@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.},
}

@article {pmid42849550,
year = {2026},
author = {Wang, Z and Zhang, H and Tian, P and Li, S and Li, L and Tian, K and Shi, X and Wu, C and Fan, Y and Lv, YE},
title = {The Gut-Lumbar Axis: A Comprehensive Review of Mechanisms, Clinical Evidence, and Future Therapeutic Perspectives.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {109667},
doi = {10.1016/j.phrs.2026.109667},
pmid = {42849550},
issn = {1096-1186},
abstract = {Low back pain (LBP) affects approximately 619 million people globally and is the leading cause of years lived with disability, yet the pathogenesis of chronic LBP remains incompletely understood despite extensive research into structural and biomechanical factors. Emerging evidence suggests that the gut microbiota, through its influence on systemic inflammation, immune regulation, metabolic homeostasis, and neuromodulation, plays a previously unrecognized role in lumbar spine pathology. While prior frameworks such as the "gut-disc axis" and "gut-spine axis" have addressed intervertebral disc degeneration or vertebral bone metabolism in relative isolation, we propose the "gut-lumbar axis" as an integrative framework that systematically unifies the intervertebral discs, vertebrae, paraspinal musculature, and neural structures of the lumbar spine within a single physiological and pathological continuum. This review synthesizes current evidence on the bidirectional communication between intestinal microbiota and lumbar spine health, covering intervertebral disc degeneration, chronic LBP, lumbar spinal stenosis, and vertebral osteoporosis. Multiple pathways linking gut dysbiosis to lumbar pathology are identified, supporting the gut-lumbar axis as a paradigm-shifting framework. However, large-scale longitudinal cohorts and well-designed randomized controlled trials are urgently needed to translate these findings into clinical practice. Microbiome-targeted therapies, including probiotics, dietary interventions, and fecal microbiota transplantation, hold promise as novel adjunctive strategies for managing chronic lumbar spine disorders, and key knowledge gaps for future investigation are highlighted.},
}

@article {pmid42849604,
year = {2026},
author = {Xiao, J and Khan, S and Shukla, PK and Johnson, D and LeDoux, MS and Khan, MM},
title = {Genetic risk for dystonia reprograms host-microbiome interactions and gut-brain communication.},
journal = {Experimental neurology},
volume = {},
number = {},
pages = {116054},
doi = {10.1016/j.expneurol.2026.116054},
pmid = {42849604},
issn = {1090-2430},
abstract = {Dystonia is a neurological movement disorder characterized by involuntary, sustained, or intermittent muscle contractions that result in twisting movements, repetitive motor patterns, or abnormal postures. While genetic mutations such as TOR1A[+/∆GAG] are known contributors, the environmental and peripheral factors influencing disease onset and progression remain poorly understood. Emerging evidence implicates the gut microbiome in shaping neurodevelopment and host behavioral function, yet its contribution to dystonia pathobiology is largely unexplored. Here, we longitudinally profiled the gut microbiome of a Tor1a[+/∆GAG] mouse model using 16S rRNA gene sequencing and uncovered early emerging, persistent disruptions in microbial diversity and community composition that coincided with progressive motor impairment. Mutant mice exhibited alterations in key commensal taxa, and molecular signatures indicative of compromised gut-barrier integrity. Parallel transcriptomic profiling of colonic tissues revealed coordinated dysregulation of pathways governing epithelial stress responses, endoplasmic reticulum homeostasis, lipid signaling, autophagy, and DNA damage and repair, suggesting a previously unrecognized epithelial stress state in Tor1a[+/∆GAG] mouse model. Integrative microbial-host interaction correlation analyses uncovered associations between specific dysbiotic taxa and host signaling pathways. These peripheral perturbations coincided with longitudinal motor deficits, identifying an age-dependent association between gut dysbiosis and neurobehavioral dysfunction. Together, our findings provide an experimental framework for investigating the relationship among microbiome perturbations, gut-barrier disruption, and neuronal vulnerability in a genetic model of dystonia. These findings reveal a previously underexplored peripheral dimension of DYT1 dystonia and provide a foundation for future studies to determine whether microbiome and intestinal alterations functionally contribute to disease pathobiology.},
}

@article {pmid42849708,
year = {2026},
author = {Ford, JG and O'Neill, E and Tolland, C and Travison, TG and Singer, K and Charbonneau, MR and Easson, DD and Jacques, PF and Toledo, GV and Rosen, CJ and Schott, EM and Kiel, DP and Sahni, S},
title = {Synbiotic to Attenuate Resorption of the Skeleton (STARS): Design and participant recruitment of a randomized, double-blind, placebo-controlled trial to test the efficacy of SBD111 medical food in older women.},
journal = {Contemporary clinical trials},
volume = {},
number = {},
pages = {108501},
doi = {10.1016/j.cct.2026.108501},
pmid = {42849708},
issn = {1559-2030},
abstract = {Osteoporosis and related fractures pose a costly public health challenge. Primary prevention of bone loss is largely limited to non-pharmacologic options without consistent guidelines. Prior studies have demonstrated that modification of the gut microbiome can influence bone homeostasis. The Synbiotic To Attenuate Resorption of the Skeleton (STARS) trial aimed to evaluate the efficacy, safety, and mechanistic effects of daily intake of SBD111, a fruit and vegetable-derived synbiotic medical food on the skeleton, gut microbiome, and inflammation biomarkers in women aged ≥60 years. This 18-month, investigator-initiated, single-site, randomized, double-blind, placebo-controlled trial had an enrollment goal of 220 women, a primary endpoint of proportionate change in lumbar spine bone mineral density (BMD) relative to baseline, and secondary outcomes including Quantitative Computed Tomography derived volumetric BMD and vertebral compressive strength, gut microbiome function, and bone and inflammatory biomarkers. Recruitment approaches included simultaneous digital and traditional methods beginning August 2024. As of July 2025, there were 42 enrolled participants (32 via digital, 10 via traditional); baseline demographics, eligibility, and enrollment rates were similar across recruitment strategies. Digital recruitment achieved over three times faster enrollment (2.9 vs. 0.9 enrollments/month) and was nearly 10 times more staff-efficient (0.05 vs. 0.48 cumulative weekly full-time equivalent) despite greater cost per enrollment ($548 vs. $173). These findings demonstrate the feasibility and efficiency of digital recruitment of older adults, offering valuable insights for future nutrition and microbiome clinical trials. The STARS trial is positioned to provide high-quality evidence for skeletal health maintenance in older women using SBD111.},
}

@article {pmid42849840,
year = {2026},
author = {Chelladurai, and Premkumar, R and Jenivi, A and Mohanapriya, },
title = {Comment on "Breastfeeding, early-life feeding practices and adolescent gut microbiota: Long-term associations in a birth cohort".},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105176},
doi = {10.1016/j.clnesp.2026.105176},
pmid = {42849840},
issn = {2405-4577},
}

@article {pmid42849841,
year = {2026},
author = {Qi, YL and Yan, Y and Li, XM and Li, YL and Liao, LZ and Liu, J and Ma, JW and Ma, JH and Chen, H},
title = {Gut Microbiota and nutrition as Emerging Modulators of Immune Checkpoint Inhibitor Therapy: Current Evidence, Challenges, and Future Perspectives.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {105168},
doi = {10.1016/j.clnesp.2026.105168},
pmid = {42849841},
issn = {2405-4577},
abstract = {Immune checkpoint inhibitors (ICIs), a major class of cancer immunotherapies, have transformed the treatment of advanced cancers, yet durable benefit remains limited by primary or acquired resistance and immune-related adverse events (irAEs). Increasing evidence implicates the gut microbiome and nutritional state as modifiable host factors that may shape both therapeutic efficacy and toxicity. Here, we critically review the emerging evidence linking microbial ecology, dietary exposure, immunonutrition and ICI outcomes, with particular emphasis on the diet-microbiome-metabolite-immune axis. Clinical cohorts and preclinical models indicate that microbiome composition and, increasingly, microbial function and metabolic cross-talk are associated with ICI responsiveness, while microbiome perturbations may also influence susceptibility to irAEs. Dietary patterns and nutritional status likewise correlate with treatment outcomes, with dietary fibre and Mediterranean-style dietary patterns providing early clinical signals, whereas evidence for specific immunonutrients and restrictive dietary strategies remains inconsistent or insufficient. Mechanistically, dietary substrates can reshape microbial communities and metabolite production, thereby modulating immune-cell states and antitumour responses. However, these effects are highly context dependent and cannot be inferred from individual taxa or metabolites alone. We further examine emerging strategies that integrate nutritional optimization with microbiome modulation as a potential means of simultaneously improving efficacy and therapeutic tolerability. Despite substantial mechanistic progress, clinical evidence remains predominantly observational or early phase, and no microbiome-informed dietary intervention has yet established a reproducible benefit in prospective trials. Future studies should therefore move beyond descriptive associations towards evaluating causal, biomarker-guided and patient-stratified interventions integrating longitudinal dietary, microbiome, metabolomic and immune profiling.},
}

