@article {pmid42562299,
year = {2026},
author = {Park, J and Miller, AS and Pore, G and Banginwar, M and Lee, S and Li, J and Jung, E and Wagner, A and Smith, J and Malone, C and Schoultz, I and Salihovic, S and Reardon, C and Gareau, MG},
title = {Oral exposure to perfluorooctanoic acid disrupts the microbiota-gut-liver axis and enhances the severity of chemically induced colitis in mice.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {409},
number = {},
pages = {128915},
doi = {10.1016/j.envpol.2026.128915},
pmid = {42562299},
issn = {1873-6424},
abstract = {Inflammatory bowel diseases (IBD) affect millions of patients worldwide and impair quality of life. Although genetic and environmental factors are known to disrupt the gastrointestinal (GI) epithelial barrier and increase susceptibility to IBD, the precise contribution of specific environmental exposures remains unclear. Per- and polyfluoroalkyl substances (PFAS), or "forever chemicals," are widely used in consumer products and contaminate food and water sources, resulting in chronic oral exposure worldwide. Perfluorooctanoic acid (PFOA), a common PFAS, has been epidemiologically associated with the development of IBD, particularly in older adults. Here, we assessed the effects of oral PFOA exposure on the GI tract, liver, and susceptibility to colitis. C57BL/6 mice were exposed to PFOA (0.1 or 1.0 mg/kg) beginning at weaning (postnatal day [P]21) for a time course of 4 or 8 weeks. GI physiology/pathology (Ussing chambers; histology), expression of pro-inflammatory cytokines (qPCR), microbiota composition (16S sequencing), bile acid production (qPCR; LC/MS), and liver pathology (histology) were assessed. Colitis susceptibility was evaluated in genetically predisposed (IL10 knockout) mice, and in chemically induced (dextran sodium sulfate [DSS]) mouse models following PFOA exposure (8 weeks at 1.0 mg/kg). Oral PFOA exposure increased intestinal permeability, mildly increased cytokine expression, altered gut microbiota composition, disrupted liver and serum bile acids, and caused hepatic hypertrophy in the high dose and longer exposure. Although PFOA did not increase disease susceptibility in genetically predisposed IL10 KO mice, it significantly worsened DSS-induced colitis, but only in male mice. Together, these findings demonstrate that early-life PFOA exposure disrupts the gut-liver axis and may contribute to colitis development in a sex-dependent manner.},
}

@article {pmid42606386,
year = {2026},
author = {Ghisleni, G and Dow, E and Iovino, T and Colman-Vega, PJ and Dicesare, A and Guanella, E and Bacchi, YM and Colombo, A and Leccese, M and Marzucchi, M and Gorla, ME and Caracciolo, A and Sala, A and Makarycheva, P and Rubrica, SC and Ferrier, A and Armanni, A and Fumagalli, S and Wood-Charlson, E and Bruno, A},
title = {Fantastic microbes and where to find them: evaluating learning-by-doing outcomes in a crowdfunded metagenomics workshop.},
journal = {FEMS microbiology letters},
volume = {373},
number = {},
pages = {},
doi = {10.1093/femsle/fnag093},
pmid = {42606386},
issn = {1574-6968},
support = {//University of Milano-Bicocca/ ; //Society for Experimental Biology/ ; //DOE/ ; DE-AC02-05CH11231//U.S. Department of Energy Office of Science/ ; DE-AC02-06CH11357//U.S. Department of Energy Office of Science/ ; DE-AC05-00OR22725//U.S. Department of Energy Office of Science/ ; DE-SC0012704//U.S. Department of Energy Office of Science/ ; },
mesh = {*Metagenomics/education ; Humans ; Computational Biology/education ; Learning ; Citizen Science ; Students/psychology ; },
abstract = {Metagenomics offers a powerful framework for authentic, interdisciplinary learning, yet it remains underrepresented in undergraduate education due to technical and infrastructural barriers. We hypothesized that a research-based, learning-by-doing metagenomics workshop supported by accessible bioinformatics tools could enhance students' perceived skills, self-efficacy, and conceptual understanding of metagenomic analysis. To test this hypothesis, we designed and evaluated a hybrid hands-on workshop in which undergraduate and postgraduate students analyzed real environmental shotgun metagenomic datasets generated from soil samples collected during a citizen science initiative. Using the graphical workflow platform KBase, participants completed an end-to-end metagenomic analysis, from quality control and assembly to genome reconstruction, taxonomic classification, functional annotation, and scientific presentation of results. Educational outcomes were assessed through validated retrospective pre-post questionnaires, self-efficacy scales, and an open-ended conceptual understanding task. Participants showed significant increases in perceived metagenomic skills and confidence in performing metagenomic analyses, while gains in perceived learning showed a positive trend. Conceptual understanding improved across educational levels, particularly among participants with limited prior experience. Together, these findings demonstrate that authentic, data-driven metagenomics activities can effectively lower barriers to computational biology and foster meaningful learning through hands-on research experiences.},
}

*Metagenomics/education
Humans
Computational Biology/education
Learning
Citizen Science
Students/psychology

@article {pmid42632989,
year = {2025},
author = {Nadezhda, I and Maria, P and Andrey, S and Alina, A and Sergey, G and Marina, S and Irina, D},
title = {Effects of Tumor-associated E. coli Metabolites on Migration of Colorectal Cancer Cells.},
journal = {Archives of Razi Institute},
volume = {80},
number = {6},
pages = {1621-1632},
pmid = {42632989},
issn = {2008-9872},
mesh = {Humans ; *Cell Movement/drug effects ; *Colorectal Neoplasms/microbiology/physiopathology ; *Escherichia coli/metabolism/physiology ; Cell Line, Tumor ; *Gastrointestinal Microbiome ; },
abstract = {INTRODUCTION: Colorectal tumors have a close connection with the gut microbiome. A correlation between rearrangement in microbiome composition and disease progression has already been shown. However, the mechanisms underlying interactions between microorganisms and cancer cells, as well as the immediate effects of tumor-associated microbiomes on cancer cells, remain unclear.

MATERIALS & METHODS: In this work, we investigated the effects of metabolites produced by tumor-associated Escherichia coli strains on the migration of human colorectal cancer cell lines (HCT116, SW480 and HT29).

RESULTS: We identified differences in some biochemical enzyme activity of E. coli strains and in the spectrum of synthesized organic acids between tumor-associated strains and the probiotic E. coli M-17 strains. Most strains associated with colorectal cancer were unable to utilize sucrose. Specifically, tumor-associated E. coli produced more fumaric, malic and maleic acids, whereas the E. coli M-17 produced more short-chain fatty acids such as propionic, 2-oxobutyric, and α-ketoglutaric acids (AKGs). Upon exposure to metabolites from tumor-associated E. coli strains, HCT116 and SW480 cells showed an increased migration activity, whereas HT29 cells showed decreased migration activity in both 2D and 3D culture models. Immunocytochemistry assay revealed a decrease in E-cadherin in HCT116 and SW480 cells and focal adhesion kinase (FAK)- in HT29, which explains the different effects of E. coli metabolites on migratory capacity of colorectal cancer cells.

CONCLUSION: Therefore, these results suggest that the effect of tumor-associated E. coli strains on cancer cells migration depends on their innate type of migration and enhances FAK-dependent single-cell migration accompanied by the loss of E-cadherin in cancer cells with initially low FAK expression. In contrast, this effect was not observed in cancer cells exhibiting a collective migration phenotype.},
}

Humans
*Cell Movement/drug effects
*Colorectal Neoplasms/microbiology/physiopathology
*Escherichia coli/metabolism/physiology
Cell Line, Tumor
*Gastrointestinal Microbiome

@article {pmid42633152,
year = {2026},
author = {Anto, L and Gao, L and Lee, J and Garcia, C and Otoko, O and Hickey, E and Mishra, N and Kim, S and Noh, SG and Kim, MB and Kang, H and Mihori, S and Ranjitkar, S and Kohan, AB and Park, YK and Provatas, AA and Mathias, C and Kwon, OS and Clark, RB and Lee, JY and Nichols, FC and Blesso, CN},
title = {Fiber-Dependent Microbiome Glycine Lipids Ameliorate Steatotic Liver Disease in Mice via Mitochondrial Enhancement.},
journal = {Gastro hep advances},
volume = {5},
number = {10},
pages = {101064},
pmid = {42633152},
issn = {2772-5723},
abstract = {BACKGROUND AND AIMS: Oral and gut Bacteroidota species produce bioactive glycine lipids (GL), including the core Lipid 342, serine-glycine Lipid 654 (L654), and complex Lipid 1256 (L1256) classes. These microbiome-derived molecules are emerging modulators of host metabolism, but their dietary regulation, systemic presence, and therapeutic potential in metabolic dysfunction-associated steatotic liver disease (MASLD) remain unclear.

METHODS: Microbiome-derived GLs were quantified in murine systemic and portal blood, intestinal lymph, and in mouse and human liver using targeted mass spectrometry. Their biological effects were assessed in mouse and cell culture models of diet-induced liver disease following treatment with L654- and L1256-enriched lipid extracts.

RESULTS: L654 and L1256 species were detected in mouse serum, portal plasma, intestinal lymph, and liver, as well as in human liver tissue. A Western-type high-fat diet lowered fecal and hepatic microbiome GLs, whereas fermentable fiber supplementation restored fecal levels (∼7-fold increase), with hepatic GL content showing an inverse association with liver triglycerides. In a 22-week diet-induced MASLD model, administration of L654- or L1256-enriched lipids for 8 weeks significantly reduced hepatic steatosis and histopathological progression. Treatments enhanced mitochondrial DNA content and metabolic function in liver and HepG2 cells. L1256 increased hepatic triggering receptor expressed on myeloid cells 2 expression, associated with lipid sensing and MASLD protection, while L654 modulated splenic cluster of differentiation 4[+] (CD4[+]) effector memory T cells.

CONCLUSION: Microbiome-derived GLs are diet-sensitive molecules that protect against MASLD via mitochondrial enhancement, revealing a novel nutritional-microbial axis for liver disease intervention.},
}

@article {pmid42633169,
year = {2026},
author = {Che, Y and Kou, W and Xu, L and Liu, Z and Kuang, J and Cheng, X and Zhao, Q and Feng, H and Qiu, W},
title = {Hashimoto's thyroiditis influences tumor cell states and intratumoral microbiota in papillary thyroid carcinoma.},
journal = {iScience},
volume = {29},
number = {9},
pages = {117167},
pmid = {42633169},
issn = {2589-0042},
abstract = {Hashimoto's thyroiditis is associated with reduced lymph node metastasis in papillary thyroid carcinoma, suggesting that the autoimmune microenvironment may influence tumor progression. We utilized single-cell RNA sequencing and intratumoral 16S ribosomal RNA gene sequencing to investigate malignant epithelial cell states and microbial features in PTC with and without Hashimoto's thyroiditis. Tumors with Hashimoto's thyroiditis exhibited malignant epithelial populations enriched for innate immune signaling programs and showed increased intratumoral microbial diversity with reduced abundance of several Gram-negative bacteria, particularly Pseudomonas. Within the Hashimoto's thyroiditis subgroup, lymph node metastasis was associated with increased Gram-negative bacterial abundance. Functional experiments further showed that Pseudomonas-derived lipopolysaccharide enhanced thyroid cancer cell migration in vitro and in vivo. These findings suggest that Hashimoto's thyroiditis reshapes both epithelial transcriptional states and the intratumoral microbial environment, potentially contributing to a less aggressive tumor phenotype.},
}

@article {pmid42633292,
year = {2026},
author = {Cho, EH and Hong, SW and Seo, EH and Kim, SH},
title = {Preventive effect of ulinastatin on postoperative cognitive dysfunction through modulation of the gut microbiome: evidence from short-chain fatty acids.},
journal = {Brain, behavior, & immunity - health},
volume = {56},
number = {},
pages = {101327},
pmid = {42633292},
issn = {2666-3546},
abstract = {BACKGROUND: Increasing evidence indicates that gut dysbiosis and gut-brain axis dysfunction contribute to postoperative cognitive dysfunction (POCD) following general anaesthesia. Although ulinastatin, a urinary trypsin inhibitor, has been reported to exert anti-inflammatory and neuroprotective effects, its role in the gut microbiome and microbiome-related metabolites in POCD remains unclear.

METHODS: A total of 30 18-month-old male Sprague-Dawley rats were randomly allocated to the Ulinastatin group or the Control group. Ulinastatin (50,000 U/mL) or normal saline (1 mL) was intraperitoneally administered before general anaesthesia, which was maintained with isoflurane 1.5 vol% for 2 h. Cognitive function was assessed using the Y-maze test. Lactobacillus viable counts, short-chain fatty acid (SCFA) levels and nuclear factor erythroid 2-related factor 2 (Nrf2) expression were evaluated by microbiological analysis, enzyme-linked immunosorbent assay (ELISA) and immunohistochemical staining, respectively.

RESULTS: Y-maze performance did not differ between groups before general anaesthesia. However, a significant decline after anaesthesia was observed only in the Control group (p < 0.001). Lactobacillus viable counts showed a similar pattern, with a significant reduction in the Control group but preservation in the Ulinastatin group (p < 0.001). The Ulinastatin group had significantly higher SCFA levels in the gut, blood, and brain than did the Control group (all p < 0.001). Nrf2 expression in both the gut and brain was also significantly higher in the Ulinastatin group (both p = 0.0001).

CONCLUSION: Preoperative administration of ulinastatin prevented cognitive decline after general anaesthesia. The protective effect of ulinastatin was associated with control of gut dysbiosis.},
}

@article {pmid42633329,
year = {2026},
author = {Joglekar, KG},
title = {Gut Microbiome Composition and Response to Immune Checkpoint Inhibitors in Melanoma: A Systematic Review.},
journal = {Cureus},
volume = {18},
number = {7},
pages = {e113248},
pmid = {42633329},
issn = {2168-8184},
abstract = {Immune checkpoint inhibitors have significantly improved clinical outcomes in patients with advanced melanoma; however, treatment response remains highly variable, and reliable predictive biomarkers are lacking. Emerging evidence suggests that the gut microbiome influences host immune regulation and may contribute to this variability. This systematic review evaluated the association between gut microbiome composition and response to immune checkpoint inhibitors in melanoma, with a focus on potential biological mechanisms, predictive biomarkers, and therapeutic implications. A systematic search of the PubMed database was conducted to identify studies published between 2015 and 2025. Eligible studies included original observational investigations and secondary analyses of melanoma microbiome datasets that examined associations between gut microbiome characteristics and response to immune checkpoint inhibitors. Interventional fecal microbiota transplantation studies, dietary or probiotic intervention trials, exposure-only studies (including antibiotic, proton pump inhibitor, or Helicobacter pylori exposure without direct microbiome sequencing), non-English-language publications, and preprints were excluded. The search identified 381 records. After removal of one duplicate, 380 records were screened, and 25 studies met the inclusion criteria. Across the included studies, gut microbiome composition, microbial diversity, and metabolic function were associated with immunotherapy outcomes. Increased abundance of short-chain fatty acid-producing taxa, including Faecalibacterium prausnitzii and Akkermansia muciniphila, was frequently associated with improved treatment response, whereas dysbiosis and enrichment of pathogenic bacterial and fungal taxa were linked to reduced therapeutic efficacy and poorer survival outcomes. Microbiome-derived metabolites appear to modulate antitumor immunity through effects on dendritic cell function, antigen presentation, and T-cell activation, while longitudinal alterations in microbiome composition may serve as early indicators of treatment response. Overall, findings were heterogeneous because of differences in patient populations, sequencing methodologies, outcome definitions, and analytical approaches. Risk-of-bias assessment using the Risk Of Bias In Non-randomized Studies of Interventions (ROBINS-I) tool rated 17 of the 25 included studies as having a moderate risk of bias and eight as having a serious risk of bias, primarily because of residual confounding and small single-center study designs. The gut microbiome represents a promising predictive biomarker and potential therapeutic target for melanoma immunotherapy; however, substantial methodological heterogeneity limits current clinical applicability. Large, standardized, prospective, multicenter, multi-omic studies are needed before microbiome-guided treatment strategies can be incorporated into routine clinical practice.},
}

@article {pmid42633404,
year = {2026},
author = {Veličković, M and Thairu, MW and Gao, Y and Clendinen, CS and Munoz, N and Lalli, PM and Nicora, CD and Stratton, KG and Monroe, ME and Moore, RJ and Currie, CR and Wu, R and Burnum-Johnson, KE},
title = {Deciphering taxon-specific metabolic shifts during pathogenic fungal infection in leaf-cutter ant fungal gardens.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag213},
pmid = {42633404},
issn = {2730-6151},
abstract = {Leaf-cutter ant fungal gardens are a living library of bioeconomy solutions, where the mutualist fungus Leucoagaricus gongylophorus drives lignocellulose degradation and conversion into valuable bioproducts. However, these gardens are vulnerable to infection by the specialized pathogen Escovopsis weberi, which disrupts garden stability. Despite their ecological importance, the metabolic mechanisms underlying fungal-fungal competition and community-level responses to infection remain poorly understood. To address this gap, we experimentally infected six fungal garden consortia with E. weberi, establishing an infection gradient within each consortium, which we then systematically analyzed using a multi-omics approach. Metabolomic profiling revealed infection-induced alterations in metabolite abundance, while metaproteomic analysis identified fungal-specific shifts in protein levels across a spatiotemporal scale. The integration of multi-omics datasets across all fungal garden consortia provided a comprehensive view of the underlying pathways, revealing that the pathogenic fungus exploits nutrient supplies derived from lignocellulose degradation by native fungi. Reconstruction of active pathways enabled us to trace nutrient flow and map taxon-specific metabolic shifts in response to infection. Specifically, a distinct switch from lysine synthesis by native fungi to lysine catabolism orchestrated by pathogenic fungi. These findings offer a system-level perspective of the molecular alterations driving competitive interactions between native and pathogenic species within the fungal garden consortium. This study not only highlights the power of multi-omics approaches in unraveling the complexity of microbial consortia across ecological scales but also provides an integrated road map to efficiently harness microbiome data for deeper insights into microbial interactions and community responses to perturbations.},
}

@article {pmid42633482,
year = {2026},
author = {Maksum, IP and Herlina, T and Siahaan, TJ and Rukayadi, Y and Mamuaja, MN},
title = {Comprehensive review of biosynthesis, plant function, metabolism and new therapeutic bioactivities of flavonoids.},
journal = {ADMET & DMPK},
volume = {14},
number = {},
pages = {3404},
pmid = {42633482},
issn = {1848-7718},
abstract = {BACKGROUND AND PURPOSE: Flavonoids are polyphenolic secondary metabolites synthesized via the phenylpropanoid pathway, serving as a vital biological "immune system" for plants by providing UV-B protection, antimicrobial defence, and pollinator attraction.

EXPERIMENTAL APPROACH: This review examines how these plant-based survival tools translate into potent therapeutic agents for human health through a literature review using Google Scholar, Scopus and ScienceDirect, with keywords alone or in combination with other terms.

KEY RESULTS: Current research demonstrates that flavonoids possess diverse bioactivities, including antioxidant, anti-inflammatory neuroprotective properties, with significant efficacy in mitigating cardiovascular disease, diabetes and cancer. Despite these benefits, the clinical application of flavonoids is currently hindered by limited bioavailability, which prevents consistent therapeutic concentrations in the human body, and a lack of standardized regulatory dosing.

CONCLUSION: This paper identifies three critical pillars for future innovation in the development of structural analogs to (a) improve intestinal absorption, (b) explore drug synergy for enhancing conventional medical treatments and (c) evaluate the microbiome interactions to facilitate personalized nutrition. By integrating plant biochemistry with clinical pharmacology, flavonoids can be transitioned from general dietary components into precise, evidence-based therapies.},
}

@article {pmid42633730,
year = {2026},
author = {Del Águila, Á and Beales, JT and Fisher, JL and Lozier, NR and Dama, K and Valentine, YA and Tapp, ZM and Sardesai, SD and Williams, NO and Gatti-Mays, ME and Stover, DG and Sudheendra, PK and Wesolowski, R and Duff, AF and Ni, A and Bailey, MT and Pyter, LM},
title = {The gut microbiome in chemotherapy-induced fatigue: Exploring clinical associations and modulation via fecal microbiota transplantation in female mice.},
journal = {International immunopharmacology},
volume = {188},
number = {},
pages = {117318},
doi = {10.1016/j.intimp.2026.117318},
pmid = {42633730},
issn = {1878-1705},
abstract = {BACKGROUND: Fatigue is a common and debilitating side effect of chemotherapy, negatively affecting treatment adherence and survival. Chemotherapy alters gut microbiome composition, and accumulating evidence suggests that gut microbes contribute to chemotherapy-induced fatigue. Because the gut microbiome is modifiable through targeted interventions, such as fecal microbiota transplantation (FMT), microbiome modulation has emerged as a potential strategy to mitigate treatment-related toxicities. To understand the impact of FMT interventions across the gut-brain axis, studying rodent chemotherapy models that simultaneously capture behavioral side effects and gastrointestinal pathology is warranted.

METHODS: Patient-reported fatigue and diarrhea were assessed in breast cancer patients before and during chemotherapy (n = 67). In parallel, mice were treated with chemotherapy (5-fluorouracil [5-FU] or paclitaxel) with or without FMT derived from pre-chemotherapy fecal material. Outcomes included fatigue (in-cage locomotion and voluntary wheel running), gut microbiome composition (16S rRNA sequencing), intestinal and brain gene/protein expression (RT-qPCR, single-cell RNA sequencing, and/or multiplex electrochemiluminescence assay), and circulating inflammatory markers.

RESULTS: In patients, increased fatigue during chemotherapy was associated with worse diarrhea and shifts in gut microbiome composition. In mice receiving 5-FU, FMT produced mild-to-moderate benefits, most notably preserving body mass, with milder and transient benefits for fatigue. FMT partially normalized gut bacterial taxa, reduced 5-FU-induced colonic Il1b expression, and prevented chemotherapy-related increases in brain Aqp4. FMT did not attenuate other inflammatory effects induced by 5-FU or paclitaxel.

CONCLUSION: These findings are consistent with a role for gut microbes in chemotherapy-induced fatigue and suggest that FMT is not universally beneficial, with effects varying by chemotherapy drug.},
}

@article {pmid42633795,
year = {2026},
author = {Roy, N and Hong, E and Kwak, YS and Chung, EH and Lee, JH and Kim, JS and Choi, K},
title = {Functional Characterization of Wheat Seed Endophytic Bacteria Reveals Plant Growth-Promoting Traits and Potential Biocontrol Activity Against Fusarium Pathogens.},
journal = {The plant pathology journal},
volume = {},
number = {},
pages = {},
doi = {10.5423/PPJ.OA.06.2026.0083},
pmid = {42633795},
issn = {1598-2254},
abstract = {Seed-associated microbiota are emerging as key determinants of early plant establishment and resilience, yet their functional potential in wheat remains underexplored. Here, we isolated and functionally characterized culturable bacterial endophytes from seeds of Triticum aestivum cvs. Saekeumkang, Baeggang, and Ariheuk to assess plant growth promotion and pathogen suppression. Sixteen bacterial strains, belonging to Pseudomonadota, Actinomycetota, and Bacillota, were identified using 16S rRNA gene sequencing. Functional assays revealed the high prevalence of plant growth-promoting traits, with all isolates producing indole-3-acetic acid and 56.25% exhibiting phosphate-solubilizing activity, whereas siderophore production was restricted to Pseudomonas poae WSSR12. Despite this apparent functional redundancy, in planta assays demonstrated strong strain-specific effects on seedling biomass. Neobacillus cucumis WSSR17 consistently induced the highest increase in fresh weight. In parallel, dual culture assays against multiple Fusarium pathogens revealed that only one isolate, Calidifontibacillus erzurumensis WSSR11, showed consistent antifungal activity across all tested Fusarium strains. Notably, isolates combining multiple functional traits did not always correspond to the strongest growth promotion, underscoring the importance of host-microbe compatibility and trait expression in planta. Collectively, these findings reveal a functionally diverse seed endophytic community with complementary roles in plant growth and disease suppression. We propose that rational selection and combination of complementary strains, particularly N. cucumis WSSR17 (growth promotion), C. erzurumensis WSSR11 (biocontrol), and P. poae WSSR12 (multifunctional nutrient mobilization) could enable the development of targeted, multi-strain bioinoculant strategies for wheat. This study advances our understanding of seed microbiome functionality and provides a foundation for microbiome-informed crop improvement.},
}

@article {pmid42633880,
year = {2026},
author = {Vergés-Roger, C and Andrés-Blasco, I and Salgado-Borges, J and Cerdá-Ibáñez, M and Zanón-Moreno, V and Mora-Sáez, S},
title = {Nutrition and microbiota in ocular surface and dry eye disease.},
journal = {Archivos de la Sociedad Espanola de Oftalmologia},
volume = {},
number = {},
pages = {502652},
doi = {10.1016/j.oftale.2026.502652},
pmid = {42633880},
issn = {2173-5794},
abstract = {Nutrition plays a crucial role in the prevention and management of dry eye disease (DED. Polyunsaturated fatty acids ω-3 and ω-6, known for their anti-inflammatory properties, improve ocular surface health. Similarly, antioxidants found in diets like the Mediterranean diet stabilize the tear film and reduce oxidative stress (OXs); however, food additives can negatively impact both general health and DED. The gut microbiome and the gut-eye axis play a critical role, as gut dysbiosis amplifies systemic inflammation, disrupts immune balance, and diminishes the production of protective metabolites such as short-chain fatty acids. The ocular microbiome further supports homeostasis and immunity by safeguarding against external pathogens. Factors such as diet, aging, and antibiotic use negatively impact microbial diversity. Probiotics, prebiotics, and fecal microbiota transplantation are emerging microbiota-targeted strategies for dry eye disease. However, current evidence remains limited and is largely based on preclinical and preliminary clinical studies, highlighting the need for further controlled investigations to better define their therapeutic role and clinical applicability.},
}

@article {pmid42634081,
year = {2026},
author = {Paul, P and Dajani, I and Kaul, R and Chaari, A},
title = {The Effect of Microbiome-Modulating Therapeutics on Anthropometric and Hemodynamic Biomarkers in Metabolic Syndrome: A Systematic Review, Meta-Analysis, and Meta-Regression of Clinical Trials.},
journal = {Obesity reviews : an official journal of the International Association for the Study of Obesity},
volume = {},
number = {},
pages = {e70215},
doi = {10.1111/obr.70215},
pmid = {42634081},
issn = {1467-789X},
abstract = {BACKGROUND: Metabolic syndrome (MetS) is a prevalent cardiometabolic disorder characterized by central obesity, insulin resistance, dyslipidemia, and hypertension. Microbiome-targeted therapies with probiotics, prebiotics, and synbiotics may improve outcomes by modulating metabolism, inflammation, and blood pressure.

