@article {pmid42923033,
year = {2026},
author = {Zhang, C and Chen, Q and Sun, Z and Wu, T and Zhang, Y and Huang, B and Huang, S and Zhang, Y and Han, M},
title = {Tripterygium wilfordii ameliorates complete freund adjuvant-induced rheumatoid arthritis through modulating the gut-joint axis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1828110},
pmid = {42923033},
issn = {1664-3224},
mesh = {Animals ; *Tripterygium/chemistry ; *Gastrointestinal Microbiome/drug effects ; *Arthritis, Rheumatoid/drug therapy/chemically induced/immunology/metabolism ; Rats ; *Arthritis, Experimental/drug therapy/immunology/metabolism ; Cytokines/metabolism/blood ; *Joints/drug effects/metabolism/immunology ; Male ; *Plant Extracts/pharmacology ; Synovial Membrane/metabolism ; *Drugs, Chinese Herbal/pharmacology ; Signal Transduction/drug effects ; Metabolomics ; },
abstract = {INTRODUCTION: Although Tripterygium wilfordii (TW) is a classical Chinese herbal medicine for the treatment of rheumatoid arthritis (RA), the mechanism by which it alleviates inflammation through modulation of the gut microbiota remains unclear.

METHODS: To elucidate the mechanism underlying the therapeutic effects of TW on RA, we first employed network pharmacology to predict the relevant pathways and core targets. Subsequently, an integrative multi-omics approach was applied, including gut metagenomics, gut metabolomics, serum metabolomics, and synovial transcriptomics, to investigate the alterations in gut microbiota, intestinal and serum metabolites, and synovial gene expression in a rat model of RA.

RESULTS: Our findings revealed that TW supplementation lowered serum concentrations of IL-6, IL-1β, TNF-α, and IL-10 and modulated the Th17/Treg balance in intestinal tissue. TW treatment altered gut microbiota (GM) composition, marked by increased abundance of Prevotella sp PCJ2 and Psychrobacter pasteurii, and decreased Adlercreutzia equolifaciens and Schaedlerella arabinosiphila, synergizing with keystone species (Bifidobacterium animalis, Phocaeicola sartorii, Blautia faecis) to promote gut health. Concurrently, TW elevated tryptophan metabolites (tryptophol, tryptamine, 5-hydroxykynurenamine) while reducing 4-(2-aminophenyl)-2,4-dioxobutanoic acid, restoring tryptophan metabolism. This regulation coincided with upregulated Inmt mRNA in synovium, activating the tryptophan pathway. Correlation and mediation analyses indicated that gut-derived circulating metabolites such as N-myristoyl arginine and lauramidoxide were positively correlated with synovial Jun expression, potentially participating in the modulation of the IL-17-NF-κB cascade. Consistently, upregulated synovial Socs3 may exert negative feedback suppression on JAK-STAT signaling to alleviate inflammatory responses.

DISCUSSION: These findings point to the gut microbiome and tryptophan pathway as a new therapeutic avenue for RA.},
}

Animals
*Tripterygium/chemistry
*Gastrointestinal Microbiome/drug effects
*Arthritis, Rheumatoid/drug therapy/chemically induced/immunology/metabolism
Rats
*Arthritis, Experimental/drug therapy/immunology/metabolism
Cytokines/metabolism/blood
*Joints/drug effects/metabolism/immunology
Male
*Plant Extracts/pharmacology
Synovial Membrane/metabolism
*Drugs, Chinese Herbal/pharmacology
Signal Transduction/drug effects
Metabolomics

@article {pmid42923050,
year = {2026},
author = {Byun, S and Sotzen, MR and Bento, MT and Knappenberger, MA and Asker, M and Wright, JR and Lamendella, R and Mu, C and Skibicka, KP},
title = {Semaglutide Remodels the Gut Microbiome Beyond Its Appetite-Suppressing Action: Sex-Specific Gut-Brain Axis Implications.},
journal = {Comprehensive physiology},
volume = {16},
number = {5},
pages = {e70286},
pmid = {42923050},
issn = {2040-4603},
abstract = {The gut microbiome communicates bidirectionally with the brain and peripheral metabolic organs to regulate appetite and body weight. Semaglutide (SEMA), a GLP-1 receptor agonist, produces robust weight loss by reducing food intake, largely through brain GLP-1 receptors, yet whether its effects on the gut microbiome are secondary to this centrally driven hypophagia is poorly understood. Given the profound impact of SEMA on food intake and body weight, we propose that SEMA treatment reshapes gut microbial composition and that these shifts are correlated with metabolic outcomes. Diet-induced obese rats received a 4-week SEMA treatment and gut microbial composition was analyzed using 16S rRNA gene sequencing. To differentiate the impact of reduced food intake associated with SEMA from other effects of the drug treatment on the gut microbiome, a pair-fed to SEMA group was tested. SEMA significantly reduced body weight gain and food intake in both sexes. Significant SEMA-induced changes in microbial richness and evenness were detected. Linear discriminant analysis Effect Size (LEfSe) identified enrichment of Firmicutes taxa-particularly members of the Clostridiaceae family-in SEMA-treated rats, whereas controls showed greater representation of Bacteroidota taxa. Sex-specific associations between host metabolic parameters and gut microbial composition were also identified. These findings demonstrate profound, not necessarily health positive, partly sex-specific gut microbial community shifts following GLP-1 analogue treatment. Many of the changes in the gut microbiota were not simply driven by the decreased food intake. Thus, GLP-1 analogue treatment engages the gut microbiome through both food intake-dependent (brain-to-gut) and intake-independent pathways.},
}

@article {pmid42923188,
year = {2026},
author = {Wang, X and Li, J and Cheng, Y and Liu, Y and Li, H and Tan, H and Hu, Y and Zhao, M and Liu, J},
title = {Microbiota-assisted screening for colorectal neoplasia: advanced adenoma as the key translational endpoint-a narrative review.},
journal = {American journal of translational research},
volume = {18},
number = {9},
pages = {8227-8253},
pmid = {42923188},
issn = {1943-8141},
abstract = {Microbial differences between established colorectal cancer (CRC) and cancer-free controls are reproducible, but screening translation depends on detecting advanced adenoma and early CRC in asymptomatic populations. We examined the gut microbiota as an adjunct to fecal immunochemical testing (FIT), stool deoxyribonucleic acid (DNA) testing, and colonoscopy, with advanced adenoma as the prevention-relevant endpoint. This narrative review used a structured, purposive search of PubMed, Embase, Web of Science, Scopus, and the Cochrane Library through April 10, 2026, prioritizing human neoplasia cohorts, stage-specific biomarkers, multi-omics studies, FIT comparators, and reporting standards. Across studies, microbial signals were strongest for established CRC and weaker and less consistently reported for advanced adenoma. Quantitative evidence supports selected adjunctive approaches, including fecal Fusobacterium nucleatum and multitaxon panels combined with FIT, but external validation remains sparse. The 2025 pooled analysis of 3,741 metagenomes demonstrated reproducible CRC-related features across 18 cohorts but did not report advanced-adenoma-specific accuracy. Clinical utility cannot be inferred from sensitivity, specificity, or the area under the receiver operating characteristic curve alone: prevalence-dependent positive predictive value (PPV), negative predictive value (NPV), calibration, a prespecified action threshold, decision-curve net benefit, and colonoscopy burden are decisive. Translation therefore requires a locked assay and model tested prospectively before bowel preparation in a representative screening cohort, with advanced adenoma reported separately and performance compared directly with FIT or stool DNA testing. Microbiota-based markers currently merit evaluation as adjuncts, not replacements, within established screening pathways.},
}

@article {pmid42923255,
year = {2026},
author = {Iorizzo, M and Albanese, G and Tedino, C and Succi, M and Di Donato, LM and de Nigris, A and Di Criscio, D and Ganassi, S and Ambrosone, L and De Cristofaro, A},
title = {Seasonal gut microbiota dynamics and colony performance under stationary and short-distance migratory beekeeping in Apis mellifera ligustica.},
journal = {Frontiers in insect science},
volume = {6},
number = {},
pages = {1890935},
pmid = {42923255},
issn = {2673-8600},
abstract = {Honey bee gut microbiota play important roles in host nutrition, immune regulation, and health, and their composition can vary in response to environmental conditions, diet, seasonality, and beekeeping management. In this two-year field study, we investigated seasonal variation in the gut bacterial communities of Apis mellifera ligustica colonies maintained under stationary or short-distance migratory beekeeping management. Six colonies originating from the same experimental apiary were assigned to stationary or migratory management, with three migratory colonies seasonally transferred to Mount Taburno during summer and three stationary colonies remaining at Castelpoto. Bacterial communities were characterized by high-throughput sequencing of the V1-V3 region of the 16S rRNA gene. The gut microbiota was consistently dominated by characteristic honey bee-associated taxa, particularly Gilliamella and Snodgrassella, although their relative abundances varied substantially across seasons and years. Alpha-diversity analyses based on harmonized genus-level relative abundance profiles revealed significant seasonal variation in both years, whereas no significant overall effect of management system was detected. Similarly, PERMANOVA of Bray-Curtis dissimilarities revealed significant seasonal structuring of bacterial community composition in 2022 and 2023, while stationary versus migratory management did not significantly explain overall community variation. The persistence of dominant gut-associated taxa across sampling periods indicates compositional continuity of major bacterial community members despite temporal variation, but does not by itself demonstrate functional stability or microbial resilience. Colony-performance measurements showed significantly higher annual honey production in migratory than in stationary colonies in 2022, whereas no significant differences in the investigated performance parameters were detected between management systems in 2023. Thus, the productive response was not consistent between years. Although temporal variation in gut bacterial communities occurred alongside differences in colony performance, the present study does not establish a causal or functional relationship between microbiota composition and productivity. Overall, these findings identify seasonality as the predominant factor associated with variation in the gut bacterial communities of the investigated colonies and provide no evidence for a consistent overall effect of short-distance migratory management on bacterial community diversity or structure. Further studies involving larger numbers of independent colonies and apiaries, together with direct functional analyses of the microbiome and characterization of dietary and environmental factors, are required to clarify the consequences of migratory beekeeping for honey bee microbiota and colony performance.},
}

@article {pmid42923262,
year = {2026},
author = {Astorga Gaxiola, AH and Sánchez Magaña, LM and León López, L and Reyes Moreno, C and Mora Rochín, S},
title = {Dietary, lifestyle, and host determinants of microbiota-host interactions.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1975060},
pmid = {42923262},
issn = {2813-4338},
abstract = {The gut microbiota is a dynamic ecosystem shaped by dietary factors, lifestyle factors, environmental exposures, and host characteristics, with important implications for metabolism, immune regulation, intestinal barrier function, and host-microbiota interactions. This narrative review examines how dietary patterns, specific food components, physical activity, sleep and circadian rhythms, aging, and medication exposure modulate gut microbial composition and function, with particular emphasis on interindividual variability and personalized nutrition. A literature search was conducted in Scopus, ScienceDirect, PubMed, and Google Scholar for publications from 2000 to 2026, with emphasis on recent peer-reviewed evidence. Current evidence indicates that dietary patterns and individual food components can modify microbial community structure, metabolic pathways, and bioactive metabolite production, although responses vary substantially across individuals. Physical activity may modify microbial ecology, intestinal physiology, barrier function, and microbial metabolism, whereas sleep disruption and circadian misalignment may alter microbial rhythmicity and host metabolic regulation. Aging and antibiotic exposure are associated with context-dependent changes in microbial composition, function, resilience, and, with antibiotics, the gut resistome. Across these determinants, interindividual variability emerges as a central feature driven by host characteristics, habitual diet, lifestyle, medication history, baseline microbiota, and microbial functional capacity. Personalized nutrition therefore represents a promising but evolving framework in which microbiome data may be integrated with host and environmental characteristics to predict differential responses. Future research should prioritize longitudinal human studies, standardized methodologies, multi-omics integration, and prospective validation of microbiome-informed interventions to establish clinically meaningful benefits.},
}

@article {pmid42923306,
year = {2026},
author = {Gao, X and Dong, Q and Shin, AS},
title = {Associations of colonic transit with the gut microbiota and short-chain fatty acids in health and irritable bowel syndrome.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1953842},
pmid = {42923306},
issn = {2296-861X},
abstract = {Gut bacteria are known to influence short-chain fatty acid (SCFA) levels through direct metabolic activity. Colonic transit also affects substrate contact time, fermentation duration, and SCFA absorption. But it is unclear whether some bacteria influence SCFA levels indirectly, by altering transit, rather than only directly, and whether this differs across health and irritable bowel syndrome (IBS) subtypes. Using data from 56 participants [17 healthy volunteers (HV), 15 IBS-C, 24 IBS-D] with concurrent stool metagenomes, stool SCFA, and segmental colonic transit measurements, we applied mediation analysis to test whether each bacterial taxon's association with SCFA levels may be transit-mediated statistically. Three taxa showed a potential transit-mediated association with at least one SCFA: Faecalibacterium prausnitzii in HV, Bacteroides thetaiotaomicron in IBS-C, and Phascolarctobacterium succinatutens in IBS-D. For F. prausnitzii, the transit-mediated pathway was the only detectable association with SCFA. The remaining two taxa, B. thetaiotaomicron and P. succinatutens, additionally showed a direct, transit-independent effect alongside the transit-mediated one. Separately, an analysis of direct, non-mediated effects identified 15 additional taxa (5 in HV, 2 in IBS-C, and 8 in IBS-D) whose associations with SCFA levels were not explained by colonic transit. Together, these findings suggest that colonic transit may potentially mediate specific associations between gut bacteria and SCFA levels, in addition to the direct metabolic effects of the bacteria. However, because the present study is cross-sectional, these findings should be interpreted as statistical associations rather than established biological or directional relationships. In addition, this was an exploratory post-hoc analysis of a single relatively small cohort, and independent validation will be required before the biological or clinical significance of these findings can be established.},
}

@article {pmid42923669,
year = {2026},
author = {Naghsh, N and Shahshahan, SM and Karimi, F and Tarrahi, MJ and Sami, R},
title = {Periodontal indices in patients with chronic obstructive pulmonary disease and their correlation with disease severity: A cross-sectional study.},
journal = {Caspian journal of internal medicine},
volume = {17},
number = {3},
pages = {562-571},
pmid = {42923669},
issn = {2008-6164},
abstract = {BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a chronic respiratory condition primarily influenced by oral microbiota, which is the source of the microbiome. This study evaluated selected periodontal indices in COPD patients and their relationship with COPD severity among patients referred to Khorshid Hospital and Day Clinic in Isfahan in 2023.

METHODS: This cross-sectional study involved 221 subjects diagnosed with COPD based on spirometry testing. According to spirometry values, the subjects were classified into mild, moderate, severe, and very severe COPD categories. Periodontal indices including pocket depth (PD), bleeding on probing (BOP), plaque index (PI) and clinical attachment loss (CAL), were assessed. In addition, relevant demographic and medical information, along with smoking status and severity of periodontal disease, were evaluated. The data were analyzed using one-way ANOVA, chi-square test, t-test, and rank regression with SPSS software.

RESULTS: All evaluated patients had periodontitis. Overall, higher COPD grades were associated with increased periodontal disease indices (PD, BOP, PI, and CAL) (p<0.001). Greater periodontitis severity correlated with increased COPD severity, with moderate and severe periodontitis raising the risk of severe and very severe COPD by 8.1 and nearly 62 times, respectively. In severe and very severe COPD cases, periodontal disease severity showed the highest level of association with COPD severity compared to age and pack-years of smoking.

CONCLUSION: COPD severity significantly correlated with PD, BOP, PI, and CAL. However, further clinical studies are needed to establish a definitive association between these conditions due to the shared pathophysiology of COPD and periodontal disease.},
}

@article {pmid42923709,
year = {2026},
author = {Hu, Y and Liu, Y and Yao, H and Wang, S and Gao, Y and Li, R and Sun, H},
title = {Gut microbiota-derived small molecules, peptides, and proteins in GPCR signaling: current evidence for β-arrestin involvement.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1979411},
pmid = {42923709},
issn = {1664-302X},
abstract = {Gut microbiota modulate host metabolism, immunity, barrier integrity, and neural function through diverse classes of molecules, including small molecules such as short-chain fatty acids (SCFAs), bile acids, tryptophan metabolites, and microbe-derived peptides and proteins. G protein-coupled receptors (GPCRs) constitute a major receptor system through which the host senses microbiota-derived signals. However, current research has largely focused on ligand recognition, G protein pathways and functional phenotypes, leaving an insufficient understanding of how signals are reorganized after receptor activation to generate functional selectivity. In addition to mediating GPCR desensitization and endocytosis, β-arrestin regulates receptor trafficking, sustains endosomal signaling, and orchestrates signaling scaffold assembly, thereby providing a key mechanistic framework for understanding the spatiotemporal reprogramming of microbiota-derived signaling. This review summarizes both canonical and non-canonical GPCR signaling mechanisms, delineates the roles of β-arrestin in regulating receptor fate, biased signaling, and functional outputs. By integrating the PRESTO-Tango system and the PubMed literature, we analyzed the microbiome-related evidence for the near-complete non-olfactory GPCRome (314 conventional GPCRs) in order to assess the association between distinct classes of microbiota-derived molecules and GPCR-β-arrestin signaling. Current evidence indicates that existing studies are dominated by small-molecule signals, whereas evidence for peptides and proteins remains relatively limited. Moreover, most functional studies cannot be directly interpreted as evidence for β-arrestin-dependent mechanisms. A β-arrestin-centered conceptual framework for GPCR signaling regulation may provide a basis forunderstanding how gut microbiota-associated molecules influence host physiological functions through thespatiotemporal modulation of receptor signaling.},
}

@article {pmid42923729,
year = {2026},
author = {Shrestha, A and Eline, Y and Sundstrom, K and Van Leuven, JT},
title = {Biocontrol potential of hive-associated Bacillus species against American Foulbrood disease in honeybees (Apis mellifera L.).},
journal = {Frontiers in insect science},
volume = {6},
number = {},
pages = {1870750},
pmid = {42923729},
issn = {2673-8600},
abstract = {INTRODUCTION: Honeybee (Apis mellifera L.) larvae are susceptible to Paenibacillus larvae, a spore-forming, Gram-positive bacterium that causes American Foulbrood (AFB), a destructive honeybee brood diseases. Current antibiotic treatments are inadequate because of rising pathogen resistance and residue accumulation in hive products, driving interest in biological and other natural strategies for AFB control. Most candidate biocontrol agents, however, have been evaluated only for their ability to inhibit P. larvae or protect larvae, with less attention to their effects on adult bees.

METHODS: Here we assessed the biocontrol potential of hive-associated Bacillus species against P. larvae infection. Bacteria isolated from AFB-infected combs were sequenced and screened for antagonistic activity, and active isolates, their lysates, and lysate-derived protein fractions were tested for their ability to improve larval survival during P. larvae challenge. To evaluate effects on adult bees, newly emerged workers were caged and fed the B. licheniformis lysate (ASx), and their survival and gut microbiome were compared with untreated controls and with bees fed Terra-Pro, a Terramycin-based AFB treatment.

RESULTS: Several Bacillus species - including B. zhangzhouensis, B. subtilis, B. amyloliquefaciens, B. licheniformis, and B. mojavensis - inhibited one or more P. larvae strains. The B. licheniformis lysate (ASx) and its 30 -50 kDa protein fraction improved larval survival during P. larvae challenge. In caged adults, survival of lysate-fed bees differed from untreated controls but was comparable to that of Terra-Pro-fed bees, and their gut microbiome remained similar to that of untreated controls.