@article {pmid42850030,
year = {2026},
author = {de Lima, NM and Vázquez-Campos, X and Thomsen, A and Ooi, M and Muñoz-Rojas, M},
title = {Mining Impacts on a Threatened and Burnt Swamp Ecosystem: Responses of the Microbial Soil Community.},
journal = {Environmental microbiology reports},
volume = {18},
number = {5},
pages = {e70397},
doi = {10.1111/1758-2229.70397},
pmid = {42850030},
issn = {1758-2229},
support = {PID2021-123097OA-I00//Ministerio de Ciencia e Innovación/ ; PID2024-161692OB-C33//Ministerio de Ciencia e Innovación/ ; LP180100741//Australian Research Council/ ; },
mesh = {*Soil Microbiology ; Bacteria/classification/isolation & purification/genetics ; *Mining ; *Wetlands ; Soil/chemistry ; *Microbiota ; Biodiversity ; Australia ; Ecosystem ; Eukaryota/classification/isolation & purification/genetics ; Fires ; },
abstract = {Peatlands are globally important carbon reservoirs that mitigate global warming while regulating biogeochemical cycles. However, these ecosystems are highly vulnerable to environmental disturbances, such as fire and mining. Despite the key ecological roles of soil microbes, descriptions of microbial assemblages in many peatland systems, and how they may shift under the dual disturbances of fire and mining, remain poorly addressed. Here, we assessed the composition and diversity of soil microbial communities in three mined and three unmined swamps in southeastern Australia, all affected by the unprecedented summer bushfires during 2019-2020. Bacterial and eukaryotic communities were analysed alongside soil chemical properties across a moisture gradient within each swamp. Our results revealed significant differences in communities due to mining activities, with the most pronounced differences observed within swamp communities rather than other sites along the moisture gradient. The eukaryotic community was significantly influenced by the combined effects of mining activity and fire history. The bacterial community was significantly correlated with pH. Our findings suggest that mining was associated with changes in eukaryotic diversity and bacterial community structure and functionality, with fire history potentially contributing to the observed patterns. This study underscores the critical, detrimental impacts that mining can have on peatland microbial composition.},
}

*Soil Microbiology
Bacteria/classification/isolation & purification/genetics
*Mining
*Wetlands
Soil/chemistry
*Microbiota
Biodiversity
Australia
Ecosystem
Eukaryota/classification/isolation & purification/genetics
Fires

@article {pmid42850034,
year = {2026},
author = {Arunachalam, JC and Relman, DA},
title = {What's New Is Old: "Cultural Lag" and Governance of Risk in the Life Sciences.},
journal = {Cold Spring Harbor perspectives in medicine},
volume = {},
number = {},
pages = {},
doi = {10.1101/cshperspect.a041953},
pmid = {42850034},
issn = {2157-1422},
abstract = {As advancement in the life sciences quickens, management of risks remains reactive, creating problematic delays in risk mitigation and difficulties for development of a holistic risk governance strategy. A reactive posture for addressing risk undermines biosecurity and contributes to public distrust in science. This problem is not new. A temporal offset between scientific advancement and oversight of associated risks was described more than a century ago. In 1922, the American sociologist, William Ogburn, coined the term, "cultural lag." Cultural lag was premised on the interconnectedness of technology and society and referred to a period of maladjustment between the introduction of a new technology and societal responses to mitigate its downsides. We examine the consequences of cultural lag for risk governance in the life sciences by looking at three recently introduced technologies, CRISPR-Cas9 gene editing, the proposed creation of mirror life, and microbiome engineering. Our observations lead to three recommendations for addressing cultural lag. The first recommendation is structural, namely, consolidation of governmental oversight on emerging technologies; the second is goal-oriented, that is, a call for a holistic form of horizon scanning; and the third concerns process and calls for implementation of deliberative democratic principles and practices. By pursuing an anticipatory governance regime, with policymaking closely aligned to and coordinated with technology breakthroughs, we enhance research safety and security while promoting innovation, and as a secondary benefit, help to restore public trust in science.},
}

@article {pmid42850154,
year = {2026},
author = {Dong, W and Yan, C and Korwin-Mihavics, B and Alexander, M},
title = {Context-dependent roles of ketone metabolism in intestinal inflammation.},
journal = {Trends in immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.it.2026.09.005},
pmid = {42850154},
issn = {1471-4981},
abstract = {Ketone metabolism is traditionally viewed as an alternative metabolic pathway providing energy during carbohydrate deprivation through the production and utilization of ketone bodies. Ketone bodies also function as signaling molecules regulating immune and metabolic processes. Accumulating evidence shows that ketone metabolism influences diverse diseases and immune responses, including inflammation, autoimmunity, and infection. Recently, ketone metabolism has been associated with inflammatory bowel disease (IBD), a chronic inflammatory disorder of the intestine, although reported effects are heterogeneous and context-dependent. In this review, we synthesize current evidence on ketone metabolism in IBD and intestinal inflammation, highlighting its roles in barrier integrity, immune regulation, and microbiota interactions. We also discuss potential mechanisms underlying divergent outcomes and outline key questions for future research.},
}

@article {pmid42850249,
year = {2026},
author = {Chen, S and Bahadur, A and Zhu, J and Liu, E and Gu, Y and Liang, H and Zhang, W and Li, S and Li, A and Wei, P and Liu, Q and Wu, T and Yang, P and Zou, Y and Han, M and Malard, LA},
title = {Hydrothermal regimes regulate microbiome patterns across vertical profile and their responses to alpine permafrost degradation.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42850249},
issn = {2041-1723},
support = {U23A2062//National Natural Science Foundation of China (National Science Foundation of China)/ ; U24A20586//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {*Permafrost/microbiology ; *Microbiota/genetics/physiology ; Bacteria/genetics/classification ; Soil Microbiology ; Tibet ; Metagenome ; Nitrogen/metabolism ; },
abstract = {Deciphering microbiomes across vertical profiles is critical for understanding biogeochemical cycling and potential biosafety hazards associated with permafrost degradation under climate warming. However, knowledge about microbiome patterns over key profile layers in response to degradation remains limited in the Qinghai-Tibet Plateau. Using metagenomic data obtained from 150 samples of six 15 m-depth alpine permafrost cores along a degradation gradient, we analyzed microbial community structure and functional potential across different main-layers, including the active, frozen fringe, and frozen layers. We found the recovered microbial and functional diversity decreased with profile depth, and declined only in the active layer as permafrost degraded. Interestingly, Pithoviridae, Caulimoviridae, and virulence factors related to adhesion, biofilm formation, and immune regulation were enriched in the frozen fringe layer, along with increasing relative abundance of Lavidaviridae under the degradation. Along the degradation gradient, carbohydrate-active enzymes diversity decreased in the active layer, while the ratio of nitrite reductase genes to nitrous oxide reductase genes increased in the active and the frozen fringe layers. Hydrothermal regimes emerged as the primary controls shaping microbiome distributions across the vertical profile and along the degradation gradient. Notably, hydrothermal and microbiome attributes jointly regulated carbon/nitrogen loss during the degradation. Taken together, these findings offer crucial insights into microbiome patterns, carbon/nitrogen loss and biosecurity concerning permafrost degradation under global warming.},
}

*Permafrost/microbiology
*Microbiota/genetics/physiology
Bacteria/genetics/classification
Soil Microbiology
Tibet
Metagenome
Nitrogen/metabolism