METHODS: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) in adults with MetS. Searches through April 2023 identified eligible RCTs, yielding 19 studies and 21 independent comparisons. Pooled mean differences (MDs) with 95% confidence intervals (CIs) were calculated using a random effects model. Subgroup analyses and meta-regressions examined moderators and heterogeneity.

RESULTS: A total of 19 studies comprising 21 trial comparisons were included. Microbiome-modulating interventions were associated with modest reductions in waist circumference and body weight (BW), indicating improvements in central adiposity. In contrast, effects on body mass index (BMI) were limited, and no meaningful changes were observed in systolic or diastolic blood pressure (DBP). Subgroup and meta-regression analyses suggested that higher microbial dose, longer intervention duration, and greater baseline adiposity were associated with more pronounced anthropometric responses. Moderate heterogeneity was observed across several outcomes.

CONCLUSIONS: Microbiome-targeted therapies reduced waist circumference (WC) and BW in MetS but had no effect on BMI, systolic blood pressure (SBP), or DBP. These safe interventions may complement lifestyle strategies. Larger, standardized trials with microbiome profiling are needed to refine therapeutic use. These findings support a potential adjunctive role for microbiome-targeted therapies in MetS, particularly for central adiposity, though standardized, longer duration trials with microbiome profiling are needed to clarify clinical utility.},
}

@article {pmid42634111,
year = {2026},
author = {Sturm, L and Maasoumy, B and Thimme, R and Bettinger, D},
title = {Letter: The Microbiome-Mediated Impact of Proton Pump Inhibitors on Spontaneous Bacterial Peritonitis-Authors' Reply.},
journal = {Alimentary pharmacology & therapeutics},
volume = {},
number = {},
pages = {},
doi = {10.1111/apt.70939},
pmid = {42634111},
issn = {1365-2036},
}

@article {pmid42634241,
year = {2026},
author = {Wang, R and Li, W and Xie, B},
title = {Vaginal Microbiota and Pelvic Floor Dysfunction: Mechanistic Insights and Therapeutic Implications.},
journal = {Medical science monitor : international medical journal of experimental and clinical research},
volume = {32},
number = {},
pages = {e953348},
doi = {10.12659/MSM.953348},
pmid = {42634241},
issn = {1643-3750},
mesh = {Humans ; Female ; *Microbiota/physiology ; *Vagina/microbiology ; *Pelvic Floor/physiopathology/microbiology ; Probiotics/therapeutic use ; *Pelvic Floor Disorders/microbiology/therapy/physiopathology ; Pelvic Organ Prolapse/microbiology ; Urinary Incontinence/microbiology ; Dysbiosis ; },
abstract = {Pelvic floor dysfunction (PFD) encompasses a spectrum of prevalent chronic conditions, including urinary incontinence, pelvic organ prolapse, and female sexual dysfunction, arising from the impaired integrity of the pelvic floor muscles, ligaments, and connective tissues. The vaginal microbiota (VM) plays a critical role in maintaining mucosal barrier function and homeostasis within the lower reproductive tract. The integrity of the levator hiatus and urogenital hiatus maintains the closure of the pelvic floor and the stability of the VM. Emerging evidence indicates a bidirectional relationship between PFD and the VM, mediated through anatomical, hormonal-metabolic, and immunological pathways. Recent studies indicate that some of these interventions are associated with shifts in VM composition. Emerging evidence suggests that microbiota-targeted approaches, including probiotics and VM transplantation, demonstrate potential in restoring microbial balance and modulating local inflammatory responses in the lower genital tract. Although large-scale clinical trials are lacking, several studies have demonstrated that microbiota-targeted interventions, including probiotics, VM transplantation, and estriol-containing pessaries, can improve vaginal dysbiosis and modulate local inflammatory responses, with potential implications for PFD management. This review synthesizes current evidence on the interaction among the VM, pelvic floor supports, and PFD development, with a focus on underlying mechanisms and clinical associations, and discusses the potential role of microbiome-based diagnostics and therapeutics in PFD management. This article aims to review the roles and therapeutic implications of the VM and VM dysbiosis in PFD.},
}

Humans
Female
*Microbiota/physiology
*Vagina/microbiology
*Pelvic Floor/physiopathology/microbiology
Probiotics/therapeutic use
*Pelvic Floor Disorders/microbiology/therapy/physiopathology
Pelvic Organ Prolapse/microbiology
Urinary Incontinence/microbiology
Dysbiosis

@article {pmid42634284,
year = {2026},
author = {Kuryłowicz, A and Czupryniak, L},
title = {Responders Vs. Non-Responders or How to Predict the Response to GLP-1 or GLP-1/GIP Receptor Agonist Therapy.},
journal = {Diabetes, obesity & metabolism},
volume = {},
number = {},
pages = {},
doi = {10.1111/dom.71226},
pmid = {42634284},
issn = {1463-1326},
abstract = {BACKGROUND: Glucagon-like peptide-1 receptor agonists (GLP-1RAs) and dual GLP-1/GIP receptor agonists have transformed the pharmacological management of type 2 diabetes (T2D) and obesity, yet substantial interindividual variability in treatment response remains a defining clinical challenge.

METHODS: Narrative review. PubMed was searched to 25 May 2026 (English language, human studies, 2005-2026) for biological, genetic, metabolic, hormonal, behavioural and psychosocial predictors of differential response. Evidence is organised across three clinically distinct contexts: glycaemic control in T2D; weight loss in people with overweight or obesity without T2D; and dual metabolic benefit in those with both conditions.

RESULTS: Response heterogeneity is most pronounced in obesity without diabetes, where non-response-commonly defined as less than 5% total body weight loss-affects approximately 10% of participants in controlled trials, with real-world cohorts suggesting a higher frequency in routine practice; glycaemic non-response in T2D is less common but clinically significant. Across all three contexts, early on-treatment response is the most readily actionable predictor currently available. A recent large genome-wide association study reported associations between variation in the GLP1R drug-target gene and both weight-loss efficacy and gastrointestinal tolerability, and between agent-specific GIPR variants and nausea and vomiting with tirzepatide; these self-reported, single-cohort and as-yet unreplicated findings remain hypothesis-generating rather than a basis for individual-level genotyping. Metabolic, microbiome and neuroendocrine predictors are at a comparably preliminary stage.

CONCLUSION: No single baseline characteristic reliably predicts response. Structured assessment of early on-treatment response is currently the most defensible basis for individualising therapy; genetic, metabolic and microbiome markers require prospective replication before clinical application.},
}

@article {pmid42634286,
year = {2026},
author = {Qiu, W and Tang, X and Shen, Q and Yuan, J},
title = {Plant-Microbiome Interactions for Rhizosphere Health: A Three-Step Framework for Crop Resilience.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70837},
pmid = {42634286},
issn = {1365-3040},
support = {42322708//National Natural Science Foundation of China/ ; },
abstract = {The rhizosphere is a key ecological niche where plants interact with microorganisms, and its health directly affects plant growth, development, and disease resistance. Existing theories have laid an important foundation for understanding plant-microbe interactions. Among them, the biological market theory interprets the mutualistic symbiosis between plants and microorganisms from the perspective of nutrient exchange, offering valuable insights into resource flow and interaction mechanisms within the rhizosphere. On this basis, this study further proposes the conceptual model of 'biological corporation' to integrate interaction mechanisms covering three dimensions: plant-dominated regulation, microbial functional differentiation, and signal network coordination. Within this theoretical framework, plants modulate the screening and colonisation of microbial communities via a dual-genome regulatory system. Microbial populations reshape community structure and drive functional differentiation through resource competition, cross-feeding symbiosis, and defensive strategies. Interkingdom and intrakingdom signal cascades further link the physiological and metabolic processes of plants and microorganisms, thereby facilitating the steady-state maintenance of the rhizosphere microecosystem. Based on this hierarchical symbiotic mechanism, we propose a three-step regulatory scheme for rhizosphere health restoration, and provide practical strategies including crop germplasm improvement, synthetic microbial consortium construction, and cross-kingdom signal engineering to mitigate combined biotic and abiotic stresses in farmland.},
}

@article {pmid42634304,
year = {2026},
author = {Kandula, UR and Bilal, HS},
title = {Comprehensive Overview of Gut Microbiota Alterations in Obesity and Related Chronic Diseases: A Narrative Review.},
journal = {Reviews on recent clinical trials},
volume = {},
number = {},
pages = {},
doi = {10.2174/0115748871477574260803112949},
pmid = {42634304},
issn = {1876-1038},
abstract = {BACKGROUND: Metabolic disorders, including obesity, type 2 diabetes (T2D), metabolic syndrome, Non-Alcoholic Fatty Liver Disease (NAFLD), and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), represent major global health challenges. Increasing evidence suggests that gut microbiota dysbiosis contributes to the development and progression of these disorders through mechanisms involving inflammation, insulin resistance, altered energy metabolism, and impaired intestinal barrier function. This review aimed to evaluate recent clinical evidence regarding the effects of gut microbiota-targeted interventions on microbial composition and metabolic outcomes in individuals with metabolic disorders.

METHODS: A narrative review of clinical studies published between 2021 and 2026 was conducted using the PubMed electronic database. Studies investigating dietary interventions, probiotics, prebiotics, synbiotics, Fecal Microbiota Transplantation (FMT), pharmacological therapies, bariatric surgery, and herbal formulations were included. Data regarding microbiota alterations and metabolic outcomes were extracted and qualitatively synthesized.

RESULTS: A total of 36 clinical studies were included. Across the reviewed literature, microbiotatargeted interventions consistently promoted beneficial alterations in gut microbial composition, including increased abundance of Bifidobacterium, Akkermansia, Roseburia, Eubacterium, and other short-chain fatty acid (SCFA)-producing bacteria. These microbial changes were associated with improvements in insulin sensitivity, glycemic control, body weight, liver fat accumulation, lipid metabolism, and cardiometabolic risk markers. Dietary interventions and probiotic-based therapies demonstrated the most consistent benefits, whereas FMT studies produced variable clinical outcomes despite substantial microbiome remodeling.

DISCUSSION: The findings indicate that restoration of microbial homeostasis may represent a key mechanism underlying improvements in metabolic health. Increased abundance of beneficial microbial taxa and enhanced SCFA production were consistently linked to favorable metabolic outcomes, supporting the concept that the gut microbiome plays an active role in metabolic regulation. However, variability among studies suggests that intervention efficacy may depend on baseline microbial composition, host characteristics, and treatment duration.

CONCLUSION: Current evidence supports the therapeutic potential of gut microbiota modulation in obesity, T2D, NAFLD, MASLD, and related metabolic disorders. Further large-scale, long-term clinical studies are required to establish causal relationships, identify predictive microbial biomarkers, and facilitate the development of personalized microbiome-based therapies.},
}

@article {pmid42634387,
year = {2026},
author = {Alomeir, N and Chinchilli, E and Terio, C and Zhang, L and Beck, LA and Assery, N and Mao, X and Wolf, JR and Xiao, J and Wu, T},
title = {Salivary OMICS factors associated with atopic dermatitis in early infancy.},
journal = {Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology},
volume = {37},
number = {8},
pages = {e70468},
doi = {10.1111/pai.70468},
pmid = {42634387},
issn = {1399-3038},
support = {R01DE031025/NH/NIH HHS/United States ; U01AI152011/NH/NIH HHS/United States ; },
mesh = {Humans ; *Dermatitis, Atopic/epidemiology/diagnosis/microbiology/metabolism ; Female ; Male ; *Saliva/microbiology/metabolism ; Biomarkers/metabolism/analysis ; Infant ; Prospective Studies ; Microbiota ; Cytokines/metabolism ; Infant, Newborn ; Child, Preschool ; },
abstract = {BACKGROUND: Atopic dermatitis (AD) often develops in early childhood and may persist into adulthood. Noninvasive measures to identify infants at risk for AD are limited. We investigated whether oral biomarkers and oral microbiota are associated with AD onset within the first 2 years of life.

METHODS: In this prospective cohort study, we followed 119 infants residing in Upstate New York from birth to 24 months (2018-2023). AD diagnoses were obtained from electronic health records. Saliva samples were collected at seven time points (1, 2, 4, 6, 12, 18, and 24 months) and analyzed for 5 hormones and 23 cytokines using multiplex immunoassays. Salivary microbiome profiles were characterized via metagenomic sequencing.

RESULTS: Nearly half (48%) of infants developed AD by age 2, with most cases manifesting by 12 months (42%) and peak incidence occurring between months 2-4. Infants who developed AD by 1 year demonstrated significantly elevated estradiol (p = .007) and progesterone (p = .046) at 1 month, and a significantly lower salivary cortisol level (p = .019) at 6 months. Additionally, these infants exhibited higher sIL-1ra (p = .024) and IL-9 (p = .034) in saliva at 4 months and lower IL-1α (p = .038) at 6 months. Salivary microbiome beta diversity differed significantly at 2 months between infants with and without AD by 1 year (p = .038), with lower differential abundances of Bifidobacterium breve and Veillonella atypica in early infancy prior to AD onset.

CONCLUSION: Early-life salivary biomarkers, including hormonal, cytokine, and microbiome signatures, may serve as noninvasive indicators of infants at risk for early AD onset.},
}

Humans
*Dermatitis, Atopic/epidemiology/diagnosis/microbiology/metabolism
Female
Male
*Saliva/microbiology/metabolism
Biomarkers/metabolism/analysis
Infant
Prospective Studies
Microbiota
Cytokines/metabolism
Infant, Newborn
Child, Preschool

@article {pmid42634456,
year = {2026},
author = {, },
title = {[China Wumeng Mountain Lung Cancer: Evidence Chain, Clinical and Molecular Characteristics of Regional Lung Cancer Related to Coal Pollution in the Yunnan-Guizhou Plateau].},
journal = {Zhongguo fei ai za zhi = Chinese journal of lung cancer},
volume = {29},
number = {6},
pages = {395-411},
pmid = {42634456},
issn = {1999-6187},
mesh = {Humans ; *Lung Neoplasms/epidemiology/genetics/etiology/chemically induced/pathology ; *Coal/adverse effects/analysis ; China/epidemiology ; Polycyclic Aromatic Hydrocarbons/analysis ; },
abstract = {BACKGROUND: Long-term household coal burning, differences in coal sources and mineral compositions, energy structure, and socioeconomic conditions jointly constitute the regional exposure basis for lung cancer. This study conducts a multi-sectional, multi-dimensional and multi-omics investigation on the correlation between coal-burning pollution in the "Wumeng Mountain region" and "China Wumeng Mountain lung cancer", and explores the concept boundaries, evidence chain, carcinogenic components, clinical and molecular characteristics, as well as the precise prevention and control pathways of "China Wumeng Mountain lung cancer", with the aim of providing evidences and references for the primary, secondary, tertiary and quaternary prevention of lung cancer in high-incidence areas of "China Wumeng Mountain lung cancer", as well as the screening and molecular typing management of high-risk populations.

METHODS: Based on the relatively complete evidence chain established in our previous research, covering household coal smoke exposure, coal source differences, polycyclic aromatic hydrocarbons (PAHs), stove intervention, lung cancer and tumor multi-omics characteristics, a narrative review method was applied for literature search and evidence integration. The search databases included PubMed, Web of Science, Embase, China National Knowledge Infrastructure (CNKI) and Wanfang Database, with the time range from the establishment of each database to May 2026; search terms included: Xuanwei, Fuyuan, Wumeng Mountains, household coal combustion, smoky coal, lung cancer, PAHs, methylated PAHs, stove improvement, never-smoking women, germline susceptibility, microbiome and multi-omics. The evidence integration adopted the "exposure-pollutant component-biological effect-clinical molecular characteristics-prevention transformation" evidence chain.

RESULTS: (1) PAHs/methylated PAHs, particulate matter 2.5 (PM2.5)/black carbon, inorganic minerals/metals, carbonyl compounds and mixed exposure are the main carcinogenic components of coal-burning pollution-related lung cancer; (2) It is prevalent among non-smoking women, with a high proportion of adenocarcinoma, low age of onset, easy early metastasis, multiple lung lesions and family aggregation are the clinical characteristics of coal-burning pollution-related lung cancer in the Wumeng Mountain region; (3) The total epidermal growth factor receptor (EGFR) mutation is relatively high, but the proportions of classic EGFR 19 exon deletion and L858R mutation are relatively low, while EGFR-G719X, S768I mutations, Kirsten rat sarcoma viral oncogene homolog (KRAS) G12C mutations, and anaplastic lymphoma kinase (ALK) and c-ROS proto-oncogene 1, receptor tyrosine kinase (ROS1) gene fusion mutations are significantly higher than those in non-Wumeng Mountain lung cancer; (4) Germline mutation genes ARHGEF5, MYO18B and MUC16 are potential genetic susceptibility genes for coal-burning pollution-related lung cancer in the Wumeng Mountain region, and they interact with telomere length maintenance genes POT1, TERT and TERF2, and may have a close relationship with the existence of lung cancer family aggregation in this region; (5) Indoor coal-burning pollution leads to changes in the microbial community of sputum, and long-term chronic infection of the respiratory tract jointly affect abnormal pathways related to the immune microenvironment and pollutant metabolism, increasing the risk of lung cancer.

CONCLUSIONS: China Wumeng Mountain lung cancer is a type of lung cancer related to indoor and outdoor coal-burning pollution, with a predilection for never-smoking women, high proportion of adenocarcinoma, low age of onset, multiple lung lesions, as well as special chronic respiratory infections, abnormal pollutant metabolism and immune microenvironment, as well as special driver gene and germline mutation gene mutation spectra.},
}

Humans
*Lung Neoplasms/epidemiology/genetics/etiology/chemically induced/pathology
*Coal/adverse effects/analysis
China/epidemiology
Polycyclic Aromatic Hydrocarbons/analysis

@article {pmid42634687,
year = {2026},
author = {N F Guimarães, G},
title = {Diagnostic Complexity in Pediatric Chronic Colitis With Allergic, Infectious, Histamine-Related, and Oral-Phase Contributors: A Case Report With Long-Term Follow-Up.},
journal = {Cureus},
volume = {18},
number = {7},
pages = {e113273},
pmid = {42634687},
issn = {2168-8184},
abstract = {Pediatric chronic colitis may present with overlapping gastrointestinal, allergic, dietary, and microbiome-related features, making early therapeutic decisions challenging, particularly when immunosuppression is being considered. This report describes an eight-year-old boy with chronic diarrhea and intermittent hematochezia beginning in early childhood, a history of cow's milk protein allergy, selective eating, poor mastication, inflammatory stool biomarkers, and colonoscopic findings consistent with mild chronic ileocolitis. Because the family declined systemic immunosuppression, a structured gut-focused approach was implemented over 18-24 months, including dietary elimination, reduction of dietary histamine burden, feeding therapy, digestive and diamine oxidase (DAO) support, microbiota modulation, and treatment of suspected enteric infections or overgrowth. Over time, the patient's stool normalized, bleeding resolved, inflammatory markers improved substantially, and repeat colonoscopy demonstrated mucosal healing. This case highlights the potential relevance of individualized, nonimmunosuppressive gastrointestinal strategies in selected pediatric patients with chronic Crohn-like colitis and allergic or histamine-related features, while recognizing that causality cannot be established from a single case.},
}

@article {pmid42634787,
year = {2026},
author = {Yoshimura, K and Rodriguez-Perera, DB and Dou, R and Fahrmann, J},
title = {Editorial: Cancer cell metabolism and tumor microenvironment remodel.},
journal = {Frontiers in genetics},
volume = {17},
number = {},
pages = {1921001},
pmid = {42634787},
issn = {1664-8021},
abstract = {Illustration showing interactions of cancer cells, stromal cells, immune cells, and microbiota in the tumor microenvironment, highlighting specific bioactive metabolites from each cell type and their effects on tumor survival, metabolic support, immune dysfunction, and therapy resistance.},
}

@article {pmid42634815,
year = {2026},
author = {Zhao, J and Li, D and Yang, S and Ma, X},
title = {Recent Advances (2020-2025) in Estrogen and ER-Positive Breast Cancer: Receptor Signaling, Tumor Microenvironment, Endocrine Therapy Resistance and Innovative Treatment Strategies-A Comprehensive Review.},
journal = {Cancer management and research},
volume = {18},
number = {},
pages = {622575},
pmid = {42634815},
issn = {1179-1322},
abstract = {Estrogen receptor-positive (ER+) breast cancer accounts for 70-80% of all invasive breast malignancies worldwide and remains the dominant subtype driving rising global breast cancer incidence, representing a major clinical burden in China with a 2.84% annual age-standardized incidence increase. Endocrine therapy serves as the cornerstone intervention for ER+ disease, yet primary and acquired drug resistance severely undermine long-term therapeutic efficacy, creating an urgent demand for systematic integration of updated mechanistic and translational evidence. This comprehensive review systematically summarizes high-quality literature published from 2020 to 2025, focusing on estrogen biosynthesis and metabolic dysregulation, dual genomic/non-genomic estrogen receptor signaling mediated by ERα, ERβ and GPER1, epigenetic regulatory networks, and bidirectional crosstalk between estrogen signaling and the breast tumor microenvironment (TME). We further dissect multi-layered mechanisms underlying endocrine resistance, including ESR1 mutations/fusions, aberrant activation of PI3K/AKT/mTOR and MAPK pathways, dysregulated ER co-regulators, and expansion of breast cancer stem cells. Current mainstream endocrine agents (AIs, SERMs, SERDs), CDK4/6 inhibitors, and innovative combinatorial regimens targeting drug-resistant clones are also thoroughly discussed. Core consensus from the included literature indicates that ERα acts as a major oncogenic driver while ERβ exerts tumor-suppressive functions; GPER1-mediated non-genomic signaling frequently fuels metastasis and tamoxifen resistance. ESR1 genetic alterations and TME immunosuppressive remodeling constitute the two leading causes of therapeutic failure. Emerging therapeutic candidates, including GPER1 antagonists, ESRRA modulators and epigenetic regulators, have only demonstrated context-dependent anti-endocrine resistance effects in preclinical cell and animal models; substantial contradictory mechanistic data and a complete lack of large-scale human clinical trials restrict their immediate clinical application. Throughout this review, we systematically stratify all interventions by evidence strength to distinguish standard clinical regimens from purely experimental preclinical strategies and thoroughly discuss unresolved limitations and conflicting research observations for each investigational target. Translational approaches with robust clinical validation include liquid biopsy for real-time ESR1 mutation surveillance and standardized lifestyle preventive interventions for high-risk groups, while single cell/spatial multi-omics and gut microbiome modulation remain exploratory analytical or preventive tools with unresolved technical and population variability barriers.},
}

@article {pmid42634877,
year = {2026},
author = {Valland, MES and Jacobsen, S and Bundgaard-Nielsen, C and Bor, P},
title = {Vaginal and urinary microbiomes in postmenopausal women and breast cancer survivors and their associations with genitourinary syndrome of menopause: a scoping review.},
journal = {Climacteric : the journal of the International Menopause Society},
volume = {},
number = {},
pages = {1-9},
doi = {10.1080/13697137.2026.2713393},
pmid = {42634877},
issn = {1473-0804},
abstract = {Genitourinary syndrome of menopause (GSM) is common among postmenopausal women and breast cancer survivors, particularly those receiving antiestrogen therapy. However, the role of the urinary and vaginal microbiomes in GSM remains underexplored. This study aimed to evaluate urinary and vaginal microbiome differences and their association with GSM in postmenopausal women and breast cancer survivors. A scoping review (PubMed, Embase; May 2025) identified 877 studies addressing the vaginal or urinary microbiome in postmenopausal women and 242 studies in breast cancer survivors. After screening and eligibility assessment, 18 studies involving postmenopausal women and three studies involving breast cancer survivors were included. Across 21 included studies (n = 30-1320 participants), Lactobacillus depletion and anaerobic overgrowth (e.g. Gardnerella, Prevotella, Sneathia) were associated with GSM. Postmenopausal women with low-Lactobacillus community state types (CSTs) had up to 25.9-fold higher odds of GSM. In breast cancer survivors, Lactobacillus was nearly absent (5% of samples), with increased Gardnerella and Sneathia in symptomatic women. Associations between Lactobacillus relative abundance and symptom severity were inconsistent. In conclusion, GSM appears to be associated with microbial dysbiosis characterized by anaerobic overgrowth, rather than Lactobacillus depletion alone. Estrogen suppression in breast cancer survivors may exacerbate dysbiosis and symptoms, highlighting the need for microbiome-targeted treatments.},
}

@article {pmid42634883,
year = {2026},
author = {Siddiqui, R and Khan, NA},
title = {Digital twin of the gut microbiome: toward predictive health modelling.},
journal = {Future microbiology},
volume = {},
number = {},
pages = {1-3},
doi = {10.1080/17460913.2026.2722871},
pmid = {42634883},
issn = {1746-0921},
}

@article {pmid42634926,
year = {2026},
author = {Dabravolski, SA and Vatlin, AA and Erbaeva, AZ and Herrera, C and Pavshintsev, VV and Mitkin, NA},
title = {The black soldier fly bioreactor: host-microbiome synergy in pathogen neutralization, xenobiotic remediation, and downstream feed safety.},
journal = {Journal of the science of food and agriculture},
volume = {},
number = {},
pages = {},
doi = {10.1002/jsfa.70995},
pmid = {42634926},
issn = {1097-0010},
support = {//RUDN University Scientific Projects Grant System, project № 080536-2-000/ ; },
abstract = {Black soldier fly larvae (BSFL) are critical to the circular economy, transforming hazardous organic wastes into sustainable agricultural feed. However, processing high-bioburden substrates presents severe biosafety challenges. This review synthesizes recent advancements (2021-2026) regarding the multidimensional role of the BSFL gut bioreactor in waste sanitization and xenobiotic remediation. Pathogen neutralization is driven by a synergistic, tripartite defense system: host-derived antimicrobial peptides (AMPs), biophysical lipid interactions (e.g., lauric acid), and microbiome-mediated competitive exclusion. Concurrently, the gut microbiota deploys novel enzymatic pathways to actively degrade veterinary pharmaceuticals. Despite these sanitization capabilities, a profound biosafety paradox exists: while live, culturable vegetative pathogens and parent chemical antibiotics are eradicated, the intensive selective pressure within the gut environment facilitates horizontal gene transfer, leading to the amplification of antimicrobial resistance genes (ARGs). This study critically evaluates industrial interventions - including chemical pre-treatments, abiotic stress modulation, and probiotic bioaugmentation - designed to engineer the bioreactor and mitigate these genetic and horizontal transfer risks. Finally, the study explores the downstream impacts of BSFL biomass as a functional substitute for antibiotic growth promoters in livestock, highlighting its prebiotic capacity to positively modulate animal microbiomes. Overcoming current methodological and regulatory limitations via multi-omics will cement BSFL as a biosecure pillar of sustainable agriculture. © 2026 Society of Chemical Industry.},
}