DISCUSSION: Together, these results indicate that hive-associated Bacillus species - and B. licheniformis-derived proteins in particular - are promising candidates for AFB management that improve larval survival without harming adult bees more than an existing antibiotic treatment.},
}

@article {pmid42923736,
year = {2026},
author = {Fayomi, A and Adom, E and Aryee, ANA},
title = {Cross-model metabolomic signatures of dietary anti-inflammatory (poly) phenols in nutraceutical development: a systematic review.},
journal = {Frontiers in molecular biosciences},
volume = {13},
number = {},
pages = {1824027},
pmid = {42923736},
issn = {2296-889X},
abstract = {Dietary (poly) phenols play a key role in nutraceutical development, due to their diverse positive health benefits such as antioxidant and anti-inflammatory properties. Although these bioactivities have been widely reported, the consistency of metabolomic signatures in experimental systems, ranging from in vitro models to human studies, remains unclear. This systematic review examined metabolomic responses to dietary anti-inflammatory (poly) phenols in vitro, animal, human, and mixed-model studies. Searches were conducted in PubMed, Scopus, Web of Science, and Google Scholar for studies published between 2020 and 2025. Seventy-eight eligible primary studies were included and synthesized narratively due to differences in interventions, models, sample matrices, analytical platforms, and outcomes. The synthesis showed model-dependent recurrence of several metabolomic signatures, with lipids, amino acids, and energy metabolism widely represented in the model groups, including phospholipids, sphingolipids, acylcarnitines, branched-chain and aromatic amino acids, kynurenine metabolites, TCA cycle intermediates, glycolytic metabolites, ketone bodies, and ATP markers. Changes in short-chain fatty acids were most consistent in animal and mixed-model gut studies but limited and matrix-dependent in human studies. Urolithins and ellagic acid-derived metabolites were most prominent in human and mixed-model studies, especially urinary biomarkers and microbiome-dependent metabolites. Overall, dietary anti-inflammatory (poly) phenols were associated with recurring metabolomic changes; however, these patterns were influenced by the model system, sample matrix, analytical platform, and intervention type. Further human studies are required to validate these candidate biomarkers and pathways for nutraceutical application.},
}

@article {pmid42923814,
year = {2026},
author = {Liu, H and Liu, J and Peng, S and Zhao, J and Yang, F and Zhang, L and Wang, S and Zhang, L and Sun, G},
title = {IL-10-secreting engineered macrophages alleviate DSS-induced colitis with macrophage phenotypic modulation and gut microbiota remodeling in mice.},
journal = {Bioengineering & translational medicine},
volume = {},
number = {},
pages = {e70178},
pmid = {42923814},
issn = {2380-6761},
abstract = {Ulcerative colitis (UC) is a chronic recurrent inflammatory bowel disease characterized by abdominal pain, hematochezia, and weight loss. Although remarkable progress has been made toward understanding the pathogenesis of UC, finding more effective treatments for this disease remains a challenge. Interleukin-10 (IL-10) possesses potent anti-inflammatory properties, yet its therapeutic application in UC has failed clinically due to poor targeting and a short half-life. In this study, we developed IL-10-secreting engineered macrophages (IL-10M) based on RAW264.7 cells and evaluated their therapeutic effects in a dextran sulfate sodium-induced colitis model. Intraperitoneal administration of IL-10M alleviated body weight loss, disease activity, colon shortening, and histological injury. IL-10M also reduced mucosal damage and improved tight junction-associated epithelial barrier markers. Flow cytometry further detected engineered macrophage-associated GFP signals in colonic tissues and revealed an early increase in CD206[+] endogenous colonic macrophages. Microbiome profiling showed treatment-associated compositional changes, including alterations in Bacteroides acidifaciens and Mucispirillum schaedleri, indicating microbiota remodeling after engineered macrophage treatment. Short-term safety assessment did not reveal overt hematological abnormalities or major histological injury in liver and spleen. Overall, these findings suggest that IL-10-secreting engineered macrophages may represent a promising macrophage-based strategy for mitigating intestinal inflammation in experimental colitis.},
}

@article {pmid42923893,
year = {2026},
author = {Thomas, KS and Lekshmi, SS and Gurrala, H and Ramzan, MR and Osman, AK and Sherin, Z},
title = {Emerging mechanism-driven therapies for endometriosis: From GnRH antagonists to microbiome and device-based strategies (Review).},
journal = {Medicine international},
volume = {6},
number = {6},
pages = {57},
pmid = {42923893},
issn = {2754-1304},
abstract = {Millions of women of reproductive age suffer from endometriosis, a chronic, estrogen-driven condition that causes pelvic pain, dysmenorrhea and infertility. Conventional therapy focuses on symptom suppression with hormone medications or the surgical excision of lesions; however, it is not curative. Recent developments in the understanding of the pathophysiology of endometriosis have revealed novel immunological and molecular mechanisms that are being used in experimental therapies. The present review outlines developing techniques, including targeted endocrine modulators, epigenetic treatments, anti-inflammatory and immunomodulatory drugs, antioxidants, anti-angiogenic medicines, and microbiome-based therapy. Prominent examples are new oral gonadotropin-releasing hormone receptor antagonists, selective progesterone receptor modulators and aromatase inhibitors that aim to overcome progesterone resistance. Alternative methods, such nutraceuticals and biologic and small-molecule inhibitors (such as metabolic drugs and anti-cytokine therapies) are being explored. Novel supplemental options are provided by device-based neuromodulation and improved surgical techniques (such as advanced laparoscopy, robotic excision, image-guided surgery, nerve-sparing techniques and adhesion barriers). While many of these innovations are promising, current evidence is limited by small studies and disease heterogeneity. Future directions emphasize rigorous trials with standardized outcomes, including fertility measures and combinations of therapies to achieve personalized, long-term relief.},
}

@article {pmid42924581,
year = {2026},
author = {Wang, Y and Zeng, H and Liu, N and Yang, D},
title = {Gut‑kidney axis in chronic kidney disease: Dysbiosis, uremic metabolites and therapeutic opportunities (Review).},
journal = {Molecular medicine reports},
volume = {34},
number = {6},
pages = {},
doi = {10.3892/mmr.2026.14047},
pmid = {42924581},
issn = {1791-3004},
mesh = {Humans ; *Dysbiosis/metabolism/microbiology/therapy ; *Renal Insufficiency, Chronic/metabolism/therapy/microbiology/pathology ; *Gastrointestinal Microbiome ; *Uremic Toxins/metabolism ; *Kidney/metabolism/pathology ; Animals ; Prebiotics ; Probiotics/therapeutic use ; Indican/metabolism ; Fecal Microbiota Transplantation ; },
abstract = {Chronic kidney disease (CKD) poses a notable global health burden. Beyond traditional pathways, the gut‑kidney axis has emerged as a potential contributor to disease progression. In the present narrative review, current evidence on the role of intestinal dysbiosis, characterized by reduced microbial diversity, depletion of beneficial short‑chain fatty acid producers and expansion of uremic toxin‑generating bacteria, in the accumulation of nephrotoxic metabolites (such as indoxyl sulfate, p‑cresyl sulfate and trimethylamine N‑oxide) is summarized. These toxins promote oxidative stress, inflammation and fibrosis, accelerating renal decline. By contrast, microbially derived short‑chain fatty acids exert protective effects. Although therapeutic strategies targeting the gut microbiome (including probiotics, prebiotics and adsorbents) and fecal microbiota transplantation (targeting the gut microbiome) exhibit potential in modulating toxin levels, evidence for clinical endpoint benefit remains insufficient. In the present review, mechanistic insights were critically evaluated, clinical intervention studies are systematically summarized in tabulated form and a roadmap for personalized, microbiota‑informed therapeutic strategies is proposed.},
}

Humans
*Dysbiosis/metabolism/microbiology/therapy
*Renal Insufficiency, Chronic/metabolism/therapy/microbiology/pathology
*Gastrointestinal Microbiome
*Uremic Toxins/metabolism
*Kidney/metabolism/pathology
Animals
Prebiotics
Probiotics/therapeutic use
Indican/metabolism
Fecal Microbiota Transplantation

@article {pmid42924590,
year = {2026},
author = {Zhang, T and Ren, Z and Wang, L and Man, R and Wang, L and Wang, J and Cheng, X and Peng, J and Yu, Y},
title = {Immune remodeling in inflammatory bowel disease-associated colorectal cancer: Mechanisms and immunotherapeutic implications (Review).},
journal = {International journal of molecular medicine},
volume = {58},
number = {6},
pages = {},
doi = {10.3892/ijmm.2026.6024},
pmid = {42924590},
issn = {1791-244X},
mesh = {Humans ; *Inflammatory Bowel Diseases/immunology/complications/therapy ; *Colorectal Neoplasms/immunology/therapy/etiology ; *Immunotherapy/methods ; Animals ; },
abstract = {Inflammatory bowel disease‑associated colorectal cancer (IBD‑CRC) arises in the setting of long‑standing chronic intestinal inflammation, in which immune dysregulation cannot be readily attributed to the dominance of a single inhibitory pathway or to global immunosuppression. Persistent inflammatory signaling sustains a state of prolonged immune engagement, yet with constrained effector output, potentially compromising antitumor immune surveillance and limiting the clinical benefit of immunotherapy. The present review synthetises the accumulated knowledge on the long‑term immunological alterations induced by chronic inflammation, including the integration of immune signaling, shifts in activation thresholds, metabolic reprogramming, and functional polarization of immune cells. These changes are discussed in the context of both tumor initiation and tumor maintenance to delineate the immunological evolution of IBD‑CRC. The review further examines the relationship between inflammation‑induced response constraints and the limited efficacy of immune checkpoint inhibitors, and summarizes the mechanistic barriers to immunotherapy in IBD‑CRC. Collectively, these observations suggest that relieving inhibition through a single target may be insufficient to restore effective antitumor immunity. Finally, the potential value of natural plant‑derived interventions characterized by multi‑component, low‑intensity, and long‑term modulation is discussed, particularly with respect to reducing inflammatory burden and improving immune metabolic states, thereby providing a conceptual basis for the development of combination immunotherapeutic strategies.},
}

Humans
*Inflammatory Bowel Diseases/immunology/complications/therapy
*Colorectal Neoplasms/immunology/therapy/etiology
*Immunotherapy/methods
Animals

@article {pmid42924734,
year = {2026},
author = {Minari, TP and Vilela-Martin, JF and Pisani, LP},
title = {Dietary Approaches to Obstructive Sleep Apnea: Translating Mechanistic Pathways into Clinical Practice.},
journal = {Clocks & sleep},
volume = {8},
number = {4},
pages = {},
doi = {10.3390/clockssleep8040058},
pmid = {42924734},
issn = {2624-5175},
support = {001//Conselho Nacional de Desenvolvimento Científico e Tecnológico/ ; },
abstract = {Obstructive sleep apnea (OSA) is a highly prevalent and heterogeneous sleep disorder characterized by recurrent upper airway collapse during sleep, resulting in intermittent hypoxia, sleep fragmentation, sympathetic activation, and increased cardiometabolic risk. Although obesity is the most recognized modifiable risk factor, growing evidence indicates that nutritional factors influence OSA through mechanisms extending beyond body weight regulation, including systemic inflammation, oxidative stress, endothelial dysfunction, gut microbiota alterations, and metabolic dysregulation. The emergence of precision medicine and incretin-based therapies has further highlighted the need to integrate personalized nutritional approaches into OSA management. A literature search was conducted in PubMed/MEDLINE, Scopus, and Web of Science to identify experimental studies, observational studies, randomized clinical trials, systematic reviews, meta-analyses, and international clinical guidelines addressing nutritional mechanisms, dietary patterns, gut microbiota, chrononutrition, incretin-based therapies, and precision nutrition in adults with OSA. Current evidence suggests that nutritional interventions may influence OSA through multiple biological pathways beyond weight reduction. Mediterranean and DASH dietary patterns are associated with favorable cardiometabolic effects, while dietary fiber, polyphenols, omega-3 fatty acids, and other antioxidant compounds may modulate pathways related to inflammation, oxidative stress, endothelial function, and metabolic regulation. However, evidence directly demonstrating improvements in objective respiratory outcomes remains limited and heterogeneous. Emerging research also suggests potential roles for gut microbiota modulation and chrononutrition in metabolic and sleep regulation, although most evidence remains mechanistic, observational, or indirect. In addition, glucagon-like peptide-1 receptor agonists and dual incretin agonists have demonstrated clinically relevant reductions in body weight and OSA severity, providing opportunities for integration with nutritional management. Nevertheless, evidence supporting phenotype-specific and biomarker-guided nutritional interventions remains insufficient. Nutrition represents a promising adjunctive strategy in the multidisciplinary management of OSA by targeting inflammatory, metabolic, vascular, and microbiome-related mechanisms that extend beyond weight loss alone. Future research should focus on precision nutrition approaches integrating metabolic phenotyping, biomarkers, gut microbiota, and digital health technologies to optimize personalized treatment and improve long-term clinical outcomes.},
}

@article {pmid42924817,
year = {2026},
author = {Pliaka, D and Fytros, F and Zisis, S and Zisis, V and Dimitropoulou, P and Poulopoulos, K and Charisi, C and Syrioti, A and Shinas, N and Poulopoulos, A},
title = {Adjunctive Antimicrobial Therapy in Peri-Implant Diseases: A Narrative Review.},
journal = {Reports (MDPI)},
volume = {9},
number = {4},
pages = {},
doi = {10.3390/reports9040365},
pmid = {42924817},
issn = {2571-841X},
abstract = {Background: Effective management of peri-implant disease relies primarily on mechanical removal of the bacterial biofilm. However, achieving adequate surface decontamination can be challenging due to complex implant-surface morphology and restricted access to deep peri-implant pockets. This has prompted the use of adjunctive antimicrobial agents to complement mechanical therapy and improve therapeutic outcomes. Objective: To investigate whether the adjunctive use of antimicrobial strategies improves clinical, microbiological, and radiographic outcomes in patients with peri-implant mucositis and peri-implantitis. Materials and Methods: A structured narrative review was conducted using PubMed/MEDLINE and Scopus in July 2026. No database filters concerning language, human participants or study design were applied. During the screening process, only randomized controlled clinical trials involving human participants and available as English-language full texts were selected. Eligible interventions included locally or systemically administered antibiotics, antiseptics, antimicrobial drug-delivery systems, antimicrobial photodynamic therapy (aPDT), ozone-based therapies, and microbiome-modulating adjuncts. Conventional laser therapy was not classified as an eligible antimicrobial intervention. The database searches retrieved 462 records, including 252 from PubMed and 210 from Scopus. Following duplicate removal and eligibility assessment, 100 publications representing 93 independent clinical trials were included. Results: adjunctive antimicrobial efficacy was highly variable and appeared to depend on disease severity, debridement strategy, antimicrobial agent, delivery modality, and follow-up period. Repeated or sustained local antimicrobial delivery was associated with modest, short-term benefits in several studies, whereas chlorhexidine (CHX) generally provided limited additional benefit over mechanical therapy. Evidence for systemic antibiotics remained inconsistent and insufficient to support routine use, while aPDT offered potential benefits that varied according to treatment protocol. Ozone therapy, herbal agents, and novel drug-delivery systems yielded encouraging preliminary results, although evidence remains scarce. Moreover, reductions in bleeding and probing depth (PD) did not reliably correspond to superior microbiological outcomes, radiographic bone gain, or complete disease resolution. Conclusions: Mechanical debridement (MD) and effective plaque control remain central to peri-implant disease management. Some adjunctive interventions produced modest short-term improvements in individual studies; however, the available evidence does not demonstrate durable disease control or support routine use. Therapeutic decisions should be tailored to disease severity, patient and implant characteristics, and the balance between potential benefits and antimicrobial-associated risks. Further well-designed and adequately powered randomized controlled trials with extended follow-up periods are needed to establish more definitive recommendations.},
}

@article {pmid42924825,
year = {2026},
author = {Bowler, B and Nasir, AR and Szewczyk, A and Ocanas, S and Unnikrishnan, A and Delpirou Nouh, C},
title = {Sleep and the Gut-Brain Axis: Bidirectional, Converging Mechanisms Linking Brain Health, Neuroinflammation, and Neurodegeneration.},
journal = {Pathophysiology : the official journal of the International Society for Pathophysiology},
volume = {33},
number = {4},
pages = {},
doi = {10.3390/pathophysiology33040074},
pmid = {42924825},
issn = {1873-149X},
abstract = {Sleep and the gastrointestinal (GI) tract interact in a complex and reciprocal relationship, although the molecular and physiological pathways underlying this interaction remain only partially defined. Communication between the central (CNS) and enteric nervous systems (ENS) spans neural, immune, endocrine, and metabolic pathways, including vagal nerve signaling, the hypothalamic-pituitary-adrenal (HPA) axis, gut-resident microbiota, and circulating microbial metabolites, such as bile acids with neuroinflammatory or neurotransmitter activity. In this narrative review, we synthesize evidence from animal models, observational cohorts, and intervention trials to map this bidirectional axis, focusing on several underexamined modulatory mechanisms including the interaction between the gut microbiome and the glymphatic system, the brain's perivascular waste-clearance network, which is implicated in the removal of amyloid-β (Aβ) and tau in Alzheimer's disease; neuroendocrine regulation and sex-related differences in gut microbiome composition and sleep patterns, which may help explain the divergent neurodegenerative disease risks between men and women; and age-related parallel trajectories of microbiome senescence and sleep fragmentation in older adults. We discuss melatonin, cortisol, estrogen, and ghrelin as endocrine mediators linking circadian biology to gut physiology, and we consider how environmental and lifestyle factors further perturb this system. These mechanisms form an integrative framework of the gut-brain-sleep axis and highlight priority directions for mechanistic and translational research, including significant nodes in this pathway where targeted interventions may help cognitive resilience and slow the neurodegenerative disease progression. More research clarifying these mechanisms may help identify the most promising targets, potentially leading to personalized, precision-medicine-based therapeutic strategies.},
}

@article {pmid42925028,
year = {2026},
author = {Wang, C and Wu, W and Cui, M and Zhang, S and Wang, C},
title = {Baicalin and levofloxacin exert divergent modulation on gut microbiota and metabolome crosstalk in DSS-triggered ulcerative colitis.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0177126},
doi = {10.1128/spectrum.01771-26},
pmid = {42925028},
issn = {2165-0497},
abstract = {Baicalin (BA), a bioactive flavonoid, and levofloxacin hydrochloride (LH), a fluoroquinolone antibiotic, both hold potential for ulcerative colitis (UC) treatment, yet the mechanistic differences in their regulation of gut microbiota and metabolome remain elusive. This study aimed to systematically compare their therapeutic efficacy and underlying mechanisms in a dextran sulfate sodium-induced murine colitis model, with a focus on gut microbial and metabolic modulation. Mice were randomized into Control, model, BA-treated, and LH-treated groups. Disease severity was assessed via body weight changes, disease activity index, colon length, and histopathological analysis. Western blot and enzyme-linked immunosorbent assay were employed to detect NF-κB pathway activation and pro-inflammatory cytokine levels, while 16S rRNA sequencing and metabolomics profiled gut microbiota and metabolites. Both agents markedly ameliorated colitis symptoms, suppressed NF-κB activation, and cytokine expression, with BA showing superior cytokine inhibition. BA enriched beneficial Lactobacillus, regulating isoflavone/alkaloid synthesis; LH elevated Akkermansia abundance and modulated amino acid metabolism. These findings reveal distinct therapeutic mechanisms of BA and LH, laying a foundation for personalized UC therapy and validating BA's traditional medicinal utility.IMPORTANCEUlcerative colitis remains a prevalent inflammatory bowel disease with limited microbiota-targeted therapies. Baicalin and levofloxacin both alleviate dextran sulfate sodium-induced colitis, yet their gut microbiome and metabolome regulatory mechanisms have not been directly compared. This study demonstrates that baicalin and levofloxacin exert anti-colitis effects via divergent microbiota-metabolite axes: baicalin enriches Lactobacillus and modulates isoflavone/alkaloid metabolism, while levofloxacin increases Akkermansia and reshapes amino acid metabolism. These distinct mechanisms provide new evidence for developing microbiota-based personalized strategies for ulcerative colitis treatment.},
}

@article {pmid42925049,
year = {2026},
author = {Creencia, AR and Arguelles, EDLR and Tan Gana, NH and Capanzana, RMAD and Martinez, JP and Lanceras, JC and Salaan, CAM and Del Castillo, RAM and Cadao, DFB},
title = {Bacterial community profiles of soils from the Mount Makiling Forest Reserve, Philippines.},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0093626},
doi = {10.1128/mra.00936-26},
pmid = {42925049},
issn = {2576-098X},
abstract = {The Mount Makiling Forest Reserve harbors diverse microorganisms with potential biotechnological applications, yet bacterial taxonomic profiling across its watersheds remains limited. Amplicon metagenome sequencing targeting the 16S rRNA gene revealed Proteobacteria and Acidobacteriota as dominant phyla, with Actinobacteriota, Verrucomicrobiota, Chloroflexi, Myxococcota, Methylomirabilota, Bacteroidota, Nitrospirota, and Planctomycetota present at varying abundances.},
}

@article {pmid42925152,
year = {2026},
author = {Hendricks, SF and Tan, AL and Williams, AG and Clark, MM and Buckley, KM and Strader, ME},
title = {Environmental microbial communities and host selection shape larval microbiomes.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag118},
pmid = {42925152},
issn = {1574-6941},
abstract = {Ocean warming is altering abiotic environments and biotic interactions experienced by marine organisms, where sensitive early developmental windows occur in biologically complex seawater communities. The impact of these interactions on developmental processes and fitness in hosts is not well understood, but likely contingent on the establishment of a host-associated microbiome. Here, we hypothesize that temperature and microbial exposure during embryogenesis influence larval microbiome assembly and host morphology. Strongylocentrotus purpuratus embryos were raised in low microbial richness (LMR) or high microbial richness (HMR) seawater at ambient (14 °C) or elevated (18 °C) temperature, then collected at 2, 4, and 6 days post-fertilization (dpf) following multiple feedings. Higher microbial diversity was observed in larvae that developed in HMR seawater when compared to LMR. Differences in relative abundances of dominant microbial families between seawater and larvae suggest some degree of host selectivity in microbiome assembly. Temperature did not strongly alter microbiome composition, but both temperature and microbial condition led to differences in larval morphology by 6 dpf, potentially due to enrichment of microbes with chemoheterotrophic functions. By linking how temperature and microbial communities interact with host development, we contribute novel insights into how early-life environmental conditions impact holobiont formation and morphology.},
}

@article {pmid42925422,
year = {2026},
author = {Rostami, M and Roudsari, MB and Abasi, M and Khaneshi, N and Gerayeli, M and Yousefi, M and Amini, A and Alizadeh, A and Fazel, F},
title = {The Potential Role of Postbiotics in Periodontitis Treatment and Preventive Dentistry.},
journal = {Current microbiology},
volume = {83},
number = {12},
pages = {},
pmid = {42925422},
issn = {1432-0991},
mesh = {Humans ; *Periodontitis/therapy/microbiology/prevention & control/drug therapy ; *Probiotics/administration & dosage/therapeutic use ; *Preventive Dentistry/methods ; Microbiota/drug effects ; },
abstract = {Postbiotics, the bioactive molecules of probiotics and inactive microbial cells, have emerged as promising supplementary method in dental health treatment, specifically targeting disorders such as periodontitis. The definition, mechanisms of action and therapeutic potential of postbiotics in periodontitis are discussed in detail in this review. The capacity of postbiotics to control pathogenic bacteria development, increase immune responses and restore microbial balance, demonstrates the many roles of postbiotics in antimicrobial activity and anti-inflammatory effects in controlling the oral microbiome. Importantly, postbiotics have potential advantages over live probiotics such as greater stability and safety, without the need for microbial colonization. Postbiotics have shown potential in reducing gingival inflammation, as evidenced by clinical studies, thus offering a promising adjunct to conventional periodontal therapies. Current data, however, are limited, heterogeneous, and insufficient to support strong therapeutic claims. As research advances, the standardized addition of postbiotics to common dental care and hygiene products needs to be rigorously validated by large-scale clinical trials.},
}