@article {pmid42850252,
year = {2026},
author = {Yang, J and Cai, X and He, F and Zhang, J and Zhang, Z and Yi, Z and Xie, C and Xu, B},
title = {Metabolic immune checkpoints (MICs) in cancer: from molecular mechanisms to challenges and opportunities in clinical translation.},
journal = {Signal transduction and targeted therapy},
volume = {11},
number = {1},
pages = {},
pmid = {42850252},
issn = {2059-3635},
support = {320.6750.2023-11-21//Ministry of Health of China | Wu Jieping Medical Foundation/ ; 82473253//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {Humans ; *Neoplasms/immunology/therapy/genetics/pathology/metabolism ; Metabolic Reprogramming ; *Tumor Microenvironment/immunology/genetics ; *Immune Checkpoint Proteins/immunology/genetics ; Animals ; },
abstract = {Metabolic reprogramming is a core feature of tumor cells in adapting to microenvironmental stress and acquiring malignant phenotypes. It not only supports rapid proliferation but also mediates immune escape by reshaping the immune microenvironment. In recent years, the "metabolism-immune axis", serving as a central hub for the crosstalk between metabolic regulation and immune suppression, has provided a new perspective for understanding tumor immune evasion. This review systematically discusses how metabolic pathways, including glucose, lipid, and amino acid metabolism, along with mitochondrial function and other related processes, shape the immunosuppressive tumor microenvironment by regulating immune cell function, immune checkpoint expression, and immune signaling networks, thereby promoting tumor immune escape. The concept of "metabolic immune checkpoints (MICs)" is innovatively proposed and classified into three categories based on their mechanisms of action: (1) MIC-I: metabolic modification-type immune checkpoints, exemplified by posttranslational modifications of immune checkpoint molecules such as PD-L1 lactylation, acetylation and glycosylation, etc.; (2) MIC-II: metabolic enzyme-dependent immune regulatory nodes, represented by enzymes such as indoleamine 2,3-dioxygenase 1 and others that directly influence immune cell function; and (3) MIC-III: microbial metabolite-coupled immune regulatory targets, including receptors for microbe-derived metabolites such as short-chain fatty acid receptors. By integrating molecular interaction networks of key targets such as lactate dehydrogenase A and ATP citrate lyase, this review explores synergistic therapeutic strategies that combine small-molecule inhibitors targeting MICs with immune checkpoint blockade. This highlights how metabolic intervention can restore immune cell function and reverse exhaustion. Current key challenges in clinical translation include limitations in metabolic dynamic monitoring technologies, lack of patient stratification biomarkers and insufficient specificity in microbiome regulation. Future directions will focus on personalized treatment guided by multiomics, integrating single-cell metabolic flux analysis, deep learning-driven target prediction, and synthetic microbiome engineering, driving tumor immunotherapy into the era of precision metabolic regulation. By integrating the fundamental mechanisms of MICs with translational medical research, this review not only provides a systematic paradigm but also establishes a foundation for the development of new-generation precision combination therapies.},
}

Humans
*Neoplasms/immunology/therapy/genetics/pathology/metabolism
Metabolic Reprogramming
*Tumor Microenvironment/immunology/genetics
*Immune Checkpoint Proteins/immunology/genetics
Animals

@article {pmid42850295,
year = {2026},
author = {Hastak, P and Andersen, CR and Crammond, P and Zhang, ZH and Phetsouphanh, C and van Bockel, D and Walsh, C and Judd, LM and Stinear, TP and Lohani, A and Shrestha, S and Louie, R and Bass, F and Delaney, A and Hammond, N and Venkatesh, B and Finfer, S and Tedla, N and Kelleher, AD and Sasson, SC},
title = {Expanded proinflammatory CD4 T cells expressing toll like receptor 4 in trauma associated acute lung injury.},
journal = {Communications biology},
volume = {9},
number = {1},
pages = {},
pmid = {42850295},
issn = {2399-3642},
mesh = {*Acute Lung Injury/immunology/etiology/metabolism ; *Toll-Like Receptor 4/metabolism/genetics ; *CD4-Positive T-Lymphocytes/metabolism/immunology ; Humans ; *Wounds and Injuries/complications/immunology ; COVID-19/immunology/complications ; Male ; Female ; Bronchoalveolar Lavage Fluid/microbiology ; SARS-CoV-2 ; Cytokines/blood ; Inflammation ; Microbiota ; },
abstract = {Acute lung injury (ALI) is characterised by hypoxia and inflammation that derives from diverse aetiologies. Delineating the molecular pathogeneses may identify treatable subgroups and inform clinical trials. Using a multi-omics approach, we analysed trauma-associated ALI (n = 9), COVID-19 ALI (n = 11), ICU controls (n = 13) using scRNA-seq, serum cytokine profiling, and bronchoalveolar lavage (BAL) microbiome analysis. We identified a population of activated CD4[+] T cells expressing Toll-like receptor 4 (TLR4) and downstream NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome complex, predominantly in trauma-associated ALI (23% of CD45[+] Cells) compared to COVID-19 ALI (14%) and ICU controls (15%). Serum IL-1RA and IL-6 were upregulated in trauma ALI, along with TLR4-binding ligand hyaluronan. TLR4 expression on CD4[+] T cells was confirmed by spectral cytometry. Lung microbiome analysis revealed distinct diversity in trauma-associated ALI compared to COVID-19 ALI. These findings highlight TLR4-mediated inflammation in trauma-associated ALI and suggest potential precision medicine approaches for ALI management.},
}

*Acute Lung Injury/immunology/etiology/metabolism
*Toll-Like Receptor 4/metabolism/genetics
*CD4-Positive T-Lymphocytes/metabolism/immunology
Humans
*Wounds and Injuries/complications/immunology
COVID-19/immunology/complications
Male
Female
Bronchoalveolar Lavage Fluid/microbiology
SARS-CoV-2
Cytokines/blood
Inflammation
Microbiota

@article {pmid42850677,
year = {2026},
author = {Burghard, V and Wende, S and Kahlenberg, G and Häuser, H and Kätzel, R and Kolb, S and Ulrich, A},
title = {The core taxa connectivity in leaf microbiomes in ash trees stands is modulated by host-related and environmental factors.},
journal = {Environmental microbiome},
volume = {21},
number = {1},
pages = {},
pmid = {42850677},
issn = {2524-6372},
support = {2219WK22I4//Fachagentur Nachwachsende Rohstoffe/ ; },
abstract = {BACKGROUND: Forests cover large areas of the terrestrial land surface and play a key role in climate regulation and biodiversity conservation. Tree-associated microbial communities are integral components of forest ecosystems and contribute to plant functioning, stress tolerance, and interactions with the environment. However, the factors shaping the phyllosphere microbiome of forest trees across large environmental gradients remain less explored. Here, we investigated the bacterial leaf microbiome of Fraxinus excelsior across different climatic regions in Germany to identify its core microbiome and determine the relative importance of environmental and host-related factors shaping the phyllosphere microbiome of forest trees across large environmental gradients assembly. Therefore, 30 ash trees were sampled at each of the 12 sites across Germany, at which we assessed their leaf microbiome, leaf physio-chemical properties and a set of site parameters.

RESULTS: In total, 755 genera were detected. Only three genera Hymenobacter, Massilia and Sphingomonas were predominant across all sites. Geographical position, precipitation, tree age and the leaf and soil chemistry parameters were significant factors that explained 22.1% of variance between microbiome structures between the different sites. Seven genera were identified as the core leave microbiome of F. excelsior. The core microbiome assessed for each sampling site was mostly more diverse and differed between sites. Complex co-occurrence networks separated by sites with the identified six hub bacterial taxa proved that they were essential for the local core microbiomes. However, the network complexity differed significantly between the sampling sites.

CONCLUSION: Our findings clearly indicate the existence of an ash core microbiome on leaves that occurred at all sites but was locally differently interconnected to further microbiome members. The network analyses revealed that less frequent genera play important roles as hub taxa. Furthermore, we were also able to prove the modulating role of biotic and abiotic factors on the ash phyllosphere microbiome. An optimized core microbiome may be considered crucial for improving tolerance against plant diseases, such as ash dieback, in future.},
}

@article {pmid42850678,
year = {2026},
author = {Liu, X and Jia, Q and Tang, Q and Ding, Y and Zhang, Z and Gu, M and Huang, W and Wang, N and Zhang, L and Zhu, J},
title = {Salinity-adapted and core microbiota along the soil salinity gradients encircling the Tarim Basin.},
journal = {Environmental microbiome},
volume = {21},
number = {1},
pages = {},
pmid = {42850678},
issn = {2524-6372},
support = {32360033//The National Natural Science Foundation of China/ ; 2024TSYCJU0007//Tianshan Talent Training Program of Xinjiang Uygur Autonomous Region/ ; },
abstract = {BACKGROUND: Soil salinization affects nearly one-tenth of global drylands and imposes strong environmental filters on microbial communities. The Tarim Basin in Xinjiang, China, is one of the world's largest inland basins and an extreme saline-arid ecosystem, yet a basin-scale understanding of its microbiota remains lacking. In this study, we collected 132 soil samples along a salinity gradient spanning more than 3,000 km encircling the Tarim Basin. By combining amplicon sequencing with measurements of soil physicochemical properties, we aimed to unravel the salinity-adapted microbiota and core microbial taxa characteristic of this extreme environment.