@article {pmid42634957,
year = {2026},
author = {Laiolo, E and Hempel, CA and Abukabbos, BA and Abunayyan, OI and Alam, I and Alamoudi, T and Alkhaldi, WA and Almubarak, ZM and Alnashri, HA and Alothman, A and Alqahtani, TH and Alshaikh, KA and Alsulaimani, M and Alturki, SA and Alva Garcia, JV and Alzahrani, AH and Amin, SA and Ardan, AA and Arossa, S and Baalkhuyur, F and Bähr, S and Barozzi, A and Barreca, F and Breavington, J and Daraghmeh, N and Dhillon, M and Dix, M and Dunn, N and English, K and Ezeta Watts, MA and Frappi, S and Havlik, MN and Imam, KA and Kamau, A and Kateb, HA and Lim, KK and Liu, W and Mann, H and Marchese, F and Martynova, A and Menzies, J and Moret, A and Muniz-Barreto, M and Nolan, MKB and Odobel, C and Ogieglo, JM and Parry, AJ and Pedraza-Pohlenz, R and Pluma, N and Qutub, A and Rabaoui, LJ and Re, E and Rivera Rosas, DE and Roch, C and Rodrigue, M and Tayib, FW and Terraneo, TI and Thomson, J and Villela, H and Vimercati, S and Angulo-Preckler, C and Frühe, L and Klein, SG and Mineta, K and Schmidt-Roach, S and Steckbauer, A and Benzoni, F and Daffonchio, D and Fox, MD and Johnson, MD and Agusti, S and Aranda, M and Berumen, M and Gao, X and Gojobori, T and Peixoto, R and van der Zwan, FM and Pieribone, V and Qurban, M and Duarte, CM},
title = {Metagenomic Insights Into Red Sea Biodiversity Across the Web of Life.},
journal = {Environmental microbiology},
volume = {28},
number = {8},
pages = {e70389},
doi = {10.1111/1462-2920.70389},
pmid = {42634957},
issn = {1462-2920},
support = {BAS/1/1071-01-01//King Abdullah University of Science and Technology/ ; RGC/3/5156-01-01//National Center for Wildlife/ ; },
mesh = {*Biodiversity ; *Metagenomics ; Indian Ocean ; *Geologic Sediments/microbiology ; *Eukaryota/genetics/classification/isolation & purification ; *Seawater/microbiology ; Microbiota ; *Metagenome ; High-Throughput Nucleotide Sequencing ; Bacteria/classification/genetics/isolation & purification ; },
abstract = {Earth's biodiversity is central to ecosystem health and resilience, providing essential functions and services. The Red Sea is a recognised marine biodiversity hotspot with high endemism and unique environmental conditions that support extensive but poorly resolved biodiversity. Here, we applied metagenomic analyses to sediment samples collected from coastal to deep-sea environments during the Red Sea Decade Expedition 2022 to characterise biodiversity across the web of life. From a single shotgun assay per sample, this approach simultaneously characterised the sediment microbiome, which amplicon-based surveys recover only through parallel, targeted assays, and extended detection to higher eukaryotes. Using high-throughput sequencing, we generated 12.8 billion sequences, revealing taxa covering all domains of life. Although eukaryotic sequences represented only 0.7% of the taxonomically annotated dataset, we managed to identify 679 eukaryotic families. Prokaryotic diversity was high, as expected in a basin-scale sampling coupled with high sequencing depth, with groups covering a wide functional array. Community structure analyses revealed depth-driven stratification of open-ocean benthic microbial communities and latitudinal structuring of coastal benthic eukaryotes. Overall, this dataset provides an empirical reliability-coverage trade-off with direct consequences for the design of eDNA monitoring programmes targeting conservation-priority taxa, and clear priorities for taxa specific reference-database expansion.},
}

*Biodiversity
*Metagenomics
Indian Ocean
*Geologic Sediments/microbiology
*Eukaryota/genetics/classification/isolation & purification
*Seawater/microbiology
Microbiota
*Metagenome
High-Throughput Nucleotide Sequencing
Bacteria/classification/genetics/isolation & purification

@article {pmid42635063,
year = {2026},
author = {Aili, M and Yu, S and Wang, X and Ye, D and Fang, Y and Wu, Y and Long, Y and Wang, S and Zou, J and Ma, Q},
title = {Functional effects of microbial metabolites in dental caries.},
journal = {Critical reviews in microbiology},
volume = {},
number = {},
pages = {1-17},
doi = {10.1080/1040841X.2026.2719588},
pmid = {42635063},
issn = {1549-7828},
abstract = {Dental caries is a multifactorial disease primarily driven by the metabolic activity of microorganisms within oral biofilms. The carious process begins when fermentable carbohydrates are metabolized by microbes, leading to the production of organic acids that lower the local pH and demineralize tooth enamel. While carbohydrates are important substrates for microbial metabolism, proteins and lipids also influence microbial activity and contribute to caries development. Recent advances in microbiology and metabolomics have highlighted the role of microbial metabolites in shaping the oral microbiome and influencing caries progression. Primary metabolites such as lactate and acetate play key roles in biofilm acidification and enamel demineralization, while secondary metabolites including antimicrobial peptides (AMPs), bacteriocins, polyketides (PKs), and non-ribosomal peptides (NRPs) mediate microbial competition and regulate biofilm stability. This review explores the mechanisms by which these metabolites influence microbial competition and biofilm dynamics and discusses their potential applications in the prevention and treatment of dental caries. By understanding the interplay between microbial metabolism and oral health, new therapeutic strategies that leverage microbial metabolites, such as targeted antimicrobial agents, biofilm modulators, and metabolic interventions, hold promise for revolutionizing caries management and improving oral health outcomes.},
}

@article {pmid42635192,
year = {2026},
author = {Chen, C and Vakirlis, N and Holmer, R and de Ridder, D and Kupczok, A},
title = {Identification and Classification of Expressed Orphan Genes, Spurious Orphan Genes, and Conserved Genes in the Human Gut Microbiome.},
journal = {Genome biology and evolution},
volume = {},
number = {},
pages = {},
doi = {10.1093/gbe/evag211},
pmid = {42635192},
issn = {1759-6653},
abstract = {Orphan genes - genes lacking detectable homologs outside a species - are widespread in microbial genomes and are thought to contribute to their adaptation and molecular innovation. However, not all predicted orphan genes may represent novel functional coding sequences. False positive orphan genes, also called spurious orphan genes, can arise from gene prediction errors. We reason that orphan genes lacking detectable expression are more likely to be spurious. To test this, we combined large-scale metatranscriptomic profiling of the human gut microbiome with machine learning to distinguish expressed orphan genes from spurious ones and to compare them with conserved genes found in multiple species. Using nearly 5,000 metatranscriptome libraries, we identified ∼218,000 orphan genes supported by expression evidence, while ∼330,000 predicted orphan genes lacked detectable expression, and were classified as spurious. We extracted 154 features for sequence, structural, and evolutionary properties for each gene and trained XGBoost classifiers while accounting for genomic representation. The models achieved an area under the receiver operating characteristic curve (AUC) of 0.82 in distinguishing expressed orphan genes from spurious orphan genes and an AUC of 0.93 in distinguishing expressed orphan genes from conserved genes. SHAP-based interpretation revealed clear biological signals. Particularly, expressed orphans were present in more genomes than spurious ones and expressed orphan genes were shorter than conserved genes. This work improves orphan gene discovery and suggests that expressed orphan genes differ systematically from conserved genes and spurious orphan genes in sequence composition, structural constraints, and evolutionary signals.},
}

@article {pmid42635214,
year = {2026},
author = {Muller, E and Baum, S and Borenstein, E},
title = {MAAMOUL: metabolic network-based discovery of microbiome-metabolome shifts in disease.},
journal = {Bioinformatics (Oxford, England)},
volume = {42},
number = {Supplement_2},
pages = {},
doi = {10.1093/bioinformatics/btag467},
pmid = {42635214},
issn = {1367-4811},
support = {2266/25//Israel Science Foundation/ ; U19AG057377/NH/NIH HHS/United States ; //Raymond and Beverly Sackler Chair in Bioinformatics at Tel Aviv University/ ; //Safra Center for Bioinformatics at Tel-Aviv University/ ; },
mesh = {*Metabolic Networks and Pathways ; Humans ; *Metabolome ; *Metabolomics/methods ; *Inflammatory Bowel Diseases/metabolism/microbiology/genetics ; *Irritable Bowel Syndrome/metabolism/microbiology ; *Microbiota ; Metagenomics/methods ; *Computational Biology/methods ; *Gastrointestinal Microbiome ; },
abstract = {MOTIVATION: A central goal in human gut microbiome research is to identify disease-associated functional shifts, an objective increasingly pursued through metagenomic and metabolomic assays. However, common differential abundance analyses of genes or metabolites often yield long and difficult-to-interpret feature lists. Aggregating features into predefined pathways can improve interpretability but relies on fixed pathway boundaries that may not reflect context-specific functional changes. Moreover, even when paired metagenomic-metabolomic data are available, they are often analyzed separately or linked only through simple statistical associations.

RESULTS: We introduce MAAMOUL, a knowledge-based computational framework that integrates metagenomic and metabolomic data to identify disease-associated, data-driven microbial metabolic modules. Leveraging prior knowledge of bacterial metabolism, MAAMOUL maps disease-association scores onto a global microbiome-wide metabolic network and identifies custom modules enriched for altered genes and metabolites. Applying MAAMOUL to inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) datasets revealed significant disease-associated modules not detected by conventional pathway-level analysis. In IBD, modules reflected disrupted sulfur and aromatic amino acid metabolism and enhanced microbial nucleotide salvage, whereas in IBS they linked purine and nicotinate/nicotinamide metabolism. These results demonstrate that network-guided multi-omic integration can uncover coherent functional shifts in the gut microbiome overlooked by single-omic or purely statistical approaches.

MAAMOUL is available as an R package at https://github.com/borenstein-lab/MAAMOUL.},
}

*Metabolic Networks and Pathways
Humans
*Metabolome
*Metabolomics/methods
*Inflammatory Bowel Diseases/metabolism/microbiology/genetics
*Irritable Bowel Syndrome/metabolism/microbiology
*Microbiota
Metagenomics/methods
*Computational Biology/methods
*Gastrointestinal Microbiome

@article {pmid42635387,
year = {2026},
author = {Kuhlmann, M and Kolland, DDC and de Almeida, GP and Hoffmann, C and von Hoesslin, M and Berner, J and Wurmser, C and Akulich, A and Schulz, AM and Hackstein, CP and Ohnmacht, C and Zehn, D},
title = {A Bacterial Microbiome Is Dispensable for the Induction of CD8 T Cell Exhaustion.},
journal = {European journal of immunology},
volume = {56},
number = {8},
pages = {e70238},
doi = {10.1002/eji.70238},
pmid = {42635387},
issn = {1521-4141},
support = {//Deutsche Forschungsgemeinschaft/ ; /ERC_/European Research Council/International ; },
mesh = {Animals ; *T-Cell Exhaustion/immunology ; Mice ; *Lymphocytic choriomeningitis virus/immunology ; *CD8-Positive T-Lymphocytes/immunology ; *Lymphocytic Choriomeningitis/immunology/microbiology ; *Microbiota/immunology ; Mice, Inbred C57BL ; Programmed Cell Death 1 Receptor/immunology/metabolism/genetics ; Cytokines ; },
abstract = {Prolonged antigen exposure in chronic viral infections reduces the effector capacity of cytotoxic T cells-a phenomenon known as T cell exhaustion. Development of T cell exhaustion is driven by high viral titers, strong TCR stimulation, and high antigen concentrations associated with strong inflammatory signals. A largely unexplored factor has been the influence of the microbiome in these processes. Here, we report that T cell exhaustion progresses independently of the presence or absence of a microbiome in chronic lymphocytic choriomeningitis virus (LCMV) infections. Virus-specific CD8 T cells in germ-free mice showed high expression of the inhibitory receptor PD-1 and decreased cytokine production. Moreover, their global gene expression patterns, as determined by single-cell sequencing, were similar to those of cells in specific pathogen-free mice. In line with this, we observed similar pathogen loads with and without a microbiome. Thus, our study demonstrates that the microbiome is dispensable for the induction of T cell exhaustion and for the limited virus control seen in chronic LCMV infections.},
}

Animals
*T-Cell Exhaustion/immunology
Mice
*Lymphocytic choriomeningitis virus/immunology
*CD8-Positive T-Lymphocytes/immunology
*Lymphocytic Choriomeningitis/immunology/microbiology
*Microbiota/immunology
Mice, Inbred C57BL
Programmed Cell Death 1 Receptor/immunology/metabolism/genetics
Cytokines

@article {pmid42635401,
year = {2026},
author = {Korózs, D and Szabó, BG and Apjok, G and Lakatos, V and Jeszenszky, K and Kamotsay, K and Hajbel-Vékony, G and Tóth, Á and Sinkó, J and Reményi, P and Kintses, B},
title = {Fecal filtrate transplantation as salvage therapy for fulminant Clostridioides difficile infection in adult hematological patients during chemotherapy-induced aplasia: a pilot experience.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2718620},
doi = {10.1080/19490976.2026.2718620},
pmid = {42635401},
issn = {1949-0984},
mesh = {Humans ; Pilot Projects ; Female ; *Salvage Therapy/methods ; Male ; Middle Aged ; *Clostridioides difficile/physiology ; *Fecal Microbiota Transplantation/methods ; Prospective Studies ; Adult ; *Clostridium Infections/therapy/microbiology ; Aged ; Feces/microbiology ; *Hematologic Neoplasms/drug therapy/complications ; Treatment Outcome ; Anti-Bacterial Agents/therapeutic use ; Bacteriophages/genetics ; Antineoplastic Agents/adverse effects ; },
abstract = {BACKGROUND: Fulminant Clostridioides difficile infection (CDI) in patients with hematologic malignancies during chemotherapy-induced aplasia carries high mortality and limited treatment options. Our objective was to evaluate fecal filtrate transplantation (FFT) as a salvage therapy for fulminant CDI during aplasia, and to explore whether donor-recipient phage dynamics may contribute to clinical response.

METHODS: We conducted a single-center, prospective, protocol-defined pilot case series study including consecutive adults with hematologic malignancies, chemotherapy-induced grade-4 aplasia and fulminant CDI, refractory to ≥5 d of high-dose oral vancomycin plus intravenous metronidazole and tigecycline. FFT was prepared from a single unrelated donor using sequential centrifugation and filtration, and administered via nasogastric tube in two doses. The primary outcome was sustained clinical cure, secondary outcomes included survival and adverse events, assessed at +14 and +30 d post-FFT. 16S rRNA gene sequencing was used to assess microbiome compositions, while viral metagenomics and in vitro propagation assays were employed to characterize donor-recipient phageome interactions.

RESULTS: Three patients with adverse-risk acute myeloid leukemia and fulminant CDI caused by genetically distinct C. difficile strains received FFT. All patients achieved clinical resolution by day +14, accompanied by improvements in abdominal distension and inflammatory markers. By day +30, one patient died from Pseudomonas aeruginosa septic shock, while two maintained remission with confirmatory follow-up. FFT was well tolerated, with no procedure-related immediate complications or FFT-attributable adverse events. Microbiome and phage profiling revealed heterogeneous responses, including shifts in bacterial community composition, with no clear evidence for a general role of donor-derived phages in CDI resolution. In contrast, we observed induction of prophages harbored by recipient-associated Clostridium species, which may have contributed to decolonization through stress-induced entry into the lytic cycle.

CONCLUSIONS: FFT was feasible, with rapid sustained CDI resolution in hematologic patients with chemotherapy-induced aplasia.

TRIAL REGISTRATION: ClinicalTrials.gov identifier NCT07172191.

SUMMARY: Prospective single-center pilot study of fecal filtrate transplantation (FFT) for fulminant-refractory C. difficile infection in three aplastic adult hematologic patients. FFT was well tolerated, achieved rapid clinical cure, and showed heterogeneous microbiome and phageome modulation, potentially contributing to therapeutic effects.},
}

Humans
Pilot Projects
Female
*Salvage Therapy/methods
Male
Middle Aged
*Clostridioides difficile/physiology
*Fecal Microbiota Transplantation/methods
Prospective Studies
Adult
*Clostridium Infections/therapy/microbiology
Aged
Feces/microbiology
*Hematologic Neoplasms/drug therapy/complications
Treatment Outcome
Anti-Bacterial Agents/therapeutic use
Bacteriophages/genetics
Antineoplastic Agents/adverse effects

@article {pmid42635403,
year = {2026},
author = {Fidilio, E and Comas Martínez, M and Flores, V and Costa Forner, MP and Xiao, X and Herance, JR and Vilallonga, R and Ciudin Mihai, A},
title = {Baseline gut microbiome ecology predicts long-term fat mass loss after bariatric surgery: evidence for a thrifty Bifidobacterium phenotype.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2719294},
doi = {10.1080/19490976.2026.2719294},
pmid = {42635403},
issn = {1949-0984},
mesh = {Humans ; *Bariatric Surgery ; *Gastrointestinal Microbiome ; Feces/microbiology ; Prospective Studies ; Female ; Male ; *Bifidobacterium/genetics/isolation & purification/classification/physiology ; Middle Aged ; Adult ; Diet, Mediterranean ; Weight Loss ; *Obesity, Morbid/surgery/microbiology ; Bacteria/classification/genetics/isolation & purification ; Phenotype ; },
abstract = {Bariatric surgery (BS) induces weight loss, but long-term success involves complex host-microbiome interactions. We evaluated the longitudinal impact of BS, microbiome resilience, and Mediterranean Diet (MedDiet) adherence up to 24 months. This prospective observational study included 85 patients with severe obesity undergoing BS and 21 normal-weight healthy controls (HC). MedDiet adherence (PREDIMED) was assessed before surgery. Fecal microbiota (16S-rRNA sequencing) and metabolomics ([1]H-NMR spectroscopy) were analyzed at baseline and at 1-, 6-, and 12-months post-BS. Clinical outcomes and fat mass, evaluated by bioimpedanciometry, were tracked up to 24 months. At baseline, patients exhibited higher microbial Shannon diversity than controls (p = 0.041), alongside a dysfunctional microbiome and metabolome characterized by a higher Firmicutes/Bacteroidetes ratio and elevated levels of branched-chain amino acids (p < 0.0001). Ordinary Least Squares (OLS) regression analysis revealed that MedDiet adherence and type 2 diabetes status significantly modulated baseline diversity. At 12 months post-BS, the gut ecosystem underwent profound remodeling, characterized by depletion of Bifidobacterium spp. and an increase in butyrate levels (p < 0.0001), establishing a novel adaptive state distinct from HC. Baseline gut ecology significantly conditioned long-term BS outcomes: patients in the highest quartile of baseline Bifidobacterium spp. lost significantly less fat mass at 24 months than those in the lowest (6.6% vs. 13.2%, p = 0.010). High baseline Bifidobacterium abundance paradoxically acts as a "thrifty microbiome," potentially maximizing energy harvest and limiting surgery-induced fat loss. Overall, BS induces adaptive microbiome restoration rather than true normalization, highlighting the potential for precision interventions prior to surgery.},
}

Humans
*Bariatric Surgery
*Gastrointestinal Microbiome
Feces/microbiology
Prospective Studies
Female
Male
*Bifidobacterium/genetics/isolation & purification/classification/physiology
Middle Aged
Adult
Diet, Mediterranean
Weight Loss
*Obesity, Morbid/surgery/microbiology
Bacteria/classification/genetics/isolation & purification
Phenotype

@article {pmid42635434,
year = {2026},
author = {Sakdinan, B and Sinha, A and Qadri, F and Khan, AI and Nelson, EJ and Shapiro, BJ},
title = {Species-specific prophage induction by ciprofloxacin in human gut metagenomes.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0030326},
doi = {10.1128/msystems.00303-26},
pmid = {42635434},
issn = {2379-5077},
abstract = {Antibiotics are known to trigger prophage induction in controlled laboratory settings, but it remains unclear whether this also occurs within microbiomes in nature. Current methods investigating the link between antibiotics and prophage induction within the human gut rely on in vitro culturing of human gut bacterial isolates. Using a metagenomic approach, we aimed to measure prophage induction, and whether it is associated with antibiotic exposure. In two independent human cohorts, we compared prophage to bacterial host read depth ratios (P:H) across known or measured antibiotic exposures. We found that induction is not broadly associated with antibiotic exposures at the level of the overall microbiome, but that ciprofloxacin increases P:H ratios in certain bacterial species. We documented heterogeneous trajectories of P:H ratios over the course of antibiotic exposure, sometimes increasing and remaining high, or returning to baseline. This study complements experimental models by providing in vivo evidence of induction in the human gut.IMPORTANCEBacteriophages are viruses that infect a bacterial host. The lytic and lysogenic cycles are the two classic outcomes of phage infection. In the lytic cycle, the phage immediately replicates and lyses its host cell to release new viral particles. In the lysogenic cycle, the phage, now called a prophage, integrates its genome into that of its host without killing it. Prophages can switch to the lytic cycle in a process called induction, in which the viral genome is replicated, the host cell is lysed, and viral particles are released. The most immediate consequence of induction is host cell death, which can impact bacterial populations and communities. Since prophages are mobile genetic elements that can move between bacteria, they are also an important vehicle for horizontal gene transfer. While induction has been well studied in vitro, whether and how induction occurs within the complex microbial ecosystem in humans is less well characterized. Understanding prophage induction in vivo is therefore critical in corroborating in vitro observations.},
}

@article {pmid42635437,
year = {2026},
author = {Escudero-Jiménez, Á and Galán-Ros, J and Huertas-López, F and Pérez-Sarabia, A and Ribeiro, D and Postigo-Corrales, F and Albaladejo-González, A and Díaz-López, MI and López-Abellán, MD and García-Rodríguez, J and Beltrán-Videla, MA and Arroyo, AB and Hurtado López, AM and Tapia-Abellán, A and Corral San Miguel, R and Rodríguez-Braun, E and Feliciangeli, E and Sánchez-Espinosa, A and Conesa, A and Luengo-Gil, G and Conesa-Zamora, P},
title = {Integrative microbiome-methylome analysis links bacterial taxa to colorectal cancer histological subtypes.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0062226},
doi = {10.1128/msystems.00622-26},
pmid = {42635437},
issn = {2379-5077},
abstract = {Colorectal cancer (CRC) arises through distinct molecular and histological routes that may be shaped by interactions between the mucosa-associated microbiota and host epigenetic regulation. We analyzed paired tumor and adjacent non-tumor colorectal mucosa from CRC patients stratified by histological subtype (conventional vs serrated-pathway groups). Microbiota composition was profiled by Illumina sequencing, and host DNA methylation was assessed using genome-wide CpG arrays with targeted validation. Alpha diversity showed modest tumor-non-tumor differences, with variation by anatomical location driven by distal tumors. Differential abundance testing identified tumor-associated genera, and linear discriminant modeling highlighted taxa with high discriminatory power, including Bacteroides, Eubacterium, Fusobacterium, and Acinetobacter. Methylome ordination separated tumor from non-tumor samples and revealed prominent contributions of zinc finger (ZNF) loci. Integrative latent-variable modeling (PLS/sparse partial least squares and multi-block sparse partial least squares discriminant analysis) supported coordinated microbiome-methylome variation distinguishing tumor from non-tumor mucosa, prioritized a limited set of bacterial and methylation signals, and suggested partial discrimination between conventional and serrated tumor profiles, particularly in the methylome block. Focusing on Fusobacterium, methylation changes in selected host loci were associated with its abundance, and qPCR-based quantification of Fusobacterium nucleatum correlated with CpG methylation at ZNF788. F. nucleatum levels were also associated with serrated/microsatellite instability-related CRC features and more advanced disease. These findings identify subtype-aware microbiome-methylome signatures in CRC and highlight ZNF788 methylation as a candidate epigenetic correlate of intratumoral F. nucleatum burden.IMPORTANCEColorectal cancer does not develop in a single way, and different tumor types may interact differently with bacteria living on the bowel lining. This study examined both tissue-associated bacteria and DNA methylation, an epigenetic mark that helps regulate genes, in paired tumor and nearby non-tumor tissue from patients with colorectal cancer. By analyzing these two layers together, we identified microbial and host methylation patterns linked to tumor tissue and to serrated-pathway cancers. In particular, Fusobacterium nucleatum was associated with serrated/microsatellite instability-related features, more advanced disease, and methylation of the host gene ZNF788. These findings suggest that combining microbiome and epigenetic information may help explain why colorectal cancer subtypes behave differently and may support future subtype-aware biomarkers.},
}

@article {pmid42635566,
year = {2026},
author = {Clark, J and Krueger, Q and Carrier, TJ and Moran, Y and Reitzel, AM},
title = {Is a Commensal Here, a Pathogen There? Genotype Specific Responses by the Sea Anemone Nematostella vectensis to Vibrio Species.},
journal = {Molecular ecology},
volume = {35},
number = {16},
pages = {e70517},
doi = {10.1111/mec.70517},
pmid = {42635566},
issn = {1365-294X},
support = {2044826//National Science Foundation/ ; 2526917//National Science Foundation/ ; 2020669//Israel Binational Science Foundation/ ; //Center for Computational Intelligence to Predict Health and Environmental Risks (UNC Charlotte)/ ; },
mesh = {Animals ; *Sea Anemones/microbiology/genetics/immunology ; Genotype ; *Vibrio/pathogenicity/physiology/genetics ; *Symbiosis/genetics ; Host-Pathogen Interactions/genetics ; },
abstract = {Animals rely on diverse molecular mechanisms to maintain beneficial microbial associations while also defending against pathogens, yet the extent to which these responses vary among genotypes of a single species remains poorly understood. Using individuals from different locations of the sea anemone Nematostella vectensis, we compared transcriptional responses to a commensal (Vibrio diabolicus) and pathogen (Vibrio coralliilyticus) bacterium. We find striking genotype-specific divergence: individuals from Nova Scotia mounted a strong transcriptional response to V. diabolicus, whereas the North Carolina and Florida individuals showed almost no response to this same bacterium. In contrast, all individuals regardless of location exhibited a large transcriptional response to the pathogen V. coralliilyticus. These responses involved key immune pathways (e.g., cGAS-STING, NF-κB, and proteostasis-related stress responses), suggesting that different genotypes deploy distinct molecular responses when encountering the same bacterium. The robust, immune-like response of the individuals from Nova Scotia to a bacterium considered commensal in other populations indicates that V. diabolicus may not function as a commensal across the species range. Such genotype-by-microbe specificity points to potential local adaptation to particular bacterial partners that underscores the complexity of holobiont regulation across heterogeneous environments and stresses the importance of assessing additive, synergistic, and antagonistic interactions across hologenomic mosaics.},
}