Humans
*Periodontitis/therapy/microbiology/prevention & control/drug therapy
*Probiotics/administration & dosage/therapeutic use
*Preventive Dentistry/methods
Microbiota/drug effects

@article {pmid42925435,
year = {2026},
author = {Su, Z and Han, L and Song, F and Wang, Y and Lin, Y},
title = {β-defensin 130 Counteracts ETEC-K88 Infection in Mice: Mechanistic Insights from Gut Microbiome and LC-MS-Based Metabolomic Correlation Analysis.},
journal = {Current microbiology},
volume = {83},
number = {12},
pages = {},
pmid = {42925435},
issn = {1432-0991},
support = {BW20250003//Binzhou Municipal Medical and Health Science and Technology Project/ ; ZR2023QC043//Natural Science Foundation of Shandong Province/ ; },
mesh = {Animals ; *beta-Defensins/administration & dosage/pharmacology ; Mice ; *Enterotoxigenic Escherichia coli/drug effects ; *Escherichia coli Infections/drug therapy/microbiology ; *Gastrointestinal Microbiome/drug effects ; Metabolomics ; Chromatography, Liquid ; *Anti-Bacterial Agents/administration & dosage/pharmacology ; Mass Spectrometry ; Disease Models, Animal ; },
abstract = {β-defensin 130 is a potential antimicrobial peptide candidate against enterotoxigenic Escherichia coli (ETEC)-K88 infection, but its in vivo mechanism remains unclear. In this study, the antibacterial activity of β-defensin 130 against ETEC-K88 was first evaluated in vitro, and membrane damage was observed by morphological disruption and PI uptake. Then, an ETEC-K88-infected mouse model was established and treated with β-defensin 130. Based on 16 S rDNA sequencing and LC-MS metabolomics, ETEC-K88 infection was shown to reduce gut microbial diversity and alter community structure. Correlation analysis revealed significant microbiota-metabolite interactions, β-defensin 130 treatment was associated with increased gut microbial diversity and partial recovery of the gut microbial community, increased beneficial Bacteroidota/Firmicutes, decreased pathogenic Proteobacteria, and partial reversal of infection-associated metabolic disturbances (e.g., upregulating L-tryptophan and linoleic acid). Collectively, these findings suggest that β-defensin 130 may alleviate ETEC-K88 infection by disrupting bacterial membranes, modulating gut microbiota, and partially restoring metabolic homeostasis, supporting its further development as a potential antimicrobial agent.},
}

Animals
*beta-Defensins/administration & dosage/pharmacology
Mice
*Enterotoxigenic Escherichia coli/drug effects
*Escherichia coli Infections/drug therapy/microbiology
*Gastrointestinal Microbiome/drug effects
Metabolomics
Chromatography, Liquid
*Anti-Bacterial Agents/administration & dosage/pharmacology
Mass Spectrometry
Disease Models, Animal

@article {pmid42925522,
year = {2026},
author = {Javed, A and Chrysostomou, D and Marchesi, JR and Roberts, L and Hart, AL and Powell, N and Williams, HRT and Hicks, LC and Mullish, BH and Alexander, JL},
title = {Fecal microbiota transplant in the treatment of inflammatory bowel diseases: new perspectives on delivery, mechanism, and clinical positioning.},
journal = {Inflammatory bowel diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/ibd/izag219},
pmid = {42925522},
issn = {1536-4844},
support = {//National Institute of Health Research (NIHR) Imperial Biomedical Research Centre (BRC)/ ; MR/Z504002/1//Medical Research Council (MRC) Clinician Scientist/ ; PG_25008//Bowel Research U.K./ ; },
abstract = {The gut microbiota, a complex and dynamic community of microorganisms, has emerged as a crucial determinant of human health and well-being in recent years. This microbial ecosystem plays a pivotal role in various physiological processes, including nutrient metabolism, immune system regulation, and intestinal homeostasis. Disruptions in the composition and function of the gut microbiota have been implicated in a wide range of diseases, such as Clostridioides difficile infection (CDI) and inflammatory bowel diseases (IBD). The elucidation of the fundamental relationship between human disease and the gut microbiome has positioned fecal microbiota transplantation (FMT) as a transformative strategy in modern clinical practice. However, while FMT is increasingly explored for a diverse range of systemic diseases, its clinical implementation is relatively limited beyond the management of recurrent CDI. This review examines the evolving role of FMT within the therapeutic framework of chronic inflammation, focusing specifically on IBD. We compare the variable clinical outcomes in IBD with the highly successful model of recurrent CDI, highlighting mechanistic and clinical determinants of response in a different disease context. Additionally, we evaluate the progression of delivery strategies, from conventional fecal suspensions to standardized oral capsule formulations, and their implications for efficacy, safety, and scalability. Furthermore, we explore the diversifying clinical scenarios where FMT may be incorporated in the treatment paradigm of IBD, including primary treatment of active inflammation, prevention of relapse, and its place in combination with current immunosuppressive therapies.},
}

@article {pmid42925771,
year = {2026},
author = {Pradeep, A and Mathew, AI and Koyyappurath, S and Vemula, PK and Bhat, SG and Narayanan, S},
title = {An exploratory study of gut microbiota and humoral immune responses following bacterial ghost administration in rats.},
journal = {Vaccine},
volume = {95},
number = {},
pages = {129284},
doi = {10.1016/j.vaccine.2026.129284},
pmid = {42925771},
issn = {1873-2518},
abstract = {The rise of multidrug-resistant pathogens necessitates innovative immunotherapeutic approaches. Bacterial ghosts (BGs) are non-viable empty cell envelopes retaining antigenic determinants, offer a safe and potent immunomodulatory alternative to live bacterial vaccines. This exploratory study examined the selected tolerability parameters, humoral immune responses, and gut microbiota profiles potential of Staphylococcus aureus-derived ghost cells (GCs) in Sprague Dawley rats. Animals received three doses at one-week intervals via oral and intramuscular (IM) administration at low (10[6] units/mL) and high (10[9] units/mL) doses over a 21-day period. Hemocompatibility, serum biochemistry, and histopathology of key organs provided preliminary insights into the tolerability of the formulation under the experimental conditions. Serum immunoglobulin profiling revealed increases in GC-specific IgG and IgA levels with oral administration, while IM delivery showed less systemic variations in antibody production. qRT-PCR analyses indicated a minimal but detectable pro-inflammatory cytokine expression, notably TNF-α, especially in high-dose IM groups. Gut microbiome analysis via 16S rRNA sequencing identified differences in microbial diversity indices and the relative abundance of selected bacterial taxa across experimental groups. Histological assessments of gut tissue indicated mild, non-pathological mucosal changes only at high oral doses. Overall, the findings provide preliminary observations on humoral immune responses, selected tolerability parameters, and gut microbiota profiles following GC administration. These preliminary findings encourage further investigation of BGs as engineerable platforms with potential applications in immunomodulation, mucosal vaccine development, and microbiome-targeted interventions.},
}

@article {pmid42918359,
year = {2026},
author = {Elmetwalli, A and Algehainy, NA and Altemani, FH and Alanazi, MA and Altemani, AH},
title = {From ecosystem engineering to living computers: integrating dual-paradigm bacterial therapeutics for solid tumor microenvironment reprogramming.},
journal = {International journal of pharmaceutics},
volume = {},
number = {},
pages = {127586},
doi = {10.1016/j.ijpharm.2026.127586},
pmid = {42918359},
issn = {1873-3476},
abstract = {Recent advances in tumor microbiome biology and synthetic biology have made bacteria attractive therapeutic agents capable of reprogramming tumor-associated microbial ecosystems and serving as programmable living systems in solid tumors. In this review, we construct a dual-paradigm framework combining engineered bacterial therapeutics and ecosystem editing. In the first paradigm, phage-mediated targeting, competitive displacement, and metabolic reprogramming are used to alter tumor-associated microbial communities. In the second paradigm, engineered bacteria are equipped with environmental sensors, genetic logic circuits, and therapeutic payloads. We discuss the mechanistic interplay of these strategies in terms of ecological niche formation, bacterial colonization, immune and metabolic remodeling, and microbiome-host feedback. Clinical experience still varies across platforms due to differences in bacterial strain, attenuation, route of administration, tumor biology, treatment context, and patient characteristics. Major translational challenges include biocontainment, genetic stability, manufacturing and potency control, predictive biomarker validation, and product-specific regulatory requirements. We propose an additional hypothesis-generating framework for patient stratification and adaptive treatment monitoring. These concepts together provide a structured framework for exploring bacterial therapeutics as components of precision oncology, while highlighting the need for prospective clinical validation.},
}

@article {pmid42918410,
year = {2026},
author = {Charlier, P and Armengaud, J and Gebelin, M and Lhortolary, S},
title = {Reconstructing skin microbiome of G. Clemenceau (1929): paleoproteomic analysis of his bath sponge.},
journal = {Annales pharmaceutiques francaises},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.pharma.2026.10.003},
pmid = {42918410},
issn = {2772-803X},
abstract = {Paleoproteomic analysis of a bath sponge belonging to Georges Clemenceau explores the possibility of reconstructing the skin microbiome of a historical figure from a preserved personal item. Using high-resolution mass spectrometry and a cascade proteotyping strategy, several microorganisms were identified, dominated by environmental bacteria of the genus Pseudomonas and opportunistic fungi such as Aspergillus and Exophiala. Traces of Escherichia coli, human proteins, marine organisms, and plants were also detected. Overall, the results suggest that the sponge does not accurately reflect Clemenceau's stable skin microbiome, as microorganisms typically associated with human skin are absent, likely due to taphonomic biases and preservation phenomena. On the contrary, the object appears as a complex microenvironment that has accumulated contamination over time related to humidity, the domestic and coastal environment, as well as the conditions of use and storage. The presence of opportunistic microorganisms, notably Exophiala sideris, even suggests a potential risk of skin infections in an elderly diabetic individual. This study thus demonstrates that everyday objects can constitute unique biological archives for paleopathology, not for precisely reconstructing an individual microbiota, but for documenting dermatological hygiene practices, microbial environments, and the infectious risks associated with reusable, damp objects at the beginning of the 20[th] century.},
}

@article {pmid42918601,
year = {2026},
author = {Tian, H and Liu, J and Zhang, Y},
title = {Metagenomic Insights into Microplastic Micro-interfaces: Transforming Pollutants and Spreading Resistance.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {129408},
doi = {10.1016/j.envpol.2026.129408},
pmid = {42918601},
issn = {1873-6424},
abstract = {Microplastic micro-interfaces (MPMI) in wastewater treatment plants (WWTPs) serve as critical hubs for microbial colonization, pollutant transformation, and antibiotic resistance gene (ARG) dissemination. In this study, a large-scale genome-resolved metagenomic approach was employed to reconstruct 463 high-quality metagenome-assembled genomes (MAGs) from biofilms established on polyethylene terephthalate (PET), polyethylene (PE), and polypropylene (PP) within a municipal WWTP. Taxonomic profiling revealed that MPMI selectively enriched strict anaerobes and uncultured taxa, driving a profound ecological shift from the surrounding water and indicating the formation of localized hypoxic micro-niches. Functionally, the MPMI microbiome constructed a highly integrated metabolic network. Key dominant lineages were found to synergistically couple aromatic hydrocarbon degradation (via the shikimate pathway and β-oxidation) with complex carbon, nitrogen, and sulfur cycling, while deploying energy-efficient nucleotide salvage strategies to ensure biofilm stabilization under nutrient stress. Crucially, horizontal gene transfer (HGT) emerged as a fundamental mechanism for functional diversification, facilitating the active cross-genomic exchange of key adaptive traits associated with pollutant metabolism and biofilm regulation. Furthermore, MPMI harbored a highly diverse resistome comprising 36 ARG categories and 289 subtypes, highlighted by the critical genomic co-localization of mobile elements and clinical resistance markers (e.g., mcr-5.1, mupA) in core colonizers. Ultimately, these genomic insights elucidate the MPMI as a profound ecological hotspot driving the concurrent adaptation of metabolic networks and the resistome, thereby exacerbating the risks of ARG dissemination in aquatic environments.},
}

@article {pmid42918681,
year = {2026},
author = {Syal, A and Cohen, SJ},
title = {Early-Onset Colorectal Cancer: Epidemiology, Etiologic Pathways, and Emerging Prevention Strategies.},
journal = {Clinical colorectal cancer},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.clcc.2026.09.005},
pmid = {42918681},
issn = {1938-0674},
abstract = {Early-onset colorectal cancer (EOCRC), defined as CRC diagnosed before age 50, is rising globally despite declining incidence in older adults, representing a growing public health concern. This review synthesizes current evidence on EOCRC epidemiology, molecular features, etiologic hypotheses, and clinical implications, with an emphasis on life-course risk. Epidemiologic data demonstrate a strong birth cohort effect, implicating generational exposures in disease pathogenesis. Younger patients more often present with symptomatic, advanced-stage disease and show a predominance of distal and rectal tumors. Molecular analyses reveal modest differences from late-onset CRC, including lower BRAF mutation rates and predominance of microsatellite-stable, chromosomal instability tumors, without a defining molecular signature. Current evidence supports a multifactorial etiologic model involving metabolic dysfunction, Western dietary patterns, microbiome disruption, antibiotic exposure, and environmental factors. These exposures likely interact with genetic and epigenetic susceptibility over time to accelerate established colorectal carcinogenesis pathways rather than produce a distinct biologic entity. Among these, obesity and diet have the strongest epidemiologic support, while other contributors remain under investigation. Clinically, EOCRC highlights limitations of age-based screening and the need for improved symptom recognition, earlier diagnosis, and risk-stratified screening approaches. Prevention strategies should extend beyond midlife screening to target modifiable exposures earlier in life. EOCRC may often reflect accelerated carcinogenesis within established pathways, although conflicting molecular findings and potential biologic subsets warrant further investigation.},
}

@article {pmid42918754,
year = {2026},
author = {B Sant'Anna-Silva, AC and Del Bove, C and Efthymiou, G and Henry, E and Henry, L and Kundnani, J and Rossignol, R and Zimmermann, S},
title = {Meeting Report of the 6th edition of metabolism and cancer symposium.},
journal = {Oncogenesis},
volume = {15},
number = {1},
pages = {},
pmid = {42918754},
issn = {2157-9024},
abstract = {The 6th International Meeting "Metabolism and Cancer" was held at the Convention Center in La Grande Motte, France, on October 8-10, 2025. The three-day conference brought together 240 participants from eleven countries and featured 29 scientific presentations, including 15 invited lectures delivered by leading investigators in the field of oncometabolism. The program was structured into four thematic sessions: (i) diet, cachexia, microbiome, and microenvironment; (ii) stem cells and metabolic plasticity; (iii) epigenetics, epitranscriptomics, and metabolism; and (iv) metabolic control of drug resistance, therapy, and biomarkers. This meeting report highlights key conceptual advances and emerging directions discussed during the conference. Future progress in cancer metabolism will depend on elucidating the cross-talk between tumors and peripheral tissues, as organism-level metabolic regulation is likely to critically influence tumor growth, plasticity, and treatment sensitivity. Moving forward, a systems-level integration of metabolic, genomic, and spatial data is poised to redefine cancer metabolism from a descriptive field into a source of actionable vulnerabilities for precision oncology.},
}

@article {pmid42918850,
year = {2026},
author = {Zhang, C and Cai, D and Aihara, K and Chen, L},
title = {CauTrigger: deciphering biological system state transitions by hierarchical causal decomposition.},
journal = {Nature methods},
volume = {},
number = {},
pages = {},
pmid = {42918850},
issn = {1548-7105},
support = {T2350003, 12131020, 42450084, T2542018, 12326614, and 12426310//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {Biological systems exhibit complex hierarchical regulation, with interactions across multiple layers governing transitions between states. Identifying the causal architecture underlying these state transitions remains challenging because confounding can produce spurious associations in observational data. Here we present CauTrigger, a hierarchical deep latent variable model that integrates do-calculus to identify potential causal triggers and predict perturbation outcomes across multiple regulatory layers. By disentangling causal and spurious latent factors, CauTrigger recursively reconstructs the underlying regulatory hierarchy and enables interpretable reasoning from observational data. Across synthetic and real-world datasets with multilayer regulatory structures, CauTrigger outperforms existing methods in identifying causal triggers and forecasting system-level responses. Applied to single-cell multi-omics and gut microbiome datasets, CauTrigger prioritizes candidate causal triggers and uses in silico perturbations to generate testable hypotheses about biological state transitions and inform potential strategies for state navigation. Together, these results establish CauTrigger as a general-purpose framework for causal discovery in complex biological systems.},
}

@article {pmid42918855,
year = {2026},
author = {Mohamed, AR and Ochsenkühn, MA and Haydon, TD and Abdelrazig, S and Coe, LSY and Mochales-Riaño, G and Jo, WS and Healy, AR and Abrego, D and Raina, JB and Burt, JA and Amin, SA},
title = {Steroid hormones produced by coral-associated Endozoicomonas influence coral immune response during thermal stress.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {42918855},
issn = {2058-5276},
abstract = {The coral microbiome is believed to play a crucial role in sustaining corals and enabling adaptation to perturbations. A ubiquitous group of coral-associated bacteria, known as Endozoicomonas, are hypothesized to provide essential metabolites to corals, although detailed dynamics of the interactions between host and microbe are poorly understood. Here multi-omics and laboratory validation experiments reveal that Endozoicomonas encodes genes for the metabolism of coral-derived testosterone and converts ubiquitous cholesterol into testosterone and progesterone, both important steroids that accumulate within the coral holobiont during thermal stress. Field sampling along a natural temperature gradient showed general suppression of coral steroid hormones under thermal stress and during white syndrome manifestation. Provision of testosterone or progesterone to corals during laboratory thermal stress induced transcriptional reprogramming of the coral innate immune response, suggesting microbial involvement in host immune modulation. These findings highlight a previously unrecognized potential mechanism of microbial contribution to coral resilience.},
}

@article {pmid42918965,
year = {2026},
author = {Rodrigues, RS and Fontenele, PA and Rocha, JC and Setti, AS},
title = {The Gut-Immune-Endometrial Axis in Reproductive Failure: a Structured Narrative Review of Intestinal Dysbiosis, Systemic Inflammation, and Chronic Endometritis.},
journal = {Reproductive sciences (Thousand Oaks, Calif.)},
volume = {},
number = {},
pages = {},
pmid = {42918965},
issn = {1933-7205},
abstract = {Chronic endometritis (CE) is a persistent inflammatory condition of the endometrium characterized by stromal plasma cell infiltration and is increasingly recognized in women with infertility, recurrent implantation failure (RIF), and recurrent pregnancy loss (RPL). Although traditionally considered a localized infectious process, heterogeneous treatment responses and recurrence suggest that broader immunological mechanisms may contribute in selected patients. This structured narrative review synthesizes clinical and mechanistic evidence relevant to a possible gut-immune-endometrial axis. A structured PubMed/MEDLINE search was conducted from database inception to December 31, 2025, and reference lists of relevant reviews and key primary studies were screened. Evidence was synthesized thematically across clinical, immunological, and translational domains. CE is associated with infertility and RPL, whereas findings in RIF populations are heterogeneous and strongly dependent on diagnostic criteria. CE is characterized by plasma cell infiltration, pro-inflammatory signaling, and activation of pathways including toll-like receptor 4 (TLR4)-nuclear factor kappa B (NF-κB). Separately, intestinal dysbiosis and barrier dysfunction may permit systemic translocation of microbial products such as lipopolysaccharide, thereby promoting low-grade inflammatory signaling. However, no direct human study has yet linked gut dysbiosis or endotoxemia to histologically confirmed CE within the same cohort. The proposed axis should therefore be regarded as a hypothesis-generating framework rather than an established causal pathway. CE is biologically heterogeneous and may arise from infectious, local microbial, immune-mediated, or systemic-inflammatory mechanisms that can overlap. Reverse causality and shared confounding factors are also plausible. At present, the model does not justify routine microbiome testing or gut-directed treatment for CE, but it defines priorities for prospective studies integrating microbiome profiling, systemic immune markers, and standardized endometrial phenotyping.},
}

@article {pmid42918974,
year = {2026},
author = {Sharma, R and Kumar, G and Thakur, A},
title = {Gut-brain axis in Alzheimer's disease: neuroinflammatory mechanisms and immunopharmacological interventions.},
journal = {Inflammopharmacology},
volume = {},
number = {},
pages = {},
pmid = {42918974},
issn = {1568-5608},
abstract = {Despite being defined pathologically by amyloid-β plaques, chronic neuroinflammation and neurofibrillary tangles, the drugs that target these processes directly (lecanemab and donanemab) have only modest effects on the clinical course of Alzheimer's disease (AD) and significant safety concerns have been identified, so there is renewed interest in upstream, systemic contributors to disease. This review aims to provide a synthesis of the latest mechanistic and clinical evidence that gut microbiota dysbiosis is associated with Alzheimer's disease with a specifically immunopharmacological focus. We will explore how the gut-brain axis pathways (vagal, immune, endocrine and microbial-metabolite signaling) converge to trigger microglial and astrocytic activation via toll-like receptor 4/NF-κB and complement-primed NLRP3 inflammasome signaling, which is also directly activated by amyloid-β and tau. Then we review the immunopharmacological interventions intended to break this axis - probiotic supplementation (some consistent benefit - although mild) and sodium oligomannate, with strong preclinical and case report signals that need human trials (in 2026) and polyphenols and GLP-1 receptor agonists, which have a persistent disconnect between mechanistic promise and clinical efficacy, including a definitive null result for semaglutide in 2026. Translative directions are addressed to nanotechnology-based delivery systems for improving bioavailability and blood-brain barrier penetration, as well as emerging precision-medicine, AI-driven approaches in the selection of treatments based on microbiome information. It is our opinion that because the gut-brain-immune axis is a mechanistically supported and potentially highly scalable therapeutic target, complementary to amyloid and tau therapies, the development of future therapies should match the inflammatory, metabolic and microbial phenotypes.},
}