RESULTS: Our results showed that bacterial communities, rather than fungal communities, were strongly shaped by soil salinity. Extremely saline soils exhibited reduced bacterial diversity and were enriched in halophilic and halotolerant taxa, including Natronomonas, Salinimicrobium, Stenotrophomonas, Salinibacter, Halorussus, and Halomicrobium. In contrast, taxa such as Arthrobacter, Rubrobacter, Rubellimicrobium, and Fusarium declined with increasing salinity. Soil cation concentrations (Na[+], K[+], Ca[2+], Mg[2+]), major anions (Cl[-], SO4[2-]), and electrical conductivity all increased significantly along the salinity gradient. Despite this strong environmental filtering, we identified a set of potential core microbiota consistently present across all soils, dominated by Halomonas, Salinimicrobium, Natronomonas, Rubrobacter, and members of the Palleronia-Pseudomaribius group. Their persistent occurrence across the basin suggests that these taxa play key roles in sustaining ecosystem functions within the extreme saline-arid environments of the Tarim Basin.

CONCLUSIONS: Our basin-scale analysis reveals that soil salinity significantly contributes to microbial community assembly in the Tarim Basin, selecting for specialized halophilic and halotolerant taxa while reducing overall bacterial diversity. The discovery of core microbiota with known salt-adaptation mechanisms highlights the presence of a stable microbial backbone across heterogeneous saline landscapes. These findings provide new ecological insights into how extreme salinity shapes microbiome structure and identify candidate microbial groups potentially contributing to ecosystem stability and plant stress resilience in arid saline environments.},
}

@article {pmid42850765,
year = {2026},
author = {Clausen, DS and Willis, AD},
title = {Modeling complex measurement error in microbiome experiments to estimate relative abundances and detection effects.},
journal = {Biostatistics (Oxford, England)},
volume = {27},
number = {1},
pages = {},
doi = {10.1093/biostatistics/kxag036},
pmid = {42850765},
issn = {1468-4357},
support = {R35 GM133420/NH/NIH HHS/United States ; },
mesh = {*Microbiota ; *Models, Statistical ; Humans ; *Biostatistics/methods ; },
abstract = {Accurate estimates of microbial species abundances are needed to advance our understanding of the role that microbiomes play in human and environmental health. However, laboratory-constructed microbiomes demonstrate that intuitive estimators of microbial relative abundances are biased. To address this, we propose a method to estimate relative abundances, species detection effects, and/or cross-sample contamination in microbiome experiments. We show that certain experimental designs result in identifiable model parameters, and present consistent estimators and asymptotically valid inference procedures that are robust to misspecification of the working likelihood. Notably, our procedure can estimate relative abundances on the boundary of the simplex. We demonstrate the utility of the method for comparing experimental protocols, removing cross-sample contamination, and estimating species' detectability.},
}

*Microbiota
*Models, Statistical
Humans
*Biostatistics/methods

@article {pmid42850800,
year = {2026},
author = {Sharkey, T and Eisner, M and Common, J and Rajan, N},
title = {Towards Personalised Therapeutics for Epidermal Differentiation Disorders: Integrating Host Genetics, Immuno-Endotypes and the Skin Microbiome.},
journal = {The British journal of dermatology},
volume = {},
number = {},
pages = {},
doi = {10.1093/bjd/ljag447},
pmid = {42850800},
issn = {1365-2133},
abstract = {Epidermal differentiation disorders (EDDs), are a rare, heterogeneous grouping of monogenic disorders. EDDs, comprising the previously termed congenital ichthyosis, are characterised by epidermal barrier dysfunction, cutaneous inflammation, and associated morbidity. Immunomodulatory therapies, particularly repurposed biologics, are an emerging approach for management. However, clinical implementation has been impeded by a variable and unpredictable response rate, reflecting the genetic and immunological heterogeneity of EDD as well as raising questions over other contributory pathogenic mechanisms. Patient genotyping and immune profiling have revealed a shared immune polarisation across EDD subtypes, predominantly Th17, with some subtypes demonstrating a mixed immuno-endotype with contribution from Th2 or lL-36 mediated signalling. This improved immunological understanding has informed the repurposing of established biologics targeting IL-4R, IL-17, IL-12/23, alongside emerging interest in JAK inhibitors. Metagenomic microbiome profiling has revealed a homeostatic disruption across EDD subtypes with depleted commensal organisms, including Cutibacterium acnes and Malassezia species, and enrichment of pathobiont Staphylococcus and Corynebacterium species. Patients may be further stratified into dysbiotic groupings, with pathogenic variant and phenotypic severity influencing microbial composition. Ecological dysbiosis may contribute to immune polarisation through an "outside-inside-outside" model of host-microbe interactions, potentially underlying the variable response rates to repurposed biologics. In this review, we propose a "host genome and microbiome" framework for personalised EDD clinical management, integrating the EDD genotype and immuno-endotype ("Host genome"), and cutaneous microbiome as candidate simultaneous stratifiable elements. Genomic diagnosis, spurred by recent EDD reclassification, provides mechanistic context. Immuno-endotyping may enable a rational biologic selection but requires prospective validation. Microbiome profiling may guide emerging therapeutics or serve as a biomarker. We propose that a route to therapeutic restoration in EDD may require simultaneous targeting of the host-microbe axis. Delineation of the complex interplay between host genetics, immuno-endotypes, epidermal barrier dysfunction, and skin microbiome is a key priority for future research to bring this approach to the clinic.},
}

@article {pmid42850916,
year = {2026},
author = {Zhang, K and Zeng, Y and Wu, J and Liu, Y and Zhang, Y and Liao, Z and Li, Y and Zhong, J and Xie, Z and Chen, T},
title = {C. butyricum Combined With Resmetirom Provides Therapeutic Benefits in MASH Associated With Gut-Liver-Brain Axis Modulation.},
journal = {Liver international : official journal of the International Association for the Study of the Liver},
volume = {46},
number = {11},
pages = {e70905},
doi = {10.1111/liv.70905},
pmid = {42850916},
issn = {1478-3231},
mesh = {Animals ; Mice ; *Liver/metabolism/drug effects/pathology ; *Gastrointestinal Microbiome/drug effects ; Male ; Diet, High-Fat ; Disease Models, Animal ; *Clostridium butyricum ; Mice, Inbred C57BL ; Brain/metabolism/drug effects ; *Brain-Gut Axis/drug effects ; Intestinal Barrier Function ; *Probiotics ; },
abstract = {BACKGROUND AND AIMS: Resmetirom has emerged as a major advance in MASH pharmacotherapy as the first approved liver-targeted THR-β agonist; however, variable therapeutic efficacy and adverse responses may limit its clinical benefits. This study investigated whether C. butyricum could provide additional therapeutic benefits when combined with resmetirom and attenuate nausea/vomiting-like responses in association with changes across the gut-liver-brain axis.

METHODS: In this study, we established a high-fat diet-induced MASH mouse model and administered C. butyricum, resmetirom, or their combination. Comprehensive biochemical, histological, molecular, 16S rRNA sequencing-based microbiome profiling, and gut-brain axis-related analyses were performed to evaluate the effects of combination therapy on hepatic metabolism, inflammation, fibrosis, intestinal barrier integrity, gut microbiota remodelling, microbial metabolites, and resmetirom-associated adverse responses.

RESULTS: Combined treatment with C. butyricum and resmetirom produced additional therapeutic benefits compared with either monotherapy, markedly improving hepatic steatosis, lipid accumulation, insulin resistance, inflammation, oxidative stress, and fibrosis in MASH mice. At the molecular level, combination treatment was associated with increased hepatic THR-β expression and coordinated changes in AMPK-related lipid metabolism, NRF2/HO-1 antioxidant, and TLR4/MyD88/NF-κB inflammatory markers. Furthermore, combination therapy restored intestinal barrier integrity, alleviated MASH-associated gut microbial dysbiosis, increased beneficial bacterial taxa, and increased faecal butyrate levels. Notably, C. butyricum attenuated resmetirom-induced nausea/vomiting-like responses, accompanied by reduced colonic and cerebral 5-HT/SP signalling, decreased brain Htr3a and Tacr1 mRNA expression, and suppressed neuronal FOS activation. Faecal butyrate levels were inversely associated with hepatic lipid burden and brain 5-HT/SP levels.