Animals
*Sea Anemones/microbiology/genetics/immunology
Genotype
*Vibrio/pathogenicity/physiology/genetics
*Symbiosis/genetics
Host-Pathogen Interactions/genetics

@article {pmid42636375,
year = {2026},
author = {Nickodem, CA and Tran, PQ and Neeno-Eckwall, E and Naing, N and Sanford, GR and Silva, EM and Hite, JL},
title = {Soil management practices shape the abundance, diversity, and spread of antimicrobial resistance.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {35},
pages = {e2605731123},
doi = {10.1073/pnas.2605731123},
pmid = {42636375},
issn = {1091-6490},
support = {58-5090-2-035//U.S. Department of Agriculture (USDA)/ ; 2023-6701-40057//U.S. Department of Agriculture (USDA)/ ; AD00001395//U.S. Department of Agriculture (USDA)/ ; },
mesh = {*Soil Microbiology ; *Soil/chemistry ; Agriculture/methods ; *Drug Resistance, Bacterial/genetics ; Anti-Bacterial Agents/pharmacology ; Animals ; Metagenomics ; *Drug Resistance, Microbial/genetics ; Bacteria/genetics/drug effects ; Phylogeny ; Interspersed Repetitive Sequences ; },
abstract = {Agricultural soils are critical hotspots of antimicrobial resistance genes (ARGs). Yet, the environmental factors shaping these reservoirs and the hazards they pose to humans and livestock remain poorly understood. Because management practices introduce antibiotics, heavy metals, and nonantibiotic biocides, they can rapidly select for resistance. Most studies have examined components of management practices in isolation, overlooking the multiple stressors of modern industrial agriculture. Here, we used a large-scale field experiment to examine how multiple stressors from soil and crop management interact to shape antimicrobial resistance. We combined shotgun metagenomics, phylogenomics, and risk-score analyses to quantify the diversity of ARGs, mobile genetic elements (MGEs), and the transmission potential of drug-resistant pathogens. Relative to other management systems, intensive, chemically reliant monoculture systems, typical of the US Corn Belt, create strong selective pressures promoting more abundant and diverse ARGs and MGEs. These systems therefore carry greater potential to transmit ARGs, including those with relevance to both livestock and public health such as tetA and blaPAM, likely mediated by integration and excision. In contrast, less-intensive, lower-input systems with diverse crop rotations maintained resistomes with lower abundance, diversity, and transmission potential. Our results suggest that these patterns could arise due to the divergent effects of management practices on overall soil microbial diversity, an ecological barrier that can suppress ARGs. This study highlights the need to understand the combined stressors of agricultural practices, beyond antimicrobial use, to design effective strategies to mitigate antimicrobial resistance.},
}

*Soil Microbiology
*Soil/chemistry
Agriculture/methods
*Drug Resistance, Bacterial/genetics
Anti-Bacterial Agents/pharmacology
Animals
Metagenomics
*Drug Resistance, Microbial/genetics
Bacteria/genetics/drug effects
Phylogeny
Interspersed Repetitive Sequences

@article {pmid42636377,
year = {2026},
author = {Nearing, JT and Kuntz, T and Perdomo, V and Nickols, WA and Branck, T and Bhosle, A and Badri, DV and Huttenhower, C and Jackson, M and Thompson, KN},
title = {Gut microbiome-metabolome interactions during varied low-carbohydrate food consumption.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {35},
pages = {e2533462123},
doi = {10.1073/pnas.2533462123},
pmid = {42636377},
issn = {1091-6490},
support = {Hills internal funding HSPH//Hills Pet Nutrition Inc./ ; },
mesh = {Animals ; Dogs ; *Metabolome ; Feces/microbiology/chemistry ; *Gastrointestinal Microbiome/physiology ; *Diet, Carbohydrate-Restricted ; *Dietary Carbohydrates/metabolism ; Cross-Over Studies ; Male ; },
abstract = {Low-carbohydrate (LC) foods have been associated with weight loss, insulin resistance, and reduced inflammation. Gut microbes may drive these effects by changing the host's immune and metabolic state, yet the optimal replacement strategies (e.g., protein vs. fat) and the biochemical impacts are still uncertain. Thus, we conducted a randomized cross-over study in canines (n = 35) using a high-carbohydrate food for 4 wk, followed by two 5-wk intervals of LC foods replacing carbohydrates with fat or protein. Feces and blood samples collected after each interval underwent metabolome profiling, as well as shotgun metagenomic and metatranscriptomic sequencing from feces. We observed strong associations between food and overall fecal and serum chemical and gut microbial composition. Bifidobacterium spp. were significantly reduced during consumption of either LC food, whereas many species from Firmicutes increased. In addition to broad taxonomic changes, we also found that several microbially associated metabolites (tryptophan derivatives, secondary bile acids, and short-chain fatty acid fermentation) shifted in abundance in response to differing LC foods. Broadly, we also identified a strong trend toward decreased amino acids in the feces of dogs fed LC foods, particularly the high fat food. Coupled with decreased fecal dipeptide levels and increased fecal ammonia, these findings indicate a broad metabolic shift within the gut microbiome, potentially toward protein catabolism. Together, the data suggest that diverse carbohydrate replacement strategies induce extensive gut reprogramming, with some changes dependent on whether carbohydrate energy was replaced with fat or protein.},
}

Animals
Dogs
*Metabolome
Feces/microbiology/chemistry
*Gastrointestinal Microbiome/physiology
*Diet, Carbohydrate-Restricted
*Dietary Carbohydrates/metabolism
Cross-Over Studies
Male

@article {pmid42636549,
year = {2026},
author = {Eley, V and Martin, E and Amoako, A and Hartel, G and McCarthy, K and Woods, C and Lu, Y and Tan, J and Nanan, R and Lipman, J and Roberts, J and Tang, MLK and Callaway, L and Navarro, S},
title = {Cefazolin administration prior to caesarean delivery and breastmilk microbiome: a nested cohort within a randomised clinical trial.},
journal = {International journal of obstetric anesthesia},
volume = {68},
number = {},
pages = {105222},
doi = {10.1016/j.ijoa.2026.105222},
pmid = {42636549},
issn = {1532-3374},
abstract = {OBJECTIVES: Consistent with guidelines, anaesthetists administer pre-incision cefazolin to patients having caesarean delivery in Australia. These antibiotics may impact the breastmilk microbiome. We hypothesised that the breastmilk microbiome of mothers administered cefazolin would differ from those administered placebo.

METHODS: In this nested cohort within a randomised clinical trial, samples were collected from adult females having caesarean delivery. Patients received cefazolin 2 g in 100 mL normal saline (cefazolin group) or 100 mL normal saline (placebo group) prior to skin incision. Breastmilk samples were collected by participants on post-operative day 14 and 30 and immediately frozen. Microbial composition of samples was assessed via long-read 16S rRNA sequencing.

RESULTS: From the cefazolin group, there were 12 samples (day 14) and 13 (day 30). From the placebo group, there were 11 (day 14) and 9 (day 30). Full-length 16S rRNA sequencing yielded sufficient reads to characterise the breastmilk microbiota at both time points. Cefazolin exposure was associated with alterations in the composition, including increased abundances of the aerobic species Roseateles spp. and Cutibacterium acnes and a predominance of Gram-negative taxa. These shifts suggest suppression of Gram-positive commensals. The resulting microbial communities appeared relatively static and enriched with less-characterised, environmentally associated genera, indicating that cefazolin may potentially disrupt normal breastmilk microbial maturation by creating niches preferentially occupied by antibiotic-tolerant taxa.

CONCLUSIONS: In this small, restricted sample, cefazolin exposure prior to delivery exerted modest effects on the breastmilk microbiome. The clinical implications require further evaluation in a larger, diverse population.},
}

@article {pmid42636661,
year = {2026},
author = {Zeng, Y and Tao, Q and Fan, J and Wang, Y and Tao, R and Rao, J and Zeng, F and Jiang, F and Zhang, C and Xiong, X and Cheng, X},
title = {Desert-derived Ensifer sp. SA403 enhances potato salt tolerance by reshaping rhizosphere microbiome functions and host responses.},
journal = {Microbiological research},
volume = {313},
number = {},
pages = {128695},
doi = {10.1016/j.micres.2026.128695},
pmid = {42636661},
issn = {1618-0623},
abstract = {Soil salinization increasingly threatens global food security, and potato (Solanum tuberosum L.), a moderately salt-sensitive crop, is particularly vulnerable to saline soils. Plant growth-promoting rhizobacteria (PGPR) offer a promising strategy to improve crop performance, yet how PGPR interact with native microorganisms to enhance potato salt tolerance remains poorly understood. In this study, we identified a desert-derived PGPR strain, Ensifer sp. SA403, which substantially enhanced potato performance under high salinity across sterile, non-sterile and field conditions. Physiologically, inoculation with SA403 reduced shoot Na[+] accumulation and increased the K[+]/Na[+] ratio; notably, these effects were markedly stronger in non-sterile substrates than under sterile conditions, indicating that SA403-mediated ion homeostasis relies on cooperation with the resident microbiota rather than on the strain acting alone. Metagenomic profiling indicated that SA403 strain reshaped rhizosphere communities, significantly enriching beneficial taxa such as Priestia and Bradyrhizobium, and upregulated functional pathways involved in glutathione and sulfur metabolism. Furthermore, host transcriptomic analyses showed that SA403 modulated plant responses to salt stress, with differentially expressed genes enriched in jasmonic acid signaling, ethanolamine metabolism and amino-acid biosynthesis pathways. Field trials on saline soils confirmed that SA403 significantly increased seedling emergence and tuber weight. Together, our results demonstrate that SA403 functions as a biological mediator that optimizes rhizosphere microecology and coordinates ion balance and host signaling to enhance potato salt tolerance. These findings support the potential of SA403 as a robust PGPR-based tool for sustainable potato production on saline soils.},
}

@article {pmid42636663,
year = {2026},
author = {Wang, D and Huang, Z and Sun, S and Song, W and Li, Y and Sun, K and Li, Z and Feng, J},
title = {Multi-omics reveal microbial functional traits and antifungal metabolites associated with lower Pseudogymnoascus destructans loads in bat cave soils.},
journal = {Microbiological research},
volume = {313},
number = {},
pages = {128696},
doi = {10.1016/j.micres.2026.128696},
pmid = {42636663},
issn = {1618-0623},
abstract = {White-nose syndrome, caused by Pseudogymnoascus destructans (Pd), is a major fungal disease threatening hibernating bats. Cave soils can serve as environmental reservoirs for Pd, yet the microbial and biochemical mechanisms underlying naturally low Pd burdens in some cave environments remain poorly understood. Here, we integrated soil microbiome profiling, metagenomics, metabolomics, multi-omics network analysis, and in vitro validation to investigate the ecological and functional basis of differential Pd loads in hibernating bat caves in Northeast China. The three caves shared cold, humid, and weakly acidic microenvironments, but differed significantly in electrical conductivity, soil water content, nutrient availability, and extracellular enzyme activities. Soil microbial communities showed significant inter-cave variation in composition, diversity, and niche breadth, with stochastic processes contributing substantially to community assembly. Environmental variables, particularly pH and Pd load, were important predictors of microbial community structure. Functional analyses revealed that the low-Pd Gezi Cave was enriched in genes associated with organic carbon degradation, nitrogen input and retention, and secondary metabolism. Metabolomic profiling further identified cave-specific metabolite signatures, among which Biochanin A, 4-Hydroxybenzaldehyde, Vanillin, and Arachidonic acid were negatively correlated with Pd loads. Integrated pathway and network analyses showed that differential genes and metabolites jointly mapped to secondary metabolite biosynthesis, aminobenzoate degradation, and flavonoid degradation pathways, forming a microbe-metabolite-functional gene coupling network involving key taxa such as Rhodococcus, Pseudorhodoplanes, and Rhodoplanes. In vitro assays confirmed that 4-Hydroxybenzaldehyde, Coumarin, and Vanillin inhibited Pd growth. Structural equation modelling further indicated that environmental heterogeneity was associated with variation in Pd loads through microbial functional attributes and metabolite profiles. These findings suggest that naturally low-Pd cave soils are associated with coordinated environmental filtering, microbial functional specialization, and antifungal metabolite production, providing mechanistic insight into microbial and biochemical constraints on Pd persistence in cave reservoirs.},
}

@article {pmid42636689,
year = {2026},
author = {Wang, D and Di, D and Jiang, B and Wang, Y and Jiang, Z and Zhang, J and Wang, L and Li, X and Jing, Y and Liu, B and Zhang, H and Sun, M and Xin, S},
title = {The Enterococcus-putrescine-hadh axis drives mitochondrial redox imbalance and endothelial barrier breakdown in aortic dissection.},
journal = {Redox biology},
volume = {96},
number = {},
pages = {104310},
doi = {10.1016/j.redox.2026.104310},
pmid = {42636689},
issn = {2213-2317},
abstract = {Growing evidence indicates that gut microbiota-derived metabolites contribute to aortic dissection (AD), yet the molecular mechanisms linking microbial metabolism to endothelial barrier failure remain unclear. Untargeted metabolomics identified putrescine as a markedly elevated circulating metabolite in AD patients, and higher putrescine levels were associated with disease severity and adverse clinical characteristics. Targeted polyamine metabolomics further confirmed putrescine as the most prominently altered metabolite among the measured polyamine-related metabolites. Integrated microbiome-metabolome analysis suggested that Enterococcus may represent an important contributor to elevated putrescine levels through AguA-associated metabolism. In vivo administration and fecal microbiota transplantation showed that increased putrescine was associated with impaired endothelial barrier integrity, aggravated mitochondrial injury, enhanced vascular leakage, and accelerated AD progression. Mechanistically, CHX chase, surface plasmon resonance, molecular docking, and pull-down assays supported a direct interaction between putrescine and the mitochondrial fatty acid β-oxidation enzyme 3-hydroxyacyl-CoA dehydrogenase (HADH), involving Ala107 and Ser137, and showed that putrescine was associated with reduced HADH stability. In endothelial cells, putrescine impaired fatty acid oxidation, mitochondrial ultrastructure, and oxidative phosphorylation, promoted cytoskeletal remodeling and biomechanical dysfunction, and compromised barrier homeostasis. In human aortic endothelial cells, NMN and Mito-TEMPO partially rescued mitochondrial dysfunction and the loss of barrier-associated proteins, indicating that mitochondrial redox imbalance, particularly mtROS accumulation, serves as a downstream amplifier of putrescine-HADH-associated endothelial injury. Collectively, these findings support the existence of a functional Enterococcus-associated putrescine-HADH pathway linking microbial metabolism to mitochondrial dysfunction, redox imbalance, and endothelial barrier disruption in AD, and nominate putrescine as a potential metabolic biomarker and therapeutic target.},
}

@article {pmid42636890,
year = {2026},
author = {Guha, L and Malik, JA and Bose, B},
title = {Living drug carriers: Microbial and bioengineered platforms redefining precision therapeutic and immunomodulatory delivery.},
journal = {Journal of controlled release : official journal of the Controlled Release Society},
volume = {},
number = {},
pages = {115274},
doi = {10.1016/j.jconrel.2026.115274},
pmid = {42636890},
issn = {1873-4995},
abstract = {Microbial living therapeutics are a new class of drug-delivery materials that combine synthetic biology, immunomodulation, and advanced formulations to achieve controllable therapeutic effects in space and time. In the broad field of living drug-delivery systems, therapeutic platforms include engineered microorganisms, mammalian immune cells, stem cells, viral vectors, extracellular-vesicle-producing cells, and hybrid bioengineered living materials. This review focuses on engineered microbial living drug carriers, including genetically modified bacteria and probiotic platforms, because these systems uniquely integrate programmable biosensing, in situ therapeutic synthesis, adaptive immunomodulation, and controllable drug delivery within a single living chassis. Designed microbes and consortia possess other unique functions, such as microenvironment sensing, programmed control of gene expression, and long-lasting in situ manufacturing of therapeutic payloads not available with small-molecule or biologic drugs. Recent progress in microbial chassis engineering, genetic circuit design, and biocontainment has enabled fine-tuning of immune responses, metabolic pathways, and tissue-specific signaling in a wide range of diseases from cancer to autoimmune and inflammatory diseases, to metabolic and endocrine disorders, neuro-immunological conditions (e.g., amyotrophic lateral sclerosis), infectious diseases including infectious threats without existing approved vaccines (Zika virus) as well as rare genetic disorders. Advances in formulation science, including encapsulation technologies, biomaterial-microbe hybrids, and stimuli-responsive release platforms, have enabled overcoming key translation challenges concerning microbial viability, biodistribution, safety, and controlled activation in complex physiological milieus like the gut (for enteric pathogens), tumor microenvironment (for oncolytic organisms), or injured tissues (for tissue-targeting organisms). Increasing numbers of clinical-stage LBP studies are now conducted under good manufacturing practice, standardized QC, and clinical conditions, ranging from emerging PK, biodistribution, and biomarker-driven studies to those adapted to living entities. The addition of host microbiome profiling, multi-omics analysis, and computational modeling is anticipated to increase therapeutic predictability and patient stratification. Taken together, these advances position live microbial therapeutics as programmable biological medicines with the potential for adaptive, context-specific administration and warrant further clinical development and increased integration within precision medicine-informed therapeutic approaches.},
}

@article {pmid42636957,
year = {2026},
author = {Niu, M and Luo, Y and Yangyang, C and Almulla, AF and Carvalho, AF and Li, J and Zhang, Y and Maes, M},
title = {A shift toward proteolytic gut fermentation links systemic inflammation to clinical phenotypes in major depressive disorder.},
journal = {Progress in neuro-psychopharmacology & biological psychiatry},
volume = {},
number = {},
pages = {111900},
doi = {10.1016/j.pnpbp.2026.111900},
pmid = {42636957},
issn = {1878-4216},
abstract = {BACKGROUND: The "Neuro-Immune-Metabolic-Oxidative Stress" (NIMETOX) theory identified systemic dysregulation in Major Depressive Disorder (MDD), yet the precise gut-derived metabolic triggers initiating this cascade remain elusive. This study investigated the interplay between fecal short-chain fatty acids (SCFAs), systemic immune activation, and clinical phenotypes to identify a potential "gut-immune biotype" for MDD.

METHODS: Fecal SCFA profiles and serum immune-inflammatory markers were quantified in 102 patients with MDD and 38 matched healthy controls. A multistage statistical approach was employed: binary logistic regression and linear discriminant analysis were utilized to evaluate the joint discriminative performance of the biomarkers, while multivariable regression models were applied to examine associations with clinical phenotypes, including the overall severity of depression (OSOD), physiosomatic symptoms, and recurrence of illness (ROI).

RESULTS: MDD patients exhibited a significant depletion of protective straight-chain SCFAs (acetate, propionate, butyrate) and an elevation in branched-chain SCFAs (BSCFAs), indicating a pathological shift from saccharolytic to proteolytic fermentation. This metabolic shift correlated with elevated acute phase inflammatory index (API) and epidermal growth factor (EGF). A multidimensional model combining BSCFAs, acetate, API, and EGF discriminated MDD from controls with adequate accuracy (AUC = 0.871). Furthermore, elevated BSCFAs and decreased protective SCFAs were strongly associated with higher OSOD, more severe physiosomatic symptoms, and increased ROI. Notably, 5-HT1A agent use remained associated with higher BSCFA levels after adjustment for MDD status.

CONCLUSION: MDD is characterized by a distinct "gut-immune biotype" tightly linked to toxic proteolytic gut fermentation. This metabolic-immune fingerprint provides a systems biology explanation for MDD and highlights the need for microbiome-targeted interventions in precision psychiatry.},
}

@article {pmid42637124,
year = {2026},
author = {Li, X and Zhou, J and Liu, X and Liu, L and Chen, Q and Xiang, Q and Gu, Y and Zhao, K and Zou, L and Wang, Q and Yu, H and Yu, X},
title = {Rhizobia block Cd absorption in peanut via rhizosphere microbiome assembly and N-regulated host defense.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {129012},
doi = {10.1016/j.envpol.2026.129012},
pmid = {42637124},
issn = {1873-6424},
abstract = {Cadmium (Cd) contamination severely threatens peanut (Arachis hypogaea L.) production and symbiotic nitrogen fixation (SNF). Although rhizobia inoculation can alleviate heavy metal toxicity in plants, how nitrate (NO3[-]) regulates Cd translocation and the defense of the "rhizobia-root-nodule" system remains unclear. Here, we investigated the mechanisms by which the peanut rhizobium, Rhizobium sp. HM13, mitigates Cd toxicity and sustains SNF under varying NO3[-] levels (N- and N+) via field and pot trials. Field trials showed that HM13 reduced rhizosphere bioavailable Cd and decreased seed Cd accumulation by 49.9%. Rhizosphere sequencing revealed that HM13 enriched functional taxa, particularly Actinobacteriota, Bacillus, and Bradyrhizobium, enhancing network complexity and stability. Pot experiments confirmed that HM13's Cd-blocking effect was strongly modulated by NO3[-]. Under N+ conditions, Cd stress reduced nitrogenase activity; nitrate supply induced premature nodule senescence, disrupted the symbiotic Cd-exclusion barrier, resulting in increased Cd accumulation in pods. Conversely, under N- conditions, robust symbiotic nitrogen fixation strengthened the root-nodule Cd-exclusion barrier, sustaining nitrogenase activity and reducing pod Cd by 38.6-41.8%. Physiologically, HM13 established a synergistic root-nodule defense network. Roots intercepted Cd via the POD-CAT-GSH-PRO pathway, while nodules protected nitrogenase activity through GR-FLA-mediated redox regulation. Overall, Rhizobium sp. HM13 is a dual-functional strain sustaining SNF and blocking Cd. This study elucidates the nitrogen-regulated SNF-antioxidant defense mechanism, providing theoretical and technical support for safe peanut production in Cd-contaminated farmlands.},
}

@article {pmid42632130,
year = {2026},
author = {Hao, X and Wu, L and Zeng, W and Gong, Q and Zhan, M and Miao, H and Yuan, C and Peng, Y},
title = {Isotopic and genomic interrogation unravels the sustaining mechanism of nitrate-dependent Fe(II) oxidation via organic carbon-driven internal iron cycle.},
journal = {Water research},
volume = {307},
number = {},
pages = {126727},
doi = {10.1016/j.watres.2026.126727},
pmid = {42632130},
issn = {1879-2448},
abstract = {Nitrate-dependent Fe(II) oxidation (NDFO) offers a promising approach for wastewater denitrification, but its sustainability is constrained by substantial Fe(II) demand and the resultant iron encrustation. By harnessing organic carbon in low C/N wastewater to drive dissimilatory Fe(III) reduction, this study establishes a self-sustaining internal iron cycle that overcomes this limitation. The organic carbon initiates the N/Fe co-metabolic cycle by reducing nitrate and Fe(III) to produce nitrite and Fe(II). The regenerated Fe(II) subsequently supports microbially mediated nitrite reduction to N2, completing the cycle. Without external Fe(II) supplementation, the system achieved 96% total nitrogen removal at a C/N ratio of 2.0, sustained by dynamic Fe(II)/Fe(III) transformations. Integrated DNA-SIP and metagenomic analyses revealed that organic carbon reshaped the microbiome, shifting functional dominance from autotrophic Thiobacillus to mixotrophic Thauera, which possesses genetic potential for both denitrification and Fe(III) reduction. This shift established a narG-nirS-dominated denitrification pathway, a genomic feature associated with high system performance. Furthermore, organic carbon alleviated iron encrustation and enhanced iron availability, with siderophore-related genes showing increased abundance, suggesting a potential role in reducing crust formation on cell surfaces. Overall, this study demonstrates that the inherent organic carbon in low C/N wastewater serves as a functional resource to drive a self-sustaining iron cycle, mitigating encrustation and eliminating external Fe(II) dependence for sustainable NDFO.},
}

@article {pmid42632242,
year = {2026},
author = {Zhang, F and Zhu, S and Wang, Y and Xia, H and Zhang, L and Wang, L and Zhao, X and He, L and Li, Q and Liu, Y and Zhang, G},
title = {Metallic micronutrients mitigate herbicide-microplastic stress on soil microbial functions in cornfields.},
journal = {Journal of hazardous materials},
volume = {516},
number = {},
pages = {143349},
doi = {10.1016/j.jhazmat.2026.143349},
pmid = {42632242},
issn = {1873-3336},
abstract = {Both herbicides and microplastics disrupt microbial functions in soils, but the pathways through which metallic micronutrients alleviate such disturbances are poorly understood. A nationwide survey in cornfields was conducted to reveal relationships among pollutants, micronutrients and microbial functions, followed by field experiments to verify the mitigating effects of these micronutrients. The survey demonstrated that acetochlor, atrazine and fiber-microplastics were negatively correlated with the functional genes nirS, cbbL and phoD, whereas soil pH was positively correlated with these genes. Structural modeling (SEM) indicated that fiber-shaped microplastics synergistically amplified the suppressive effects of atrazine and acetochlor on cbbL and phoD abundances, primarily through nirS downregulation, soil pH decline, and reduced microbial diversity. Consistently, field experiments showed that the herbicide thiencarbazone-methyl·isoxaflutole, when combined with biodegradable microplastics, inhibited nirS expression, thereby decreasing the abundances of cbbL and phoD. SEM analysis based on the survey suggested that zinc supplementation exerted an antagonistic effect against combined contamination by elevating nirS abundance. This mitigation effect was further verified by field variance analysis, which showed that zinc addition significantly enhanced nirS and cbbL abundances. Overall, this study provides a targeted strategy for alleviating the combined suppressive impacts of herbicides and microplastics on soil microbial functions during maize production.},
}

@article {pmid42632425,
year = {2026},
author = {Halliwell, B},
title = {Ergothioneine as an Emerging Food-Derived Bioactive Compound Protecting against Age-related Diseases: Issues Needing More Research.},
journal = {The American journal of clinical nutrition},
volume = {},
number = {},
pages = {101488},
doi = {10.1016/j.ajcnut.2026.101488},
pmid = {42632425},
issn = {1938-3207},
abstract = {Ergothioneine (ET) is a chemically-stable, tasteless, odourless, highly water-soluble diet-derived compound that is avidly absorbed and retained by the human body using a selective transporter, organic cation transporter novel 1, OCTN1 (often called the ET transporter, ETT). A substantial and growing body of evidence supports a role for ET in maintaining human health and protecting against age-related diseases, especially neurodegenerative diseases, and multiple studies indicate that low blood/plasma/serum ET levels increase the risk of developing age-related diseases. Despite the growing interest in ET, much fundamental work remains to be done to investigate its metabolism, actions (if any) on the genome, lipidome, metabolome and proteome, intracellular and intercellular transport (especially in the brain), precise mechanisms of cytoprotection, interactions with the microbiome, mycobiome and human pathogens, and identifying the factors that control body ET levels. This narrative review explores these issues and suggests what research needs to be done to improve our understanding of ET biology.},
}