@article {pmid42918987,
year = {2027},
author = {Piloto-Sardiñas, E and Wu-Chuang, A and Cabezas-Cruz, A},
title = {Predictive Functional Profiling of Allergy-Associated Microbiota with PICRUSt2.},
journal = {Methods in molecular biology (Clifton, N.J.)},
volume = {3092},
number = {},
pages = {143-156},
pmid = {42918987},
issn = {1940-6029},
mesh = {*Microbiota/genetics ; Humans ; *Hypersensitivity/microbiology ; RNA, Ribosomal, 16S/genetics ; *Computational Biology/methods ; *Software ; Phylogeny ; Workflow ; Metabolic Networks and Pathways ; },
abstract = {Functional profiling of host-associated microbiota is essential for elucidating its role in immune dysregulation, such as in allergic diseases. Predictive bioinformatics tools like PICRUSt2 (Phylogenetic Investigation of Communities by Reconstruction of Unobserved States, version 2) enable the inference of microbial metabolic potential from 16 S rRNA gene amplicon data. This chapter describes the computational workflow for using PICRUSt2 to analyze allergy-associated microbiota. The protocol begins with a standardized amplicon sequence variant (ASV) table and its corresponding taxonomy and sequence files. Users execute the core PICRUSt2 pipeline to predict gene family abundances (EC numbers, KO categories) and reconstruct MetaCyc metabolic pathways. Predicted pathway abundances are then analyzed for differential abundance between sample groups using statistical methods in R, and metabolic interaction networks are constructed for visualization. The workflow is executed in a standard Unix command-line environment and is compatible with output from upstream pipelines such as QIIME 2. This protocol provides a standardized method to generate testable hypotheses about microbiome function in allergy research from widely available 16 S rRNA data.},
}

*Microbiota/genetics
Humans
*Hypersensitivity/microbiology
RNA, Ribosomal, 16S/genetics
*Computational Biology/methods
*Software
Phylogeny
Workflow
Metabolic Networks and Pathways

@article {pmid42919035,
year = {2026},
author = {Jia, Y and Wang, T and Wang, X and Zhou, Y and Xu, H and Qu, L and Liu, B and Lin, L and Ma, Z and Wang, G},
title = {Temporal variation and functional potential of epiphytic bacterial communities associated with the brown alga Sargassum fusiforme.},
journal = {Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]},
volume = {57},
number = {1},
pages = {},
pmid = {42919035},
issn = {1678-4405},
mesh = {*Sargassum/microbiology ; *Bacteria/classification/genetics/isolation & purification/metabolism ; RNA, Ribosomal, 16S/genetics ; *Microbiota ; Biodiversity ; Phylogeny ; DNA, Bacterial/genetics ; Seasons ; Seaweed/microbiology ; Edible Seaweeds ; },
abstract = {The brown alga Sargassum fusiforme is an economically and nutritionally important marine macroalga widely cultivated in East Asian coastal waters. Its surface harbors diverse epiphytic bacterial communities, yet their temporal variation and functional characteristics remain insufficiently understood. In this study, we investigated the epiphytic bacterial communities associated with S. fusiforme throughout a seven-month mariculture cycle and compared them with those of eight sympatric macroalgae from three major phyla (Phaeophyta, Rhodophyta, and Chlorophyta) using 16S rRNA gene amplicon sequencing. After quality filtering and optimization, a total of 1,203,660 high-quality sequences (comprising 452,840,609 bases) were retained across all samples. Alpha diversity differed among the sampled macroalgal host species, with the Chao index ranging from 272.1 (Sargassum horneri) to 792.8 (Polysiphonia senticulosa), and temporal variation in S. fusiforme showed the highest species richness in November (Chao = 535.9) and lowest in December (Chao = 254.8). Beta diversity analyses revealed distinct bacterial community patterns associated with both sampling months and macroalgal species. Proteobacteria, Bacteroidota, and Firmicutes were the dominant bacterial groups across all samples, with a core microbiome of 33 OTUs consistently detected across all months. Functional prediction using FAPROTAX indicated that epiphytic bacterial communities potentially participate in carbon, nitrogen, and sulfur cycling, with chemoheterotrophy and related metabolic processes being predominant. Culturable epiphytic bacteria (84 isolates) exhibited diverse extracellular enzyme activities, including alginate, starch, chitin, cellulose, and carrageenan degradation. Additionally, 15.5% of isolates produced indole-3-acetic acid (IAA) and 77.4% displayed acyl-homoserine lactone (AHL)-related signaling activity. Collectively, our findings reveal pronounced temporal variation and host-associated differences in the epiphytic bacterial communities of S. fusiforme across a cultivation cycle and highlight the functional potential of seaweed-associated bacteria as a source of microbial resources for future ecological and biotechnological investigations.},
}

*Sargassum/microbiology
*Bacteria/classification/genetics/isolation & purification/metabolism
RNA, Ribosomal, 16S/genetics
*Microbiota
Biodiversity
Phylogeny
DNA, Bacterial/genetics
Seasons
Seaweed/microbiology
Edible Seaweeds

@article {pmid42919156,
year = {2026},
author = {Shanmugam, G and Jeon, J},
title = {EzMAP v2.0: an integrated platform for microbiome analysis with advanced functional and network modules.},
journal = {BMC bioinformatics},
volume = {27},
number = {1},
pages = {},
pmid = {42919156},
issn = {1471-2105},
mesh = {*Microbiota ; *Software ; Machine Learning ; Algorithms ; *Computational Biology/methods ; },
abstract = {BACKGROUND: Amplicon-based microbiome studies generate complex datasets that require streamlined processing and analysis. While EzMAP provided a user-friendly platform integrating QIIME2 with downstream statistical and functional analyses, its adoption was limited by installation issues, restricted user flexibility, and lack of advanced analytical modules.

RESULTS: We present EzMAP v2.0, a major update to the Easy Microbiome Analysis Platform (EzMAP), featuring improved accessibility, enhanced usability, and expanded analytical capabilities. Installation has been simplified across operating systems, resolving dependency conflicts common in the previous version. EzMAP v2.0 introduces a dual-mode framework: Easy Mode with automated parameter selection (including a smart-trim algorithm for DADA2 truncation based on per-base quality profiles) suitable for novice users, and Expert Mode with full parameter control for advanced users. Functional prediction modules (Tax4Fun and FunGuild) have been optimized for stability and accuracy. EzMAP v2.0 incorporates machine learning through a Random Forest module for predictive modeling and feature selection at user-specified taxonomic levels, and a novel ANCOM-BC + Random Forest consensus module that combines compositional differential abundance with predictive feature importance to identify high-confidence biomarkers. Microbial co-occurrence network analysis using SparCC enables identification of correlated taxonomic associations, with hub analysis to identify potential keystone taxa. We demonstrate EzMAP v2.0 capabilities through application to a publicly available rhizosphere microbiome dataset, comparing Easy Mode and Expert Mode outputs across diversity, differential abundance, biomarker identification, consensus analysis, and co-occurrence network modules. Both modes detected significant treatment effects on community structure (PERMANOVA P < 0.001) and identified hundreds of differentially abundant ASVs per stress comparison, with the consensus module identifying high-confidence biomarkers supported by both ANCOM-BC and Random Forest analyses. Differences from previously published findings on this dataset are documented and attributed to known sources of pipeline-dependent variation in microbiome analyses.

CONCLUSION: EzMAP v2.0 consolidates upstream processing, downstream statistics, functional prediction, machine learning, and ecological network analysis within a single, user-friendly framework. By lowering technical barriers and broadening analytical scope, EzMAP v2.0 provides an integrated and methodologically transparent solution for microbiome research.},
}

*Microbiota
*Software
Machine Learning
Algorithms
*Computational Biology/methods

@article {pmid42919172,
year = {2026},
author = {Jorquera, R and Ejsmentewicz, T and Lagos, R and Bravo, N and Issotta, F and Hernández-Oliveras, A and Villarroel-Espíndola, F and González-Stegmaier, R},
title = {Evaluating 16S metagenomics data analysis pipelines using an Ion Torrent sequencer for human gut microbiome research.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {42919172},
issn = {1471-2180},
support = {internal grant ID FALP-LMT-2021//Fundacion Arturo Lopez Perez/ ; internal grant ID FALP-LMT-2022//Fundacion Arturo Lopez Perez/ ; },
mesh = {Humans ; *RNA, Ribosomal, 16S/genetics ; *Metagenomics/methods ; Software ; *High-Throughput Nucleotide Sequencing/methods ; *Gastrointestinal Microbiome/genetics ; Feces/microbiology ; *Bacteria/genetics/classification/isolation & purification ; Computational Biology/methods ; Sequence Analysis, DNA/methods ; DNA, Bacterial/genetics ; },
abstract = {BACKGROUND: High-throughput 16S rRNA gene amplicon sequencing is essential for characterizing gut dysbiosis in translational research. However, microbiome profiles vary widely across sequencing platforms, library preparation protocols, targeted hypervariable regions (HVRs), and bioinformatics workflows. For users of the Ion Torrent S5 platform, there is currently no consensus methodology for performing open-source analyses as an alternative to proprietary frameworks. This study evaluates the proprietary Ion Reporter™ software against eight open-source pipelines based on QIIME2 and the SILVA database, accounting for data compositionality. Benchmarking was performed using a commercial human fecal reference material (ZymoBIOMICS™ D6323) characterized via DNA-shotgun sequencing (the ZB-Shotgun profile), as the reference standard.

RESULTS: Poisson regression modeling showed that using two primer sets for library preparation yielded a 30 % lower expected read count than a single primer set (IRR = 0.6986, p < 0.001). Across all configurations, the choice of denoising algorithm (DADA2 vs. Deblur) significantly affected alpha diversity calculations. At the phylum level, hierarchical clustering of Bayes factors (BFs) indicated that multi-region Ion Reporter workflows produced stable consensus predictions. Conversely, at the species level, single-HVR open-source pipelines significantly outperformed multi-region approaches.

CONCLUSIONS: Open-source pipelines that combine targeted HVR2 or HVR4 inputs with state-of-the-art denoisers outperform proprietary Ion Reporter options, providing superior taxonomic resolution and precision for species-level microbiome profiling. This study establishes a traceable, reproducible, and cost-effective framework that empowers independent researchers to maximize the utility of Ion Torrent 16S rRNA data in healthcare and gastrointestinal research without relying on restrictive software ecosystems.},
}

Humans
*RNA, Ribosomal, 16S/genetics
*Metagenomics/methods
Software
*High-Throughput Nucleotide Sequencing/methods
*Gastrointestinal Microbiome/genetics
Feces/microbiology
*Bacteria/genetics/classification/isolation & purification
Computational Biology/methods
Sequence Analysis, DNA/methods
DNA, Bacterial/genetics

@article {pmid42919357,
year = {2026},
author = {Huang, Y and Zhang, F and Zhang, J and Zhang, W and Wang, N and Wang, X and Wei, Z and Jiang, G and Raza, W},
title = {Microbial volatile humulene orchestrates plant-microbe alliance to establish disease-suppressive rhizosphere.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.71689},
pmid = {42919357},
issn = {1469-8137},
support = {1630052025029//Chinese Academy of Tropical Agricultural Sciences/ ; CATASCXTD202519//Chinese Academy of Tropical Agricultural Sciences/ ; 32571909//National Natural Science Foundation of China/ ; 42350610257//National Natural Science Foundation of China/ ; 42377124//National Natural Science Foundation of China/ ; 42477122//National Natural Science Foundation of China/ ; },
abstract = {Microbial volatile organic compounds (mVOCs) suppress growth and virulence traits of soil-borne pathogens, yet their ecological roles in disease suppression remain unclear. Here, we show that the sesquiterpene humulene from Streptomyces acts as a multifunctional regulator that suppresses bacterial wilt through coordinated inhibition of Ralstonia solanacearum, plant metabolic reprogramming, and rhizosphere microbiome modulation. We combined in vitro pathogen assays, pot experiments, microbiota transplantation, rhizosphere 16S rRNA profiling, root-exudate metabolomics, and plant and pathogen transcriptomics to investigate the direct and microbiome-mediated effects of humulene. Humulene reduced disease severity and pathogen abundance via a microbiome-dependent mechanism. Microbiota transplantation confirmed that the humulene-conditioned microbiome retains transferable disease-suppressiveness. Humulene also selectively enriched antagonistic Streptomyces, not by direct growth promotion, but by reprogramming tomato root exudation to produce lipid-derived petroselinic acid, which promoted Streptomyces growth, humulene production, and pathogen suppression. Root transcriptomics further revealed activation of lipid metabolic pathways involving alternative fatty acid desaturation and oxylipin signaling. Together, humulene functions as an ecological signal that integrates pathogen suppression, host lipid metabolism, and microbiome assembly to establish a disease-suppressive rhizosphere, enabling microbiome-informed control of bacterial wilt.},
}

@article {pmid42919400,
year = {2026},
author = {Roca, C and Greenwald, MA and Zorn, BT and Sun, L and Chen, G and Freeman, AF and Boucher, RC and Olivier, KN and Wolfgang, MC},
title = {Respiratory microbiome dysbiosis in STAT3 hyper-IgE syndrome (Job syndrome).},
journal = {Orphanet journal of rare diseases},
volume = {21},
number = {1},
pages = {},
pmid = {42919400},
issn = {1750-1172},
support = {T32HL166141/HL/NHLBI NIH HHS/United States ; U01HL156655/HL/NHLBI NIH HHS/United States ; U01HL156655/HL/NHLBI NIH HHS/United States ; U54HL185005/HL/NHLBI NIH HHS/United States ; SUN22F0//Cystic Fibrosis Foundation/ ; Clinical Center Bench-to-Bedside program/NH/NIH HHS/United States ; Clinical Center Bench-to-Bedside program/NH/NIH HHS/United States ; },
mesh = {Humans ; *Job Syndrome/microbiology/genetics/metabolism ; *Microbiota/genetics/physiology ; *STAT3 Transcription Factor/genetics/metabolism ; *Dysbiosis/microbiology ; Bronchoalveolar Lavage Fluid/microbiology ; Male ; Female ; },
abstract = {STAT3 hyper-IgE syndrome (STAT3-HIES), historically known as Job syndrome, is a rare primary immunodeficiency caused by dominant-negative mutations in STAT3. STAT3-HIES is characterized by impaired mucosal immunity, connective tissue abnormalities, and recurrent cutaneous and pulmonary infections. Although STAT3-dependent immune and epithelial pathways are central to airway host defense, the respiratory microbiome in STAT3-HIES remains poorly defined. To address this question, we profiled upper and lower respiratory tract microbiomes using 16S rDNA gene sequencing of oral rinse samples from eight STAT3-HIES participants and eight matched healthy controls, and bronchoalveolar lavage fluid (BALF) samples from eight STAT3-HIES participants and six healthy controls that passed sequencing quality thresholds. Oral rinse samples from STAT3-HIES participants showed lower phylogenetic diversity and significantly altered microbial community structure compared with controls. In BALF, α-diversity was comparable between groups, but β-diversity differed significantly, indicating altered lower airway microbial community composition in STAT3-HIES. Differential abundance analysis identified enrichment of the genus Rothia in STAT3-HIES BALF, and Rothia relative abundance positively correlated with BALF IL-1β, IL-1RA, and IL-8. Although limited by cohort size, these findings provide the first characterization of respiratory microbiome alterations in STAT3-HIES and suggest that impaired STAT3-dependent immune pathways may influence airway microbial ecology and inflammatory responses.},
}

Humans
*Job Syndrome/microbiology/genetics/metabolism
*Microbiota/genetics/physiology
*STAT3 Transcription Factor/genetics/metabolism
*Dysbiosis/microbiology
Bronchoalveolar Lavage Fluid/microbiology
Male
Female

@article {pmid42919413,
year = {2026},
author = {Moreno, ML and Taft, DH and Tompkins, TA and Dahl, WJ},
title = {Efficacy of yeast mannan supplementation on increasing stool frequency in adults: a randomized controlled trial.},
journal = {Trials},
volume = {27},
number = {1},
pages = {},
pmid = {42919413},
issn = {1745-6215},
support = {PRO00067834//Lallemand/ ; },
mesh = {Humans ; *Mannans/administration & dosage/adverse effects ; Double-Blind Method ; Feces/microbiology ; *Dietary Supplements ; *Defecation/drug effects ; *Saccharomyces cerevisiae/chemistry ; Gastrointestinal Transit/drug effects ; Treatment Outcome ; Adult ; Time Factors ; Quality of Life ; *Gastrointestinal Microbiome/drug effects ; },
abstract = {BACKGROUND: Yeast mannans are microbial-available substrates that may improve laxation and specifically modulate gut microbiota composition. The aim of this study is to determine the effect of yeast mannan supplementation on stool frequency in adults. Secondary aims will assess gastrointestinal tolerance and quality of life, whole gut transit time, fecal microbiota composition, and fecal and urinary levels of microbial-generated metabolites.

METHODS: A 6-week, double-blinded, parallel, randomized trial will evaluate the effect of 12 g of yeast mannan (Saccharomyces cerevisiae cell wall fraction containing mannan-oligosaccharides and mannoproteins) or control (maltodextrin and yeast protein) supplementation on mean daily stool frequency in adults (n = 60). Participants will complete a daily survey of stool frequency, gastrointestinal symptoms, and quality of life, any adverse events, and compliance with supplement intake during the 2-week baseline and 4-week intervention periods; gastrointestinal tolerance will be assessed weekly. Capsules containing radiopaque markers will be administered, and all stools will be collected during the last 3 days of baseline and intervention. Whole gut transit time will be estimated using the 80% recovery of radiopaque markers method. Per period, 24-h urine will be collected, and metabolomics will be determined by LC-MS/MS. For the primary outcome, change from baseline daily stool frequency between groups will be compared, and between-group comparisons of secondary outcomes using appropriate generalized linear regression models, and for those outcomes with repeated measures, linear mixed effect models. Fecal microbiome using whole metagenome sequencing data will be processed using metaphlan4, Braken, or another tool appropriate for estimating the relative abundance of microbial species. Additional analysis using tools such as humann3 will enable functional assignment of reads. Resulting relative abundance and normalized functional data will be further analyzed using a combination of tools in R software, including phyloseq and vegan packages.

DISCUSSION: In accordance with our pilot open-label study, the hypothesis is that yeast mannans will increase daily stool frequency, be highly tolerable, and demonstrate specific modulation of the microbiota, supporting its prebiotic properties. Additionally, yeast mannan supplementation may decrease whole gut transit time and mitigate the microbial production of inflammatory microbial-generated metabolites.