CONCLUSIONS: C. butyricum combined with resmetirom provides additional therapeutic benefits and attenuates nausea/vomiting-like responses in MASH, accompanied by coordinated changes across the gut-liver-brain axis. This combination strategy provides a potential microbiota-based adjunctive approach for optimizing the therapeutic benefits of resmetirom in MASH.},
}

Animals
Mice
*Liver/metabolism/drug effects/pathology
*Gastrointestinal Microbiome/drug effects
Male
Diet, High-Fat
Disease Models, Animal
*Clostridium butyricum
Mice, Inbred C57BL
Brain/metabolism/drug effects
*Brain-Gut Axis/drug effects
Intestinal Barrier Function
*Probiotics

@article {pmid42850929,
year = {2026},
author = {Osuji, IE and Akanmu, AO and Babalola, OO},
title = {Amplicon Characterization of Fungal Diversity and Functional Prediction of Glycine max L. Rhizosphere Microbiome Under Different Organic Fertilization.},
journal = {MicrobiologyOpen},
volume = {15},
number = {5},
pages = {e70437},
doi = {10.1002/mbo3.70437},
pmid = {42850929},
issn = {2045-8827},
support = {CRP/ZAF22-93//International Centre for Genetic Engineering and Biotechnology/ ; },
mesh = {*Rhizosphere ; *Glycine max/microbiology ; *Fungi/classification/genetics/isolation & purification ; *Soil Microbiology ; Animals ; *Fertilizers/analysis ; Cattle ; DNA, Fungal/genetics ; Manure/microbiology ; Biodiversity ; *Mycobiome ; Phylogeny ; Soil/chemistry ; DNA, Ribosomal Spacer/genetics ; Sequence Analysis, DNA ; *Microbiota ; },
abstract = {The rhizosphere microbiome is extremely important for soil health and plant productivity, with fungi primarily acting as the drivers of soil ecosystem functions. This study explores the fungal diversity and predicted functional potential of the soybean (Glycine max L.) rhizosphere under different organic fertilization treatments, including cattle dung, poultry waste, untreated control, and bulk. Fungal communities were profiled using ITS rRNA gene amplicon sequencing on the Illumina NovaSeq. 6000 platform following DNA extraction from rhizosphere soil. Raw sequences were processed and analyzed using QIIME 2 version 2019.1. Significant differences in fungal richness were observed among treatments. Bulk soil and cattle dung-amended soils showed the highest richness (Chao1 = 1603.33 and 1456.64, respectively), whereas poultry waste-amended soil exhibited the lowest richness (Chao1 = 957.93) and the lowest evenness (Pielou's index = 0.560), and the untreated control showed intermediate richness (Chao1 = 1242.11). The dominant phyla include Ascomycota, Basidiomycota, and Zygomycota, with enrichment in organic matter degradation and plant symbiosis. Beta-diversity analysis showed the greatest compositional divergence between cattle dung and poultry waste (ANOSIM R = 0.74), none of the pairwise comparisons reached conventional statistical significance (p > 0.05), indicating ecologically relevant but statistically subtle shifts in community structure. LEfSe identified Hypocreales as a significant biomarker of cattle dung and Onygenales of poultry waste, consistent with FUNGuild predictions of enriched dung/wood-saprotrophic and keratinolytic functions, respectively. FUNGuild predictions showed increased saprotroph and symbiotroph diversity in organically amended soils. Organic fertilizers enrich beneficial fungi, enhancing ecosystem functions in sustainable soybean cultivation.},
}

*Rhizosphere
*Glycine max/microbiology
*Fungi/classification/genetics/isolation & purification
*Soil Microbiology
Animals
*Fertilizers/analysis
Cattle
DNA, Fungal/genetics
Manure/microbiology
Biodiversity
*Mycobiome
Phylogeny
Soil/chemistry
DNA, Ribosomal Spacer/genetics
Sequence Analysis, DNA
*Microbiota

@article {pmid42850991,
year = {2026},
author = {Guan, S and Qi, C and Liu, X and Li, B and Zhang, Y and Gao, H and Chen, Q and Cheng, L and Zhang, X},
title = {gutMDisorder v3.0: an updated database for dysbiosis of the gut and oral microbiota in phenotypes and interventions.},
journal = {Nucleic acids research},
volume = {},
number = {},
pages = {},
doi = {10.1093/nar/gkag985},
pmid = {42850991},
issn = {1362-4962},
support = {62531007//National Natural Science Foundation of China/ ; },
abstract = {Microbiota plays an essential role in host health, and dysbiosis of microbial communities has been widely associated with diverse phenotypes and intervention responses. With the rapid development of microbiome research, microbiome studies are no longer restricted to gut-derived samples, and the oral microbiota has emerged as another important microbial habitat closely connected with both local and systemic conditions. To meet the growing need for integrative resources across body sites, we updated gutMDisorder to version 3.0. In this version, the scope was expanded from gut microbiota to both gut and oral microbiota in humans and mice. We extensively reviewed previous publications and newly published studies, resulting in 13 402 manually curated literature-based associations under diverse comparison conditions. In addition, raw sequencing datasets from gut and oral samples were collected and reprocessed using standardized workflows, yielding 22 241 raw data-based associations, and corresponding host metadata were manually curated. To facilitate data exploration, gutMDisorder v3.0 provides sample-source-aware browsing, improved filtering options, interactive visualizations for raw data-based associations, and downloadable resources. The backend processing and frontend rendering logic were also optimized to improve page responsiveness and user experience. The database is freely available at https://bio-computing.hrbmu.edu.cn/gutMDisorder/.},
}

@article {pmid42851078,
year = {2026},
author = {Doumbia, B and Luo, S and Yang, S and Wang, C and Jia, Y and Kuprin, AV and Geng, A and Zhu, D and Sun, J and Ezenwanne, BC and Xie, R and Dar, MA},
title = {Harnessing bacterial symbionts of beetles for the valorization of lignin into value-added byproducts: Recent advances and future perspectives.},
journal = {Insect science},
volume = {},
number = {},
pages = {},
doi = {10.1111/1744-7917.70378},
pmid = {42851078},
issn = {1744-7917},
support = {32250410285//National Natural Science Foundation of China/ ; 2023YFC3403600//National Key R&D Program of China/ ; WGXZ2023020L//Foreign Expert Program, of Ministry of Science and Technology (MoST) of China/ ; 124012400285-7//Ministry of Science and Higher Education of the Russian Federation/ ; },
abstract = {Lignin is the most abundant renewable aromatic heteropolymer in nature and is highly recalcitrant due to its complex structure. The gut systems of beetles function as an evolutionarily optimized microreactor wherein mechanical pretreatment, physicochemical gradients, and selectively maintained microbial consortia act synergistically to transform, mineralize, and metabolize lignin as an energy source. Beetle-associated bacterial symbionts represent a promising yet underexploited resource for lignin valorization into value-added products. This review provides emerging evidence of lignin degradation by beetles in association with their gut symbionts and indicates the diversity of gut bacteria involved in lignin depolymerization. We further discuss the mechanisms by which beetles and their gut bacteria metabolize lignin, the lignin-transforming capacities of the bacterial symbionts and their potential application in the valorization of waste lignin into added-value byproducts. Finally, we assess the emerging research trends on the bioprospection of lignin-degrading bacteria from underexplored beetle species. Despite significant advantages, several key challenges remain unresolved, including difficulties in isolation and culturing of key gut bacteria in vitro, limited biochemical validation of candidate enzymes and the unresolved linking of specific genes or taxa to in situ lignin transformation. Future studies should integrate discovery-driven microbial ecology, multi-omics, predictive modeling and precision genome engineering to convert the complexity of beetle gut bacterial communities into a practical blueprint for scalable lignin valorization, and the biomanufacturing of high-value products from lignin-based waste.},
}

@article {pmid42851311,
year = {2026},
author = {Saloni, T and Chaithra, N and Umamaheshwari, S},
title = {Harnessing probiotics against candidiasis: a systematic review of experimental and mechanistic evidence.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1894309},
pmid = {42851311},
issn = {2235-2988},
mesh = {*Probiotics/therapeutic use/pharmacology ; Humans ; Biofilms/drug effects/growth & development ; *Candidiasis/therapy/microbiology ; Animals ; *Candida/drug effects/growth & development ; Antifungal Agents/pharmacology/therapeutic use ; Microbiota ; Virulence ; Lactobacillus ; },
abstract = {BACKGROUND: Candida species are among the most important opportunistic fungal pathogens responsible for superficial mucosal infections and life-threatening invasive candidiasis, particularly in immunocompromised individuals. The increasing prevalence of antifungal resistance, biofilm-associated tolerance, and the emergence of multidrug-resistant species such as Candida auris have highlighted the need for alternative or adjunctive therapeutic strategies. Probiotics have emerged as promising microbiome-based interventions owing to their ability to inhibit Candida growth, suppress virulence traits, restore microbial homeostasis, and modulate host immune responses.

METHODS: This systematic review comprehensively evaluated the experimental and mechanistic evidence regarding the anti-Candida activity of probiotics and probiotic-derived products. A systematic literature search was conducted in PubMed, Scopus, and Web of Science for studies published between 1 January 2015 and 5 January 2026 in accordance with PRISMA 2020 guidelines. Studies meeting the predefined eligibility criteria were included in the qualitative synthesis.