@article {pmid42632547,
year = {2026},
author = {Abdelaziz, AM and Eladawy, RM},
title = {Immunopharmacological reprogramming of innate immune memory in Alzheimer's disease: From microglial priming to therapeutic resilience.},
journal = {Biochemical pharmacology},
volume = {},
number = {},
pages = {118381},
doi = {10.1016/j.bcp.2026.118381},
pmid = {42632547},
issn = {1873-2968},
abstract = {Alzheimer's disease (AD) is increasingly recognized as a disorder driven by dysregulated innate immunity rather than merely amyloid‑β accumulation. Microglia, the brain's resident innate immune cells, acquire long‑term functional memory, a process known as trained immunity or innate immune memory, through epigenetic and metabolic reprogramming. In AD, chronic exposure to amyloid‑β and tau aggregates locks microglia into a maladaptive primed state characterized by altered histone modifications (H3K4me3, H3K27ac), sustained glycolysis via the HIF‑1α/mTOR axis, and impaired phagocytic function, perpetuating neuroinflammation and neurodegeneration. This review critically synthesizes recent advances that define the molecular architecture of microglial immune memory, including epigenetic rewiring, immunometabolic shifts, and intercellular crosstalk with astrocytes and the gut microbiome. We evaluate the emerging immunopharmacological toolbox designed to reverse maladaptive priming and restore neuroprotective resilience, focusing on small‑molecule NLRP3 inflammasome inhibitors (HT‑6184, DFV890, BGE‑102), TREM2 agonists (VG‑3927, MNA‑001), metabolic modulators (metformin, rapamycin), trained immunity‑based vaccination (BCG), specialized pro‑resolving mediators (maresin 1, resolvin D1, lipoxin A4), and senolytics. Clinical‑stage agents and their mechanisms of action are highlighted. We argue that the next generation of AD therapeutics must move beyond target suppression toward the functional reprogramming of brain innate immunity, and we propose a biomarker-guided, patient-stratified framework that integrates multimodal immunopharmacology, combining NLRP3 inhibition, TREM2 agonism, metabolic reprogramming, and resolution pharmacology to restore immune homeostasis. Harnessing the plasticity of innate immune memory offers a transformative paradigm for disease‑modifying therapy in AD.},
}

@article {pmid42632573,
year = {2026},
author = {de Castilhos, V and Cruz, JC and Braga, A and Gabana, ADA and Bertagnolli, AC and Cerva, C and Varela, APM and Klain, V and Mayer, FQ},
title = {The Role of Microbiota in Bovine Tuberculosis: Characterizing Bacterial Communities Across Lungs, Gut, and Lymph Nodes.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {108795},
doi = {10.1016/j.micpath.2026.108795},
pmid = {42632573},
issn = {1096-1208},
abstract = {Animals with bovine tuberculosis (bTB) develop granulomatous lesions as part of a complex immune response to chronic antigenic stimulus involving innate and adaptive mechanisms; however, the association of the microbiota with the development of and susceptibility to bTB remains poorly understood. This study characterizes the bacterial communities at different body sites involved in the pathophysiology of bTB, highlighting the gut-lung axis and their association with disease. Lungs, gut, thoracic, and mesenteric lymph nodes samples were collected from 31 bovines from a single herd (n = 19 bTB; n = 12 controls). The samples were analyzed using high-throughput sequencing of the 16S rRNA gene. A significant difference in beta diversity was observed between the bTB and control groups only in the thoracic lymph nodes (p < 0.05), whereas no significant differences were detected in the other sites. LEfSe and GLM analyses showed different taxa significantly enriched in the control group: Eubacterium ventriosum, Lacticaseibacillus, Paucibacter, Clostridioides, Bdellovibrio/Bdellovibrionaceae and Rhodobacteraceae, some of them suggested by previous findings as taxa of interest in their potential as preventive or diagnostic candidates. Additionally, analysis of microbial correlations along the gut-lung axis identified distinct phylum-level associations between bTB and healthy groups, suggesting altered microbial patterns in bTB. These findings contribute to the understanding of bovine microbiota composition across organs, their association with bTB and the pathogenesis of bTB, highlighting microbial candidates for future validation for microbiota-based interventions and laying the groundwork for future studies exploring host-microbiota-pathogen interactions in the context of bTB.},
}

@article {pmid42632665,
year = {2026},
author = {Zhuang, Y and Sun, T and Hu, F and Bi, Y and Lv, X and Ma, T},
title = {Dietary resveratrol improves meat quality in lambs via the rumen-muscle axis mediated by reshaped microbial metabolism.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 2},
pages = {119868},
doi = {10.1016/j.foodres.2026.119868},
pmid = {42632665},
issn = {1873-7145},
mesh = {Animals ; *Resveratrol/pharmacology/administration & dosage ; *Rumen/microbiology/metabolism/drug effects ; *Diet/veterinary ; *Muscle, Skeletal/metabolism/drug effects ; Sheep ; Animal Feed/analysis ; *Red Meat/analysis ; *Gastrointestinal Microbiome/drug effects ; Fatty Acids, Volatile/metabolism ; Amino Acids/metabolism ; },
abstract = {Resveratrol (RSV) is a plant-derived polyphenol known to enhance host health and growth in animals. In this study, we used integrated metagenomic and metabolomic approaches to show that dietary RSV reshapes the rumen microbiome and its metabolism. Specifically, RSV upregulated volatile fatty acid (VFA) and amino acid synthesis pathways while suppressing methanogenesis in finishing lambs. These microbial metabolic changes propagated along a rumen-muscle axis, driving compositional improvements, as evidenced by elevated polyunsaturated fatty acids (gamma-linolenic acid) and key amino acids (Ser, Ala, Ile, and Leu), as well as enhanced meat quality traits, including reduced drip loss, increased eye muscle area, and improved color stability. Microbiota-muscle correlation analyses further linked the signature rumen microbes with muscle nutritional indicators. Our findings delineate a clear microbe-metabolite-tissue pathway through which RSV influences mutton quality, offering a mechanistic basis for microbiome-guided strategies to optimize meat production in ruminants.},
}

Animals
*Resveratrol/pharmacology/administration & dosage
*Rumen/microbiology/metabolism/drug effects
*Diet/veterinary
*Muscle, Skeletal/metabolism/drug effects
Sheep
Animal Feed/analysis
*Red Meat/analysis
*Gastrointestinal Microbiome/drug effects
Fatty Acids, Volatile/metabolism
Amino Acids/metabolism

@article {pmid42632691,
year = {2026},
author = {Rahman, AU and Valentino, V and Cobo-Díaz, JF and Sequino, G and Ordóñez, AA and Ercolini, D and De Filippis, F},
title = {Metagenomic profiling reveals how ecological and processing drivers shape the beef microbiome from farm to fork.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 2},
pages = {119939},
doi = {10.1016/j.foodres.2026.119939},
pmid = {42632691},
issn = {1873-7145},
mesh = {Animals ; Cattle ; *Microbiota/genetics ; *Red Meat/microbiology ; *Food Handling/methods ; *Metagenomics/methods ; *Food Microbiology ; Farms ; *Bacteria/genetics/classification/isolation & purification ; Seasons ; Biofilms ; },
abstract = {Meat processing environments harbor complex microbial ecosystems that may be transferred to the final product, thus influencing product quality and safety. Several factors may affect microbiome composition, such as seasonality and sanitation procedures. In this study, we carried out a metagenomic analysis over two seasons across four beef processing facilities, following beef carcasses from farm-to-fork. The pre-maturation environment was dominated by Corynebacterium xerosis and Acinetobacter johnsonii in summer, and by Bifidobacterium pseudolongum and Cutibacterium acnes in winter, whereas meat maturation environments were colonized by a specialized lactic acid bacterial community. The long-term maturation stage was led by Carnobacterium divergens and Carnobacterium maltaromaticum, whereas Pseudolactococcus carnosus and Pseudolactococcus paracarnosus prevailed during the retail stage. The environmental microbiome exhibited broad metabolic potential, in contrast to the specialized, low-diversity profiles of mature meat. Routine sanitation practices did not fully remove detectable microbial DNA signatures from environmental surfaces and were associated with shifts in taxonomic and functional profiles, including a greater representation of biofilm-associated genes. We also identified a diverse phage community, and statistical modeling revealed strong negative predictive associations with Listeria monocytogenes, Salmonella enterica, and Staphylococcus aureus. Collectively, our findings demonstrate that the beef processing microbiome is shaped by the interaction of multiple ecological forces. Understanding these interactions provides a comprehensive framework for ecology-based strategies to improve meat quality, safety, and shelf-life.},
}

Animals
Cattle
*Microbiota/genetics
*Red Meat/microbiology
*Food Handling/methods
*Metagenomics/methods
*Food Microbiology
Farms
*Bacteria/genetics/classification/isolation & purification
Seasons
Biofilms

@article {pmid42632698,
year = {2026},
author = {Shi, Y and He, H and Niu, M and Fan, Y and Yu, M and Ma, Y and Wang, P and Gao, Z and Chen, X},
title = {Microbial co-occurrence network and spatial metabolism underlie wheat cultivar effects on medium-high temperature Daqu fermentation.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 2},
pages = {119943},
doi = {10.1016/j.foodres.2026.119943},
pmid = {42632698},
issn = {1873-7145},
mesh = {*Triticum/microbiology/metabolism ; *Fermentation ; Metabolomics ; *Microbiota/physiology ; Hot Temperature ; Taste ; *Food Microbiology ; },
abstract = {Although wheat cultivar is widely accepted to shape Daqu quality, it remains unclear which cultivar-linked microbial property - taxonomic composition, spatial niche differentiation, or the topology of cross-domain interactions - is the proximate driver of flavor-precursor accumulation. To address this gap, four wheat cultivars (GS19, QM725, QM838 and ZM) were used as natural perturbations, and depth-resolved (core/surface) 16S/ITS profiling, untargeted metabolomics and volatilomics were combined across the 90-day fermentation-maturation trajectory of medium-high-temperature Daqu. Of the four cultivars, only QM725 produced a microbiome with high node density and a positive-edge-dominated topology (88.73% positive correlations versus 76.98% in ZM), here termed a "cooperative-network" phenotype. This phenotype was spatially partitioned into two complementary metabolic compartments: the surface (Group P) was enriched in glycerophospholipid and arachidonic-acid metabolism, driving ester and floral-note formation; the core (Group X) was enriched in α-linolenic-acid and amino-acid metabolism, promoting the accumulation of aldehydes/ketones and higher alcohols. QM725-specific flavor markers (2-heptanone, 6-methyl-5-hepten-2-ol, methyl 13,16-octadecadiynoate) mapped onto these compartments. Co-occurrence analysis further identified an unclassified Thermoactinomycetaceae lineage as a network-level negative regulator of key alcohols and aldehydes, whereas Lactobacillus and Bacillus form complementary co-occurrence modules linking amino-acid metabolism to flavor-precursor accumulation through decarboxylation and Strecker degradation pathways, consistent with our previous bioaugmentation evidence that wheat-origin Bacillus strains causally modulate Daqu protease/amylase activities and amino-acid pools. These results identify cultivar-driven differences in microbial co-occurrence network and spatial metabolism as a hitherto underused dimension of Daqu quality, and introduce a transferable network-phenotype criterion for cultivar selection in Baijiu production.},
}

*Triticum/microbiology/metabolism
*Fermentation
Metabolomics
*Microbiota/physiology
Hot Temperature
Taste
*Food Microbiology

@article {pmid42632709,
year = {2026},
author = {José, S and Gil, D and Cruz, C and Brandão, J and Valério, E},
title = {Azole antifungals in food and environmental matrices: occurrence and comparative assessment with predicted no effect concentrations (PNECs).},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 2},
pages = {119972},
doi = {10.1016/j.foodres.2026.119972},
pmid = {42632709},
issn = {1873-7145},
mesh = {*Azoles/analysis ; *Antifungal Agents/analysis ; Wastewater/chemistry ; *Food Contamination/analysis ; Humans ; Environmental Monitoring ; },
abstract = {Azole antifungals are widely used to treat fungal infections in humans, animals, and plants, and as fungicides to protect crops and post-harvest commodities. Their extensive use favors environmental dissemination, with residues frequently detected in surface waters, wastewater effluents, soils, and food-related matrices. Given that many fungal infections originate from environmental sources, the presence of antifungals in these settings may contribute to the selection and spread of antifungal resistance, representing a growing One Health concern. This systematic review aimed to evaluate the occurrence of azole antifungals in environmental and food-related matrices and to assess their potential ecological, public -health, and food-system risks by comparing reported concentrations with available Predicted No Effect Concentration (PNEC) values. The systematic literature review was conducted in accordance with PRISMA guidelines, where studies reporting the detection of azole antifungals in surface water, food, wastewater effluents, and soil were included. A total of 83 studies met the inclusion criteria. Voriconazole, clotrimazole, ketoconazole, and fluconazole were among the most frequently detected medical azoles across surface water, wastewater effluents, food, and soil samples, while several agricultural azoles were also detected in matrices directly connected with crop production and aquatic food chains. Concentrations in surface waters often exceeded PNEC values, indicating potential risks to environmental quality, antifungal efficacy, and food-system sustainability, as and human health. In addition, conventional wastewater treatment processes reveal to be insufficient for the complete removal of these compounds, facilitating their persistence and reintroduction into the environment and, potentially, into agricultural systems through irrigation, sludge application, and aquatic trophic transfer. In conclusion, the widespread presence of azole antifungals in environmental matrices, including food products, together with their incomplete removal by conventional wastewater treatment processes, may contribute to the selection, emergence, and dissemination of antifungal resistance. These findings highlight the need for integrated surveillance across water, soil, wastewater, food products, and agricultural inputs, as well as more efficient treatment technologies, residue monitoring, integrated pest management, and responsible microbiome-based innovations to reduce antifungal contamination and associated food-sector risks.},
}

*Azoles/analysis
*Antifungal Agents/analysis
Wastewater/chemistry
*Food Contamination/analysis
Humans
Environmental Monitoring

@article {pmid42632744,
year = {2026},
author = {Zhao, X and Xiao, S and Ma, X and Qi, Y and Liu, Z and Xu, X and Chang, C and Wu, J and Gong, Z and Shao, B and Liu, X},
title = {Modulating stress responses via the microbiota-gut-brain axis: a pathway-focused review of GABA, 5-HT, and kynurenine metabolites.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 2},
pages = {119908},
doi = {10.1016/j.foodres.2026.119908},
pmid = {42632744},
issn = {1873-7145},
mesh = {*gamma-Aminobutyric Acid/metabolism ; Humans ; *Kynurenine/metabolism ; *Serotonin/metabolism ; *Gastrointestinal Microbiome/physiology ; Animals ; *Brain/metabolism ; *Brain-Gut Axis/physiology ; *Stress, Psychological/metabolism ; Dysbiosis ; *Stress, Physiological ; },
abstract = {Stress is a major risk factor for human anxiety, depression, and other neuropsychiatric disorders, yet nutritional strategies that target upstream biological mechanisms remain insufficiently developed. Growing evidence indicates that host-microbiota co-regulated metabolites act as functional mediators within the microbiota-gut-brain axis, shaping individual vulnerability or resilience to stress. In this review, we synthesize current preclinical and human evidence with a focus on three metabolite systems of high mechanistic relevance-γ-aminobutyric acid, serotonin, and kynurenine-pathway metabolites. We discuss how microbial activity, host metabolism, and dietary inputs interact to modulate brain-relevant signaling under stress. We highlight neuroendocrine, neuroimmune, and neural pathways through which these systems may act, including stress-induced disruptions in intestinal and blood-brain barrier integrity and amplification of inflammatory signaling. Evidence across models suggests that stress-associated dysbiosis alters GABAergic and serotonergic signaling and shifts tryptophan metabolism toward neuroactive kynurenines, thereby biasing neural excitability, synaptic plasticity, and affect-related behaviors. We further evaluate food-based psychobiotic strategies-such as targeted whole-food matrices, fermented foods, and selected probiotic strains-that can reprogram microbial metabolism to restore neurotransmitter balance and attenuate inflammation. Finally, we propose a translational framework emphasizing strain- and pathway-specific mechanisms, standardized metabolite quantification, and biomarker-guided personalization to advance microbiome-metabolite interventions for stress-related brain dysfunction.},
}

*gamma-Aminobutyric Acid/metabolism
Humans
*Kynurenine/metabolism
*Serotonin/metabolism
*Gastrointestinal Microbiome/physiology
Animals
*Brain/metabolism
*Brain-Gut Axis/physiology
*Stress, Psychological/metabolism
Dysbiosis
*Stress, Physiological

@article {pmid42632882,
year = {2026},
author = {Yoon, D and Ottavio, B and Yun, C and Jung, SY and Beydoun, MA and Launer, LJ and Song, M},
title = {Association between self-reported oral health issues and autoimmune diseases: evidence from UK biobank.},
journal = {BMC oral health},
volume = {26},
number = {1},
pages = {},
pmid = {42632882},
issn = {1472-6831},
support = {ZIA AG000522/AG/NIA NIH HHS/United States ; },
mesh = {Humans ; Female ; *Autoimmune Diseases/epidemiology ; *Self Report ; United Kingdom/epidemiology ; Middle Aged ; *Oral Health/statistics & numerical data ; Male ; *Mouth Diseases/epidemiology ; UK Biobank ; Aged ; Risk Factors ; },
abstract = {BACKGROUND: Oral microbiome dysbiosis may contribute to autoimmune disease development, but epidemiological evidence linking oral health and autoimmune disease risk is limited.

OBJECTIVES: To evaluate the association between self-reported oral health issues by questionnaire-defined as the presence of painful or bleeding gums, mouth ulcers, toothache, dentures, or loose teeth-and the risk of incident autoimmune diseases in the UK Biobank cohort.

MATERIALS AND METHODS: Individuals reporting any oral health issues (painful/bleeding gums, mouth ulcers, toothache, dentures, and loose teeth) were classified as any self-reported oral health issues; others as no self-reported oral health issues. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for any autoimmune diseases and 39 types of autoimmune diseases using Cox regression models with Bonferroni correction. We investigated associations of the type and number of self-reported oral health issues with autoimmune diseases.

RESULTS: Among 451,404 participants (mean age: 56.4 years, 54.2% female), any self-reported oral health issues (N = 177,198; 39.3%) were associated with an increased risk of any autoimmune diseases (HR 1.11, 95% CI 1.09-1.14). Painful gums showed the strongest association (HR 1.39, 95% CI 1.31-1.47), followed by mouth ulcers (1.23, 1.18-1.27) and toothache (1.21, 1.15-1.27). Risk increased with the number of self-reported oral health issues (per 1-issue increase: HR 1.09, 95% CI 1.08-1.11, P-trend < 0.001). For specific autoimmune disease, primary biliary cholangitis (HR 1.65, 95% CI 1.24-2.19), rheumatism (1.48, 1.23-1.77), lichen planus (1.35, 1.15-1.57), Sjögren's disease (1.30, 1.11-1.52), pernicious anemia (1.28, 1.12-1.46), rheumatoid arthritis (1.18, 1.12-1.26), and psoriasis (1.16, 1.07-1.26) were identified.

CONCLUSIONS: Self-reported oral health issues were associated with an increased risk of incident autoimmune diseases, suggesting that oral health indicators may serve as clinically relevant markers of autoimmune disease risk.},
}

Humans
Female
*Autoimmune Diseases/epidemiology
*Self Report
United Kingdom/epidemiology
Middle Aged
*Oral Health/statistics & numerical data
Male
*Mouth Diseases/epidemiology
UK Biobank
Aged
Risk Factors

@article {pmid42628725,
year = {2026},
author = {Niazi, SA and Zhang, Y},
title = {Apical Periodontitis: A Hidden Non-Communicable Disease in Global Health - a Narrative Review of Longitudinal Research.},
journal = {Journal of endodontics},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.joen.2026.08.028},
pmid = {42628725},
issn = {1878-3554},
abstract = {Apical periodontitis (AP) is a highly prevalent oral disease increasingly recognized as a hidden non-communicable disease (NCD) with systemic consequences. This narrative review integrates the findings from longitudinal studies on a well-characterized AP cohort to elucidate the link between AP systemic conditions. Evidence highlights AP as a reservoir for low-grade bacteremia and systemic inflammatory burden. Elevated baseline levels of inflammatory markers including fibroblast growth factor-23, interleukin-1β, high-sensitivity C-reactive protein, and asymmetric dimethylarginine were observed in AP patients, correlating with lesion size and microbial profiles in both root canal and blood microbiomes. AP is also associated with altered metabolic syndrome indicators - such as hemoglobin A1C, triglycerides, low-density lipoprotein and shifts in serum metabolomic profiles involving glucose, lipid, branched-chain amino acid, and tryptophan metabolism. Importantly, successful endodontic treatment can lead to significant reductions in inflammatory biomarkers, improved metabolic syndrome (MetS) indicators, and improved glucose and lipid metabolism. Collectively, these findings position AP as an important NCD which impacts beyond the oral cavity via linking to systemic conditions and related cardiometabolic risks, highlighting the importance of its timely diagnosis and successful management.},
}

@article {pmid42628727,
year = {2026},
author = {Fouad, AF},
title = {Comprehensive Microbiome Analyses for Regenerative Endodontic Therapy.},
journal = {Journal of endodontics},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.joen.2026.08.016},
pmid = {42628727},
issn = {1878-3554},
abstract = {Comprehensive microbiome analyses include the study of all microbial taxa, including bacteria, archaea, viruses, and fungi, as well as their functional activities and antibiotic resistance gene expression. Regenerative endodontic therapy (RET) presents a clinical situation where the most effective antimicrobial approaches are needed in order to ensure clinical success. In this paper, different contemporary technologies for the identification of endodontic microorganisms, such as with next generation sequencing (NGS), and their functional characterization, such as with whole genome sequencing (WGS), are described. The role of transcriptomics, as well as resistome analysis, are also discussed. Furthermore, the manner in which all this work and knowledge could be incorporated into clinical endodontics in general, and RET as a special treatment, is outlined.},
}

@article {pmid42628828,
year = {2026},
author = {Hela, A and Donthineni, PR and Singh, S and Basu, S and Arunasri, K},
title = {Tear film Microbiota in Meibomian gland dysfunction: Compositional changes and their correlation with meibum lipids and tear film parameters.},
journal = {Experimental eye research},
volume = {},
number = {},
pages = {111212},
doi = {10.1016/j.exer.2026.111212},
pmid = {42628828},
issn = {1096-0007},
abstract = {Meibomian gland dysfunction (MGD) is the leading cause of evaporative dry eye disease. The multifactorial pathogenesis of MGD remains poorly understood, with limited understanding of the interplay between the microbiome and meibum lipid composition. This study investigates the ocular microbiota and lipid profiles in patients with MGD (n = 20, diagnosed according to DEWSIII criteria) and in Healthy Controls (HC, n = 24). Bacterial isolates from the tear film wash, cultured on blood agar, were assessed for their ability to form biofilms. Meibum collected from the upper and lower eyelids of the same patients was profiled for lipidomics (LC-MS/MS). Bacteria were identified through 16S rRNA gene sequencing and BLAST search analysis. MGD samples showed an increased abundance of Gram-negative bacteria and a significant reduction in the Genus Bacillus. Biofilm-forming capacity was markedly higher in MGD isolates. MGD meibum revealed increased levels of phospholipids and cholesteryl esters. Lipid pathway enrichment analysis (LIPEA) of the differentially abundant lipids linked them to glycerophospholipid metabolism, ferroptosis, autophagy, inflammation, and apoptosis. Spearman correlation analysis between MGD and HC revealed positive correlations between the abundance of biofilm formers and the percentage of polar lipids, total bacterial counts and reduced lipid layer thickness, suggesting their potential interactions in MGD. The results of the study indicate that MGD is characterized by an altered ocular surface microbial composition, increased biofilm-forming capability, and disrupted lipid composition.},
}

@article {pmid42628955,
year = {2026},
author = {Mai, HT and Nguyen, CC and Nguyen, TTB and Vo, HTN and Pham, TT and Nguyen, NT and Nguyen, NT and Doan, HL and Vu, HT and Nguyen, MD and Nguyen, NTB and Ta, HTK and Nguyen, AH and Pham, TD and Tran, VC and Nguyen, ATV},
title = {Clinical, microbiological, and immune marker improvement with adjunctive vaginal-spray spore-forming probiotics in women with vaginal infections.},
journal = {Beneficial microbes},
volume = {},
number = {},
pages = {1-21},
doi = {10.1163/18762891-bja00131},
pmid = {42628955},
issn = {1876-2891},
abstract = {Symptomatic vaginal and cervicovaginal conditions include bacterial vaginosis (BV), vulvovaginal candidiasis (VVC), and other sexually transmitted infection (STI)-related conditions with overlapping clinical features. Adjunctive probiotic therapies are increasingly explored to complement standard antimicrobial treatment. This randomised, double-blind, controlled trial examined clinical, microbiological, and immune marker patterns associated with the adjunctive use of vaginal-spray spore-forming probiotics (LiveSpo X-Secret; Bacillus subtilis ANA46, Bacillus clausii ANA39, Heyndrickxia coagulans ANA40; 1 × 109 cfu/ml) in women with BV, VVC, and STI-related co-infections. A total of 120 symptomatic women were randomised (1:1; n = 60 per group) to receive either physiological saline spray (Control) or probiotic spray (LiveSpo X-Secret) for 28 days, in addition to standard treatment. Outcomes included clinical signs and symptoms, pathogen positivity and relative load (real-time PCR), vaginal microbiota composition (16S rRNA sequencing), and IL-1β, IL-8, and secretory IgA (ELISA) at days 7 and 28 versus baseline. No adverse events were reported. Symptom improvement was observed from day 7. By day 28, the X-Secret group showed a substantial reduction in the proportion of patients with ≥3 symptoms/signs (from 68.18% to 4.55%; OR = 6.42, P = 0.0147). Multi-pathogen positivity decreased from 50 to 11.36%. Gardnerella vaginalis relative load decreased 275-fold more in the X-Secret group than in the Control group, calculated based on 2ΔCt (P = 0.0185). Stratified subsample microbiome analysis indicated increased lactobacilli dominance and reduced dysbiosis-associated genera (Prevotella, Gardnerella). IL-1β and IL-8 levels decreased by 62.98% (P < 0.0001) and 42.95% (P = 0.0002), respectively, while sIgA increased by 65.67% (P < 0.0001). In summary, this two-arm randomised study describes clinical, microbiological, and immune marker patterns associated with adjunctive vaginal-spray Bacillus spore probiotic versus saline spray, both in combination with standard treatment. While causal inferences cannot be drawn, these findings highlight the need for further aetiology-specific and longer-term studies. The trial was prospectively registered at ClinicalTrials.gov (NCT06165354).},
}

