothers increased milk B-vitamins, while macronutrients, oligosaccharides, bioactive proteins, and microbiome composition were physiologically buffered. Metabolomic and proteomic analyses revealed shifts in vitamin-related metabolites, triglyceride profiles, and intracellular protein representation. In a MISAME-III subset, maternal and infant blood showed concordant changes. Postnatal BEP improved infant growth only in the more undernourished cohort. Improved milk micronutrient quality across settings supports extending maternal supplementation into lactation.},
}

@article {pmid42849016,
year = {2026},
author = {Martignoni, MM and Bordenstein, SR and Karakoç, C and Tyson, RC and Brown, SP and Garnier, J},
title = {An eco-evolutionary consumer-resource theory of host-microbe symbioses.},
journal = {Journal of evolutionary biology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jeb/voag100},
pmid = {42849016},
issn = {1420-9101},
abstract = {Symbiotic associations between microorganisms and hosts are universal, diverse, and dynamic. Yet, our ability to represent this complexity mathematically remains limited. We propose extending consumer-resource theory to incorporate evolutionary processes to advance our understanding of symbioses, from pairwise interactions to complex host-microbe assemblages. The resulting eco-evolutionary framework captures feedbacks between host-microbe interaction structure, biotic resource availability, and selection acting across biological scales. Importantly, this approach relaxes the assumption of separated ecological and evolutionary timescales, so that both processes unfold simultaneously. The coupling between ecological and evolutionary dynamics allows key properties of symbioses, such as ecological dependence and functional integration, to emerge from evolving resource-mediated interactions, rather than being imposed a priori. We illustrate the framework with a mathematical model of mycorrhizal symbiosis. The proposed consumer-resource formulation provides a unified basis for linking ecological and evolutionary dynamics in host-microbe symbioses, with implications for both basic theory and applied management.},
}

@article {pmid42849098,
year = {2026},
author = {Wen, Y and Huang, X and Zhang, L and Zhang, S and Li, M and Zou, K},
title = {Seasonal dynamics of plastic-degradation-associated microbiomes in an anthropogenically impacted Pearl River Estuary: A genome-resolved metagenomic study.},
journal = {Marine pollution bulletin},
volume = {233},
number = {Pt 3},
pages = {120421},
doi = {10.1016/j.marpolbul.2026.120421},
pmid = {42849098},
issn = {1879-3363},
abstract = {Estuarine sediments are important sinks for plastic debris and potential reservoirs of microbial functions involved in plastic transformation. Here, metagenomic sequencing and genome-resolved analyses were used to characterize the seasonal distribution and environmental associations of microbial taxa and genes potentially associated with plastic degradation in the Pearl River Estuary. The screened taxa differed between wet and dry seasons, with Priestia and Staphylococcus showing higher relative abundances in the dry season, whereas Vibrio, Photobacterium, Methylobacterium, and Ralstonia were more abundant in the wet season. Microbial community dynamics were associated with variation in organic matter, pH, temperature, and nitrogen variables, with the leading environmental predictors differing between microbial communities and seasons. Genome-resolved analysis recovered 150 non-redundant medium- to high-quality metagenome-assembled genomes (MAGs), of which 42 carried putative plastic-degradation-associated gene homologs identified through comparison with PlasticDB. Approximately 60% of these 42 MAGs belonged to Pseudomonadota, and three Burkholderiaceae MAGs harbored multiple candidate homologs. KEGG annotations further identified genes related to alkane oxidation, fatty acid degradation, ester hydrolysis, and aromatic-compound metabolism, providing a broader metabolic context for these genomes. Together, these findings characterize seasonal variation in the screened microbial communities and identify candidate microbial hosts and genes for investigating plastic transformation in estuarine sediments.},
}