RESULTS: Eighteen studies met the predefined eligibility criteria. Most studies investigated Lactobacillus species, followed by Bifidobacterium, Saccharomyces, and probiotic-derived metabolites or postbiotics, using predominantly in vitro models with limited in vivo evidence. Across studies, probiotics consistently demonstrated anti-Candida activity through inhibition of fungal growth, adhesion, yeast-to-hyphal transition, biofilm formation, and virulence-associated gene expression. Additional mechanisms included the production of antimicrobial metabolites, competitive exclusion, immune modulation, enhancement of epithelial barrier function, and restoration of microbial homeostasis. Emerging evidence also supports the antifungal potential of postbiotics and activity against non-albicans Candida species and Candida auris, although available evidence remains limited. Considerable heterogeneity in probiotic strains, experimental models, methodologies, and outcome measures precluded quantitative meta-analysis.

CONCLUSIONS: Current evidence supports probiotics and postbiotics as promising microbiome-based strategies for reducing Candida pathogenicity; however, the available evidence remains predominantly preclinical. Well-designed clinical studies are required to establish strain-specific efficacy, optimal formulations, dosing strategies, safety, and therapeutic applicability before routine clinical implementation.

https://www.crd.york.ac.uk/prospero/view/CRD420261278363, identifier CRD420261278363.},
}

*Probiotics/therapeutic use/pharmacology
Humans
Biofilms/drug effects/growth & development
*Candidiasis/therapy/microbiology
Animals
*Candida/drug effects/growth & development
Antifungal Agents/pharmacology/therapeutic use
Microbiota
Virulence
Lactobacillus

@article {pmid42851327,
year = {2026},
author = {Langellotti, L and Schena, CA and Covino, M and Alfieri, S and Rosa, F},
title = {From microbiome signatures to precision oncology in colorectal cancer.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1926171},
pmid = {42851327},
issn = {2234-943X},
}

@article {pmid42851354,
year = {2026},
author = {Lewandowski, R},
title = {Transient short-chain fatty acid exposure and the temporal question of epithelial barrier immunity.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1930311},
pmid = {42851354},
issn = {1664-3224},
mesh = {*Fatty Acids, Volatile/metabolism/immunology ; Humans ; Animals ; Intestinal Barrier Function ; *Intestinal Mucosa/immunology/metabolism/microbiology ; *Immunity, Mucosal ; *Gastrointestinal Microbiome/immunology ; },
abstract = {Studies of microbiome-targeted interventions often use persistence of an administered organism or endpoint metabolite abundance as markers of biological consequence, but host barriers may be altered by microbial chemistry after the initiating exposure has disappeared. Short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate, provide a tractable model for this temporal problem because they connect microbial fermentation to epithelial metabolism, G protein-coupled receptor signaling, tight-junction regulation, immune tone, and chromatin-associated gene regulation. This Perspective argues that SCFA biology should be used to distinguish three outcomes at the host-microbial interface: exposure-dependent modulation, reversible epithelial reprogramming, and durable barrier imprint. Current evidence supports robust epithelial responses to SCFAs and makes persistence biologically plausible through chromatin-associated regulation and epithelial immune memory, but it does not yet establish whether brief adult SCFA exposure can alter later barrier behavior after withdrawal. Clarifying this conversion step will provide a common temporal framework for dietary, prebiotic, probiotic, postbiotic, and microbiota-transfer studies by distinguishing intervention delivery and engraftment from epithelial persistence.},
}

*Fatty Acids, Volatile/metabolism/immunology
Humans
Animals
Intestinal Barrier Function
*Intestinal Mucosa/immunology/metabolism/microbiology
*Immunity, Mucosal
*Gastrointestinal Microbiome/immunology

@article {pmid42851468,
year = {2026},
author = {Sun, W and Liu, H and Shao, A and Li, R and Ma, W and Zheng, M and Yan, S and Liu, S and Wu, M and Sun, D},
title = {Engineered bacteria and engineered probiotics for intestinal disease therapy: a bibliometric and knowledge mapping analysis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1970221},
pmid = {42851468},
issn = {1664-302X},
abstract = {OBJECTIVE: Engineered bacteria and engineered probiotics are emerging living therapeutic platforms for intestinal diseases, supported by advances in synthetic biology, genetic engineering, and microbiome technologies. This study aimed to characterize the research landscape, knowledge structure, research hotspots, and emerging trends of engineered bacteria and engineered probiotics for intestinal disease therapy using bibliometric and knowledge mapping approaches.

METHODS: Publications were retrieved from the Web of Science Core Collection and Scopus databases. After publication type restriction, thematic relevance screening, database merging, and duplicate removal, 499 publications published between 2015 and 2026 were included. The search was completed on July 3, 2026; therefore, records from 2026 represent a partial-year dataset. R, Python, VOSviewer, and CiteSpace were used to analyze annual publication trends, country/region, institution, author and journal distributions, keyword co-occurrence and bursts, co-cited references, and research frontiers.

RESULTS: Publication output increased markedly over the study period, reaching 109 publications in 2025; 64 records were retrieved for 2026 by the cutoff date. China had the highest publication output, whereas the United States had the highest total link strength, and Asia contributed 361 publications. Keyword analysis identified inflammatory bowel disease, gut microbiota, probiotics, engineered bacteria, engineered probiotics, synthetic biology, intestinal barrier, drug delivery, colorectal cancer, and immunotherapy as major research hotspots. Co-cited reference and timeline analyses indicated a shift in research attention from conventional probiotic-mediated anti-inflammatory effects, mucosal immune regulation, and intestinal barrier protection toward bacterial chassis selection, enhanced colonization, self-regulated genetic circuits, probiotic-based biomaterials, sustained-release delivery systems, and engineered bacteria-mediated antitumor therapy.

CONCLUSION: The bibliometric evidence indicates that recent research attention is increasingly focused on programmable living therapeutic strategies. Environmental sensing, local therapeutic delivery, sustained activity, and multifunctional design features are capabilities reported in the underlying literature and represented among the emerging themes identified in this analysis, rather than therapeutic performance directly established by the bibliometric data. Future research should further address biosafety, genetic stability, spatiotemporal controllability, intestinal colonization, delivery efficiency, and clinical translation.},
}

@article {pmid42851568,
year = {2026},
author = {Enwere, M and Bryan, NS and Onu, A and Neufeld, M and El-Hussein, MT and Yakub, I and Omale, C and Onyedike, O and Atim, T and Agbeyomi, O and Davies, E and Okeke, UE and Holmes, L},
title = {The microbiome-nitric oxide axis in cancer immunotherapy: a targeted qualitative systematic review of mechanistic and translational evidence.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1904698},
pmid = {42851568},
issn = {1664-3224},
mesh = {Humans ; *Neoplasms/therapy/immunology/metabolism/microbiology ; *Nitric Oxide/metabolism/immunology ; Animals ; *Gastrointestinal Microbiome/immunology ; *Immunotherapy/methods ; *Immune Checkpoint Inhibitors/therapeutic use ; Fecal Microbiota Transplantation ; Translational Research, Biomedical ; },
abstract = {BACKGROUND: Immune checkpoint inhibitors (ICIs) have transformed cancer treatment, but responses vary substantially among patients. Clinical studies have associated features of the gut microbiome with ICI outcomes, while experimental evidence suggests that microbial metabolites and nitric oxide (NO)-related pathways may influence antitumor immunity and tumor vascular biology. This qualitative systematic review evaluated the evidence supporting a proposed microbiome-NO-ICI framework.

METHODS: Five databases were searched for peer-reviewed studies published between January 2000 and August 2025. Fifty-four distinct primary studies met the eligibility criteria, comprising 21 clinical studies, 19 animal studies and 14 in vitro mechanistic studies. Evidence was synthesized narratively according to study type and thematic domain.

RESULTS: Several clinical cohorts associated enrichment of Akkermansia muciniphila, Faecalibacterium prausnitzii, Bifidobacterium species and other short-chain fatty acid-producing taxa with favorable ICI outcomes; however, the reported microbial signatures varied across cohorts and analytical platforms. Microbial-transfer experiments and early non-randomized fecal microbiota transplantation studies provide proof-of-concept evidence that microbiome composition can influence antitumor immune responses, although the clinical intervention evidence remains preliminary. Animal and cellular studies indicate that microbial metabolites, host nitric oxide synthase pathways and reactive nitrogen signaling can affect immune-cell function, vascular regulation and tumor hypoxia. Direct clinical evidence linking microbiota-mediated nitrate reduction or dietary nitrate supplementation to improved ICI outcomes is lacking. Human dietary nitrate studies conducted outside oncology demonstrate increased circulating nitrate and nitrite and measurable vascular effects but do not establish anticancer or ICI efficacy.