@article {pmid42629014,
year = {2026},
author = {Nissen, L and Casciano, F and Di Nunzio, M and Bordoni, A and Gianotti, A},
title = {Simulation of insect enriched bread consequences on gut microbiota.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 1},
pages = {119750},
doi = {10.1016/j.foodres.2026.119750},
pmid = {42629014},
issn = {1873-7145},
mesh = {Animals ; *Bread/microbiology/analysis ; Fermentation ; *Gastrointestinal Microbiome/physiology ; Humans ; *Gryllidae ; *Food, Fortified ; Bacteria/classification/metabolism ; Colon/microbiology ; },
abstract = {Insect powders are newly regulated in Europe and can be used to fortify protein-enriched bakery products. Because protein sources influence gut microbial balance, assessing their impact on the human microbiome is essential. This study investigated how cricket (Acheta domesticus) powder affects colon microbiota and whether sourdough fermentation improves protein-enriched breads. Using an in vitro gut model combining Infogest® digestion with MICODE© colon microbiota fermentation, four bread prototypes were examined. Metabolomic and microbiomic analyses showed that sourdough breads with insect powder increased some beneficial bacteria (Bifidobacteriaceae), contained opportunists (Clostiridium group I), reduced sulfurate producers (Desulfovibrio spp.), and enhanced production of acetate and butyrate. However, they also reduced certain beneficial taxa (Verrucomicrobiaceae) and increased the level of Enterobacteriaceae. Acetate, butyrate, and hexanoate correlated positively with lactic acid bacteria, as both increased after colon microbiota fermentation of insect sourdough bread Although further studies are needed, sourdough processing appears the most promising approach for producing cricket-enriched protein breads. These findings highlight both benefits and risks of insect-based protein fortification, showing modulation of different core groups of the colon microbiota.},
}

Animals
*Bread/microbiology/analysis
Fermentation
*Gastrointestinal Microbiome/physiology
Humans
*Gryllidae
*Food, Fortified
Bacteria/classification/metabolism
Colon/microbiology

@article {pmid42629059,
year = {2026},
author = {Lv, J and Qu, Y and Yan, Q and Cheng, K and Wu, Q and Zhang, J and Duan, X and Han, S and Tian, H and Shi, L},
title = {Polygonatum kingianum polysaccharides ameliorate cognitive impairments in alcohol-exposed obese mice in a sex-specific manner by regulating the gut microbiome and metabolome.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 1},
pages = {119827},
doi = {10.1016/j.foodres.2026.119827},
pmid = {42629059},
issn = {1873-7145},
mesh = {Animals ; *Polygonatum/chemistry ; Male ; *Gastrointestinal Microbiome/drug effects ; *Polysaccharides/pharmacology ; Female ; Mice ; Diet, High-Fat/adverse effects ; *Ethanol/adverse effects ; *Metabolome/drug effects ; *Cognitive Dysfunction/drug therapy/metabolism ; Mice, Inbred C57BL ; Mice, Obese ; Sex Factors ; Hippocampus/drug effects ; Obesity ; },
abstract = {High-fat diet and alcohol are often co-exposed in real life, contributing to cognitive deficits and posing a significant yet modifiable public health challenge. We extensively evaluated the efficacy of polysaccharides extracted from Polygonatum kingianum (PP) in mitigating cognitive deficits in high-fat-diet-induced obese mice exposed to alcohol in females and males. PP alleviated cognitive deficits assessed via open-field and Y-maze tests, with a more pronounced efficacy in females, accompanied by restored hippocampal histopathology and improved synaptic integrity markers. PP also ameliorated metabolic dysregulation (i.e., hyperglycemia, dyslipidemia, oxidative stress), improved colon morphology and tight junction proteins (ZO-1, Claudin-1). Sex-specific alterations were significantly prominent in remodeling gut microbiome and fecal metabolome induced by PP. For instance, Parabacteroides goldsteinii, Bacteroides caecimuris, and the families Staphylococcaceae and Prevotellaceae were elevated in females while Lactobacillus spp. and Clostridium spp. exclusively elevated in males. Mendelian randomization using large-scale human GWAS data demonstrated causal relationships between certain gut bacteria and cognitive function. Metabolomics identified largely non-overlapping sets of PP-regulated metabolites and pathways in females and males. Correlation analysis linked microbiota to microbiota-derived metabolites and network pharmacology identified core targets (e.g., BCL2, CASP3, TNF, STAT3, PTGS2, PPARG) involved in PP's cognition protection benefits. Molecular docking validated the binding ability of core targets to 8 pharmacokinetically favorable metabolites regulated by PP in each sex, reinforcing the sex-specific mechanism. Collectively, our findings provide novel insights into the benefits of PP in alleviating diet-induced cognitive deficits and underscore the necessity of considering sex as a critical biological variable in developing microbiome-targeted nutritional therapies.},
}

Animals
*Polygonatum/chemistry
Male
*Gastrointestinal Microbiome/drug effects
*Polysaccharides/pharmacology
Female
Mice
Diet, High-Fat/adverse effects
*Ethanol/adverse effects
*Metabolome/drug effects
*Cognitive Dysfunction/drug therapy/metabolism
Mice, Inbred C57BL
Mice, Obese
Sex Factors
Hippocampus/drug effects
Obesity

@article {pmid42629065,
year = {2026},
author = {Liu, F and Luo, Z and Jabeen, S and Liu, G and Li, P and Wu, T and Li, W},
title = {Structural programmability of jujube polysaccharides: Extraction, molecular architecture, and microbiota-mediated fermentation Design for gut-Brain-Axis-Relevant Applications.},
journal = {Food research international (Ottawa, Ont.)},
volume = {242},
number = {Pt 1},
pages = {119833},
doi = {10.1016/j.foodres.2026.119833},
pmid = {42629065},
issn = {1873-7145},
mesh = {*Fermentation ; *Polysaccharides/chemistry/isolation & purification/metabolism ; *Ziziphus/chemistry ; *Gastrointestinal Microbiome/physiology ; Humans ; *Brain/physiology ; Pectins/chemistry ; },
abstract = {Jujube polysaccharides (JPs) are heterogeneous food pectic glycans, but how extraction and post-isolation modification define their molecular architecture and microbiota-accessible functionality remains insufficiently integrated. This review critically synthesizes evidence linking extraction conditions to JP structural templates and evaluates how post-isolation remodeling tunes molecular weight, RG-I/HG balance, side-chain architecture, esterification, charge, conformation, and assembly state. Using an evidence-stratified framework, we distinguish direct JP findings from mechanisms inferred from broader pectin and dietary-fiber literature. We propose that backbone architecture, RG-I-associated side chains, esterification, and supramolecular organization may shape microbial accessibility, fermentation kinetics, selective utilization, short-chain fatty acid production, and gastrointestinal substrate availability. This structure-microbiota-metabolite perspective supports a validation pipeline based on defined JP fractions, matched pectin controls, standardized fermentation models, and causal microbiome designs. Gut-brain-axis relevance is discussed as an indirect, evidence-limited downstream implication rather than an established JP mechanism.},
}

*Fermentation
*Polysaccharides/chemistry/isolation & purification/metabolism
*Ziziphus/chemistry
*Gastrointestinal Microbiome/physiology
Humans
*Brain/physiology
Pectins/chemistry

@article {pmid42629157,
year = {2026},
author = {Wilborn, D and Constantinou, A and Franz, A and Schwarzer, R and Menzel, P and Engelhardt, G and Tomova-Simitchieva, T and Amin, R and Zhou, G and Hillmann, K and Kottner, J and Ralle, J and Konietschke, F and Blume-Peytavi, U},
title = {Maternal and Infant Skin Microbiome Synchrony and Divergence: A Longitudinal Study of Skin Microbial Ecology and Early-Life Assembly.},
journal = {Experimental dermatology},
volume = {35},
number = {8},
pages = {e70349},
doi = {10.1111/exd.70349},
pmid = {42629157},
issn = {1600-0625},
mesh = {Humans ; Female ; Longitudinal Studies ; Pregnancy ; *Skin Microbiome ; Infant ; *Skin/microbiology ; Infant, Newborn ; Adult ; *Microbiota ; Biodiversity ; },
abstract = {During pregnancy and after childbirth, women's skin undergoes significant changes which may affect the skin's functional and structural characteristics and microbial diversity. Like their mothers, the newborns also experience various skin challenges in the months following birth. Temporal changes in skin microbiome in special groups such as pregnant women and newborns, as well as the interrelation between their skin's microbial diversity, have not been investigated. We followed women from pregnancy through 6 months after delivery, and their infants from 4 weeks to 6 months of age to investigate their skin characteristics and the microbiome, and potential associations. We enrolled 109 pregnant females residing in Berlin, Germany, with 93 mothers-infant pairs completing the study. Microbiome investigations included DNA isolation as single-site sampling using volar forearm skin swabs. Bioinformatic analysis involved OTU clustering at 97% sequence identity, taxonomic assignment using NCBI reference databases, and calculation of biodiversity metrics, including relative abundance of the dominant bacterial phylotypes, bacterial diversity and Shannon diversity index. The maternal skin microbiome showed mild to moderate changes throughout pregnancy and the 6 months postpartum period. In infants, alpha diversity significantly increased (mean species richness from 82.6 at 4 weeks to 116.1 at 6 months), although it did not reach maternal diversity levels (145.4 at 6 months postpartum). Regarding the microbiome consistency of the included women and infants, the within-pair similarity was always significantly higher than between-pair similarity for both time points. Therefore, we conclude that there is likely a relationship between the microbiome of the mother and that of her child.},
}

Humans
Female
Longitudinal Studies
Pregnancy
*Skin Microbiome
Infant
*Skin/microbiology
Infant, Newborn
Adult
*Microbiota
Biodiversity

@article {pmid42629271,
year = {2026},
author = {Brix, F and Demetrowitsch, T and Jensen-Kroll, J and Roeder, N and Rohmann, N and Hasler, M and Kosch, R and Waschina, S and Szymczak, S and Schreiber, S and Laudes, M and Zacharias, HU and Schwarz, K},
title = {Corrigendum to "Educational inequalities are associated with distinct metabolomic and gut microbiome patterns in adults" [Soc. Sci. Med. 403 (2026) 119454].},
journal = {Social science & medicine (1982)},
volume = {},
number = {},
pages = {119701},
doi = {10.1016/j.socscimed.2026.119701},
pmid = {42629271},
issn = {1873-5347},
}

@article {pmid42629340,
year = {2026},
author = {Wan, X and Zhou, Y and Yang, J and Guo, G and Lei, M and Chen, T},
title = {Engineering Plant-Microbiome Interaction Networks for Predictive Soil Bioremediation Under the Stress-Stability Paradox.},
journal = {Physiologia plantarum},
volume = {178},
number = {4},
pages = {e71082},
doi = {10.1111/ppl.71082},
pmid = {42629340},
issn = {1399-3054},
support = {2023YFD1702300//National Key Research and Development Program of China/ ; 4257072380//National Natural Science Foundation of China/ ; },
mesh = {*Biodegradation, Environmental ; *Plants/microbiology/metabolism ; *Soil Microbiology ; *Microbiota/physiology ; Soil/chemistry ; Soil Pollutants/metabolism ; Metals, Heavy/metabolism ; Stress, Physiological ; },
abstract = {Soil pollution poses a profound threat to ecosystem and human health. This review proposes a novel framework centered on engineering biological interaction networks for efficient and sustainable soil decontamination, moving beyond the traditional single-species paradigm. We dissect the architecture and dynamics of key interactions, including plant-plant, plant-microbe, and microbe-microbe interactions, within remediation contexts, elucidating how mechanisms like mutualism, competition, and cross-kingdom signaling govern the fate of heavy metals, organic pollutants, and complex mixtures. Crucially, we explore how these natural networks can be actively engineered through strategies such as targeted bioaugmentation, precision biostimulation, and rational plant community assembly to enhance remediation outcomes. Furthermore, we highlight how cutting-edge multi-omics, synthetic ecology, and computational modeling are transitioning the field from descriptive ecology to predictive network design, enabling the decoding of the soil black box and the rational construction of tailored, resilient remediation consortia. Finally, we discuss the ecological challenges of introducing designed networks and outline a future road map toward precision restoration ecology, where theory-guided interaction network management enables effective, stable, and ecologically sound soil clean-up. This network-centric paradigm represents a fundamental shift from experience-based trial-and-error to a principled design approach for restoring soil health.},
}

*Biodegradation, Environmental
*Plants/microbiology/metabolism
*Soil Microbiology
*Microbiota/physiology
Soil/chemistry
Soil Pollutants/metabolism
Metals, Heavy/metabolism
Stress, Physiological

@article {pmid42629403,
year = {2026},
author = {ELHindi, S and Abdalla, S and Azab, MM and Bendary, MM},
title = {Impact of Infant Feeding Mode on Gut Microbiome Composition in Early Life: Evidence from an Egyptian Cohort.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42629403},
issn = {2045-2322},
mesh = {Humans ; *Breast Feeding ; Infant ; Egypt ; *Gastrointestinal Microbiome/genetics ; RNA, Ribosomal, 16S/genetics ; Feces/microbiology ; Male ; Female ; *Bacteria/classification/genetics ; Biodiversity ; Cohort Studies ; },
abstract = {The infant gut microbiome develops rapidly in early life, shaping immune maturation and metabolic pathways. Data from Middle Eastern populations remain limited. We studied Egyptian infants aged 1 to 6 months to assess feeding related differences in gut microbiome composition. Stool samples were collected and the gut microbiota was profiled using 16S rRNA gene sequencing targeting the V3-V4 region. Sequence processing, denoising, and taxonomic assignment were performed in QIIME2. Differentially abundant taxa between feeding groups were identified using LEfSe. Alpha and beta diversity, and co-occurrence networks were analyzed. Feeding mode was the dominant factor shaping microbiome composition and diversity. Artificial feeding showed Actinobacteria dominance, near absence of Bacteroidetes, and lowest diversity. Breastfeeding was associated with a more balanced phylum distribution, detectable Bacteroidetes, increased Proteobacteria, and significantly higher richness and diversity. Mixed feeding showed the highest alpha diversity and a Firmicutes dominated profile, consistent with a transitional microbial state. Beta diversity clearly separated breastfed from artificially fed infants, with mixed feeding intermediate. Genus level signatures differed by feeding mode. Artificial feeding enriched Bifidobacterium. Breastfeeding enriched facultative anaerobes including Escherichia Shigella and Enterobacter. Mixed feeding enriched fermentative genera such as Subdoligranulum and Eubacterium. Network analysis revealed structured co-variation among anaerobic commensals in breastfed infants and denser opportunistic connectivity in artificially fed infants. Feeding mode strongly influences gut microbiome development in Egyptian infants. Exclusive breastfeeding is associated with greater microbial richness and broader ecological structure, whereas formula feeding is linked to reduced diversity and a narrower community profile. Mixed feeding reflects an intermediate configuration. These findings support breastfeeding promotion for optimal early immune development.},
}

Humans
*Breast Feeding
Infant
Egypt
*Gastrointestinal Microbiome/genetics
RNA, Ribosomal, 16S/genetics
Feces/microbiology
Male
Female
*Bacteria/classification/genetics
Biodiversity
Cohort Studies

@article {pmid42629862,
year = {2026},
author = {Luo, HN and Wu, ZX and Guan, JY},
title = {Frequency locking to environmental forcing suppresses oscillatory extinction in phage-bacteria interactions.},
journal = {Physical review. E},
volume = {114},
number = {1-1},
pages = {014412},
doi = {10.1103/rch2-2hsr},
pmid = {42629862},
issn = {2470-0053},
mesh = {*Bacteriophages/physiology ; *Models, Biological ; *Bacteria/virology/growth & development ; *Extinction, Biological ; *Environment ; },
abstract = {Bacteriophage-bacteria interactions are central to microbial ecology, influencing evolution, biogeochemical cycles, and pathogen behavior. Most theoretical models assume static environments and passive bacterial hosts, neglecting the joint effects of bacterial traits and environmental fluctuations on coexistence dynamics. This limitation hinders the prediction of microbial persistence in dynamic ecosystems such as soils and oceans. Using a minimal ordinary differential equation framework, we demonstrate that environmental fluctuations can suppress destructive oscillations through resonance, promoting coexistence where static models otherwise predict collapse. Counterintuitively, we find that lower bacterial growth rates are helpful in enhancing survival under high infection pressure, elucidating the observed postinfection growth reduction. Our studies highlight bacterial hosts as active builders of ecological dynamics and environmental variation as a potential stabilizing force. Our findings thus bridge a theory-experiment gap and provide a framework for predicting microbial responses to environmental stress, which might have potential implications for phage therapy, microbiome management, and climate-impacted community resilience as well.},
}

*Bacteriophages/physiology
*Models, Biological
*Bacteria/virology/growth & development
*Extinction, Biological
*Environment

@article {pmid42630122,
year = {2026},
author = {Xu, Y and Shen, H},
title = {Overcoming Resistance to Immune Checkpoint Blockade: Mechanistic Insights and Emerging Therapeutic Directions.},
journal = {Iranian journal of immunology : IJI},
volume = {23},
number = {3},
pages = {1},
doi = {10.22034/iji.2026.111387.3205},
pmid = {42630122},
issn = {1735-367X},
abstract = {Immune checkpoint inhibitors have revolutionized cancer therapy by delivering long-lasting responses in a subset of patients across many cancer types. Yet, their effectiveness is often limited by high rates of primary and acquired resistance. This resistance is driven by complex interactions among tumor-intrinsic alterations, immunosuppressive factors within the tumor microenvironment, and host-related determinants. This review critically examines the biological mechanisms underlying resistance to immune checkpoint inhibitors, including defects in antigen presentation, dysregulated interferon signaling, activation of oncogenic pathways, compensatory upregulation of alternative immune checkpoints, and microbiome-associated immune modulation. In addition to defining these challenges, this review also highlights emerging opportunities for overcoming these obstacles. Emerging opportunities to circumvent resistance include biomarker-guided patient stratification, rational combination therapies that engage complementary immune pathways, modulation of the tumor microenvironment, and integration of multi-omics approaches to identify predictive resistance signatures. The central conclusion of this review is that effective clinical translation will necessitate a paradigm shift from discrete pathway inhibition toward integrated precision immuno-oncology strategies that combine molecular profiling, immune-contexture analysis, and mechanism-based combination therapies. Such integrated approaches may improve patient selection, overcome resistance, and expand the proportion of patients who achieve durable responses to immune checkpoint blockade.},
}

@article {pmid42630173,
year = {2026},
author = {Liu, Y and Wang, L and Han, Z and Wang, Z and Jia, W},
title = {Systemic inflammatory biomarkers in gastroesophageal reflux disease: current evidence and future perspectives.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1893763},
pmid = {42630173},
issn = {2296-858X},
abstract = {Gastroesophageal reflux disease (GERD) is a common gastrointestinal disorder that affects a large proportion of the population and is associated with impaired quality of life and increased healthcare utilization. Although GERD has traditionally been attributed to excessive reflux and dysfunction of the anti-reflux barrier, growing evidence indicates that inflammatory and immune-related processes also contribute to symptom development, mucosal injury, and disease progression. Accordingly, peripheral blood-derived inflammatory biomarkers, including the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), and systemic immune-inflammation index (SII), have been investigated as simple and readily available indicators of systemic inflammation. Clinical studies have suggested that these hematological indices may be associated with the presence of GERD, endoscopic phenotypes, and disease severity, although reported values and cutoff thresholds remain inconsistent. In addition, chronic low-grade inflammation, impaired epithelial barrier function, obesity-associated metabolic inflammation, and alterations in the microbiome are increasingly recognized as interacting mechanisms that may influence both local esophageal injury and systemic inflammatory responses. However, published findings remain inconsistent, and the clinical utility of these biomarkers has yet to be clearly established. This review provides an overview of the inflammatory mechanisms involved in GERD and evaluates current evidence regarding the potential role of hematological inflammatory biomarkers in clinical practice. Their strengths, current limitations, and priorities for future research are also discussed.},
}

@article {pmid42630190,
year = {2026},
author = {Ray, S and Francis, GA and Jeyakumar, SS and Chavan, P and Supreethee, S and Vashishth, R},
title = {Millet: a functional powerhouse against chronic lifestyle disease.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1884184},
pmid = {42630190},
issn = {2296-861X},
abstract = {Chronic lifestyle diseases such as cardiovascular disease, type 2 diabetes, and obesity are increasing globally, now accounting for more than two-thirds of deaths worldwide. In this context, millets are regaining attention as nutrient-dense, climate-resilient grains from traditional diets. They are rich in protein, dietary fiber, essential vitamins, minerals, and bioactive compounds that contribute to improved metabolic health and overall well-being. This review compiles and synthesizes current scientific evidence on the nutritional composition, bioactive profile, and disease-modulating mechanisms of millets. It also explores the role of millets in gut microbiome modulation, particularly their prebiotic potential in stimulating the production of short-chain fatty acids (SCFAs) and enhancing gut barrier integrity. Furthermore, the review highlights innovative food applications, including the incorporation of millets into modern food products such as fortified flours, breakfast cereals, snack bars, and beverages. Millets have demonstrated the ability to blunt postprandial blood glucose spikes by up to 15%, reduce cholesterol levels by nearly 10%, and promote natural calorie regulation, thereby supporting weight management and metabolic balance. Their prebiotic fibers nourish beneficial gut bacteria, contributing to improved gut health and immune defense. By integrating traditional knowledge with modern nutritional science, millets emerge as promising functional foods for preventing and managing chronic lifestyle disorders. Promoting millet-based diets offers a sustainable and health-promoting approach to address the growing burden of non-communicable diseases.},
}

@article {pmid42630261,
year = {2026},
author = {Colom, J and Baig, A and Kalmar, L and Belkhiri, A and Travers, A and Gigante, AM and Connerton, PL and Connerton, IF and Grant, AJ and Holmes, M and Barrow, PA and Atterbury, RJ},
title = {The pig as a preclinical model for human phage therapy of polybacterial enteric infections.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1857948},
doi = {10.3389/fmicb.2026.1857948},
pmid = {42630261},
issn = {1664-302X},
abstract = {BACKGROUND: Diarrhoeal disease remains a leading cause of morbidity and mortality among children in low-and-medium-income countries (LMIC). Polybacterial infections and increasing antimicrobial resistance complicate treatment, underscoring the need for alternative approaches. Bacteriophage therapy offers a targeted treatment capable of combating multiple pathogens simultaneously. Here, we report use of a bacteriophage cocktail targeting Enterotoxigenic E. coli, Salmonella and Campylobacter in a polybacterial porcine model of infant enteric disease.

METHODS: Weaned pigs were challenged with all three pathogens and subsequently treated with a cocktail of three phages. Pathogen loads, phage titres, clinical scores and fecal microbiome composition were measured and compared with untreated pathogen-challenged controls and unchallenged sentinel animals.

RESULTS: Phage-treated pigs exhibited significant reductions in E. coli and Salmonella burdens, each decreasing by >1.8 log10 CFU/g relative to unchallenged controls (p < 0.05). Treatment produced corresponding increased in bacteriophage titres and led to significant improvements in clinical scores. Conversely, Campylobacter loads remained largely unchanged following phage administration. Microbiome analysis showed differences between challenged and unchallenged pigs (p = 0.09), and between pathogen-challenged and phage-treated pigs (p = 0.5), although these were not statistically significant.