TRIAL REGISTRATION: NCT ID NCT06911177. Registered on 04 April 2025.},
}

Humans
*Mannans/administration & dosage/adverse effects
Double-Blind Method
Feces/microbiology
*Dietary Supplements
*Defecation/drug effects
*Saccharomyces cerevisiae/chemistry
Gastrointestinal Transit/drug effects
Treatment Outcome
Adult
Time Factors
Quality of Life
*Gastrointestinal Microbiome/drug effects

@article {pmid42919532,
year = {2026},
author = {Islam, T and Ali, S and Rabbee, MF},
title = {Mechanisms of nematicide evasion in plant-parasitic nematodes: From molecular adaptation to evolution-aware management.},
journal = {Pesticide biochemistry and physiology},
volume = {224},
number = {},
pages = {107336},
doi = {10.1016/j.pestbp.2026.107336},
pmid = {42919532},
issn = {1095-9939},
mesh = {Animals ; *Nematoda/drug effects/genetics/physiology ; *Antinematodal Agents/pharmacology ; Rhizosphere ; *Plant Diseases/parasitology/prevention & control ; Drug Resistance ; *Plants/parasitology ; Adaptation, Physiological ; },
abstract = {Plant-parasitic nematodes (PPNs) cause substantial global crop losses, yet the effectiveness of chemical nematicides is declining due to adaptive responses in nematode populations. Current understanding of nematicide resistance remains incomplete, often limited to target-site mutations and metabolic detoxification. This review addresses this gap by providing an integrated perspective on how PPNs evade nematicides across molecular, physiological, and ecological scales. We synthesize established resistance mechanisms alongside underexplored strategies, including cuticle remodeling, behavioral avoidance, and microbiome-assisted protection. Here, we incorporate the environmental and rhizosphere dynamics, highlighting how soil heterogeneity and microbial communities influence nematicide efficacy and resistance evolution. The review also examines cross-resistance and sub-lethal exposure as critical drivers of adaptive responses. Importantly, we propose integrated evolution-aware management (IEAM) as a sustainable framework that combines chemical, biological, and host-mediated strategies to reduce selection pressure and prolong control efficacy. This study is necessary to move beyond conventional single-target approaches toward holistic, evolution-informed nematode management. By linking mechanistic insights with agroecosystem processes, it provides a comprehensive foundation for developing durable and environmentally sustainable control strategies.},
}

Animals
*Nematoda/drug effects/genetics/physiology
*Antinematodal Agents/pharmacology
Rhizosphere
*Plant Diseases/parasitology/prevention & control
Drug Resistance
*Plants/parasitology
Adaptation, Physiological

@article {pmid42919547,
year = {2026},
author = {Li, X and Yang, Q and Ijaz, M and Zhou, T and Tian, Z and Yan, J and Li, B},
title = {Synergistic control of rapeseed sclerotinia stem rot by Penicillium oxalicum CAD211 and biosynthesized silver nanoparticles through host defense activation and rhizosphere microbiome remodeling.},
journal = {Pesticide biochemistry and physiology},
volume = {224},
number = {},
pages = {107351},
doi = {10.1016/j.pestbp.2026.107351},
pmid = {42919547},
issn = {1095-9939},
mesh = {Rhizosphere ; *Silver/chemistry/pharmacology ; *Ascomycota/drug effects ; *Penicillium/metabolism ; *Plant Diseases/microbiology/prevention & control ; *Metal Nanoparticles/chemistry ; *Brassica rapa/microbiology ; Microbiota/drug effects ; Brassica napus/microbiology ; Soil Microbiology ; },
abstract = {Sclerotinia stem rot (SSR), caused by Sclerotinia sclerotiorum, severely threatens rapeseed production, while prolonged fungicide use raises safety concerns, highlighting the need for sustainable alternatives. Herein, an indigenous Penicillium oxalicum strain CAD211 was isolated and used to biosynthesize spherical AgNPs (12.73-25.48 nm) with potent dose-dependent antifungal activity against S. sclerotiorum. In vitro assays showed that 20 μg mL[-1] AgNPs significantly inhibited mycelial growth and sclerotial germination of S. sclerotiorum. Under controlled pot conditions, the combined application of CAD211 and AgNPs achieved complete disease suppression through synergistic antagonism and restored rapeseed fresh and dry weights to 2.14- and 1.79-fold of the sole S. sclerotiorum-inoculated plants, respectively, while maintaining soil Ag content within the environmental safety threshold. Furthermore, the combined treatment reactivated the host oxidative burst, restored antioxidant enzyme activity, and ultimately contributed to an interactive network among rapeseed, S. sclerotiorum, soil nutrients and the rhizosphere microbiome. Specifically, it elevated soil organic matter (SOM) and available phosphorus (AP) contents to optimize rhizosphere nutrient supply, reshaped microbial community structure, enhanced microbial diversity, and enriched potentially beneficial taxa (Acidovorax, Cellvibrio and Sphingomonas). Furthermore, gene expression analysis uncovered the core dual molecular mechanism whereby the combined treatment suppressed the key S. sclerotiorum virulence genes (SsdchA, SsPKS12, SsPKS13, SsTHR1 and SsSCD1) and activated host defense genes (BnaA07.MKK9 and BnCYP71A13), while restoring the expression of growth-related genes (BnaC04.BIL1 and BnaA10.HY5), thereby balancing plant immunity and growth. Overall, this study provides a potential sustainable strategy for controlling soil-borne fungal diseases under controlled pot conditions, although further field validation is needed.},
}

Rhizosphere
*Silver/chemistry/pharmacology
*Ascomycota/drug effects
*Penicillium/metabolism
*Plant Diseases/microbiology/prevention & control
*Metal Nanoparticles/chemistry
*Brassica rapa/microbiology
Microbiota/drug effects
Brassica napus/microbiology
Soil Microbiology

@article {pmid42919552,
year = {2026},
author = {Feng, Y and Han, C and Du, Z and Wang, P and Yuan, D and Zhang, B},
title = {Chronic bifenthrin exposure disturbs intestinal homeostasis in common carp via mitochondrial dysfunction, epithelial barrier injury, gut dysbiosis, and metabolic reprogramming.},
journal = {Pesticide biochemistry and physiology},
volume = {224},
number = {},
pages = {107356},
doi = {10.1016/j.pestbp.2026.107356},
pmid = {42919552},
issn = {1095-9939},
mesh = {Animals ; *Pyrethrins/toxicity ; *Carps/metabolism ; *Mitochondria/drug effects/metabolism ; Homeostasis/drug effects ; *Insecticides/toxicity ; Intestinal Barrier Function/drug effects ; *Dysbiosis/chemically induced ; Intestinal Mucosa/drug effects/metabolism ; *Intestines/drug effects ; Gastrointestinal Microbiome/drug effects ; },
abstract = {Bifenthrin is a widely used pyrethroid insecticide that is frequently detected in aquatic environments, yet the mechanisms underlying its chronic intestinal toxicity in fish remain poorly understood. In this study, common carp (Cyprinus carpio) were chronically exposed to bifenthrin at concentrations of 0, 0.1, 1, and 2 μg/L for 30 d, and intestinal toxicity was comprehensively evaluated through biochemical, molecular, histopathological, microbiome, and metabolomic analyses. Bifenthrin exposure significantly altered the activities of digestive enzymes, induced histopathological damage, disrupted oxidative homeostasis, impaired mitochondrial function, and enhanced apoptosis. It also compromised intestinal barrier integrity, with altered tight junction protein expression and increased serum diamine oxidase and D-lactate levels. Furthermore, elevated intestinal and serum lipopolysaccharide levels together with increased pro-inflammatory cytokine levels indicated persistent intestinal inflammation. Moreover, bifenthrin markedly altered the intestinal microbial community, with increased abundance of potential opportunistic bacteria and decreased abundance of several dominant commensal taxa. Metabolomic analysis revealed extensive metabolic reprogramming characterized by disrupted energy metabolism, lipid mediator imbalance, and altered redox-related metabolism, providing insights into the metabolic basis underlying bifenthrin-induced intestinal dysfunction. Integrated microbiome-metabolome correlation analysis further linked gut dysbiosis to metabolic signatures associated with intestinal damage. Collectively, these results demonstrate that chronic bifenthrin exposure causes coordinated disruption of intestinal homeostasis in common carp. This study provides new mechanistic insights into bifenthrin-induced intestinal toxicity and improves our understanding of the chronic toxicological effects of bifenthrin in freshwater fish.},
}

Animals
*Pyrethrins/toxicity
*Carps/metabolism
*Mitochondria/drug effects/metabolism
Homeostasis/drug effects
*Insecticides/toxicity
Intestinal Barrier Function/drug effects
*Dysbiosis/chemically induced
Intestinal Mucosa/drug effects/metabolism
*Intestines/drug effects
Gastrointestinal Microbiome/drug effects

@article {pmid42919557,
year = {2026},
author = {Ren, Z and Hu, Z and Bao, Y and Qin, W and Qin, J and Wan, H and Tan, H and Chen, H},
title = {Enterococcus mundtii regulates SfCYP6B39 expression to modulate chlorantraniliprole resistance in Spodoptera frugiperda.},
journal = {Pesticide biochemistry and physiology},
volume = {224},
number = {},
pages = {107362},
doi = {10.1016/j.pestbp.2026.107362},
pmid = {42919557},
issn = {1095-9939},
mesh = {Animals ; *Spodoptera/microbiology/genetics/drug effects/metabolism ; *Insecticide Resistance/genetics ; *ortho-Aminobenzoates/pharmacology ; *Enterococcus/physiology ; *Insecticides/pharmacology ; Cytochrome P-450 Enzyme System/metabolism/genetics ; Symbiosis ; *Insect Proteins/genetics/metabolism ; },
abstract = {Microbiota-mediated adaptation is increasingly recognized as an important driver of insecticide resistance. Here, we demonstrate that gut symbionts promote chlorantraniliprole resistance in Spodoptera frugiperda through transcriptional regulation of host detoxification pathways. Resistant populations exhibited a distinct gut microbial community dominated by Enterococcus mundtii, accompanied by elevated cytochrome P450 (P450) activity and widespread upregulation of detoxification genes. Disruption of the gut microbiota reduced resistance, suppressed P450 activity, and downregulated multiple P450 genes, whereas recolonization with E. mundtii SC1 restored these effects. Functional analyses employing RNA interference and transgenic Drosophila melanogaster identified SfCYP6B39 as a key gene contributing to resistance. Molecular docking and molecular dynamics simulations further revealed that chlorantraniliprole can stably bind to SfCYP6B39. Mechanistically, E. mundtii SC1 promotes SfCYP6B39 overexpression via the transcription factors CncC and BR-C, forming a microbe-host regulatory axis that links symbiont presence to detoxification gene activation. Collectively, these findings demonstrate that gut symbionts enhance insecticide resistance through transcriptional reprogramming of host detoxification networks, providing mechanistic insight and suggesting microbiome-targeted strategies for sustainable pest management.},
}

Animals
*Spodoptera/microbiology/genetics/drug effects/metabolism
*Insecticide Resistance/genetics
*ortho-Aminobenzoates/pharmacology
*Enterococcus/physiology
*Insecticides/pharmacology
Cytochrome P-450 Enzyme System/metabolism/genetics
Symbiosis
*Insect Proteins/genetics/metabolism

@article {pmid42919656,
year = {2026},
author = {Zhang, D and Chu, H and Zhang, Y and Wang, Y and Zhang, Y and Guo, Y and Wan, P and Yue, H and Sun, G and Chao, Y and Zhang, J and Ge, C and Xie, F and Xie, Z and Guo, Q and Geng, M},
title = {Sodium oligomannate remodels gut redox adaptation and promotes microbiota-derived indole-3-propionic acid production to alleviate Alzheimer's disease.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2026-339603},
pmid = {42919656},
issn = {1468-3288},
}

@article {pmid42919671,
year = {2026},
author = {Rutkowska, N and Drożdżyński, P and Boruta, T and Sekuła, B and Marchut-Mikołajczyk, O},
title = {Bacillaceae Within Galium aparine L.: A Plant-Associated Treasure of Biosynthetic Diversity and Growth-Promoting Potential.},
journal = {Environmental microbiology reports},
volume = {18},
number = {5},
pages = {},
doi = {10.1111/1758-2229.70447},
pmid = {42919671},
issn = {1758-2229},
support = {SONATA-BIS 2025/58/E/NZ8/00097//Narodowe Centrum Nauki/ ; },
mesh = {Biosurfactants ; *Endophytes/isolation & purification/metabolism/genetics/classification ; *Galium/microbiology/growth & development ; Phylogeny ; Bacillus/isolation & purification/metabolism ; },
abstract = {Endophytic bacteria are key components of plant microbiomes, enhancing host growth, stress tolerance, and defence mechanisms. Ten cultivable strains affiliated with Bacillaceae, including putative novel Priestia and Bacillus species, were previously isolated from Galium aparine L.'s tissues. All tolerated diverse levels of abiotic stresses, produced ammonia and auxins, as well as all exhibited strong hydrolytic enzyme activities (amylase, protease, xylanase, and pectinase), indicating robust metabolic versatility. These bacteria stand out as prolific producers of industrially relevant compounds. Priestia megaterium GR4 demonstrated high production of hydrolytic enzymes and biosurfactants, and most strains synthesized and accumulated polyhydroxyalkanoates (PHA), highlighting their potential as sustainable bioplastic producers. UPLC-MS/MS confirmed koranimine production by Peribacillus frigoritolerans GR2. Previous genome mining studies revealed diverse biosynthetic gene clusters, including those for surfactin and fengycin. Overall, G. aparine endophytes represent powerful biological factories capable of producing a wide range of valuable compounds, including enzymes, biosurfactants and biopolymers, with strong potential for applications in industrial biotechnology, sustainable agriculture, and biocontrol.},
}

Biosurfactants
*Endophytes/isolation & purification/metabolism/genetics/classification
*Galium/microbiology/growth & development
Phylogeny
Bacillus/isolation & purification/metabolism

@article {pmid42919800,
year = {2026},
author = {Bhuiyan, MNI},
title = {Microbiome Continuum: Connecting Environmental, Host-Associated and Engineered Microbiomes Through One Health and Artificial Intelligence.},
journal = {Environmental microbiology reports},
volume = {18},
number = {5},
pages = {},
doi = {10.1111/1758-2229.70445},
pmid = {42919800},
issn = {1758-2229},
mesh = {*Artificial Intelligence ; *Microbiota ; Humans ; Animals ; *One Health ; Climate Change ; Gene Transfer, Horizontal ; Ecosystem ; *Host Microbial Interactions ; Multiomics ; },
abstract = {Microbiomes are increasingly understood as interconnected ecological systems spanning soil, water, plants, animals, humans and engineered environments rather than as isolated host-associated communities. This microbiome continuum provides a mechanistic perspective for One Health by linking microbial cells with the movement of metabolites, genes, signalling molecules and ecological functions across environmental boundaries. Here, we critically examined the biological processes that maintain this continuity, including dispersal, horizontal gene transfer (HGT), metabolic exchange, environmental exposure and host-microbe communication. We consider how climate change and anthropogenic disturbance reshape these interactions and influence antimicrobial resistance (AMR), non-communicable disease, ecosystem function and pathogen emergence. We further evaluate how artificial intelligence (AI), including machine learning and deep learning, can integrate multi-omics and longitudinal data, while emphasizing that predictive performance does not establish causality and that AI remains dependent on data quality, biological knowledge and experimental validation. Engineered microbiomes offer opportunities for targeted intervention, but ecological stability, biosafety, HGT and translational uncertainty remain important constraints. We propose a One Health Microbiome Intelligence Framework (OH-MIF) as a conceptual architecture for cross-domain integration, with emphasis on standardized data, causal validation, equitable participation and human oversight.},
}

*Artificial Intelligence
*Microbiota
Humans
Animals
*One Health
Climate Change
Gene Transfer, Horizontal
Ecosystem
*Host Microbial Interactions
Multiomics

@article {pmid42919965,
year = {2026},
author = {Blaser, MJ and Bushman, FD and Dominguez-Bello, MG and Elinav, E and Khare, S and Knight, R and Kwon, JH and Mazmanian, SK and Osman, M and Segata, N and Spector, T and Wargo, JA and Hourigan, SK},
title = {The human microbiome and chronic disease: ten strategic priorities for research and public health.},
journal = {Nature medicine},
volume = {},
number = {},
pages = {},
pmid = {42919965},
issn = {1546-170X},
}

@article {pmid42919974,
year = {2026},
author = {Lindgaard, C and Hvidt, AK and Keller, AK and Thingholm, L and Kristensen, SS and Lyskjær, I},
title = {Microbiome interactions in renal cell carcinoma: evidence, challenges and opportunities.},
journal = {Nature reviews. Urology},
volume = {},
number = {},
pages = {},
pmid = {42919974},
issn = {1759-4820},
abstract = {Renal cell carcinoma (RCC) is a heterogeneous malignancy with limited predictive biomarkers to guide treatment. Emerging evidence suggests that the microbiome might influence systemic immunity, therapeutic response and clinical outcomes. In metastatic RCC, the gut microbiome has been linked to the efficacy of immune checkpoint inhibitors, whereas the existence of a tumour microbiome remains a topic of debate. Circulating microbial DNA in blood has been proposed as a minimally invasive window into systemic immune status, offering a potential tool for monitoring treatment response, but its role in RCC is largely unexplored. Evidence from mechanistic studies, primarily from other solid cancer types, suggests that microbiome-immune crosstalk, microbial metabolites and functionally redundant pathways across taxa could modulate tumour biology. However, progress in RCC microbiome research remains limited by small cohorts, methodological variability and challenges in working with samples with a low microbial biomass, which are highly prone to contamination. Emerging spatial and multi-omics technologies now enable high-resolution mapping of these complex interactions, offering the potential to transform our understanding of the cancer microbiome. A structured roadmap is required to overcome technical and analytical challenges in RCC microbiome studies, enabling the identification of clinically relevant microbial signatures and their role in shaping tumour immunity.},
}

@article {pmid42919990,
year = {2026},
author = {Han, K and Li, X},
title = {Biodegradable microplastics in soil-plant systems: bibliometric analysis and structured evidence synthesis of carbon cycling, rhizosphere microbiomes and plant responses.},
journal = {Environmental geochemistry and health},
volume = {48},
number = {16},
pages = {},
pmid = {42919990},
issn = {1573-2983},
mesh = {*Rhizosphere ; *Plants/metabolism/drug effects ; *Microbiota/drug effects ; Soil Microbiology ; *Carbon Cycle ; *Microplastics/metabolism/toxicity ; Bibliometrics ; *Soil Pollutants/toxicity/metabolism ; Soil/chemistry ; Biodegradation, Environmental ; *Biodegradable Plastics ; },
abstract = {Biodegradable microplastics (Bio-MPs) are increasingly used in agriculture, yet their effects in soil-plant systems remain strongly context dependent. We combined Web of Science bibliometric analysis with structured evidence synthesis covering 2010 to 9 June 2026. Of 1,513 records retrieved, 1,392 were retained for bibliometric analysis after 121 documented exclusions. All 1,392 bibliometric records were further screened using predefined eligibility criteria, yielding 121 records for detailed evidence assessment and 105 unique original experimental studies for structured evidence synthesis. PLA and PBAT occurred in 69 (65.7%) and 30 (28.6%) studies, respectively, whereas only six studies (5.7%) used field settings. Research expanded rapidly after 2020 and increasingly addressed rhizosphere processes, microbial communities, carbon cycling and greenhouse-gas emissions. Across experimental studies, Bio-MP effects varied with polymer identity, dose, aging state, soil properties and plant-rhizosphere conditions. Soil carbon responses reflected competing processes involving polymer-derived carbon release, microbial assimilation, stimulation of native soil organic matter turnover, respiratory losses and carbon stabilization, rather than a consistent increase or decrease in soil carbon. Plant responses commonly involved altered nutrient acquisition, oxidative balance, photosynthesis and root development; among studies with extractable response directions, negative or decreasing plant/root effects occurred in 17 of 31 studies. Microbiome responses were predominantly mixed or context dependent (36 of 49 studies), and taxonomic shifts were reported much more frequently than direct functional validation. The evidence base therefore supports viewing Bio-MPs as both carbon inputs and ecological stressors whose consequences depend on environmental context, rather than as uniformly benign substitutes for conventional plastics. Major uncertainties remain because field-scale, time-resolved, carbon-fate and functionally validated microbiome studies are still limited.},
}

*Rhizosphere
*Plants/metabolism/drug effects
*Microbiota/drug effects
Soil Microbiology
*Carbon Cycle
*Microplastics/metabolism/toxicity
Bibliometrics
*Soil Pollutants/toxicity/metabolism
Soil/chemistry
Biodegradation, Environmental
*Biodegradable Plastics

@article {pmid42920144,
year = {2026},
author = {Ali, SS and Khan, K and Hassan, HE and Ali, A and El Aziz, FA and Schagerl, M and El-Shanshoury, AE and Abd El-Emam, MM},
title = {Engineering adaptive polysaccharide biomaterials: integrated biotechnology framework for regenerative medicine.},
journal = {Journal of biological engineering},
volume = {20},
number = {1},
pages = {},
pmid = {42920144},
issn = {1754-1611},
abstract = {Natural polysaccharides are versatile building blocks for regenerative biomaterials because of their structural diversity, generally favorable biocompatibility and biodegradability, chemical tunability, and capacity for biologically relevant interactions. Advances in biotechnology and materials engineering have expanded their role from primarily structural matrices to multifunctional platforms that can influence cellular, immune, and biochemical processes during tissue repair. This review presents an integrated biological engineering framework linking polysaccharide source and molecular architecture with extraction and purification, chemical functionalization, crosslinking, advanced fabrication, biological recognition, and translational performance. Particular emphasis is placed on structure-function relationships, stereospecific glycan-receptor interactions, immune-instructive biomaterials, protein-mediated cell-material interactions, microbiome-responsive systems, and emerging artificial intelligence-assisted approaches for biomaterial design. The importance of material purity is also critically considered, particularly the potential for residual endotoxin contamination to confound interpretation of immunomodulatory responses and compromise reproducibility. Representative applications in skin, musculoskeletal, cardiovascular, neural, and other regenerative systems illustrate how material composition, scaffold architecture, biofunctionalization, and manufacturing strategy collectively influence biological performance. Finally, challenges associated with scalable manufacturing, batch-to-batch reproducibility, sterilization, storage stability, quality control, regulatory translation, and clinical implementation are examined. By integrating molecular design, biological mechanisms, fabrication, and translational requirements, this review provides engineering principles for the development of adaptive polysaccharide biomaterials and identifies priorities for advancing reproducible and clinically translatable regenerative technologies.},
}

@article {pmid42920146,
year = {2026},
author = {Camus, L and Franz, J and Gerlach, D and Lange, A and Power, JJ and Navarro-Díaz, M and Stahl, J and Krismer, B and Rapp, J and Bilici, K and Otto, M and Klages, LJ and Starostin, V and Ham, S and Kalinowski, J and Angenent, LT and Link, H and Heilbronner, S},
title = {Amino acid availability influences Staphylococcus aureus interaction with the nasal microbiota in a strain- and community-specific manner.},
journal = {Microbiome},
volume = {14},
number = {1},
pages = {},
pmid = {42920146},
issn = {2049-2618},
mesh = {*Staphylococcus aureus/growth & development/metabolism/classification ; Animals ; Mice ; Humans ; *Microbiota ; *Nose/microbiology ; *Amino Acids/metabolism ; *Staphylococcal Infections/microbiology ; *Microbial Interactions ; Germ-Free Life ; Tyrosine/metabolism ; Female ; },
abstract = {BACKGROUND: Only some individuals carry Staphylococcus aureus in the nose, predisposing them to endogenous infections. While microbial cooperation and competition are known to shape environmental and intestinal microbial communities, their impact on pathogen colonization within the nasal microbiome is largely unknown.

RESULTS: Using a newly curated nasal strain collection and systematic pairwise interaction analysis, we investigated competitive and collaborative traits between diverse S. aureus strains and nasal communities. Our experiments revealed that nasal species strongly modulate S. aureus growth in a strain- and community-specific manner both in vitro and in gnotobiotic mice. Nutrient-dependent interactions emerged as key drivers. In one example, we found that tyrosine provided by synthetic communities supported proliferation of an auxotrophic S. aureus strain. Screening of a large collection of S. aureus strains identified tyrosine dependency in 8% of strains, with colonization impaired in the absence of supportive communities, indicating broader relevance of this interaction.