CONCLUSION: The microbiome-NO-ICI axis should be regarded as a testable integrative model linking microbial ecology, immune regulation and tumor vascular biology. Current evidence supports biological plausibility but is insufficient to establish NO- or microbiome-directed interventions as effective adjuncts to ICI therapy. Prospective mechanistic studies and biomarker-driven clinical trials are required before therapeutic translation.},
}

Humans
*Neoplasms/therapy/immunology/metabolism/microbiology
*Nitric Oxide/metabolism/immunology
Animals
*Gastrointestinal Microbiome/immunology
*Immunotherapy/methods
*Immune Checkpoint Inhibitors/therapeutic use
Fecal Microbiota Transplantation
Translational Research, Biomedical

@article {pmid42851677,
year = {2026},
author = {Plaza-Diaz, J and Voidarou, CC and Bezirtzoglou, E and Stavropoulou, E},
title = {Editorial: Rodent model organisms: therapeutic treatments and drugs interaction with the gut microbiome, volume II.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1962495},
doi = {10.3389/fmicb.2026.1962495},
pmid = {42851677},
issn = {1664-302X},
}

@article {pmid42851762,
year = {2026},
author = {Ye, G and Yu, X and Ismaiah, MJ and Ke, R and Zeng, Z and Wang, J and Lan, S and Yu, H and Liu, H and Xie, S and Leung, KS and Zhang, L and Lee, JC and Habimana, O},
title = {Structured succession of a cross-kingdom microbiome drives degradation and detoxification of oolong tea waste.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1871476},
pmid = {42851762},
issn = {2813-4338},
abstract = {The spontaneous aerobic degradation of oolong tea waste offers a promising but underexplored route for sustainable waste valorization. In this study, we used whole-genome metagenomic sequencing to examine microbial succession and functional gene dynamics over a 35-day degradation period. Our results uncovered a three-phase ecological progression: an initial mesophilic phase (Days 0-7) dominated by Pseudomonadota, which reached 93.4% relative abundance and specialized in simple substrate utilization; a thermotolerant transition (Days 8-15, 30-33°C) characterized by increased abundance of glycoside hydrolases (GH5, GH13); and a maturation phase (Days 16-35) marked by the emergence of lignocellulose-degrading taxa such as Cellulomonas and Microbacterium, accompanied by a 78% reduction in antibiotic resistance genes. Profiling of carbohydrate-active enzymes revealed a sequential shift from pectinases (GH28) to hemicellulases (GH43), while mobile genetic elements declined substantially during the maturation phase. These results indicate that tea waste degradation follows structured microbial succession patterns influenced by abiotic factors and suggests a potential self-purification capacity through the attenuation of antibiotic resistance genes. This study establishes a foundation for optimizing composting processes and designing targeted bioaugmentation strategies to enhance tea waste valorization.},
}

@article {pmid42851936,
year = {2026},
author = {Tao, YT and Wang, L and Zheng, HW and Yu, LS},
title = {Characterization of the Middle Ear Microbiome in Meniere's Disease by 16S rRNA Gene Sequencing Compared to Chronic Suppurative Otitis Media.},
journal = {World journal of otorhinolaryngology - head and neck surgery},
volume = {},
number = {},
pages = {},
pmid = {42851936},
issn = {2589-1081},
abstract = {OBJECTIVE: To investigate the middle ear microbiome in Meniere's disease (MD) patients.

METHODS: Middle ear smears from 10 MD patients (ME group) and 10 chronic suppurative otitis patients (OE group) were collected during surgery and processed via 16S rRNA gene sequencing.

RESULTS: The ME group demonstrated significant differences in alpha diversity (Shannon/Simpson index, p < 0.01) and beta diversity (ANOSIM/PERMANOVA, the Bray-Curtis distance matrix, R = 0.144, p < 0.05; R [2] = 0.107, p < 0.05) compared to OE group, and the PERMDISP showed lower heterogeneity in the ME group (p < 0.01). Ruminococcus, Ochrobactrum, and Halomonas at the genus level were enriched in the ME group, and the difference reached marginal significance. The linear discriminant analysis effect size analysis (LefSe) identified Bacteroides, Halomonas, and Prevotella as significantly enriched in ME, while Neisseriales was downregulated (|LDA| > 2, p < 0.05). BugBase phenotype analysis revealed that facultatively anaerobic bacteria and bacteria containing mobile genetic elements were significantly reduced in the ME group compared to the OE group (p < 0.05). The proportion of anaerobes was higher in the ME group (p = 0.123). Nine KEGG metabolic pathways were enriched in the ME group, though the difference was not significant after correction.

CONCLUSION: These findings suggested that inner ear inflammation resulted from middle ear dysbiosis may contribute to MD pathogenesis, offering novel perspectives for MD etiology and therapies.},
}

@article {pmid42852269,
year = {2026},
author = {Shao, T and Liu, JM},
title = {Intermittent fasting-associated microbiome remodeling and functional modulation by Lacticaseibacillus rhamnosus HN001.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1947132},
pmid = {42852269},
issn = {2296-861X},
abstract = {OBJECTIVE: The gut microbiome is a critical regulator of host metabolism, yet how intermittent fasting (IF) remodels the gut ecosystem independent of dietary composition remains unclear. This study aimed to isolate the effect of feeding rhythm on the gut microbiome and identify specific microbial taxa mediating IF-induced metabolic changes.

METHODS: We employed a family-based 'shared meal' model that strictly standardized dietary composition across all participants. Five healthy adults (3 males, 2 females) from a single family participated in a pilot, hypothesis-generating 4-week 16:8 IF intervention with longitudinal fecal sampling for 16S rRNA sequencing and untargeted metabolomics. To functionally test a candidate Lacticaseibacillus-associated mechanism, C57BL/6 J mice were subjected to a 1-week 16:8 IF protocol with or without daily oral supplementation of Lacticaseibacillus rhamnosus HN001. Plasma beta-hydroxybutyrate (betaOHB) and peptide YY (PYY) were measured by ELISA.

RESULTS: IF was associated with body weight loss in humans (2.1 +/- 0.4 kg, 95% CI: 1.3 to 2.9 kg, p < 0.05) without a significant reduction in caloric intake. In the primary paired genus-level DESeq2 analysis accounting for participant identity, no genus remained significant after false-discovery-rate correction, although Lacticaseibacillus showed a directional decrease after IF, consistent in direction with the original exploratory unpaired analysis. Predicted microbial functional and fecal metabolomic changes were consistent with altered microbial energy metabolism. In mice, IF significantly elevated plasma betaOHB (p = 0.0046) and reduced body weight, whereas HN001 supplementation reversed these IF-associated effects under the conditions tested.

CONCLUSION: In this pilot, hypothesis-generating human cohort, IF was associated with coordinated microbiome and metabolomic remodeling, including a directional Lacticaseibacillus signal that motivated subsequent functional testing. In mice, L. rhamnosus HN001 supplementation reversed IF-associated weight loss and ketosis, supporting the functional plausibility of a Lacticaseibacillus-associated mechanism. The human observations require confirmation in larger, independent cohorts with time-matched non-fasting controls and species-resolved microbiome measurements.},
}

@article {pmid42852270,
year = {2026},
author = {Brown, J and Norby-Adams, L and Ghanem, N and Lewis, A and Goldenberg, JZ and Weir, T and Vita, AA},
title = {Correction: Clinical evidence for microbial-derived polyphenol metabolites in health and disease: a scoping review.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1993867},
doi = {10.3389/fnut.2026.1993867},
pmid = {42852270},
issn = {2296-861X},
abstract = {[This corrects the article DOI: 10.3389/fnut.2026.1859472.].},
}

@article {pmid42852271,
year = {2026},
author = {Jahan-Mihan, A and Salamat, S and Nodarse, R and Shangraw, R and Labyak, C and Snyder, J and Berg, K and Leftwich, J},
title = {Maternal obesity, diet, and the gut microbiome: implications for offspring cardiometabolic programming.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1909112},
pmid = {42852271},
issn = {2296-861X},
abstract = {Maternal obesity is associated with adverse pregnancy and long-term offspring outcomes. The maternal gut microbiome may contribute through altered microbial functions, barrier integrity, immune signaling, and metabolite production. Pregnancy itself entails microbial and metabolic remodeling, but obesity and obesogenic dietary patterns may modify these adaptations. Evidence from human cohorts and animal models links maternal obesity with context-dependent differences in microbial composition and function, reduced butyrate-producing capacity, altered bile acid and short-chain fatty acid profiles, and heightened inflammation. These changes may influence placental function and early-life microbial assembly through delivery-related exposures, breastfeeding, human milk oligosaccharides, and shared environmental and dietary factors. Maternal diets high in saturated fat and refined carbohydrate tend to be associated with less favorable microbial and cardiometabolic profiles, whereas fiber-rich, plant-diverse dietary patterns may support short-chain fatty acid production and metabolic resilience. However, causal inference is limited by heterogeneity, confounding, and inconsistent findings. Probiotic, prebiotic, and synbiotic interventions show potential, but clinical results-particularly for gestational diabetes prevention-remain mixed. This narrative review integrates evidence on diet-microbiome interactions in maternal obesity, microbial metabolites and immune pathways, early-life colonization, and implications for offspring obesity and cardiometabolic risk. Overall, the maternal microbiome is a plausible but incompletely validated target; well-powered longitudinal studies and pregnancy-specific randomized trials are needed before precision microbiome strategies can be incorporated into routine care.},
}