CONCLUSION: This study demonstrates the first use of phage therapy to target polybacterial enteric infections in a pig model of human disease. Simultaneous reductions in pathogen load and improved clinical outcomes highlight the potential of bacteriophage cocktails as treatments for bacterial enteric infections of relevance to children in low and middle-income countries, and to livestock health.},
}

@article {pmid42630413,
year = {2026},
author = {Mu, S and Wang, Y and Qin, W and Mao, M and Wang, Y and Zhang, Y and Wang, Y},
title = {A systemic epithelial-immune-neural framework for pediatric atopic dermatitis-allergic rhinitis comorbidity.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1864351},
doi = {10.3389/fimmu.2026.1864351},
pmid = {42630413},
issn = {1664-3224},
mesh = {Humans ; *Dermatitis, Atopic/immunology/epidemiology ; *Rhinitis, Allergic/immunology/epidemiology ; Comorbidity ; Child ; Animals ; },
abstract = {Atopic dermatitis (AD) and allergic rhinitis (AR) commonly coexist in childhood and are associated with an important clinical burden. Their frequent coexistence and substantial mechanistic overlap suggest that pediatric AD-AR comorbidity may involve patterns more complex than simple co-occurrence. However, existing models do not provide an operational approach for determining whether reproducible coupling between AD and AR disease activity extends beyond shared susceptibility and disease-specific responses occurring in parallel. In this Hypothesis and Theory article, we propose the systemic epithelial-immune-neural framework as an operational and falsifiable model for investigating pediatric AD-AR comorbidity. The framework integrates four interacting proposed mechanistic domains-epithelial barrier and alarmin signaling, type 2 immune activation, neuroimmune signaling, and microbiome regulation-and distinguishes established organ-specific mechanisms from candidate cross-organ coupling. It also separates core mechanisms from external inputs, contextual modifiers, and observable outcomes, and translates the proposed relationships into directed edges, feedback loops, testable predictions, and falsification criteria. Current evidence supports the biological plausibility of the framework and demonstrates substantial mechanistic overlap between AD and AR, but direct pediatric evidence for reproducible cross-organ coupling between AD and AR disease activity remains limited. The framework should therefore be regarded as a research model rather than a new diagnostic classification, composite network score, or separate treatment pathway. Clinical assessment and management should remain grounded in validated, guideline-based approaches for AD and AR. By organizing shared mechanisms and clinical observations into explicit and testable claims, the framework provides a structured basis for investigating the existence, potential mechanisms, heterogeneity, and clinical relevance of cross-organ coupling in pediatric AD-AR comorbidity.},
}

Humans
*Dermatitis, Atopic/immunology/epidemiology
*Rhinitis, Allergic/immunology/epidemiology
Comorbidity
Child
Animals

@article {pmid42630427,
year = {2026},
author = {Snelling, TJ and Johnson, CA and Warren, HE and Taylor-Pickard, J and Huntington, JA and Sinclair, LA},
title = {Modulation of the rumen microbiome and metabolism in dairy cows by altering the concentrate feeding pattern and the inclusion of Saccharomyces cerevisiae yeast.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1884444},
doi = {10.3389/frmbi.2026.1884444},
pmid = {42630427},
issn = {2813-4338},
abstract = {Dairy cattle are typically fed a total mixed ration (TMR), which is prepared in an automated mixer wagon. On-farm, effective TMR mixing can often be neglected due to lack of time or training. This leads to a disbalance of intake and potentially detrimental effects on health and production. Using dietary treatments to simulate this effect, this study determined the response of rumen metabolism and microbiome to different concentrate allocations in combination with a live Saccharomyces cerevisiae supplement (yeast supplementation, YS). The 4 × 4 Latin square design consisted of four dairy cows fitted with permanent rumen cannulae, which were fed a partial mixed ration with dietary concentrates (4 kg per cow per day) in an even or an uneven pattern of allocation (concentrate allocation, CA). YS was included in the TMR at a rate of 10 g per cow per day. Rumen metabolism was determined by measuring the pH, volatile fatty acids (VFAs), and ammonia nitrogen (NH3-N). The rumen microbial community was characterised using 16S rRNA gene amplicon sequencing. Both CA and YS had no effect (p > 0.05) on the dry matter intake, milk yield, or composition. CA did not affect the rumen NH3-N and VFA concentrations (p > 0.05). YS inclusion tended to increase the rumen pH (p = 0.088), acetate (p = 0.076), and valerate (p = 0.091). YS significantly increased the total VFA (p = 0.033) and propionate concentrations (p < 0.016). CA had little overall effect on the rumen microbiome beta diversity. However, there was a reduction in the relative abundance of a Prevotellaceae feature associated with an uneven pattern of CA. Bray-Curtis clustering of the microbiome was observed with YS (p = 0.002), driven by a decrease of Gammaproteobacteria and Prevotellaceae features and an increase of a Christensenellaceae feature (LDA > 2.0).},
}

@article {pmid42630435,
year = {2026},
author = {Peng, P and Cai, J and Zhang, L and Lu, Y and Kuang, P},
title = {The subgingival microbiome in periodontitis: from ecological dysbiosis and metabolic reprogramming to precision interventions.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1906205},
doi = {10.3389/fmicb.2026.1906205},
pmid = {42630435},
issn = {1664-302X},
abstract = {Periodontitis is a dysbiosis-driven chronic inflammatory disease characterized by complex interactions among the subgingival microbiome, microbial metabolism, and host immune responses. Accumulating evidence indicates that disease progression is not solely determined by the enrichment of specific periodontal pathogens but is critically associated with ecological disruption and functional reprogramming of the subgingival microbial community. During the transition from periodontal health to disease, microbial metabolism shifts from carbohydrate utilization toward proteolysis and amino acid fermentation, resulting in altered production of short-chain fatty acids, polyamines, volatile sulfur compounds, hydrogen sulfide, and nitric oxide. These metabolic alterations contribute to inflammasome activation, immune dysregulation, osteoclastogenesis, and progressive periodontal tissue destruction. Beyond local pathology, periodontal microorganisms and their metabolites can disseminate through the oral-systemic axis, thereby influencing the pathogenesis of multiple systemic disorders. Recent advances in multi-omics technologies have further revealed that metabolic reprogramming represents a critical mechanistic link connecting ecological dysbiosis with host inflammatory responses. Consequently, therapeutic strategies are evolving from conventional antimicrobial approaches toward precision microbiome-based interventions, including probiotics, postbiotics, bacteriophages, predatory bacteria, metabolic modulation, and oral microbiome transplantation. In this review, we integrate current evidence on microbial ecology, metabolism, and host interactions and propose the Ecological Dysbiosis-Metabolic Reprogramming-Host Crosstalk framework. This framework highlights metabolic reprogramming as the central bridge linking microbial dysbiosis to host inflammatory damage and provides a conceptual basis for the development of precision periodontal medicine.},
}

@article {pmid42630507,
year = {2026},
author = {Cox-Holmes, AN and Green, GBH and Potier, ACE and Wang, Y and Chen, D and Morrow, CD and McFarland, BC},
title = {Microbial and metabolic signatures of humanized microbiome mice associate with Tlr2 expression and Th17 immune programming.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1879544},
doi = {10.3389/fimmu.2026.1879544},
pmid = {42630507},
issn = {1664-3224},
mesh = {Animals ; *Th17 Cells/immunology/metabolism ; Mice ; *Toll-Like Receptor 2/genetics/metabolism/immunology ; Humans ; *Gastrointestinal Microbiome/immunology ; Germ-Free Life ; Fecal Microbiota Transplantation ; },
abstract = {INTRODUCTION: The gut microbiota plays a critical role in immune system development. However, whether normal variation in healthy human microbiota alone can establish distinct baseline immune states that influences responses to disease and therapy remains unclear.

METHODS: To address this, we employed a humanized microbiome (HuM) mouse model where fecal matter is transplanted from healthy human donors into gnotobiotic mice. Our previous studies found that HuM mouse lines have differential responses to glioma immunotherapy, so we sought to define how microbiota composition mediates host immunity prior to disease development.

RESULTS: Despite being genetically identical and disease-free, HuM mice exhibited distinct microbiota-driven immune profiles. Mice harboring responder-associated microbiota (HuM2) had higher proportions of gram-positive gut bacteria and decreased acetate and propionate compared to nonresponder-associated (HuM1) mice. Single-cell RNA-sequencing of colonic CD45[+] cells from HuM2 mice had a higher portion of B cells and neutrophils, an increase in Tlr2 in the lamina propria, and a systemic increase in Th17 cells compared to HuM1.

DISCUSSION: Together, these findings reveal a microbiota dependent program associating gram-positive enrichment and altered metabolite production to TLR2-associated immune activation and Th17 response. Our results demonstrate that human microbiome variation alone correlates with distinct baseline immune profiles that may predispose hosts to differential immunotherapy responses.},
}

Animals
*Th17 Cells/immunology/metabolism
Mice
*Toll-Like Receptor 2/genetics/metabolism/immunology
Humans
*Gastrointestinal Microbiome/immunology
Germ-Free Life
Fecal Microbiota Transplantation

@article {pmid42630573,
year = {2026},
author = {Nie, Q and Hu, X and Zhang, Y and Pan, L and Zhang, X and Zhou, Y and Fu, T and Zheng, L and Xiao, F and Liu, Y and Du, S and Liu, J and Liu, L and Xiong, X and Wu, Y and Fan, D and Tao, L and Ren, F},
title = {Gut microbiota-driven immunomodulation in tuberculosis: targeting dysbiosis to overcome drug resistance.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1889315},
doi = {10.3389/fimmu.2026.1889315},
pmid = {42630573},
issn = {1664-3224},
mesh = {Humans ; *Dysbiosis/immunology ; *Gastrointestinal Microbiome/immunology/drug effects ; Animals ; *Antitubercular Agents/therapeutic use/adverse effects ; *Immunomodulation ; *Tuberculosis/immunology/microbiology/drug therapy ; *Mycobacterium tuberculosis/immunology/drug effects ; *Tuberculosis, Multidrug-Resistant/immunology/microbiology/therapy ; Host-Directed Therapy ; },
abstract = {Tuberculosis (TB) remains a major global health threat, hampered by the escalating prevalence of multidrug-resistant (MDR) and extensively drug-resistant (XDR) strains. Managing these resistant infections demands protracted, intricate, and frequently hepatotoxic drug regimens with poor efficacy, toxicity, and adherence issues. This landscape underscores an urgent need to move beyond a purely antimicrobial-focused paradigm. Converging lines of evidence now firmly position the gut microbiota-a pivotal orchestrator of systemic immunity, metabolic homeostasis, and drug metabolism-as a central determinant in both TB pathogenesis and therapeutic success. Our review describes a vicious cycle at the heart of contemporary TB management. A critical and often overlooked trigger is the profound and persistent gut microbiota dysbiosis induced by the anti-TB medications themselves. Far from an incidental side effect, this dysbiosis is strongly implicated as a pathological driver in preclinical models and observational studies. It undermines pulmonary host defense through the gut-lung axis, aggravates anti-tuberculosis drug-induced liver injury (ATB-DILI), and cultivates a systemic state of chronic inflammation coupled with metabolic dysregulation (such as impaired lipid metabolism). Paradoxically, this host environment fosters Mycobacterium tuberculosis persistence and disease progression. In drug-resistant TB, this vicious cycle is amplified, is associated with therapeutic failure and may contribute to the selection of resistance in correlative studies. To disrupt this cycle, we assess the translational promise of interventions targeting the microbial ecosystem. This encompasses a multi-pronged strategy: employing probiotics, prebiotics, and tailored dietary modifications to restore ecological balance; utilizing fecal microbiota transplantation (FMT) for more profound restoration; and pioneering the development of novel, narrow-spectrum antimicrobials designed to preserve commensal flora. We contend that the integration of microbiome stewardship into TB care is an indispensable evolution in our approach. By concurrently targeting the pathogen and fortifying the host's intrinsic microbial defenses, this holistic strategy presents a transformative pathway to surmount drug resistance, alleviate treatment-related toxicity, and improve patient outcomes.},
}

Humans
*Dysbiosis/immunology
*Gastrointestinal Microbiome/immunology/drug effects
Animals
*Antitubercular Agents/therapeutic use/adverse effects
*Immunomodulation
*Tuberculosis/immunology/microbiology/drug therapy
*Mycobacterium tuberculosis/immunology/drug effects
*Tuberculosis, Multidrug-Resistant/immunology/microbiology/therapy
Host-Directed Therapy

@article {pmid42630587,
year = {2026},
author = {Boutin, S and Rondeau-Leclaire, J and Roy, A and Laforest-Lapointe, I},
title = {A field-based study of phyllosphere mycobiomes in apple orchards under varying agricultural management strategies.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag203},
doi = {10.1093/ismeco/ycag203},
pmid = {42630587},
issn = {2730-6151},
abstract = {Microbial communities in the phyllosphere are key players in plant health and disease resistance, yet their response to agricultural management strategies remains poorly understood under field conditions. Here, we compare fungal community composition and diversity across conventional and organic apple orchards using ITS amplicon sequencing. Leaf samples were collected from six sites at three distinct time points during the 2023 growing season (in May, July, and August) corresponding approximately to monthly intervals throughout the summer. Flower samples were collected from the same trees in May. Our analyses reveal that agricultural management strategies are significantly associated with fungal community structure, with effects intensifying from May to July. Both types of management strategies showed enrichment for different genera known to include common apple tree pathogens: Alternaria and Podosphaera were associated with conventional sites, while Didymella and Ramularia were associated with organic sites. Although fungal alpha diversity was higher in May at conventional orchards compared to organic orchards, it declined over time at conventional sites while it remained stable at organic sites. Together, these patterns indicate that distinct management interventions impose contrasting selective pressures on the apple tree phyllosphere mycobiome, thus shaping both broad fungal community composition and the dominance dynamics of key fungal taxa. Our findings underscore the ecological relevance and inherent challenges of field-based microbiome research, and provide insights to inform the development of sustainable orchard management strategies grounded in fungal community dynamics.},
}

@article {pmid42630741,
year = {2026},
author = {Hou, L and Wu, Y and Hou, R and Li, Y and Song, Z},
title = {Perioperative microbiota at the colorectal anastomosis: local host-microbe interactions in healing and leak.},
journal = {Frontiers in surgery},
volume = {13},
number = {},
pages = {1895315},
doi = {10.3389/fsurg.2026.1895315},
pmid = {42630741},
issn = {2296-875X},
abstract = {Anastomotic leak remains a major complication after colorectal resection, but established clinical and technical risk factors do not fully explain why some repairs fail during early healing. This review treats perioperative microbiota as part of a local host-microbe wound environment at the colorectal anastomosis rather than as a broad gut microbiome signal. Literature was identified through PubMed and Web of Science searches covering 1 January 2010-6 July 2026, using terms combining colorectal anastomosis, anastomotic leak, microbiota, microbiome, and host-microbe interactions. Evidence was tiered by directness to the anastomotic wound, distinguishing stool-based proxy signals from mucosal, tissue-adjacent, and functional measurements. Stool and broader luminal profiles provide indirect signals for suture-line events unless paired with site-aware sampling. Mucosal, mucus, and tissue-adjacent studies move closer to the repair site but remain mostly exploratory and associative. Animal and in vitro work supports plausible mechanisms, including collagenase activity, biofilm-like persistence, metabolite signaling, inflammatory modulation, and extracellular matrix injury, but does not establish human clinical causality. Current evidence justifies better perioperative sampling, function-aware microbial analysis, and integration with conventional leak-risk factors; it does not justify routine microbiome-guided risk stratification or leak-prevention interventions. The most useful next step is longitudinal, site-aware human work anchored to standardized leak outcomes and surgical context.},
}

@article {pmid42630981,
year = {2026},
author = {Bi, Y and Song, W and Glymenaki, M and Hu, J and Li, X and Huang, H and Peng, Y and Ni, S and Haonon, O and Liu, Z and Daowtak, K and Shen, X and Peng, H and Phetcharaburanin, J and Tang, H and Wang, Y and Li, JV and Jiang, M and Powell, N and Zhong, VW and Holmes, E and Xianyu, Y and Liu, Z},
title = {The gut microbiome organ.},
journal = {iMeta},
volume = {},
number = {},
pages = {e70144},
doi = {10.1002/imt2.70144},
pmid = {42630981},
issn = {2770-596X},
abstract = {The human gut microbiome is increasingly viewed as an active regulator of host physiology, extending beyond earlier taxonomy-centered descriptions of a complex microbial community. Accumulating evidence supports an organ-like conceptual framework in which the gut microbiome exhibits spatially structured organization, extensive metabolic capacity, and continuous bidirectional communication with host systems. Through the production of bioactive metabolites with endocrine-like, immunomodulatory, and neuromodulatory properties, the microbiome contributes to metabolic, immune, and neuroendocrine regulation, thereby influencing systemic homeostasis and disease susceptibility. Recent advances in multi-omics, spatial biology, and computational modeling are moving the field from taxonomic association toward functional interpretation, mechanistic insight, and causal inference. These approaches are beginning to reveal microbiome-derived functional modules and host-microbe signaling networks that are shaped by host genetics, diet, medications, feeding patterns, circadian rhythms, and environmental exposures. In this review, we synthesize current mechanistic and translational evidence to conceptualize the gut microbiome as an organ-like functional system, delineate its structural and functional organization, and propose a framework for mapping, modeling, and therapeutically targeting microbiome-derived circuits to support precision medicine in metabolic, inflammatory, and selected gut-brain axis-related disorders.},
}

@article {pmid42631006,
year = {2026},
author = {Ripollés-Campos, E and Hernández-Calderón, P and Palomino-Schätzlein, M and Jorge-Bueno, L and Bono, A and Miralpeix, A and Sastre-Bataller, I and García-Villarreal, L and Tugores, A and Mariño, Z and Berenguer, M and Benítez-Páez, A and Espinós, C},
title = {Integrated multiomics analysis reveals metabolic and microbiome alterations in Wilson disease.},
journal = {iScience},
volume = {29},
number = {9},
pages = {117101},
doi = {10.1016/j.isci.2026.117101},
pmid = {42631006},
issn = {2589-0042},
abstract = {Wilson disease (WD) is a rare autosomal recessive disorder caused by mutations in ATP7B, which encodes a copper transporter. Abnormal ATP7B function leads to copper deposition, mainly in the liver and brain, resulting in hepatic, neurological, and psychiatric impairments. Metabolic alterations have been reported in patients with WD and in murine WD models. We performed a multiomics study in an in-depth phenotyped and multi-center cohort to establish gut microbiota perturbations and metabolic dysfunctions in WD. Metabolomics helped distinguish changes in the tricarboxylic acid cycle, amino acid metabolism, and dyslipidemia in patients with WD. Metataxonomics allowed the detection of attenuated pivotal bacterial species. Independent WD cohorts and in vitro assays validated the lipid metabolism alterations and loss of Akkermansia muciniphila. Our results indicate a profound metabolic dysfunction in patients with WD beyond ATP7B-linked copper toxicity. Pharmacological treatment appears detrimental for beneficial species, aggravating organ cross-talk in the gut-liver axis.},
}

@article {pmid42631058,
year = {2026},
author = {Medrano, M and Pacheco-Herrero, M and Borges, Z and Laureano, JR and Dominguez-Garcia, J and Gil-Ventura, R and Castro-Tejada, G},
title = {Characterization of the intestinal microbial profile in mild cognitive impairment and Alzheimer's disease.},
journal = {Dementia & neuropsychologia},
volume = {20},
number = {},
pages = {e20250440},
doi = {10.1590/1980-5764-DN-2025-0440},
pmid = {42631058},
issn = {1980-5764},
abstract = {UNLABELLED: Alzheimer's disease (AD) and mild cognitive impairment (MCI) are major contributors to dementia, with growing prevalence in Latin America. Evidence suggests that gut microbiota alterations may influence neurodegeneration, but data on Hispanic population are lacking.

OBJECTIVE: Characterize gut microbiota in individuals with AD, MCI, and controls in the Dominican Republic, exploring clinical, demographic, and dietary associations.

METHODS: Prospective-translational study including 88 participants aged ≥60 years. Performed clinical, cognitive, and functional assessments. Stool samples analyzed using 16S rRNA gene sequencing. Bioinformatic processing using Quantitative Insights into Microbial Ecology Version 2 (QIIME2) and R. Alpha and beta diversity, taxonomy, and differential abundance were evaluated. Dietary influences were assessed using PERMANOVA.

RESULTS: No significant differences in alpha diversity (Shannon index 4-5, Simpson index 0.94-0.99, p>0.05) or beta diversity (p>0.05) were observed between groups. Firmicutes (51.9%) and Bacteroidota (34.1%) dominated the microbiota. Higher Desulfobacterota abundance in MCI and AD (0.54 and 0.61%, respectively, vs. 0.34% in controls; p<0.05). The Firmicutes/Bacteroidota ratio was lower in men with MCI (1.09) compared to controls and AD (1.70). MCI and AD were associated with increased levels of the genera Bilophila, Odoribacter, and Parabacteroides (p<0.05) and reduced levels of Mitsuokella and Eubacterium ruminantium. Dietary interactions, e.g., mango, lettuce, and carrot, influenced specific taxa (p<0.05).

CONCLUSION: This study pioneers gut microbiota characterization in AD and MCI in the Dominican Republic, identifying microbial alterations in cognitive impairment and highlighting regional dietary and ethnic factors. Longitudinal and multi-omics studies are warranted to clarify causality and therapeutic potential.},
}

@article {pmid42631188,
year = {2026},
author = {Webb, B and Farrell, M and Montelius, C and Önning, G},
title = {Probiotics and iron bioavailability: mechanisms, clinical evidence, and translational applications-a comprehensive review of the probiotic strain Lactiplantibacillus plantarum 299v (LP299V®).},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1905459},
doi = {10.3389/fnut.2026.1905459},
pmid = {42631188},
issn = {2296-861X},
abstract = {Iron deficiency remains the most prevalent micronutrient deficiency globally, driven in large part by the limited bioavailability of non-heme iron and compounded by dietary inhibitors, inflammation-mediated hepcidin regulation, and challenges associated with conventional iron supplementation. Health effects of prolonged iron deficiency include heart irregularities, weakened immunity, and cognitive impairment. Growing evidence highlights the gut microbiome as a key modulator of nutrient absorption, with probiotics emerging as a promising adjunctive strategy. Among these, the Lactiplantibacillus plantarum strain Lp299v (LP299V®, proprietary strain of Probi®) has demonstrated consistent efficacy in enhancing non-heme iron bioavailability through multiple complementary mechanisms, including luminal acidification via organic acid production, stabilization and chelation of soluble iron complexes, facilitation of ferric-to-ferrous reduction, and potential mitigation of inhibitors such as phytates. Additional effects on host physiology, such as improved intestinal barrier function, increased short-chain fatty acid production, and attenuation of inflammation, further support its role in optimizing iron uptake. The present review gives an overview of how probiotic strains may modulate iron absorption, and more specifically focuses on describing effects obtained with the Lp299v strain. Ten peer-reviewed clinical studies have described the effects of Lp299v for increasing iron absorption. Human isotope studies show that Lp299v increases fractional iron absorption by approximately 20-50% across diverse dietary contexts, while randomized controlled trials and meta-analyses indicate meaningful improvements in iron status, particularly in populations with elevated requirements such as women of reproductive age, pregnant women, and athletes. From the mechanistic studies combined with clinical evidence, results suggest that Lp299v functions as a bioavailability enhancer rather than a substitute for iron intake. Given its versatility in delivery formats, favorable safety profile, and applicability across a range of dietary patterns and socioeconomic settings, Lp299v represents a microbiome-informed approach to addressing the persistent global burden of iron deficiency that has great potential for widespread adoption. This review aims to describe the gut microbiome as an important determinant of micronutrient bioavailability, and, more specifically, to summarize the data supporting Lp299v as a key modulator of iron absorption.},
}

@article {pmid42631497,
year = {2026},
author = {Gopal, RK and Pathoor, NN and Ganesh, PS},
title = {Eubiosis and dysbiosis in periodontitis-related systemic diseases.},
journal = {Journal of periodontology},
volume = {},
number = {},
pages = {},
doi = {10.1002/jper.70188},
pmid = {42631497},
issn = {1943-3670},
abstract = {BACKGROUND: This narrative review examines the eubiosis-dysbiosis spectrum in periodontitis and its systemic implications. Evidence is drawn from the literature through 2026; as a narrative review, some selection bias cannot be excluded. Periodontitis, affecting 10%-15% of adults globally, drives systemic health disorders through microbial dysbiosis.

OBJECTIVES: This narrative review examines microbial ecological shifts in periodontitis and their implications for cardiovascular disease (CVD), diabetes mellitus (T2D), neurodegenerative disorders, rheumatoid arthritis (RA), and other systemic conditions.

METHODS: We have synthesized the current evidence on oral microbiome transitions from eubiosis to dysbiosis, focusing on mechanistic pathways linking periodontal disease to systemic health outcomes.

RESULTS: Periodontal dysbiosis may influence systemic health through mechanisms including bacteremia, chronic inflammation, molecular mimicry, and microbiome axis interactions. Individuals with periodontitis show 1.5 to 2-fold increased cardiovascular risk, bidirectional relationships with diabetes (HbA1c reductions of 0.3%-0.5% following periodontal treatment), and associations with Alzheimer's disease, rheumatoid arthritis, and inflammatory bowel disease. Key pathogens including Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Fusobacterium nucleatum have been proposed as keystone species capable of remodeling microbial communities and potentially contributing to systemic effects.

CONCLUSIONS: Understanding the eubiosis-dysbiosis spectrum provides crucial insights into oral-systemic health connections and offers therapeutic targets for managing both periodontal and systemic diseases. Integrated medical-dental care approaches, precision medicine strategies, and microbiome-based therapeutics represent promising future directions.},
}

@article {pmid42631722,
year = {2026},
author = {Liu, F and Wang, Q and Wang, X and Ye, Y and Chen, T and Cai, B},
title = {Exploring the Nasal Microbiome-Metabolite Axis as a Potential Therapeutic Target in Parkinson's Disease-Associated Olfactory Dysfunction.},
journal = {Letters in applied microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/lambio/ovag071},
pmid = {42631722},
issn = {1472-765X},
abstract = {Olfactory impairment is a common early non-motor feature of Parkinson's disease (PD), often preceding motor symptoms by several years. However, the biological mechanisms underlying PD-associated olfactory dysfunction remain poorly understood. This study investigated the relationship between nasal microbiota, metabolites, and olfactory function in PD and explored potential therapeutic targets. A total of 66 participants, including PD patients and healthy controls, were enrolled. Nasal samples were analyzed using 16S rRNA sequencing and metabolomic profiling by GC-MS. An MPTP-induced PD mouse model was used to evaluate the effects of cholic acid supplementation. PD patients exhibited distinct alterations in nasal microbial composition and metabolic profiles, which were associated with olfactory dysfunction severity. Cholic acid showed potential as a candidate biomarker for PD-associated olfactory impairment (AUC > 0.97). In MPTP mice, cholic acid improved olfactory performance and increased TH expression in the olfactory bulb and substantia nigra, but did not significantly improve motor deficits or striatal dopaminergic neuron loss. These findings suggest a potential association between nasal microbiota-associated metabolic alterations and olfactory dysfunction in PD.},
}

@article {pmid42631832,
year = {2026},
author = {Jeyavelkumaran, R and Keerthivasan, N and Dhanapal, MS},
title = {Phyllanthus emblica as a prebiotic modulator of the gut-endocrine axis in polycystic ovary syndrome: a translational perspective on synbiotic therapeutics.},
journal = {Folia microbiologica},
volume = {},
number = {},
pages = {},
pmid = {42631832},
issn = {1874-9356},
abstract = {Polycystic Ovary Syndrome (PCOS) is a complex endocrine-metabolic disorder characterized by insulin resistance, chronic inflammation, and hyperandrogenism, with emerging evidence implicating gut microbiome dysbiosis in its pathogenesis. This review explores the therapeutic potential of Phyllanthus emblica (Amla) as a prebiotic scaffold within synbiotic systems targeting the gut-endocrine axis. Rich in polyphenols, vitamin C, and dietary fibers, Amla functions both as a microbial substrate and a bioactive modulator, promoting beneficial microbiota, enhancing short-chain fatty acid production, and regulating metabolic and inflammatory pathways. Mechanistically, synbiotic modulation improves intestinal barrier integrity, suppresses NF-κB-mediated inflammation, enhances insulin sensitivity, and restores hormonal balance, thereby improving ovarian function. Evidence from preclinical studies and indirect clinical investigations in metabolic disorders suggests that Phyllanthus emblica exhibits multi-target efficacy in modulating metabolic, endocrine, and immune pathways relevant to PCOS. However, direct clinical evidence from PCOS-specific human studies remains limited. From a translational perspective, Amla-based synbiotic formulations, particularly when integrated with advanced delivery systems, represent promising pharmacological candidates for microbiome-informed therapeutics. Overall, this systems-level framework highlights the therapeutic potential of Amla-driven synbiotics while emphasizing the need for well-designed randomized clinical trials to establish their efficacy and safety in women with PCOS.},
}