CONCLUSIONS: Our findings reveal distinct metabolic adaptations that enable S. aureus to exploit specific features of resident nasal communities, highlighting complex interspecies networks that influence colonization in the human nose. These insights may inform microbiome-editing strategies to displace S. aureus from the nasal niche. Video Abstract.},
}

*Staphylococcus aureus/growth & development/metabolism/classification
Animals
Mice
Humans
*Microbiota
*Nose/microbiology
*Amino Acids/metabolism
*Staphylococcal Infections/microbiology
*Microbial Interactions
Germ-Free Life
Tyrosine/metabolism
Female

@article {pmid42920210,
year = {2026},
author = {Dey, S and Rout, AK and Ghosh, K and Kumar, V and Saha, A and Das, BK and Behera, BK},
title = {Investigation of Polyethylene (PE) Exposure in Labeo rohita (Hamilton, 1822): Accumulation, Stress Responses and In Vitro Biodegradation of PE by a Gut-Associated Bacterium.},
journal = {Environmental toxicology},
volume = {},
number = {},
pages = {},
doi = {10.1002/tox.70207},
pmid = {42920210},
issn = {1522-7278},
abstract = {The aquatic biome is exposed to a significant threat of persistent contamination by polyethylene (PE) in the ecosystem. A critical research gap exists in PE-induced tissue-specific bioaccumulation, associated immune and stress responses in fish, followed by potential bioremediation solutions. The present study investigated the bioaccumulation of PE particles and subsequent oxidative stress in Labeo rohita induced by two different doses (0.1 and 0.5 mg/L) over 2 weeks. Additionally, the biodegradation potential of gut-associated microbial isolates was also evaluated. We found that PE accumulation was highest in the intestine (33.0 ± 2.5 particles/g), followed by gills (20.5 ± 1.9 particles/g) and liver (8.0 ± 1.4 particles/g), indicating a significant, dose- and time-dependent increase. Substantially, it triggered a tissue-wise oxidative stress response of antioxidant (SOD, CAT, GPx) and stress marker (Hsp70) genes, showing significant upregulation in gill, liver, and intestine. Furthermore, this work identified a gut-associated bacterium, Proteus vulgaris KG-SD-15807, demonstrating significant PE biodegradation capability. Quantitative analysis revealed achievement of 3.00% ± 0.16% weight loss over 30 days of incubation. Qualitative characterization through FT-IR, FE-SEM, and GC-MS analyses indicated polymer oxidation, surface erosion, and formation of distinct metabolic degradation intermediates. The present findings reveal the significant bioaccumulation and stress response due to PE in a commercially important fish, Labeo rohita. Moreover, the identified bacterium acted as a PE biodegradation agent. This research has significant implications for future explorations focused on the long-term impacts of PE in aquatic animals and the optimization of biodegradation efficiency of Proteus vulgaris for applied bioremediation.},
}

@article {pmid42920211,
year = {2026},
author = {Xie, X and Hu, Y and Qian, W},
title = {[Gallic acid regulates microbe and microbial community: process and molecular mechanism].},
journal = {Sheng wu gong cheng xue bao = Chinese journal of biotechnology},
volume = {42},
number = {10},
pages = {4341-4354},
doi = {10.13345/j.cjb.260160},
pmid = {42920211},
issn = {1872-2075},
support = {XDA28030502//the Strategic Priority Research Program of the Chinese Academy of Sciences/ ; 2021YFA0717000//the National Key Research and Development Program of China/ ; },
mesh = {*Gallic Acid/pharmacology ; *Microbiota/drug effects/physiology ; Biofilms/drug effects ; Animals ; Bacteria/drug effects/metabolism ; },
abstract = {Gallic acid, a widely distributed plant-derived phenolic acid, exhibits diverse biological functions, including stress responses, antimicrobial activity, and antioxidant properties, rendering it valuable in pharmaceutical, food, and agricultural applications. Polyphenolic compounds such as gallic acid can effectively regulate the metabolic processes of microorganisms. Elucidating how such compounds influence the composition and structure of microbial communities represents an important research direction in current microbiome studies. This study reviewed research on the mechanisms by which gallic acid disrupts microbial cell membranes, interferes with energy metabolism, inhibits biofilm development, and suppresses virulence factor production. Furthermore, it also summarized the adaptive strategies employed by microorganisms, including metabolic transformation (complete degradation and non-oxidative decarboxylation) and stress defense (efflux, biofilm formation, etc.). Gallic acid acts as both an antibiotic and a probiotic in animal- and plant-microbiome interactions, thereby modulating the species composition, community structure and functions of the microbiome, subsequently influencing host growth, development, and immune responses. Future research will focus on in-depth analysis of the molecular targets of gallic acid and its functions and applications in microbiome reprogramming.},
}

*Gallic Acid/pharmacology
*Microbiota/drug effects/physiology
Biofilms/drug effects
Animals
Bacteria/drug effects/metabolism

@article {pmid42920487,
year = {2026},
author = {Sun, M and Zang, D and Zhou, H and Chen, J},
title = {Evaluation of large language models for ICI-related liver injury with an emerging microbiome focus.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1955356},
pmid = {42920487},
issn = {2235-2988},
mesh = {*Large Language Models ; Humans ; *Chemical and Drug Induced Liver Injury/diagnosis ; *Gastrointestinal Microbiome ; *Microbiota ; },
abstract = {BACKGROUND: Immune checkpoint inhibitor-related liver injury (ICI-LI) has heterogeneous phenotypes, a complex differential diagnosis, and evolving management. Gut microbiome research provides biological plausibility for immune regulation during ICI therapy, but evidence specific to ICI-LI remains limited and is not yet clinically actionable. We evaluated whether publicly accessible large language model (LLM) chatbots can organize this mixed evidence base and communicate its uncertainty.

METHODS: We developed a disease-specific benchmark of 25 questions covering immunological mechanisms, microbiome and immune regulation, diagnosis, biomarkers, and management of ICI-LI. The benchmark addressed ICI-LI broadly and included a focused microbiome component. Four publicly available LLM platforms were evaluated using DISCERN, EQIP, the Global Quality Score, the JAMA Benchmark Criteria, and six readability indices. These instruments assessed information quality, structure, transparency, and patient-facing readability rather than factual accuracy or clinical decision-making.

RESULTS: Performance differed across DISCERN, EQIP, and JAMA scores, whereas the Global Quality Score showed limited discrimination. Question-level variation was most apparent for items requiring evidence appraisal or translation. All platforms produced structured responses, but none met the prespecified patient-facing readability benchmark. Readability was interpreted separately from clinician-facing information synthesis.

CONCLUSIONS: Disease-specific multidimensional evaluation is needed before LLM-generated information can be considered reliable for microbiome-informed clinical communication or decision support. Evaluation should emphasize evidence calibration and distinguish biological plausibility, association, and clinically actionable evidence.},
}

*Large Language Models
Humans
*Chemical and Drug Induced Liver Injury/diagnosis
*Gastrointestinal Microbiome
*Microbiota

@article {pmid42920530,
year = {2026},
author = {Huang, F and Jin, X and Xu, J and Wu, H and Gan, M and Chang, W and Tan, Q and Wang, Y and Li, R and Li, D and Zhang, X},
title = {Gut microbiome-driven longevity mechanisms in giant pandas: age-associated gut microbial shifts, functional pathways, and probiotic insights.},
journal = {Current zoology},
volume = {72},
number = {5},
pages = {616-638},
pmid = {42920530},
issn = {1674-5507},
abstract = {Microbiome-mediated longevity mechanisms in conservation wildlife remain largely uncharacterized, particularly in species with specialized diets where host-microbe coevolution plays essential compensatory roles. We conducted cross-sectional metagenomic profiling of gut microbiota in 82 captive giant pandas (Ailuropoda melanoleuca) spanning juvenile, adult, and geriatric cohorts. The cohort included 14 long-lived individuals (≥25 years). Our approach integrated enterotype analysis, functional pathway characterization, and lactic acid bacteria (LAB) isolation. Age-specific compositional shifts occurred throughout the lifespan, characterized by reciprocal dominance between Bacillota (declining from 84.77% to 10.26%) and Pseudomonadota (increasing from 12.74% to 81.86%). Streptococcus dominated adolescent microbiomes, followed by a transition to cellulose-degrading taxa in young adults. Enterotype analysis revealed 4 distinct community types with age-dependent succession patterns. Long-lived pandas exhibited elevated abundance of Akkermansia muciniphila, Bifidobacterium longum, Lactobacillus intestinalis, and Ruminococcus gnavus. Functional profiling revealed age-dependent shifts from nucleotide and amino acid biosynthesis in young animals to lipid metabolism and amino acid degradation in aged individuals. Carbohydrate-active enzyme analysis demonstrated enrichment of cellulolytic enzymes (such as GH3, GH5, and GH9) in long-lived adults. Biosynthetic gene cluster profiling revealed progressive age-associated accumulation of genes encoding NRPS, RiPP-like, arylpolyene, and terpene biosynthetic pathways. Culture-based isolation from fecal samples of long-lived giant pandas yielded 98 LAB strains representing 8 species (Lactobacillus johnsonii, Limosilactobacillus reuteri, L. intestinalis, among others), including 89 non-hemolytic strains that were sensitive to 6 common antibiotics. These findings suggest potential cross-species conservation of microbiome-longevity mechanisms, with implications for understanding physiological adaptations in specialist herbivores and applications in conservation medicine.},
}

@article {pmid42920647,
year = {2026},
author = {López, LC and Carda-Diéguez, M and Mira, A and Martínez-Moragón, E},
title = {Characterization of pulmonary bacterial composition in community-acquired pneumonia depending on sampling methods.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1938648},
pmid = {42920647},
issn = {1664-302X},
abstract = {INTRODUCTION: Community-acquired pneumonia (CAP) remains a major global health concern due to its high incidence, morbidity, mortality, and economic impact. Although Streptococcus pneumoniae is the primary bacterial cause, diverse bacterial and viral pathogens contribute to CAP etiology. Conventional microbiological methods provide limited characterization of the pulmonary microbiome, resulting in low diagnostic yield and frequent empirical antibiotic use. This pilot study aimed to characterize the pulmonary microbiome in adult CAP patients using high-throughput sequencing and to determine whether commonly used non-invasive samples accurately represent the lower respiratory tract.

METHODS: Pulmonary samples were obtained using invasive procedures (bronchoalveolar lavage, bronchial aspirate, bronchial brushing, and biopsy) and non-invasive methods (sputum, nasopharyngeal aspirate). Classical microbiological testing identified pathogens in 24.1% of cases. DNA extracted was subjected to 16S rRNA gene amplification and sequencing, and microbial composition and diversity were compared across sampling types.

RESULTS: Microbiome profiles differed significantly by sampling methodology. Non-invasive samples displayed high variability and limited correspondence with lower airway microbiota. In contrast, invasive samples demonstrated greater consistency and appeared more representative of the lower respiratory tract. The genus Ralstonia was significantly more abundant in invasive samples (p < 0.05), warranting further investigation of its potential biological and clinical relevance.

CONCLUSIONS: 16S rRNA gene sequencing provides comprehensive detection of pulmonary microorganisms and offers added value in the microbiological diagnosis of CAP. The findings highlight the importance of using invasive specimens for accurate microbiome characterization and for detecting bacterial taxa not identified by routine microbiological methods.},
}

@article {pmid42920884,
year = {2026},
author = {Chen, J and Du, J and Mu, B and Zhang, J and Shang, G and Yan, X},
title = {Microbiota-host crosstalk in ulcerative colitis: mechanistic evidence and translational prospects for traditional Chinese medicine.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1956353},
pmid = {42920884},
issn = {1663-9812},
abstract = {Ulcerative colitis (UC) is sustained by reciprocal interactions among intestinal dysbiosis, altered microbial metabolism, epithelial barrier dysfunction, and mucosal immune activation. This narrative review examines that microbiota-metabolism-barrier-immune network and evaluates how traditional Chinese medicine (TCM) may influence it. Human multi-omics studies indicate that UC-associated dysbiosis is more reproducible at the level of microbial function and metabolite output than at the level of individual taxa. Experimental studies further implicate short-chain fatty acids, bile acids, tryptophan-derived indoles, arginine, and choline-related metabolites in epithelial and immune regulation. Most evidence for TCM-mediated microbiota modulation, however, comes from chemically induced experimental colitis, organoid, or cell systems; human interventional evidence remains limited. We therefore grade mechanistic evidence from association through microbiota dependence, candidate strain/metabolite sufficiency, host-target validation, and integrated causal-chain validation. This distinction avoids treating genus-level relative-abundance changes as proof of microbial benefit or mediation. Emerging clinical trials of indigo naturalis, Curcumin-QingDai, Andrographis paniculata extract, curcumin, and selected multicomponent Chinese herbal therapies provide short-term efficacy signals, but results are preparation- and dose-dependent and do not yet establish microbiota-mediated clinical efficacy. Translation will require chemically standardized products, rigorous safety surveillance, strain- and function-resolved microbiome measurements, explicit experiments separating direct herbal actions from microbiota-dependent effects, and clinical trials incorporating endoscopic, histological, pharmacokinetic, microbial, metabolic, and long-term safety outcomes.},
}

@article {pmid42921015,
year = {2026},
author = {Seneff, S},
title = {Do small hydrogen-containing gas molecules support low deuterium in mitochondrial water?.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1933444},
pmid = {42921015},
issn = {1664-302X},
abstract = {Deuterium is a natural heavy isotope of hydrogen, containing a neutron as well as a proton, making it twice as heavy. Mitochondrial ATP synthase nanomotors are highly sensitive to deuterium, because it impedes the flow of protons through the nanomotors and causes the γ C-terminal helix to unwind. It appears that metabolic processes have evolved to devise ways to reduce the deuterium load in the mitochondria, primarily, we argue, by exploiting several small hydrogen-containing molecular gases. We propose that, when a gas is produced, deuterium, due to its extra weight, tends to stay behind in the aqueous medium, so the gas becomes deuterium-depleted. Furthermore, many of the enzymes that synthesize and/or metabolize these small gas molecules fractionate out deuterium by exploiting proton tunneling. We hypothesize that the gut microbes play a crucial role in producing deuterium-depleted gas molecules, such as hydrogen gas (H2), methane (CH4), ammonia (NH3), hydrogen sulfide (H2S), trimethylamine (TMA), formaldehyde (HCHO), and methanethiol (CH3SH). Gut microbial metabolism of TMA likely provides a low-deuterium source of one-carbon (1C) units to fuel the methylation pathway in the host. The glutamate-glutamine exchange that takes place between astrocytes and neurons plausibly capitalizes on NH3 to preferentially deliver [1]H (protons) to neuronal mitochondria. Red blood cells actively import NH3 while the cation NH4 [+] is excreted in the urine, possibly as a strategy to fractionate out deuterium. In this paper, we investigate how small molecular hydrogen-containing gases are handled in metabolism, from a perspective that considers that these gases may serve a useful role in reducing the deuterium content in the mitochondria. Our hypothesis awaits validation by expert researchers who can perform appropriate experiments to test the hypothesis.},
}

@article {pmid42921244,
year = {2026},
author = {Deng, Y and Wei, D and Gu, S and Yu, M and Yao, J and Zhao, M and Qin, L and Kou, T},
title = {Evidence boundaries and integrated disease management of microbial disease risks in protected Cymbidium faberi production: a translational framework and validation agenda.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1952084},
doi = {10.3389/fpls.2026.1952084},
pmid = {42921244},
issn = {1664-462X},
abstract = {Cymbidium faberi (C. faberi) is an economically and culturally important orchid in East Asia, yet direct species-specific evidence for microbial diseases under protected cultivation remains limited. This critical narrative review synthesizes evidence on orchid diseases, protected-crop disease ecology, plant pathogen detection and diagnosis, biological control, and plant microbiome interactions. Direct C. faberi studies comprise one localized anthracnose-oriented report, baseline studies of root- and rhizosphere-associated microorganisms, and candidate antagonistic endophytes. However, they do not establish a contemporary pathogen inventory, species-resolved epidemiology, disease-associated microbiome dynamics, or validated management efficacy. Evidence from related Cymbidium species, other orchids, protected crops, and general plant-pathology systems is therefore interpreted according to host proximity, pathogen biology, production environment, and management relevance. Within this synthesis, disease risk is organized provisionally in a disease-complex framework in which environmental filtering, pathogen pressure, host status, and microbiome resilience are considered jointly; the framework does not assume that stable multi-pathogen synergistic pathogenesis has been demonstrated. A node-based translational Integrated Disease Management framework links mother-plant accession, clonal propagation, potting, vegetative growth, flowering, abnormal-batch disposition, and release decisions. The principal research gaps are pathogen isolation and causal confirmation, species-resolved pathogen surveillance, quantitative microclimate and inoculum thresholds, microbiome-function testing, and prospective validation of diagnostic and prediction tools. The framework is intended as a provisional decision-support and research-prioritization structure rather than a validated C. faberi-specific management standard.},
}

@article {pmid42921249,
year = {2026},
author = {Zhang, M and Zhang, S and Ren, X},
title = {Gut microbiota-host immunity crosstalk in psoriasis: from dysbiosis to cutaneous inflammation.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1957850},
doi = {10.3389/fimmu.2026.1957850},
pmid = {42921249},
issn = {1664-3224},
mesh = {Humans ; *Psoriasis/immunology/microbiology/therapy/metabolism ; *Dysbiosis/immunology ; *Gastrointestinal Microbiome/immunology ; Animals ; *Skin/immunology/metabolism/microbiology ; Intestinal Barrier Function ; Immunity, Innate ; Th17 Cells/immunology ; Inflammation/immunology ; },
abstract = {Psoriasis is a chronic inflammatory skin disease driven by the IL-23/IL-17 axis. Evidence accumulated over the past decade indicates that its pathogenesis extends beyond the skin and involves bidirectional communication between the intestinal microbiota and host immunity. This narrative review organizes current evidence along a proposed sequence running from gut dysbiosis and intestinal barrier damage, through altered microbial metabolites, to reprogrammed host immune responses and cutaneous inflammation. We summarize the gut microbiota changes reported in patients with psoriasis and the clinical evidence for impaired intestinal permeability. We describe how microbiota-derived metabolites-short-chain fatty acids (SCFAs), tryptophan/kynurenine metabolites, and bile acids-modulate Th17/Treg balance and innate immunity through the aryl hydrocarbon receptor (AhR) and G protein-coupled receptors. We then review clinical data on microbiome-directed interventions, chiefly probiotics and fecal microbiota transplantation (FMT), and close with the outstanding issues in causal inference, methodological heterogeneity, and standardization of interventions. The current evidence is consistent with the gut-skin axis hypothesis. The direction of causality between the microbiota and psoriasis, the dose-response relationship, and the clinical benefit of microbiome-directed therapy nonetheless remain to be confirmed in prospective cohorts and well-designed randomized controlled trials.},
}

Humans
*Psoriasis/immunology/microbiology/therapy/metabolism
*Dysbiosis/immunology
*Gastrointestinal Microbiome/immunology
Animals
*Skin/immunology/metabolism/microbiology
Intestinal Barrier Function
Immunity, Innate
Th17 Cells/immunology
Inflammation/immunology

@article {pmid42921282,
year = {2026},
author = {Alva, R and Shenoy, D and Shetty, V},
title = {From Chlorophyll to Micro Biome: Wheatgrass's Role in Gut Health-A Comprehensive Review.},
journal = {International journal of preventive medicine},
volume = {17},
number = {},
pages = {98},
doi = {10.4103/ijpvm.ijpvm_320_25},
pmid = {42921282},
issn = {2008-7802},
abstract = {BACKGROUND: Wheatgrass (Triticum aestivum) is a nutrient-dense microgreen increasingly recognized as a functional food due to its high content of bioactive compounds, including chlorophyll, vitamins, minerals, flavonoids, phenolic compounds, and polysaccharides. While wheatgrass has been associated with antioxidant, anti-inflammatory, antidiabetic, anticancer, and immunomodulatory effects, its specific role in gut health and gut microbiome modulation remains insufficiently explored.

OBJECTIVE: This review aims to critically evaluate the existing scientific evidence on the effects of wheatgrass consumption on gut health, with particular emphasis on its potential influence on gut microbiota composition, function, and gut-related health outcomes.

METHODS: A comprehensive literature search was conducted using PubMed, Scopus, and other scientific databases up to June 2025. Studies assessing wheatgrass intake in relation to gastrointestinal health, inflammatory biomarkers, or microbiota-related outcomes were included.

RESULTS: No human or animal intervention studies directly examining the effects of wheatgrass on gut microbiome composition were identified. However, mechanistic, and phytochemical studies suggest that wheatgrass-derived polysaccharides and phenolic compounds may support gut health through prebiotic, antioxidant, and immunomodulatory mechanisms. Available clinical and preclinical evidence indicates that wheatgrass supplementation may reduce gastrointestinal inflammation, enhance mucosal integrity, and promote the growth of beneficial gut microorganisms.