@article {pmid42849177,
year = {2026},
author = {Tang, S and Yang, Y and Wang, Y and Gong, S and Li, N and He, Z and Ni, J and Wang, J and Liu, Y and Chan, JWY and Chu, WCW and Mok, VCT and Chen, Z and Huang, B and Wing, YK},
title = {Deciphering the heterogeneity of prodromal α-synucleinopathy: linking brain biotyping and gut dysbiosis in isolated REM sleep behaviour disorder.},
journal = {EBioMedicine},
volume = {133},
number = {},
pages = {106503},
doi = {10.1016/j.ebiom.2026.106503},
pmid = {42849177},
issn = {2352-3964},
abstract = {BACKGROUND: Isolated/idiopathic REM sleep behaviour disorder (iRBD) is a specific prodrome of α-synucleinopathies. We previously identified two distinct clinical-neuroimaging biotypes in iRBD: Biotype 1, marked by widespread cortical-subcortical-cerebellar atrophy with motor and cognitive deficits, and Biotype 2, with preserved brain structure and neurocognition. Converging evidence implicates the gut-brain axis in early α-synucleinopathy, yet its role in these divergent iRBD phenotypes remains unexplored.

METHODS: We analysed faecal microbiota using shotgun metagenomic sequencing and structural neuroimaging data from 167 participants (42 Biotype 1, 50 Biotype 2, 75 controls). Microbial features and brain structure were compared across groups. Gut-brain associations were assessed using sparse partial least squares regression to link microbiome features with neuroanatomical patterns.

FINDINGS: Overall microbial composition did not significantly differ between Biotype 1 and Biotype 2, and both biotypes showed depletion of short-chain fatty acid-producing bacteria. Relative to the shared dysbiotic background, Biotype 1 displayed more pronounced taxon- and pathway-level alterations, including enrichment of Collinsella aerofaciens, Cloacibacillus evryensis, and Mogibacterium sp. BX12, which were associated with Biotype 1-specific brain atrophy. Biotype 2 showed milder dysbiosis with fewer differentially abundant species. These patterns were consistent in sensitivity analyses and fully adjusted models.

INTERPRETATION: Beyond a shared depletion of short-chain fatty acid-producing bacteria, iRBD biotypes exhibit differences in taxonomic and functional profiles, with these differences being more pronounced in Biotype 1. These findings support a role for the gut-brain axis in early α-synucleinopathy and its phenotypic heterogeneity.

FUNDING: This study was funded by the Health and Medical Research Fund of the Food and Health Bureau (Ref No.: 05162876 and 10210686) and Research Grants Council (RGC-CRF Ref No.: C4044-21G) of Hong Kong.},
}

@article {pmid42849234,
year = {2026},
author = {Makatjane, KA and Xu, J and Guo, W and Liu, G and Wang, Y and Lin, H and Fang, Z and Li, T and Zhou, H},
title = {Dietary Cupplant (Silphium perfoliatum L.) flavonoid supplementation is associated with changes in cecal microbial diversity and community structure in broiler chickens.},
journal = {Poultry science},
volume = {105},
number = {12},
pages = {107876},
doi = {10.1016/j.psj.2026.107876},
pmid = {42849234},
issn = {1525-3171},
abstract = {Cupplant (Silphium perfoliatum L.) contains flavonoids that may influence the intestinal microbiota, but their effects in broilers remain poorly defined. We examined cecal microbial responses to dietary Cupplant flavonoids. Two hundred forty one-day-old broilers were assigned to four diets containing 0 (CH), 100 (S1), 200 (S2), or 300 (S3) mg/kg flavonoid extract, with five replicate cages per treatment. At day 42, cecal digesta from six birds per treatment were characterized using 16S rRNA gene amplicon sequencing; one cage per treatment contributed two sampled birds. QIIME2/DADA2 processing yielded 1,601,918 retained reads and 2,735 amplicon sequence variants. Observed ASVs, Chao1 richness, and Shannon diversity were higher in S3 than CH (adjusted P < 0.05), although responses were non-monotonic. Global Bray-Curtis PERMANOVA showed treatment-associated differences in community composition (pseudo-F(3,20) = 2.997, R[2] = 0.310, P = 0.001), while PERMDISP was non-significant (P = 0.168). All pairwise PERMANOVA comparisons remained significant after multiplicity correction. False-discovery-rate (FDR)-controlled metagenomeSeq identified six genera in the CH-S1 comparison and three in CH-S3, with Escherichia-Shigella, Desulfovibrio, and Anaerotignum recurring in both contrasts; CH-S2 had no FDR-significant genera. Reconstructed FDR-controlled networks retained only 6.8-12.0 % of nominal edges, and βNTI, NST, and iCAMP results did not support a monotonic dose-dependent shift in community assembly. Descriptive final body weight and average daily gain values were similar across treatments, but cage-level growth inference was not possible from the archived data. Cupplant flavonoid supplementation was associated with non-linear changes in cecal microbial diversity and composition, warranting confirmation in cage-aware, adequately powered studies.},
}