@article {pmid42631876,
year = {2026},
author = {Ebrahim, RA and Raghu, SV and Das, SP},
title = {The underexplored mycobiome: insights from Drosophila into human health and disease.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {9},
pages = {},
pmid = {42631876},
issn = {1572-9699},
mesh = {Animals ; Humans ; *Drosophila melanogaster/microbiology/physiology ; *Mycobiome ; *Gastrointestinal Microbiome ; Disease Models, Animal ; },
abstract = {Drosophila melanogaster serves as a powerful and experimentally tractable genetic model for microbiome research due to its relatively simple gut community, ease of genetic manipulation, and the ability to generate germ-free flies. Despite extensive research on bacterial components of the human microbiome, the role of the mycobiome in host health and disease remains largely underexplored, presenting a significant knowledge gap. Although yeasts form a minor component of the Drosophila gut microbiome, they serve as a critical dietary source of essential micronutrients that drive larval development, growth, and metabolic rate. Furthermore, live yeasts directly shape adult fly behaviour, including oviposition, mating, and aggression, while interacting with gut bacteria to regulate lipid metabolism. Drosophila can be used as an invaluable tool for modelling neurodegenerative disorders, offering platforms for high-throughput screening and dissecting disease mechanisms. Despite these advantages, translation to human clinical contexts requires careful consideration of the fly's evolutionary limitations, including its exclusive reliance on the innate immune system, the absence of an adaptive immune system, the absence of certain vertebrate-specific genes and physiological pathways, and fundamental differences in brain architecture, neuronal organisation, and neurotransmission. Nevertheless, Drosophila provides essential mechanistic insights that are accelerating our understanding and guiding the development of novel therapeutic strategies against mycobiome-associated, metabolic, and neurological disorders. It also advances our understanding of the mycobiome's integral role in shaping insect behaviours, development, ecology, and overall health. These studies can significantly influence the understanding of fungi in human health and their roles in various disease conditions.},
}

Animals
Humans
*Drosophila melanogaster/microbiology/physiology
*Mycobiome
*Gastrointestinal Microbiome
Disease Models, Animal

@article {pmid42631903,
year = {2026},
author = {Ahmadi, P and Mozaffari-Jovin, S and Faraj, TA and Razavi, FT and Javanmardi, Z and Fadaee, A and Doulabi, H and Esmaeili, SA},
title = {"IL-40: A novel immunoregulatory axis at the crossroads of inflammation, tissue remodeling, and cancer immunity".},
journal = {Immunologic research},
volume = {74},
number = {1},
pages = {},
pmid = {42631903},
issn = {1559-0755},
mesh = {Humans ; *Neoplasms/immunology ; Animals ; *Inflammation/immunology ; Autoimmune Diseases/immunology ; *Interleukin-1/immunology/metabolism ; },
abstract = {Interleukin-40 (IL-40), encoded by the C17orf99 gene, is a recently identified B cell-associated cytokine that bridges innate and adaptive immune responses. Since its discovery in 2017, IL-40 has emerged as a pleiotropic immunoregulatory factor with broad implications in human diseases. Elevated IL-40 levels are consistently reported across systemic and organ-specific autoimmune disorders, including rheumatoid arthritis, systemic lupus erythematosus, Sjögren's syndrome, systemic sclerosis, and autoimmune thyroid diseases. In these conditions, IL-40 correlates with disease activity, inflammatory burden, and adverse outcomes. Mechanistically, beyond B-cell differentiation and IgA production, IL-40 induces neutrophil extracellular trap (NET) formation (NETosis), triggering extracellular release of peptidylarginine deiminase 4. PAD4 catalyzes citrullination of intracellular proteins, converting arginine to citrulline residues, generating neoepitopes that break immune tolerance and drive anti-citrullinated protein antibody (ACPA) production-a hallmark of rheumatoid arthritis and related autoimmunities. Beyond autoimmunity, dysregulated IL-40 is observed in viral infections (COVID-19, Epstein-Barr virus), sepsis, and pneumonia, suggesting roles in host defense, systemic inflammation, and immunopathology. IL-40 deficiency impairs IgA homeostasis and alters gut microbiota, implicating it in mucosal immunity and microbiome crosstalk. In oncology, aberrant IL-40 expression is reported in solid tumors (breast cancer, hepatocellular carcinoma) and hematologic malignancies (acute/chronic myeloid leukemias, Hodgkin lymphoma), indicating context-dependent functions in tumor biology. Elevated IL-40 in obesity, metabolic syndrome, type 2 diabetes, and allergic diseases further implicates this cytokine in low-grade chronic inflammation and hypersensitivity. Overall, IL-40 represents a promising immunoregulatory cytokine with diagnostic and therapeutic potential across immune-mediated diseases and cancer. However, current evidence remains largely observational and animal-based, while mechanistic and clinical investigations are scarce. Future research should prioritize identifying IL-40 receptor(s) and downstream signaling pathways through well-designed cellular and molecular studies, alongside large-scale multicenter trials, to fully elucidate its biological functions and clinical utility.},
}

Humans
*Neoplasms/immunology
Animals
*Inflammation/immunology
Autoimmune Diseases/immunology
*Interleukin-1/immunology/metabolism

@article {pmid42631930,
year = {2026},
author = {Choi, W and Mangal, U and Cha, JK and Cho, H and Ryu, JH and Kim, JY and Koh, WG and Lee, KJ and Kim, KW and Choi, SH and Traverso, G and Hong, J},
title = {A Mucosa-Inspired Dynamic Biointerface Engineering a Biofilm-Preventive Niche Against Pathogenic Microbiome Dysbiosis.},
journal = {Advanced materials (Deerfield Beach, Fla.)},
volume = {},
number = {},
pages = {e74745},
doi = {10.1002/adma.74745},
pmid = {42631930},
issn = {1521-4095},
support = {//Korea-US Collaborative Research Fund/ ; RS-2024-00468036//Ministry of Science and ICT and Ministry of Health & Welfare/ ; 2025-RISE-10-101//Regional Innovation System & Education/ ; //Regional Anchor company-Academia Partnership Innovation Development/ ; //Institute for Project-Y Seed/ ; RS-2024-00438634//Korea Health Technology R&D Project through the Korea Health Industry Development Institute/ ; //Nano & Material Technology Development Program through the National Research Foundation of Korea/ ; RS-2024-00449435//Ministry of Science and ICT/ ; RS-2021-NR059601//National Research Foundation of Korea/ ; RS-2023-00217709//National Research Foundation of Korea/ ; RS-2025-00522998//National Research Foundation of Korea/ ; },
abstract = {A stable symbiosis within the microbiome-host axis is essential for human health. However, preventing microbiome dysbiosis using biomaterials remains challenging due to their unpredictable influence on microbiome evolution. Inspired by the defensive niche of symbiotic mucosa, we have developed a biointerface that forms an engineered mucosa-inspired dynamic niche to prevent pathogenic dysbiosis. This biointerface features a dynamic zwitterionic network that emulates the mucosa's biophysical defensive functions. Notably, by leveraging its dynamic niche, the biointerface restricts microbial attachment and aggregation, thereby preventing biofilm formation. Comprehensive metagenomic analyses reveal that microbial communities adapt to this biofilm-preventive dynamic biointerface compositionally and functionally. In particular, Gram-negative bacteria were relatively reduced, along with decreased abundance of pathways associated with virulence and biofilm formation. Consequently, the mucosa-inspired biointerface intrinsically prevents the development of pathogenic dysbiosis. This study demonstrates the groundbreaking potential of material-based niche engineering to guide the ecological shifts of microbial communities from the material scale.},
}

@article {pmid42632035,
year = {2026},
author = {Chen, LC and Chen, YC and Sun, PW and Cheng, YP and Lin, SC and Guo, JW},
title = {Systemic Interventions Targeting Epidermal Barrier Function: Translational Insights from Oral Probiotics.},
journal = {Skin pharmacology and physiology},
volume = {},
number = {},
pages = {1},
doi = {10.1159/spp/aetag003},
pmid = {42632035},
issn = {1660-5535},
abstract = {The epidermal barrier is increasingly recognized as a dynamic and pharmacologically targetable system that extends beyond its traditional role as a passive structural defense. In inflammatory skin diseases such as atopic dermatitis and psoriasis, barrier dysfunction contributes not only to increased permeability and environmental susceptibility but also to complex bidirectional interactions involving immune dysregulation, microbial imbalance, oxidative stress, and systemic inflammation. Emerging evidence further supports the concept of the gut-skin axis as a systemic regulatory network linking intestinal microbiota, microbial metabolites, immune signaling, and epidermal homeostasis. Microbiota-derived metabolites, including short-chain fatty acids and aryl hydrocarbon receptor-related microbial metabolites, have been implicated in the regulation of keratinocyte differentiation, lipid metabolism, and epithelial integrity. Within this framework, oral probiotics have attracted increasing attention as biologically plausible systemic modulators of skin barrier function. Experimental and translational studies suggest that probiotics may improve transepidermal water loss, barrier-associated protein expression, inflammatory signaling, and microbial homeostasis through immune and metabolic mechanisms. However, current evidence remains heterogeneous because of strain-specific variability, inconsistent study methodologies, and limited standardized barrier-associated endpoints. Consequently, the clinical utility of microbiome-targeted therapy remains substantially stronger at the mechanistic and preclinical level than at the level of standardized large-scale clinical validation. Current evidence is also considerably more developed in atopic dermatitis than in psoriasis and other inflammatory dermatoses. Future progress will likely depend on integrated multi-omics analyses, functional barrier phenotyping, host-genetic stratification, and longitudinal therapeutic monitoring to enable precision barrier-centered interventions and personalized dermatologic strategies.},
}

@article {pmid42624068,
year = {2026},
author = {Wang, Z and Yan, Y and Han, IL and Lee, J and Li, G and He, P and Onnis-Hayden, A and Tooker, NB and Meng, Z and Miller, MW and McCullough, K and Klaus, S and Sabba, F and Jimenez, JA and Bott, CB and deBarbadillo, C and Giometto, A and Weinberger, KQ and Gu, AZ},
title = {Artificial intelligence-assisted phenotypic monitoring and diagnostic of wastewater microbiome management towards sustainability.},
journal = {Water research},
volume = {307},
number = {},
pages = {126624},
doi = {10.1016/j.watres.2026.126624},
pmid = {42624068},
issn = {1879-2448},
abstract = {Wastewater resource recovery facilities (WRRFs) rely on functional microbiome to remove pollutants and safeguard water sustainability towards United Nation's Sustainable Development Goals (SDGs). However, conventional DNA-based and operator experience-based monitoring approaches often fail to provide early warning of functional instability, leading to sudden WRRF performance loss and increased risk of regulatory noncompliance, primarily due to the lack of precise, functionality-driven monitoring systems. Here, we develop an artificial intelligence(AI)-assisted single-cell Raman spectroscopy (SCRS) platform and assemble a large Ramanome database (46,892 single cells across 12 WRRF configurations) for high-resolution phenotypic monitoring and diagnostics of wastewater microbiomes for a reliable and sustainable WRRF system. Our results demonstrate that Ramanome-defined operational phenotypic units (OPUs) and their associated phenotypic metrics (e.g., phenotypic diversity, network structures) can serve as robust phenotypic signals for accurate WRRF performance monitoring, complementing the conventional taxonomy-based signals (e.g., 16S rRNA). Moreover, our explainable AI models accurately identify key functional phenotypes and OPUs (accuracy 0.95-1.00) and enable quantitative diagnosis of WRRF health across regulatory compliance levels (accuracy 0.55-1.00). Overall, this function-driven SCRS-AI framework establishes a robust and scalable platform for predictive microbiome monitoring, diagnostics, and management, advancing sustainable wastewater treatment innovations in alignment with the SDGs.},
}

@article {pmid42624113,
year = {2026},
author = {Wang, Y and Xie, S and Li, C and Huang, R and Zheng, Z and Chen, S and Wu, Y and Zhang, H and Yang, R and Chan, YL and Sun, Y and Chan, FKL and Chan, NY and Ng, SC and Su, Q},
title = {Faecalibacterium prausnitzii-derived L-arginine ameliorates insomnia by inhibiting POMC-ACTH-cortisol axis.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102997},
doi = {10.1016/j.xcrm.2026.102997},
pmid = {42624113},
issn = {2666-3791},
abstract = {Insomnia is associated with gut microbial dysbiosis, but the specific microbial metabolites mediating gut-brain communication remain elusive. Here, we integrate metagenomic sequencing from 171 individuals (primary insomnia, post-COVID insomnia, and controls) with functional pathway analysis and preclinical validation. We identify Faecalibacterium prausnitzii depletion and reduced L-arginine biosynthesis as consistent features in both insomnia subtypes, accompanied by elevated cortisol levels. Genomic and in vitro analyses confirm that F. prausnitzii is a key microbial contributor to L-arginine production. In a chronic mild stress mouse model, administration of either F. prausnitzii or L-arginine restores sleep duration, normalizes corticosterone levels, and reverses stress-induced gut dysbiosis. Mechanistically, L-arginine suppresses POMC gene expression and dampens adrenocorticotropic hormone (ACTH)-stimulated corticosterone release, implicating the POMC-ACTH-cortisol axis as a key target. These findings uncover a gut-brain axis driven by F. prausnitzii-derived L-arginine that modulates sleep through endocrine signaling, positioning this metabolite as a potential therapeutic avenue for insomnia.},
}

@article {pmid42624114,
year = {2026},
author = {Jang, LG and Huh, JW and Kim, S and Lee, JY and Hwang, HS and Yoon, J and Lee, HG and Kim, TI and Lee, YC and Jee, SH and Kim, JF},
title = {Mouth-to-gut microbial transmission signatures enable robust, non-invasive diagnosis of gastrointestinal cancers.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.07.007},
pmid = {42624114},
issn = {1934-6069},
abstract = {The human microbiome is spatially compartmentalized, yet oral bacteria can ectopically colonize distal sites such as the gut, potentially influencing disease. By analyzing paired oral and fecal microbiomes from 507 participants across healthy controls and patients with metabolic disorders or gastrointestinal cancers, we established a quantitative mouth-to-feces (MF) index to measure MF microbial transmission. The MF index revealed elevated mouth-to-gut transmission in cancer and a strong association with host metabolic and inflammatory indicators. Using transmitted taxa, we developed a random forest classifier that accurately distinguished gastric/colorectal cancer from healthy controls across seven independent cohorts, even when trained solely on oral microbiome data. When benchmarked against the conventional screening test, the MF-based model achieved markedly higher sensitivity than the fecal occult blood test. These findings uncover disease-specific transmission signatures and highlight MF microbial profiling as a generalizable, non-invasive framework for gastrointestinal cancer diagnosis and risk stratification.},
}

@article {pmid42624237,
year = {2026},
author = {Iqbal, H and Baig, AM and Shi, X and Shi, R and Zeb, A and Khan, S and Liu, J and Wu, Z and Hussain, S and Liu, W},
title = {Photoaging-Induced Phytotoxicity of Tire Wear Particles on Tomato (Solanum lycopersicum L.): Evidence from Oxidative Stress, Metabolic Reprogramming, and Microbial Shifts.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {129002},
doi = {10.1016/j.envpol.2026.129002},
pmid = {42624237},
issn = {1873-6424},
abstract = {Tire wear particles (TWPs) undergo intricate photoaging processes that substantially alter their physicochemical properties and enhance their environmental behavior and ecological effects. However, the combined effects of particle size and exposure concentration of photoaged TWPs on plant growth and rhizosphere microbial communities remain inadequately characterized. In this study, a 30-day tomato cultivation experiment was conducted using UV-aged TWPs of two sizes (100 and 200 μm) applied at two concentrations (0.1% and 1%, w/w). The results revealed distinct size- and concentration-dependent phytotoxicity. The highest concentration of 100 μm TWPs (1%, w/w) induced the most pronounced inhibitory effects, reducing shoot biomass by 77.1% and net assimilation rate by 62.1%, while increasing malondialdehyde (MDA) content by 72%. UV photoaging altered TWP surface morphology, chemical composition, and hydrophilicity, promoting the leaching of heavy metals. Furthermore, UV-aged TWPs disrupted soil nutrient cycling and enzyme activities, triggered extensive metabolic reprogramming in tomatoes, particularly in carbon metabolism and TCA cycle, and reduced rhizosphere bacterial and fungal diversity, shifting microbial communities toward more stress-tolerant taxa. Integrated analyses demonstrated that the phytotoxicity of UV-aged TWPs was linked to oxidative stress, metabolic disturbance, impaired soil function, and microbial community shifts. These findings advance the understanding of UV-aged TWP toxicity and underscore the necessity of incorporating particle size and aging status into environmental risk assessments.},
}

@article {pmid42624309,
year = {2026},
author = {Huang, P and Li, S and Liu, Y and Li, J and Liu, B and Li, N and Wang, C and Xia, C and Liu, F},
title = {Schisandrin B protects against oxaliplatin-induced liver injury by suppressing ferroptosis via the canonical KEAP1-Nrf2 and non-canonical microbiota-driven Lactobacillus reuteri-CLA-Nrf2 axes.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {108408},
doi = {10.1016/j.phrs.2026.108408},
pmid = {42624309},
issn = {1096-1186},
abstract = {Ferroptosis is a critical contributor to chemotherapy-induced liver injury. Schisandrin B (SchB), a bioactive compound from Schisandra chinensis, exerts hepatoprotection, but the underlying mechanisms in oxaliplatin (OXA)-induced liver injury are unclear. In this study, OXA treatment induced hepatic dysfunction, lipid accumulation, and gut dysbiosis, with marked depletion of Lactobacillus reuteri (L. reuteri). A lipidomic analysis showed that SchB reversed OXA-induced linoleic acid (LA) metabolic reprogramming, particularly PE (18:0_18:2) and PE (18:2_18:2) accumulation. A targeted quantification revealed that OXA increased the levels of the LA-derived oxidation products 9-HODE and 13-HODE, which were significantly reduced by SchB treatment. Mechanistically, SchB mitigated OXA-induced DILI by suppressing ferroptosis through the dual-targeted activation of Nrf2. Notably, in addition to the canonical KEAP1-dependent mechanism, an important gut microbiota-mediated pathway appeared to contribute substantially to Nrf2 activation. SchB reshaped the gut microbiota by enriching L. reuteri, which metabolized the accumulated LA into conjugated linoleic acid (CLA). The CLA contributed to Nrf2 activation via a microbiome-dependent non-canonical pathway. Nrf2 knockout rats and FMT experiments further confirmed the causal roles of Nrf2 and L. reuteri in SchB-mediated hepatoprotection against lipid peroxidation. Importantly, in microbiota-depleted rats with OXA-induced liver injury, CLA supplementation partially restored Nrf2 activation and attenuated lipid peroxidation, indicating that CLA positively affected the microbiota-dependent hepatoprotective pathway associated with SchB. Collectively, these findings identify SchB as a potent therapeutic candidate against OXA-induced liver injury and highlight a microbiota-driven L. reuteri-CLA-Nrf2 axis as a key non-canonical pathway regulating gut-liver metabolic crosstalk and ferroptosis to maintain hepatic homeostasis.},
}

@article {pmid42624437,
year = {2026},
author = {Kyriazopoulou, E and Stylianakis, E and Damoraki, G and Spyrou, A and Symbardi, S and Chrysos, G and Adamis, G and Giamarellos-Bourboulis, EJ},
title = {Development of antibiotic-associated diarrhea in sepsis patients is associated with dysbiosis at baseline: Data from the PROGRESS Controlled Trial.},
journal = {International journal of antimicrobial agents},
volume = {},
number = {},
pages = {107979},
doi = {10.1016/j.ijantimicag.2026.107979},
pmid = {42624437},
issn = {1872-7913},
abstract = {The randomized PROGRESS trial (ClinicalTrials.gov NCT03333304) proved that early stop of antibiotics in sepsis guided by procalcitonin (PCT) changes leads, among others, to decrease of the incidence of antibiotic-associated diarrhea (AAD) and preservation of gut microbiome diversity. We aimed to explore an association of AAD with baseline microbiome composition. Patients with sepsis were followed-up for 28 days for AAD development. As PCT guidance led to decrease of AAD, only patients of the comparator arm, i.e. under treatment with standard-of-care (SoC) duration of antimicrobials, were considered for this exploratory analysis. In case of diarrhea, Clostridioides difficile infection was thoroughly investigated and excluded. Fecal samples were collected before initiation of antimicrobials and microbiome analysis was done by 16S rRNA Nanopore sequencing. Shannon diversity index was similar at baseline in 31 AAD (3.01; Q1-Q3, 2.49-3.49) and 54 non-AAD (2.83; Q1-Q3, 2.16-3.27; p: 0.456) patients. Relative abundance of Bacillota was lower (p: 0.038) and of Pseudomonadota higher (p: 0.019) in AAD patients. Abundance of the butyrate-producing anaerobic genus Faecalibacterium ≥ 0.15% was protective against AAD whereas abundance of Pseudomonas at baseline ≥ 0.75% (ORadj, 5.70; 95% CI, 1.70-19.06; p: 0.005) and Enterococcus at baseline ≥ 2.1% (ORadj, 7.16; 95% CI, 2.12-24.25; p: 0.002), were independent risk factors. Development of AAD in sepsis patients is associated with dysbiosis before start of antimicrobial treatment.},
}

@article {pmid42624662,
year = {2026},
author = {Outeiro, TF and Tolosa, E},
title = {How (We Think) Parkinson's disease begins.},
journal = {Parkinsonism & related disorders},
volume = {},
number = {},
pages = {108943},
doi = {10.1016/j.parkreldis.2026.108943},
pmid = {42624662},
issn = {1873-5126},
abstract = {Parkinson's disease (PD) is a complex heterogeneous neurodegenerative syndrome that is clinically defined. However, how it begins at the molecular and systems level remains unresolved. In this review, we cover selected evidence from neuropathology, imaging, genetics, microbiome and immune studies to examine competing and complementary models of PD initiation. We discuss classical pathology-staging concepts alongside brain-first and periphery-first subtypes, olfactory and gut routes, and threshold and multifocal models that posit parallel central and peripheral involvement. Emerging work on microbiome dysbiosis, endotoxin exposure, environmental toxicants at the nose-brain interface, genetically defined cellular vulnerabilities, and neuroinflammation, suggest these factors may act as potential upstream drivers of alpha-synuclein (aSyn) aggregation and spread. This supports a view in which PD comprises multiple initiating biologies leading to phenotypes that converge on a shared degenerative cascade. Altogether, we posit that understanding how PD starts impacts on our ability for performing biology-based subtyping, prodromal stratification, and for devising mechanism-based early preventive strategies.},
}

@article {pmid42624708,
year = {2026},
author = {Li, G and Du, Y and Huang, X and Luo, R and Zhou, H and Song, K},
title = {Associations between post-bariatric surgery gut microbiota changes and type 2 diabetes remission: a narrative review.},
journal = {Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.soard.2026.07.013},
pmid = {42624708},
issn = {1878-7533},
abstract = {Bariatric surgery is accompanied by substantial remodeling of the gut microbiota, which has been associated with type 2 diabetes mellitus (T2DM) remission. This review summarizes evidence from recent years on how surgery-induced microbial changes contribute to metabolic improvement. Key findings include a sustained increase in beneficial bacteria such as Akkermansia muciniphila and short-chain fatty acids (SCFAs)-producing taxa, coupled with a decrease in proinflammatory organisms. These shifts enhance intestinal barrier function, reduce systemic inflammation, modulate immune responses, and alter bile acid metabolism and SCFAs signaling-collectively improving glucose homeostasis and insulin sensitivity. We conclude that gut microbiota restructuring is a plausible contributor to the metabolic benefits of bariatric surgery, offering insights for future microbiome-targeted therapies in T2DM.},
}

@article {pmid42624765,
year = {2026},
author = {Kao, CM and Fritz, SA},
title = {The Role of Decolonization in Prevention of Staphylococcus aureus Infection.},
journal = {Infectious disease clinics of North America},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.idc.2026.07.002},
pmid = {42624765},
issn = {1557-9824},
abstract = {Staphylococcus aureus is a common skin commensal with significant pathogenic potential. S aureus is a leading cause of healthcare-associated infections, such as central-line associated bloodstream infections and surgical site infections, as well as skin and soft tissue infections. S aureus colonization is a significant risk factor for subsequent infection; thus, surveillance and decolonization with topical antimicrobials and antiseptics remain the mainstay of prevention. However, widespread implementation of decolonization protocols in hospitals and the community has been associated with antimicrobial resistance and microbiome perturbation. Thus, novel methods of S aureus decolonization and prevention remain a public health priority.},
}

@article {pmid42624857,
year = {2026},
author = {Sewunet, T and Razavi, M and Hanrott, K and Norris, V and Kricker, J and Giske, CG},
title = {Impact of the anti-inflammatory macrolide glasmacinal on the gut microbiota of healthy adults: an open-label trial.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42624857},
issn = {2041-1723},
mesh = {Humans ; *Macrolides/pharmacology/administration & dosage ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; Adult ; Female ; *Gastrointestinal Microbiome/drug effects/genetics ; Male ; *Anti-Inflammatory Agents/pharmacology ; Anti-Bacterial Agents/pharmacology ; Azithromycin/pharmacology ; Healthy Volunteers ; Phylogeny ; Enterobacteriaceae/drug effects/genetics/isolation & purification ; Bacteria/genetics/drug effects/classification/isolation & purification ; Young Adult ; },
abstract = {Glasmacinal (EP395) is an oral macrolide, with immunomodulatory properties like antibiotic macrolides (such as azithromycin), but with negligible in vitro antimicrobial activity, which is being developed as a potential treatment to reduce exacerbations in respiratory conditions. In an open-label healthy participant trial (ClinicalTrials.gov: NCT06118684), with the primary objective of assessing potential drug-drug interactions of glasmacinal, faecal samples were collected to evaluate the impact on the gut microbiota of daily doses of glasmacinal for 2 weeks, using both phenotypic and 16S rRNA gene sequencing. Glasmacinal produced modest effects: reduced phylogenetic richness (p < 0.0001), but not evenness, and altered beta-diversity (PERMANOVA R[2] = 0.104 p.adj=0.0018 after 1 week, and R[2] = 0.059, p.adj=0.028 after 2 weeks) with reductions in Clostridiaceae, Enterobacteriaceae, and Sutterellaceae abundance. The community shift was approximately 10% after 1-week glasmacinal, and 6% after 2-weeks. With quantitative culture, only Enterobacterales was impacted. No increase or selection of resistance to azithromycin in Enterobacterales and Bacteroides, nor increase in Candida spp. or Clostridioides difficile, were detected. Overall, glasmacinal induced limited restructuring of the gut microbiome (without the defining hallmarks of antibiotic-like dysbiosis), core anaerobic phyla of the gut (Firmicutes and Bacteroidetes) were preserved, and there was no selection of antimicrobial resistance.},
}

Humans
*Macrolides/pharmacology/administration & dosage
Feces/microbiology
RNA, Ribosomal, 16S/genetics
Adult
Female
*Gastrointestinal Microbiome/drug effects/genetics
Male
*Anti-Inflammatory Agents/pharmacology
Anti-Bacterial Agents/pharmacology
Azithromycin/pharmacology
Healthy Volunteers
Phylogeny
Enterobacteriaceae/drug effects/genetics/isolation & purification
Bacteria/genetics/drug effects/classification/isolation & purification
Young Adult