CONCLUSION: Wheatgrass is a nutritionally rich functional food with potential gut health benefits; however, direct evidence linking wheatgrass consumption to changes in gut microbiome composition and function is limited. Well-designed animal and clinical studies are needed to clarify its effects on gut microbiota diversity, short-chain fatty acid production, and overall gastrointestinal health.},
}

@article {pmid42921324,
year = {2026},
author = {Balsamo, JM and Bess, EN},
title = {Leveraging the Gut Microbiota for Mechanistically Informed Therapeutics against Body-First Parkinson's Disease.},
journal = {ACS bio & med chem Au},
volume = {6},
number = {5},
pages = {508-521},
doi = {10.1021/acsbiomedchemau.6c00110},
pmid = {42921324},
issn = {2694-2437},
abstract = {Although some symptoms of Parkinson's disease can be pharmacologically alleviated, stopping disease progression is not currently possible. Motor impairment in Parkinson's disease is associated with accumulation of aggregates of the protein α-synuclein (α-syn) in dopaminergic neurons in the brain. In some Parkinson's disease cases, these pathogenic aggregates accumulate in the intestinal lining years before motor symptoms manifest. This long prodromal period provides a window of opportunity to detect Parkinson's disease and halt its progression. Specifically, elucidating the factors involved in disease onset in the gut would enable prevention of α-syn aggregation before it spreads to the brain. In this perspective, we highlight discoveries of gut bacteria that induce aggregation of intestinal α-syn as well as efforts to decipher the molecular-level mechanisms by which this process occurs. We also showcase the rationale and potential breadth of applications focused on manipulating the gut microbiome, including biotics, fecal microbiome transplants, and microbial editing. By understanding molecular mechanisms of intestinal α-syn aggregation, the microbiome may be harnessed to control the factors responsible for their pathogenic formation and spread. Such insights will ultimately enable the development of more effective therapeutics for prevention and treatment of Parkinson's disease.},
}

@article {pmid42921377,
year = {2026},
author = {Carpenter, CM and Tian, Z and Harris, JK and Kirby, M and Lyons, T and Peterson, C and Wagner, BD and Ghosh, D},
title = {Multi-omic spectral clustering with the flag mean.},
journal = {Bioinformatics advances},
volume = {6},
number = {1},
pages = {vbag217},
doi = {10.1093/bioadv/vbag217},
pmid = {42921377},
issn = {2635-0041},
abstract = {MOTIVATION: One common goal in multi-omics studies is to identify subgroups within the study's cohort. Many methods create subgroups through unsupervised clustering, and, to our knowledge, all of these methods attempt to infer a common subspace or latent cluster across multiple views. We argue that this is a strict assumption that may not truly exist in many datasets.

RESULTS: We use the classic spectral clustering algorithm in conjunction with the flag manifold. Together, this allows for differing cluster structures across the omics profiles, leading to a novel approach for more flexible subtyping in multi-omics studies. We study a dataset on ventilator associated pneumonia in children. These data contain airway microbiome and transcriptome. Through simulation studies, we demonstrate that the flag mean of separate clustering subspaces can accurately capture the span of a joint clustering space. It is also robust to varying noise structures and number of features across omics profiles. Our proposed method also outperforms popular multi-omics clustering methods in the presence of differing group sizes. This proposed method is general enough to apply to other multi-omics studies as well as any multi-view study that uses spectral clustering.

Code for these methods are written in R and are freely available through GitHub at https://github.com/Ghoshlab/MMOC or through CRAN at https://cran.r-project.org/web/packages/MMOC/index.html.},
}

@article {pmid42921440,
year = {2026},
author = {Cotella, D},
title = {Gene, microbiome, and anti-aging doping in sport: molecular mechanisms, detection strategies, and implications for sports rehabilitation medicine.},
journal = {Frontiers in sports and active living},
volume = {8},
number = {},
pages = {1984895},
doi = {10.3389/fspor.2026.1984895},
pmid = {42921440},
issn = {2624-9367},
abstract = {Advances in gene transfer have created legitimate opportunities for tissue repair, but the same tools raise the prospect of illicit use to enhance athletic performance ("gene doping"). Evidence that elite athletes harbour a distinctive gut microbiota has raised a parallel concern that microbiome manipulation, including faecal microbiota transplantation (FMT) from high-performing donors, could be used as a form of biological enhancement ("microbiome doping"). A third, related frontier is anti-aging gene therapy (telomerase and Klotho gene delivery and partial cellular reprogramming) which targets the same muscle- and stem-cell-regenerative pathways relevant to injury recovery and has already reached unregulated human self-experimentation. This narrative review summarises the principal gene-doping targets relevant to performance and recovery (erythropoietin, myostatin/activin inhibitors, insulin-like growth factor 1, PPAR-δ/AMPK reprogramming), their delivery vectors, and current detection strategies. It then reviews athlete-associated gut microbiota signatures, notably the lactate-metabolising bacterium Veillonella atypica, and the feasibility and detection challenges of microbiota transplantation, before examining the rationale, targets, and governance challenges of anti-aging gene therapy. Attention is given to the overlap between all three frontiers and legitimate regenerative, microbiota-directed, or aging-biology therapies under investigation for musculoskeletal, metabolic, and gastrointestinal conditions, an overlap that places rehabilitation clinicians in a sensitive position, particularly with older or master athletes; across all three frontiers, the same biological pathways and delivery technologies are simultaneously being developed for legitimate therapeutic use, creating a recurring dual-use dilemma for clinicians and regulators alike. I review safety risks, the regulatory framework administered by the World Anti-Doping Agency (WADA) and its gaps regarding microbiome and longevity interventions, and the practical responsibilities of rehabilitation professionals. I conclude that interdisciplinary collaboration between molecular biologists, microbiome and aging researchers, anti-doping scientists, and clinicians is essential to keep detection methods and clinical governance aligned with the pace of innovation in these three areas, and we outline specific priorities, including clarification of the regulatory status of microbiota transfer and anti-aging gene constructs, strain-level metagenomic monitoring, and biological-age biomarkers, for achieving this alignment.},
}

@article {pmid42921543,
year = {2026},
author = {Ren, Y and Hu, Y and Qin, H and Zhang, Y and Zhao, H},
title = {Dynamic Gut-Lung Microbiome Interactions Beyond Dysbiosis Across the Course of COPD.},
journal = {International journal of chronic obstructive pulmonary disease},
volume = {21},
number = {},
pages = {649518},
doi = {10.2147/COPD.S649518},
pmid = {42921543},
issn = {1178-2005},
mesh = {Humans ; *Pulmonary Disease, Chronic Obstructive/microbiology/physiopathology/immunology/therapy/metabolism/diagnosis ; *Gastrointestinal Microbiome ; *Dysbiosis ; *Lung/microbiology/physiopathology/metabolism/immunology ; Animals ; *Bacteria/metabolism/immunology/growth & development/drug effects ; Disease Progression ; Host-Pathogen Interactions ; Fecal Microbiota Transplantation ; },
abstract = {Chronic obstructive pulmonary disease (COPD) is a heterogeneous respiratory disorder characterized by persistent airflow limitation, progressive functional decline, and recurrent exacerbations. Increasing evidence indicates that microbiome alterations in COPD extend beyond the airways and involve coordinated changes across respiratory and intestinal compartments. Importantly, these alterations are dynamic rather than static, varying across stable disease, disease progression, acute exacerbations, and distinct inflammatory phenotypes. Changes in the gut microbiome are accompanied by alterations in microbial metabolites, particularly short-chain fatty acids and tryptophan-derived metabolites, as well as impaired intestinal barrier integrity and systemic inflammatory responses. Emerging evidence from respiratory samples further suggests that airway microbial functional features and local metabolic alterations may contribute to pulmonary host responses, although respiratory microbial metabolites remain less extensively characterized. Experimental studies further suggest that microbiome-derived signals can modulate neutrophils, macrophages, T-cell balance, and innate lymphoid cells, thereby influencing pulmonary inflammation and tissue injury. Fecal microbiota transplantation studies provide additional evidence that disease-associated microbial communities can modify susceptibility to smoke-induced lung injury, supporting a potential causal contribution of the gut microbiome. Meanwhile, probiotics, dietary fiber, short-chain fatty acid supplementation, macrolides, and traditional Chinese medicine or natural products have shown preliminary microbiome-associated benefits, although clinical evidence remains limited and heterogeneous. This review summarizes dynamic airway and gut microbiome alterations across the course of COPD, integrates current evidence on microbial metabolism, intestinal barrier dysfunction, and immune responses, and evaluates emerging microbiome-related therapeutic strategies. Future studies should prioritize longitudinal multi-compartment sampling, standardized microbiome methodology, mechanistic validation, and adequately powered clinical trials to determine whether microbiome modulation can provide reproducible clinical benefit in defined COPD populations.},
}

Humans
*Pulmonary Disease, Chronic Obstructive/microbiology/physiopathology/immunology/therapy/metabolism/diagnosis
*Gastrointestinal Microbiome
*Dysbiosis
*Lung/microbiology/physiopathology/metabolism/immunology
Animals
*Bacteria/metabolism/immunology/growth & development/drug effects
Disease Progression
Host-Pathogen Interactions
Fecal Microbiota Transplantation

@article {pmid42921982,
year = {2026},
author = {Haider, K and Abbas, D and Kabir, K and Ali, MS and Ismail, AM and Sufian, M},
title = {Linking functional biodiversity, natural enemies, and insect microbiomes for sustainable biological control of agricultural pests.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.71399},
pmid = {42921982},
issn = {1526-4998},
support = {//This work was supported by Deanship of Scientific Research, Vice Presidency for Graduate Studies and Scientific Research, King Faisal University, Saudi Arabia with grant number KFU265588./ ; },
abstract = {Global agricultural pests continue to threaten crop productivity. Rising chemical resistance, environmental concerns, and the need for a sustainable food supply have increased interest in ecologically oriented pest control strategies. Furthermore, biological control has emerged as an essential component of sustainable agriculture, where habitat diversification and functional biodiversity can increase natural enemies' abundance, activity, and pest suppression. Recent studies indicate that insect microbiomes are essential for nutrition, immunity, growth, ecological adaptations, and interactions between insects and their natural enemies. Recent research suggests that microbial communities could impact host vulnerability to predators, parasitoids, and entomopathogenic fungi (EPF), which might subsequently influence biological control. Despite these progressions, functional biodiversity, natural enemy ecology, and insect microbiome research have historically developed as relatively separate fields of study. This review aims to synthesize current knowledge on ecological interactions among functional biodiversity, insect microbiomes, and biological control in agricultural systems. We examined the impact of habitat diversification on beneficial insects, the composition and functional role of microbiomes in relation to insect fitness, and the influence of microbial communities on the interaction between pests and biological control agents (BCAs). We then examined recent findings that have shown that environmental conditions, shaped by biodiversity, might affect microbiome assembly through mechanisms such as environmental microbial reservoirs, habitat complexity, and landscape-scale processes. We propose an integrated approach in which functional biodiversity directly influences biological control through ecological interactions and indirectly through the microbiome's effects on pest-natural enemy interactions. We state that biodiversity, microbiomes, and biological control are interconnected processes that should be regarded as integral components of agroecosystem functionality. Microbiome ecology may offer a new opportunity to enhance sustainable pest suppression and reduce chemical inputs in conservation biological management. Future research should focus on multitrophic, field-based, and mechanistic investigations that advance microbiome-informed biological control strategies for resilient and climate-smart agriculture. © 2026 Society of Chemical Industry.},
}

@article {pmid42921988,
year = {2026},
author = {Sun, P and Wu, Y and Wang, P and Chen, Y},
title = {Phenology-Dependent Reorganization of Nitrate Reduction Pathways in Rice Paddy Periphyton.},
journal = {Environmental microbiology},
volume = {28},
number = {10},
pages = {},
doi = {10.1111/1462-2920.70432},
pmid = {42921988},
issn = {1462-2920},
support = {U25A20807//National Natural Science Foundation of China/ ; 42177232//National Natural Science Foundation of China/ ; 41961144010//National Natural Science Foundation of China/ ; 2024YFD1701201//National Key Research and Development Program of China/ ; },
mesh = {*Oryza/microbiology/growth & development/metabolism ; *Nitrates/metabolism ; *Microbiota ; Oxidation-Reduction ; *Bacteria/metabolism/genetics/classification/isolation & purification ; Denitrification ; Nitrogen Cycle ; Soil Microbiology ; Ammonium Compounds/metabolism ; Nitrogen/metabolism ; },
abstract = {Microbiome-mediated nitrate transformation is central to nitrogen cycling in agroecosystems, yet the governing principles linking microbial functional organization to ecosystem-scale nitrogen outcomes remain poorly resolved. Here, combining [15]N tracing, high-throughput quantitative PCR arrays and multi-omics across a complete rice growth cycle with a tillering-stage survey of 15 rice-growing regions, we identify paddy-field periphyton as a temporally dynamic dissimilatory nitrate reduction (DNR) system whose associated genes are geographically widespread. Under aerobic incubation (dissolved oxygen > 5 mg L[-1]), early-stage communities are dominated by incomplete denitrifiers expressing norB/norC, producing transient N2O, whereas later-stage communities shift towards taxa active in dissimilatory nitrate reduction to ammonium (DNRA) and expressing nirB/nirD-nrfA/nrfH, promoting ammonium production. This transition suggests a phenology-associated redistribution of nitrate/nitrite-reduction pathways, redirecting nitrate-derived nitrogen from gaseous intermediate production towards ammonium retention. Metatranscriptomics confirms coordinated suppression of denitrification and activation of DNRA, indicating a microbiome-level transition from nitrogen loss to retention. Across the surveyed regions, both pathways were widespread but latitudinally structured, with the DNRA balance index showing a broadly unimodal pattern peaking at mid-latitudes. Together, these results identify periphyton as an important dual-functional DNR system linking microbiome organization to nitrogen cycling outcomes in rice paddies.},
}

*Oryza/microbiology/growth & development/metabolism
*Nitrates/metabolism
*Microbiota
Oxidation-Reduction
*Bacteria/metabolism/genetics/classification/isolation & purification
Denitrification
Nitrogen Cycle
Soil Microbiology
Ammonium Compounds/metabolism
Nitrogen/metabolism

@article {pmid42922012,
year = {2026},
author = {Vieites-Blanco, C and Caballol, M and Oliva, J},
title = {The Influence of Nitrogen on Alnus glutinosa Susceptibility to Phytophthora × alni.},
journal = {Plant disease},
volume = {},
number = {},
pages = {PDIS10252034RE},
doi = {10.1094/PDIS-10-25-2034-RE},
pmid = {42922012},
issn = {0191-2917},
abstract = {Riparian forest ecosystems face multiple anthropogenic pressures, including chronic nitrogen (N) pollution and invasive pathogens. However, the putative synergies among them are poorly understood. In the case of the keystone N-fixing tree Alnus glutinosa attacked by the exotic pathogen Phytophthora × alni, such pressures may act synergistically. N can indirectly promote susceptibility to the pathogen by affecting native soil microbiome composition and disrupting alder's symbiotic partnership with actinobacteria of the genus Frankia. In a greenhouse experiment that involved the manipulation of N through fertilization and Frankia nodulation through soil sterilization, we examined the interactive effects of nodulation, soil microbiota, and P. × alni infection on alder performance. We found that alder survival after infection was strongly influenced by the origin of the substrate in which the plants were grown. Under N-fertilization, mortality due to Phytophthora was higher in plants grown without alder soil amendments. In contrast, in soils amended with alder soil, N-fertilization did not increase alder susceptibility to the pathogen, although it significantly reduced Frankia nodulation. Nodulation was lowest in plants carrying the highest pathogen loads, showing that P. × alni infection not only kills alders but also undermines N-fixation. Our findings show that N-fertilization and P. × alni suppress nodulation and therefore can simultaneously contribute negatively to the N-fixing central function of alders in river ecosystems. Our results also seem to discard any protective role of soil microbiome or Frankia nodulation against P. × alni on alder.},
}

@article {pmid42922199,
year = {2026},
author = {Talbert, JA and Townsend, SD},
title = {From Dysbiosis to Disease: How Vaginal Microbiota Shape Group B Streptococcus Pathogenesis.},
journal = {Chembiochem : a European journal of chemical biology},
volume = {27},
number = {20},
pages = {},
pmid = {42922199},
issn = {1439-7633},
support = {R35-GM133602/NH/NIH HHS/United States ; },
mesh = {Humans ; *Vagina/microbiology ; Female ; *Dysbiosis/microbiology ; *Streptococcus agalactiae/pathogenicity ; *Streptococcal Infections/microbiology/drug therapy ; *Microbiota ; Pregnancy ; },
abstract = {Host-microbe interactions refer to the dynamic relationships between hosts, such as humans, and the microorganisms present on or inside them. These associations can be beneficial, like gut bacteria facilitating digestion, or harmful, such as pathogens leading to disease. This review focuses on the reproductive tract, specifically the vaginal microbiome. Typically, a healthy vaginal microbiome is dominated by Lactobacillus species, which help protect against infections by pathogens. Dysbiosis, or a microbial imbalance, allows pathogens to invade. One such pathogen is Streptococcus agalactiae (group B Streptococcus, GBS), which can colonize the vaginal microbiome and cause infections. GBS infection during pregnancy is particularly concerning and is a major cause of adverse pregnancy outcomes. This review will explore host-microbe interactions in the vaginal microbiome, with an emphasis on GBS infection, its virulence, and current treatment strategies.},
}

Humans
*Vagina/microbiology
Female
*Dysbiosis/microbiology
*Streptococcus agalactiae/pathogenicity
*Streptococcal Infections/microbiology/drug therapy
*Microbiota
Pregnancy

@article {pmid42922244,
year = {2026},
author = {Selim, AMF and Ibrahim, MMLG and Elbrolosy, MSM and Mansour, A and Abdeltawab, A and Ellaban, M and Eltabakh, AAE and Saraya, YS and Abdelaal, EHA and Shenishan, MEM and Elewiny, II and Mohamed, MA and Elbarbary, MIA and El Beltagy, ASA and Elshahat, EF},
title = {From Dysbiosis to Malignancy: The Female Genital Tract Microbiome in Endometrial Cancer; Insights from a Systematic Review and Meta-Analysis.},
journal = {La Clinica terapeutica},
volume = {177},
number = {6},
pages = {1698-1713},
doi = {10.7417/CT.2026.2175},
pmid = {42922244},
issn = {1972-6007},
mesh = {Female ; Humans ; *Endometrial Neoplasms/microbiology/etiology ; *Dysbiosis/complications ; *Microbiota ; *Genitalia, Female/microbiology ; },
abstract = {BACKGROUND/AIM: Emerging evidence suggests that alterations in the female genital tract microbiome may be associated with the development and progression of endometrial cancer (EC). Microbial dysbiosis may contribute to chronic inflammation, immune dysregulation, and metabolic disturbances within the endometrial microenvironment. This systematic review and meta-analysis aimed to evaluate alterations in the female genital tract microbiome in women with EC and to identify microbial patterns associated with benign, premalignant, and malignant endometrial conditions.

METHODS: A systematic review and meta-analysis was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and Meta-analysis of Observational Studies in Epidemiology (MOOSE) recommendations. Ten eligible observational studies published between 2016 and 2026 were included, comprising 775 women: 329 with benign conditions, 121 with endometrial hyperplasia, and 325 with EC. Demographic, histopathological, anatomical sampling, and microbiological data were extracted and analyzed using Review Manager, SPSS version 23, and EPI-INFO. Risk of bias was assessed using the Cochrane Collaboration tool.

RESULTS: Women with EC were older than those with benign conditions (59.2 ± 5.3 vs. 52.7 ± 4.4 years) and had a higher mean body mass index (33.8 ± 3.8 vs. 27.5 ± 2.0 kg/m²). Endometrioid carcinoma was the predominant histological subtype, and most malignant cases were low-grade and early-stage tumors. EC was associated with significant alterations in the genital tract microbiome. Several commensal taxa, including Lactobacillus, Bacteroides, Prevotella, Staphylococcus, and Enterococcus, were decreased in malignant cases, whereas potentially pathogenic or infection-associated genera, particularly Stenotrophomonas, Streptococcus, and Porphyromonas, were increased (p < 0.001). The pooled analysis demonstrated a significant association between genital tract microbial dysbiosis and EC.

CONCLUSIONS: Female genital tract microbial dysbiosis is associated with EC, characterized particularly by depletion of potentially protective microorganisms and enrichment of potentially pathogenic or infection-associated taxa. These microbial alterations may have potential as adjunctive biomarkers for EC risk stratification and early detection. However, the available observational evidence does not establish a causal role of microbial dysbiosis or infection in endometrial carcinogenesis. Large prospective studies using standardized sampling, sequencing, and analytical methods are required to clarify causality and determine the clinical utility of microbiome-based diagnostic and therapeutic approaches.},
}

Female
Humans
*Endometrial Neoplasms/microbiology/etiology
*Dysbiosis/complications
*Microbiota
*Genitalia, Female/microbiology

@article {pmid42922426,
year = {2026},
author = {Kabbashi, S and Chetty, M},
title = {Periodontal Infectogenomics in Africa: The Biological Case for a Population-Centred Research Agenda.},
journal = {Journal of periodontal research},
volume = {},
number = {},
pages = {},
doi = {10.1111/jre.70186},
pmid = {42922426},
issn = {1600-0765},
support = {//South African Medical Research Council/ ; //University of the Western Cape/ ; },
abstract = {African populations harbour the greatest human genetic diversity on earth and carry the highest global burden of severe periodontitis, yet their absence from periodontal infectogenomics represents a biological limitation of the field with profound implications for host-microbe interaction research. This Perspective builds the biological case for African populations as an urgent research priority and proposes a research roadmap integrating genomics, metagenomics and multiomics approaches.},
}

@article {pmid42922504,
year = {2026},
author = {Fu, H and Tie, J and Zhou, Y and Wang, X and Shan, Z and Qi, B},
title = {Bacterial Peptidoglycan Extends Lifespan by Activating Lysosomal Activity through V-ATPase Binding.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.28.747948},
pmid = {42922504},
issn = {2692-8205},
abstract = {UNLABELLED: Lysosomal dysfunction is a hallmark of aging, yet whether microbial components actively regulate this organelle to influence longevity remains unknown. Here, we identify bacterial peptidoglycan (PGN), a major cell wall component degraded by host lysozyme, as an evolutionarily conserved activator of lysosomal function that extends lifespan in both C. elegans and mice. We show that aging leads to an intestinal decline in lysozyme expression, which impairs bacterial cell-wall digestion and results in systemic PGN deficiency. Late-life PGN supplementation (starting at 18 months of age) significantly prolongs mouse lifespan and improves healthspan. Mechanistically, PGN localizes to lysosomes and directly binds V-ATPase subunits, enhancing ATP hydrolysis activity and promoting lysosomal acidification. This effect is abolished by V-ATPase inhibition (bafilomycin A1) or genetic disruption of lysosomal components (cup-5 and vha-12 mutants), confirming that functional V-ATPase is strictly required for lysosomal function and the longevity benefit. Importantly, PGN restores lysosomal acidification in aged cells, alleviates cellular senescence markers, and improves multiple hallmarks of aging including locomotion and muscle integrity. Collectively, these findings reveal an evolutionarily conserved mechanism whereby hosts exploit bacterial cell wall components to maintain cellular homeostasis, establishing a gut microbiome-lysosome-longevity axis with implications for microbiome-based anti-aging interventions.