@article {pmid42849293,
year = {2026},
author = {Zhou, X and Cui, G and Dong, H and Wen, S and Li, Y and Han, M and Wang, G},
title = {Genotype-dependent phosphorus acquisition responses of two soybean genotypes under combined low phosphorus and salt stress: evidence from root traits, exudates and rhizosphere microbiome.},
journal = {Plant physiology and biochemistry : PPB},
volume = {239},
number = {},
pages = {111810},
doi = {10.1016/j.plaphy.2026.111810},
pmid = {42849293},
issn = {1873-2690},
abstract = {Soil salinization and phosphorus (P) deficiency often co-occur in coastal saline-alkali soils, severely limiting crop productivity. Although root exudates are known to mediate rhizosphere microbiome assembly, the coordinated associations among root exudates, rhizosphere microbes, and P acquisition under combined salinity stress and phosphate deficiency remain unclear. In this study, we used two salt-tolerant soybean genotypes differing in P efficiency (A74, P-efficient; A6, P-inefficient) as materials. In a controlled pot experiment, four treatments were established: control (CK), low P (LP), salt (S), and combined stress (LPS). By integrating root phenotypes, P acquisition traits, root exudate metabolomics, and rhizosphere metagenomics, the genotype-dependent rhizosphere responses were investigated. Results showed that, compared to A6, A74 maintained a more extensive root-soil interface and superior P nutritional status under LP and LPS, exhibiting more robust P acquisition responses. Metabolomics and metagenomics identified 16 candidate metabolites and 12 candidate microbial taxa, respectively. Effect-size and correlation analyses prioritized naringenin and Sinorhizobium as candidate components associated with genotype-dependent P acquisition responses. KO annotation identified Sinorhizobium-associated genes with potential roles in phosphonate and phosphinate metabolism and benzoate degradation (e.g., phnJ, pcaC, and mhpD). In summary, these results support a genotype-dependent rhizosphere response pattern involving naringenin and Sinorhizobium, in which coordinated changes in root traits, exudate profiles, and microbial functional potential were associated with the stronger P acquisition response of A74 under combined stress. These findings identify candidate relationships for future functional validation under saline conditions.},
}

@article {pmid42849303,
year = {2026},
author = {Baffoni, L and Fernandez de Landa, G and Braglia, C and Braschi, G and Siroli, L and Di Gioia, D and Alberoni, D},
title = {Lactobacillus apisdorsatae sp. nov. from the giant honeybee (Apis dorsata), Lactobacillus pollinatoris sp. nov. and Lactobacillus xylocopae sp. nov., from the carpenter bee (Xylocopa violacea).},
journal = {Systematic and applied microbiology},
volume = {49},
number = {6},
pages = {126776},
doi = {10.1016/j.syapm.2026.126776},
pmid = {42849303},
issn = {1618-0984},
abstract = {Insects host diverse and distinctive communities of gut mutualistic bacteria, including lactic acid bacteria of the Lactobacillus genus. Recently, most research in the insect microbial taxonomy has focused on identifying novel Lactobacillaceae species in managed insects such as Apis mellifera and few species of Bombus spp. from North America, Europe, and China. However, the gut microbiota of wild insects remains largely unexplored. Yet, insects represent the largest animal class and a vast, untouched source of novel microbial symbionts, especially in wild populations. This study focuses on the isolation and characterization of novel Lactobacillaceae strains from wild and solitary insects, such as the carpenter bee (Xylocopa violacea), the strawberry seed beetle (Harpalus rufipes), and the giant honeybee (Apis dorsata). Full-genome sequencing and annotation, including investigation of distinctive functional traits, were performed for these strains, along with phenotypic characterization of sugar fermentation, enzymatic activity, cellular fatty acid profiles and G + C content. Phylogenetic relationships were determined using 16S rRNA gene sequences and core genome computation, which confirmed the classification of novel taxa within the Lactobacillus genus. From the aforementioned insect species, three novel Lactobacillus species were isolated and characterized: Lactobacillus xylocopae XV31L (= DSM 120036[T] = MSCL 1776[T]) and Lactobacillus pollinatoris XV13L (= DSM 104957 [T] = LMG 30141[T]) from X. violacea, and CA30L (= DSM 119968[R] = MSCL 1777[R]) from H. rufipes, and Lactobacillus apisdorsatae C449L (= VTT E-263657 [T] = MSCL 1775[T] = NCCB 101125[T]) from A. dorsata.},
}