@article {pmid42852388,
year = {2026},
author = {Laue, HE and Fleisch, AF and Calafat, AM and Lanphear, BP and Cecil, KM and Yolton, K and Buckley, JP and Karagas, MR and Madan, JC and Willis, AD and Braun, JM},
title = {Associations of Urinary Triclosan Concentrations Across Gestation and Childhood with the Adolescent Gut Microbiome.},
journal = {Environmental health perspectives},
volume = {134},
number = {6},
pages = {672-687},
pmid = {42852388},
issn = {1552-9924},
mesh = {*Triclosan/urine ; Humans ; Female ; Pregnancy ; Adolescent ; Child ; *Gastrointestinal Microbiome/drug effects ; Child, Preschool ; Male ; Infant ; *Anti-Infective Agents, Local/urine ; Ohio ; Prospective Studies ; Feces/microbiology ; },
abstract = {Research on the influence of repeated exposure to antimicrobial chemicals, such as triclosan, on the microbiome is lacking. The goal of this study was to elucidate the associations of time-varying urinary triclosan concentrations with the adolescent gut microbiome. We used data from a prospective cohort based in Cincinnati, OH (enrolled 2003-2006, n = 146), to assess the time-varying associations of urinary triclosan concentrations with adolescent (age ∼ 12 years) gut microbiome diversity and composition. Individuals ≥ 18-years-old were recruited during the second trimester of pregnancy, and urinary triclosan concentrations were measured in pregnant women up to 2 times in pregnancy and up to 7 times in the child from ages 1 through 12 years. At age ∼ 12 years, fecal microbiome diversity and composition was characterized with metagenomic sequencing. We estimated differences in the relative abundance of prevalent (≥50%) bacterial species and gene pathways using linear regression and generalized estimating equations to assess windows of heightened susceptibility adjusted for sociodemographic characteristics. Additionally, we examined sex-specific associations by including an interaction term. The adolescent median Shannon diversity was 3.5 (IQR: 3.3, 3.5). Higher gestational triclosan concentrations with lower gut microbiome diversity [β = -0.13 per 10-fold increase (95%CI: -0.24, -0.02)]. Triclosan concentrations were also positively associated with higher abundance of antibiotic resistance genes and differential abundance of some bacterial species, with the strongest associations observed in early life and at age 12 years. We also found differences depending on sex, with more significant associations observed among males. Our findings provide insight into windows of triclosan exposure that are relevant to gut microbiome composition and the impacts of antimicrobial agents.},
}

*Triclosan/urine
Humans
Female
Pregnancy
Adolescent
Child
*Gastrointestinal Microbiome/drug effects
Child, Preschool
Male
Infant
*Anti-Infective Agents, Local/urine
Ohio
Prospective Studies
Feces/microbiology

@article {pmid42852494,
year = {2026},
author = {Li, Y and Chen, J and Lin, L and Jian, Z and Liu, L and Wang, M and Wei, J and Chen, X and Yang, M and Li, T and Xiang, L and Liao, B and Jin, X and Wang, K},
title = {Gut microbiota-derived tryptophan metabolite attenuates calcium oxalate nephropathy by suppressing renal tubular cell apoptosis through the AhR-SOCS3-STAT1 axis.},
journal = {The Journal of pathology},
volume = {},
number = {},
pages = {},
doi = {10.1002/path.70135},
pmid = {42852494},
issn = {1096-9896},
support = {82570894//National Natural Science Foundation of China/ ; 82270799//National Natural Science Foundation of China/ ; 2023SCUH0054//Sichuan University/ ; CZ2026001//Project of National Outstanding Medical Doctors/ ; 2023HXFH014//Clinical Research Incubation Project of West China Hospital of Sichuan University/ ; },
abstract = {Calcium oxalate (CaOx) nephropathy is a highly prevalent urological disease worldwide. Gut microbiota dysbiosis and host metabolic dysregulation are recognized as pivotal drivers in disease pathogenesis, yet the underlying mechanisms remain incompletely understood. In this study, by integrating metagenomics and metabolomics, we identified dysregulation of tryptophan metabolites in patients with CaOx nephrolithiasis, with microbiota-derived indole-3-propionic acid (IPA) as the most discriminatory differential metabolite. Oral IPA supplementation markedly reduced renal CaOx crystal deposition and tubular injury in a CaOx nephropathy murine model. Mechanistically, IPA activated the aryl hydrocarbon receptor (AhR), which translocated to the nucleus and transcriptionally upregulated suppressor of cytokine signaling 3 (SOCS3)-a negative regulator of signal transducer and activator of transcription 1 (STAT1)-thereby suppressing STAT1 phosphorylation, alleviating oxalate-induced tubular cell injury and apoptosis, and inhibiting CaOx crystal deposition. Our findings identify tryptophan metabolite alteration as a critical metabolic signature of CaOx nephropathy and demonstrate that microbiota-derived IPA attenuates oxalate-induced renal tubular cell injury and apoptosis via the AhR-SOCS3-STAT1 axis. © 2026 The Pathological Society of Great Britain and Ireland.},
}

@article {pmid42852572,
year = {2026},
author = {Post, A and Yadlapalli, A and Webb, T and Zhang, A and Yelampalli, A and Challa, K and Indugu, N and Pitta, DW},
title = {Core microbial populations drive longitudinal development of the hindgut bacterial microbiota in Jersey calve.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0187826},
doi = {10.1128/spectrum.01878-26},
pmid = {42852572},
issn = {2165-0497},
abstract = {The early-life gut microbiome represents a critical window during which microbial succession may exert lasting effects on host metabolism and productivity. While gut microbiome-host phenotypic associations have been extensively studied in Holstein calves, such relationships are rarely reported in alternative breeds, including Jersey calves. We hypothesized that Jersey calves would exhibit age-dependent community shifts characterized by core microbial populations and breed-associated bacterial networks that may contribute to metabolic phenotype. Fecal samples were collected from dams post-calving, and Jersey calves (n = 12) were sampled longitudinally at 24-48 h and weekly through 12 weeks. Bacterial communities were profiled using the V1-V2 region of the 16S rRNA gene. The number of observed ASVs and Shannon diversity increased with age (P < 0.001), and Beta diversity revealed age-dependent structuring (weighted R[2] =0.12, P = 0.023; unweighted R[2] =0.37, P = 0.001), with calf communities gradually converging toward dams. Taxonomic analyses revealed a conserved core microbiome comprising 34 taxa accounting for over 90% of total community abundance. Neonatal samples were dominated by facultative anaerobes, including Escherichia and Streptococcus, with early colonization by Blautia and Collinsella. Calves then exhibited transient enrichment of milk-glycan-associated taxa, including Lactobacillus and Bacteroides. Weeks 3-7 stages saw preeminence of acetogens (Blautia, Dorea, Collinsella), followed by later enrichment of adult-associated fiber-degrading taxa. Collectively, these findings demonstrate a consistent age-dependent pattern of hindgut microbiome maturation among Jersey calves. The taxonomic patterns provide a foundation for investigating potential links between early-life microbial ecology and breed-specific metabolic phenotypes.IMPORTANCEThe neonatal period represents a critical window for microbial community assembly and interaction with the host. While microbial succession in Holstein calves has been studied extensively, little is known about microbiome assembly in Jersey calves. Herein, we performed longitudinal profiling of the hindgut microbiome of Jersey calves from birth through twelve weeks of age. Microbial communities underwent a structured succession broadly resembling patterns reported previously in Holsteins, with network analyses revealing microbial assemblages that shift with diet throughout the pre- and postweaning periods. Jersey calves also exhibited a notably elevated abundance of several acetate-associated taxa during early life. These findings provide the first detailed characterization of hindgut microbiome assembly in Jersey calves and identify microbial community structures potentially linked to breed-specific metabolic phenotypes. Such information is critical for designing microbiome-targeted strategies to improve calf growth, health, and feed efficiency, and for influencing milk components.},
}

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

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

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

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

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

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

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

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

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