@article {pmid42849380,
year = {2026},
author = {Khamidov, F and Jalolov, O and Ne'matov, U and Ilmira, U and Mavlyuda, Q and Malohat, S and Alkhawaja, AS and Gulkhayyo, J and Siahmansouri, H},
title = {Microbiome oncolytic virus interactions in cancer: emerging evidence and therapeutic implications for immunotherapy.},
journal = {Seminars in oncology},
volume = {53},
number = {6},
pages = {152564},
doi = {10.1016/j.seminoncol.2026.152564},
pmid = {42849380},
issn = {1532-8708},
abstract = {The tumor microenvironment (TME) is essential for the regulation of tumor progression, immune responses, and therapeutic outcomes. The importance of the tumor microbiome, a complex ecosystem of microorganisms that reside within the TME, in shaping tumor dynamics and modulating treatment responses has been underscored by recent advancements in cancer research. Oncolytic viruses (OVs) have been recognized as promising treatment options in cancer immunotherapy due to their ability to selectively target and eliminate tumor cells while protecting normal tissue. Recent preclinical studies suggest a bidirectional relationship between OVs and the microbiome, although direct evidence that OVs remodel tumor-resident microbial communities remains limited. Most available data concern the gut microbiome, where OV treatment has been associated with changes in microbial composition, while baseline or experimentally manipulated microbiota can, in turn, influence virotherapy efficacy. This review examines these emerging interactions, distinguishes direct experimental evidence from proposed mechanisms, and discusses how microbiome-informed strategies may complement OV-based immunotherapy. We also highlight the scarcity of longitudinal intratumoral and clinical microbiome data and identify the experimental steps required to establish causality.},
}

@article {pmid42849446,
year = {2026},
author = {Deng, F and Hu, J and Min, Y and Xie, S and Lin, Z and Sun, Q and Liu, H and He, S and Feng, S and Wu, L and Chen, X and Xu, L and Zhang, Z and Tang, W and Li, Z and Zhou, H and Liu, K},
title = {Microbiota-mediated naringenin release limits postoperative acute gastrointestinal injury by suppressing ferroptosis.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {103101},
doi = {10.1016/j.xcrm.2026.103101},
pmid = {42849446},
issn = {2666-3791},
abstract = {Acute gastrointestinal injury (AGI) remains a major complication after cardiopulmonary bypass, yet its microbiome-related determinants are unclear. We identify microbiota-mediated naringenin (NAR) release as a candidate modulator of AGI susceptibility. Patients who subsequently develop AGI have lower preoperative fecal NAR levels and β-glucuronidase (GUS) activity, accompanied by reduced abundance of Bacteroides vulgatus (B. vulgatus). In germ-free and conventional mice, B. vulgatus alleviates intestinal ischemia-reperfusion injury through GUS-dependent release of NAR from its glucuronide conjugate. Mechanistically, NAR engages the TLR4/MyD88-SPRR2A axis to suppress CHAC1-driven ferroptosis, thereby maintaining epithelial integrity and promoting mucosal repair in vivo and in organoids. Clinically, preoperative fecal NAR concentration and GUS activity show exploratory value as noninvasive markers for postoperative AGI risk stratification. Collectively, these findings support a microbiota-host metabolic model in which microbial NAR release may mitigate postoperative gastrointestinal injury by restricting ferroptosis, with potential implications for risk assessment and therapeutic modulation.},
}