HIGHLIGHTS: Aging reduces intestinal lysozyme activity, depleting systemic PGN bioavailabilityPGN binds V-ATPase subunits, enhancing ATP hydrolysis and lysosomal acidificationBacterial PGN supplementation extends lifespan and improves healthspanPGN maintains multi-tissue lysosomal homeostasis and reduces cellular senescence during aging.},
}

@article {pmid42922510,
year = {2026},
author = {Sun, X and Yount, KS and Batsuli, NN and Campbell, C and Jeong, S and Tollison, T and Peng, X and Darville, T and Zheng, X and O'Connell, CM},
title = {Mycoplasmal endosymbionts of Trichomonas vaginalis are associated with reduced risk for Chlamydia trachomatis endometrial infection in asymptomatic, coinfected, women.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.31.748291},
pmid = {42922510},
issn = {2692-8205},
abstract = {Trichomonas vaginalis is a protozoan parasite that causes trichomoniasis, the most common curable non-viral sexually transmitted infection, while Chlamydia trachomatis is a bacterial pathogen that can ascend to the upper genital tract and cause pelvic inflammatory disease, infertility, and ectopic pregnancy. T. vaginalis harbors bacterial endosymbionts, including Candidatus Malacoplasma girerdii , an obligate symbiont, and Metamycoplasma hominis , which can live freely or symbiotically. In a 16S rRNA sequencing study of the cervicovaginal microbiome of at-risk women, Ca. M. girerdii abundance was one of 13 features predicting the absence of coincident upper tract infection, despite no direct association between T. vaginalis infection and reduced chlamydial ascension. Investigating the relationship between these microorganisms further, we found that T. vaginalis vaginal abundance correlated positively with chlamydial burden in women whose infection was confined to the cervix, whereas a nonsignificant inverse relationship was observed in women with endometrial spread. Among participants with high chlamydial burden, Ca. M. girerdii was detected exclusively in women without endometrial infection. Both endosymbionts trended toward more frequent detection, and higher abundance, in coinfected women without endometrial spread, while M. hominis abundance correlated strongly with T. vaginalis burden in this group. These findings suggest that mycoplasmal endosymbionts of T. vaginalis , rather than T. vaginalis itself, are microbial factors limiting chlamydial ascension, and point to a three-way interaction between parasite, endosymbiont, and bacterial pathogen that shapes upper genital tract C. trachomatis infection risk.},
}

@article {pmid42922524,
year = {2026},
author = {Tantry, A and Long, W and Tran, J and Rohatgi, S and Cyphert, EL},
title = {Exploratory multi-omics analysis reveals sex-specific differences in microbial response to antibiotic exposure.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.09.01.748584},
pmid = {42922524},
issn = {2692-8205},
abstract = {UNLABELLED: Antibiotic exposure is a major driver of microbiome disruption and antimicrobial resistance gene (ARG) expansion. Yet, the role of biological sex in shaping these responses remains poorly understood. Most studies do not stratify antibiotic-induced microbiome changes by sex or integrate multi-omics datasets, limiting our understanding of how microbial, metabolic, and immune responses interact. Therefore, there remains a critical need for an integrative systems-level approach to determine how sex-specific disruptions under antibiotic pressure are paralleled across microbial, metabolic, and host immune layers. The objective of this work was to perform an exploratory study investigating how continuous antibiotic exposure reshaped the gut microbiome across sexual maturation and how these perturbations influenced downstream host responses in a sex-specific manner using an integrative multi-omics framework. Male and female mice that were exposed to continuous antibiotics were profiled over sexual maturation using shotgun metagenomics, untargeted metabolomics, and bulk RNA sequencing of the spleen to assess microbial composition, ARG dynamics, metabolic profiles, and immune responses. Overall, our results demonstrated sex-specific correlations at a systems-level that help provide valuable context to the differences observed in males and females upon antibiotic exposure.

IMPORTANCE: Antimicrobial resistance is a major global threat, and it remains unclear how continuous antibiotic exposure shapes the gut microbiome across sexual maturation and influences the host response in a sex-specific manner. In this work, we used an integrative multi-omics framework to demonstrate sex-specific correlations at a systems-level across several biological layers including taxonomic and resistome composition, host-microbe interactions through cecal metabolomic profiles, and host splenic gene expression. These results provide valuable context to understand systems-level differences in males and females following antibiotic exposure and inform sex-specific antibiotic strategies to contribute to more effective antimicrobial stewardship.},
}

@article {pmid42922528,
year = {2026},
author = {Rosado-Franco, JJ and Ellison, AL and Weerts, EM and Moore, CF and Williams, DW},
title = {Chronic Δ9-Tetrahydrocannabinol Vapor Self-Administration Modulates Gut Microbiota and the Immune and Endocannabinoid Systems in Female Sprague- Dawley Rats.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.30.748024},
pmid = {42922528},
issn = {2692-8205},
abstract = {Vaping of cannabis and its primary components, including Δ9- tetrahydrocannabinol (THC), has increased during the last decade, especially among adolescents and adults. While the behavioral consequences of THC, including anxiety, depression, and associated impacts on reward-related signaling, are well documented, evaluation of additional pathways that have implications for neuronal function remains relatively unexplored. Further, despite evidence of the impact of THC on several physiologic processes, most studies have focused on the brain even though the endocannabinoid system with which THC interacts has widespread expression and functions throughout the body. To address these gaps, we obtained biological samples from adult female Sprague-Dawley rats (N=5-6 per group; all females) that were passively exposed to THC or vehicle vapor and then allowed to self-administer vaporized THC or vehicle intermittently for nine months. Animals were euthanized, and brain and peripheral organs were collected for analyses. We evaluated genes of endocannabinoid system-related receptors, modulators, ion channels, and metabolic enzymes, along with immune and microbiome-related pathways in 9 peripheral organs, 14 brain regions, and plasma. We observed that rats exposed to chronic intermittent THC vapor administration had widespread modulation of several endocannabinoid- system genes only in the brain, with most changes occurring in the dorsal striatum and hippocampus. In contrast, endocannabinoid-system gene expression in all evaluated peripheral organs remained unchanged after THC exposure. Similar findings occurred with immune-relevant genes, where il-1β , il-6 , ccl2 , and mx1 were modulated only in the brain while expression in peripheral organs remained unchanged. Immune system modulation following chronic THC exposure significantly elevated plasma concentrations of IL-17A, gut microbiota dysbiosis, and global changes to circulating metabolites, including several amino acids, fatty acids, aminosugar, and nucleic acids. Our findings provide, for the first time, a whole-body evaluation of the molecular effects of chronic THC exposure throughout adulthood on the endocannabinoid and immune systems that have implications for cannabinoid-related behavioral effects.},
}

@article {pmid42922588,
year = {2026},
author = {Barrett, M and Anderson, J and Escandón, K and Wieking, G and Schroeder, T and Swanson, E and Graham, ML and Gale, M and Schacker, TW and Klatt, NR and Basting, CM},
title = {Spatial Transcriptomics Reveals Compartment-Specific Immune Activation Signatures in Ileal and Lymph Node Tissue in Treated HIV Infection.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.08.28.747869},
pmid = {42922588},
issn = {2692-8205},
abstract = {People with HIV (PWH) on long-term antiretroviral therapy (ART) continue to experience elevated rates of morbidities and mortality driven by persistent immune activation despite viral suppression. Known contributors include low-level HIV provirus activity, microbial translocation in part from epithelial barrier dysfunction, microbiome dysfunction, and co-infections. However, how these interact and where they predominate across tissue compartments remains incompletely defined. Here, we applied spatial transcriptomics to characterize compartment-specific transcriptional programs in ileum (epithelium, Peyer's patches, lamina propria) and inguinal lymph nodes (B Cell follicles and T cell zone) from ten PWH on long-term ART, stratified by CD4/CD8 ratio into low-ratio and high-ratio groups, with low-ratio as a proxy for immune activation and increased risk for non-AIDS related serious event. Comparison of global expression found significant differences between groups in four of five compartments. Differential expression analysis identified 483 differentially expressed genes across four of five compartments, with the greatest burden in the T-cell zone and none in the lamina propria. Gene set enrichment analysis identified 116 enriched pathways predominantly in the low-ratio group, spanning immune activation, infection-associated, and metabolic programs, with Peyer's patches showing the broadest transcriptional divergence of any compartment. Cross-compartment signals included higher expression of ORMDL3 and ARL17B in the low-ratio group implicating mitochondrial stress and inflammasome activation, lower expression of CCL3L3 and FCMR in the low-ratio group suggesting impaired immune execution, and divergent ribosomal protein programs between B-cell follicles and the T-cell zone. Cell deconvolution identified compartment-specific differences in estimated immune cell proportions, and T-cell zone gene expression showed significant associations with HIV reservoir measures and plasma markers of microbial translocation and immune activation. Together these findings support spatially heterogeneous immune activation as a feature of persistent immune dysregulation in treated HIV infection and provide compartment-resolved, hypothesis-generating evidence for the tissue-specific mechanisms driving inflammation in this population.},
}

@article {pmid42922635,
year = {2026},
author = {Rehman, L and Song, W and Rehman, A and Singh, K and Rawat, SG and Darbaniyan, F and Le, CC and Aletti, FM and Weng, J and Liu, J and Cheng, X and Tang, Y and Patchva, S and Richard, MD and Chu, F and Cao, J and Flowers, CR and Shpall, EJ and Tanner, MR and Fahrmann, J and Elinav, E and Stein-Thoeringer, CK and Jain, MD and Jenq, RR and Jain, A and Neelapu, SS and Zheng, Y and Saini, NY},
title = {Microbial valerate is associated with CAR T dysbiosis and its supplementation enhances CAR T function in B-cell lymphoma.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.09.01.748711},
pmid = {42922635},
issn = {2692-8205},
abstract = {Anaerobe-depleting antibiotic exposure is associated with inferior progression-free survival after CD19 CAR T-cell therapy in large B-cell lymphoma, yet the cellular mechanisms linking gut dysbiosis to the CAR T-cell product and whether this imprint is reversible have remained undefined. In two independent CAR-T candidate cohorts, low stool valerate at the time of CAR-T eligibility identified a multi-metabolite-deficient dysbiotic gut microbiome state marked by depletion of fiber-fermenting commensals and loss of carbohydrate-fermentation, SCFA-biosynthesis, and amino-acid metabolism pathways. Reanalysis of single-cell RNA sequencing from 42 lymphoma patients stratified by piperacillin-tazobactam/imipenem/meropenem (PIM) exposure revealed that PIM-exposed CAR T-cell products were CD4-skewed, with significantly elevated AP-1/immediate-early gene (IEG) and cellular activation signatures that together predicted inferior progression-free survival. Ex vivo conditioning of CAR T-cells with valerate produced a chromatin and transcription factor program distinct from butyrate or propionate, characterized by KLF/SP/EGR family engagement, KLF4 promoter opening, and broad induction of AP-1/IEG and MHC class II transcripts, whereas butyrate drove broader chromatin remodeling with TBX21/EOMES/NF-κB gains and KLF2 promoter closure, and propionate induced an NFY-centered program with preferential commitment to low-mitochondrial-content states. Untargeted metabolomics confirmed valerate uptake and mitochondrial β-oxidation in CAR T-cells, while dietary sodium valerate supplementation in meropenem-treated mice bearing A20 lymphoma significantly reduced tumor burden and extended survival compared with CAR T-cells alone. These findings identify stool valerate as a bedside-deployable biomarker of dysbiosis-imprinted CAR T-cell dysfunction and support ex vivo or dietary valerate supplementation as a clinically tractable strategy to improve CAR-T anti-tumor function in patients with disrupted gut microbiomes.},
}

@article {pmid42922863,
year = {2026},
author = {Shuai, W and Mithal, LB and Kremer, A and Aron, A and Sajwani, A and Huntinghouse, D and Hartmann, EM and Arshad, M},
title = {Persistence of Extended Spectrum β-Lactamase-Producing Enterobacterales in the Gut Microbiome of Healthy Newborns.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.09.01.26361559},
pmid = {42922863},
abstract = {The global prevalence of Extended-spectrum β-lactamase-producing Enterobacterales (ESBL-E) colonization is increasing. However, it is unclear whether ESBL-E persist and if that is associated with an altered gut microbial ecology especially in early life where the developing microbiome may not provide the same colonization resistance as in adults. In this study, we collected longitudinal infant gut microbiome samples at delivery and in the nonclinical home setting in Chicago, Illinois, U.S.A, aiming to disentangle how genetic factors pertaining to the ESBL-E, as well as the surrounding gut ecology, influences persistence in the infant gut microbiome. We observed not only a higher-than-expected prevalence of ESBL-E in healthy infant gut microbiomes, but also a trend of ESBL-E persistence once colonized. Microbial communities showed higher dissimilarity between ESBL-E positive and negative infant gut microbiome at earlier time points. Although dissimilarity decreased over time, we present evidence that ESBL-E persist even when traditional detection methods are negative.},
}

@article {pmid42922960,
year = {2026},
author = {Cui, M and Li, S and Wang, C and Dou, J and Zhu, Y and Chen, Q},
title = {Integrated gut microbiome and serum metabolomics identify candidate metabolic signatures of uric acid nephropathy.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1941602},
pmid = {42922960},
issn = {1664-302X},
abstract = {OBJECTIVE: To characterize the clinical, gut microbial, and serum metabolic features of uric acid nephropathy (UAN) and identify candidate metabolic signatures distinguishing UAN from uncomplicated hyperuricemia (HUA).

METHODS: This observational study enrolled 108 patients with hyperuricemia, including 57 with HUA and 51 with UAN. Clinical characteristics, metabolic comorbidities, lipid profiles, and renal function indices were compared, and multivariable linear regression identified factors independently associated with estimated glomerular filtration rate (eGFR). Fecal 16S rRNA gene sequencing was performed in 72 participants (HC, n = 10; HUA, n = 30; UAN, n = 32), whereas serum untargeted metabolomic profiling was conducted in a nested subset of 30 participants (n = 10 per group). Differential taxa and metabolites were identified using LEfSe and combined multivariate and univariate analyses. Spearman correlation and MIMOSA2 analyses assessed microbiota-metabolite-clinical associations and predicted microbial contributions to candidate metabolites.

RESULTS: Patients with UAN were older and more frequently had hyperlipidemia than those with HUA. They also had higher serum creatinine, blood urea nitrogen, total cholesterol, low-density lipoprotein cholesterol, and urinary albumin-to-creatinine ratio, together with lower eGFR, despite comparable serum uric acid concentrations. Age and total cholesterol were independently associated with lower eGFR, whereas body mass index was positively associated with eGFR. Neither microbial α-diversity nor overall β-diversity differed significantly among groups. Exploratory microbiome analyses suggested higher Faecalibacterium abundance in HC, whereas selected taxa including Streptococcus and Dialister differed between HUA and UAN. OPLS-DA separated HUA from UAN, with 217 differential metabolites identified using VIP > 1.0 and p < 0.05. Exploratory multi-omics integration further highlighted nine candidate metabolic signatures. These metabolites were enriched mainly in glutathione metabolism, arginine and proline metabolism, histidine metabolism, glycerolipid metabolism, bile secretion, and ABC transporter pathways. Integrated analyses identified nine candidate metabolites: citric acid, succinic acid, deoxycytidine, uridine, guanosine, betaine, nicotinamide, glycerol, and stearic acid. Citric acid, deoxycytidine, succinic acid, and uridine showed the broadest predicted microbial contribution profiles.

CONCLUSION: UAN was characterized by renal dysfunction, lipid metabolic abnormalities, selective gut microbial alterations, and extensive serum metabolic remodeling rather than by a further increase in circulating uric acid. The nine metabolites represent exploratory host-microbial metabolic signatures associated with hyperuricemia-related renal involvement. Their biological relevance and clinical discriminatory value require validation in larger, independent prospective cohorts.},
}

@article {pmid42922965,
year = {2026},
author = {Truffin, D and Perreau, C and Jenkins Sánchez, L and Heyse, J and Baudot, A and Vu, LD and De Beul, E and Van den Abbeele, P},
title = {Soluble prebiotic fiber and glucono-δ-lactone blends integrate compatible effects to modulate microbiota composition and metabolism ex vivo.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1923298},
pmid = {42922965},
issn = {1664-302X},
abstract = {INTRODUCTION: Prebiotics modulate the gut microbiome toward health-associated states. Because distinct candidate prebiotic compounds selectively stimulate microbial taxa and metabolic pathways, combining complementary ingredients may broaden or enhance beneficial outcomes. To investigate this concept, we evaluated the effects of microbiome-modulating blends of glucono-δ-lactone (GDL) and the resistant dextrin NUTRIOSE[®] (NUTR).

METHODS: The validated ex vivo SIFR[®] technology pipeline (systemic intestinal fermentation research) was used to assess how GDL, NUTR and their blends impacted the composition and metabolic activity of the gut microbiota of a small cohort of healthy adults (n = 6), while effects on gut barrier integrity (transepithelial electrical resistance, TEER) were evaluated via an in vitro co-culture of epithelial/immune (Caco-2/THP-1) cells.

RESULTS: GDL and NUTR induced distinct yet compatible shifts in microbial composition and metabolite output. GDL was rapidly fermented and specifically promoted Bifidobacterium adolescentis, while boosting butyrate-related taxa (Faecalibacterium prausnitzii, Anaerobutyricum hallii) and health-associated amino acid derivatives (e.g., indole-3-propionic acid). In contrast, NUTR gradually and strongly promoted propionate through stimulating Bacteroides and Parabacteroides, as well as specific Lachnospiraceae taxa. GDL/NUTR blends displayed ratio-dependent intermediate effects of the individual ingredients. Moreover, GDL/NUTR blends enhanced gut barrier integrity under LPS-induced inflammatory stress, with increases in TEER up to +24.5%.

DISCUSSION: Overall, GDL and NUTR blends compatibly integrate divergent effects, supporting their combined use for enhancing gut health through microbiome modulation.},
}

@article {pmid42923002,
year = {2026},
author = {Mostafaei, FS and Arki, MK and Sadeghi, A and Moravvej, H and Hossein-Khannazer, N and Arjmand, B and Razzaghi, Z and Bandarian, F and Razi, F and Tavirani, MR},
title = {Role of intestinal microbiota in pathogenesis and perspective therapeutics events for diabetes mellitus: A narrative review.},
journal = {Journal of diabetes and metabolic disorders},
volume = {25},
number = {2},
pages = {294},
pmid = {42923002},
issn = {2251-6581},
abstract = {PURPOSE: Diabetes mellitus is a widespread metabolic condition characterized by persistent high blood sugar, contributing significantly to global disease burden. Recent studies have turned attention to the intestinal microbiome as a critical factor influencing metabolic health and glucose control. Disruptions in normal microbial ecosystem, referred to as dysbiosis, are now linked to the development and worsening of diabetes. Gut bacteria and their metabolic outputs affect host energy use, immune responses, inflammation, digestive efficiency, and even genetic activity.

METHODS: A comprehensive search was performed in PubMed, Scopus, Web of Science, and Google Scholar using relevant keywords such as "gut microbiota," "dysbiosis," "short-chain fatty acids," "bile acids," "probiotics," and both type 1 and type 2 diabetes (T1D, T2D), along with diabetic complications.

RESULTS: Evidence indicates that an increased Firmicutes/Bacteroidetes ratio is commonly observed in T1D patients, underscoring the significance of microbial imbalance. In T2D, positive associations have been reported with genera such as Blautia and Ruminococcus, while genera like Bacteroides, Bifidobacterium, Faecalibacterium, and Roseburia show negative correlations. However, these findings are predominantly derived from cross-sectional studies, and definitive causal relationships remain to be established.

CONCLUSION: Elucidating the relationship between gut microbiota and diabetes not only clarifies the role of dysbiosis in metabolic disease and opens avenues for novel therapeutic strategies. Modulating the microbiome may improve insulin sensitivity and glycemic control. Future research could pave the way for innovative diagnostic tools, clinical assays, and treatment designed to alleviate diabetic symptoms. Nevertheless, translation of these findings into clinical practice requires further rigorous investigation.},
}

@article {pmid42154817,
year = {2026},
author = {Clardy, J},
title = {From an Interest in Molecules to a Fascination with Microbes.},
journal = {Annual review of microbiology},
volume = {80},
number = {1},
pages = {1-16},
doi = {10.1146/annurev-micro-042924-030959},
pmid = {42154817},
issn = {1545-3251},
abstract = {My scientific career has followed a meandering path centered on the structures and functions of microbial metabolites. These microbes included bacteria, fungi, and single-celled eukaryotes, and the metabolites included representatives from most metabolite families-peptides, complex carbohydrates, and lipids. The journey began with an interest in the structural complexity of microbial toxins and in microbes as chemists, and it evolved into a fixation on microbial metabolites' ability to reveal totally unexpected structure-function and host-guest relations and microbes' ability to affect human health and disease. The results described in this manuscript illustrate the power of interdisciplinary collaborations, clearly defined and soluble questions, a skilled research team, and serendipity.},
}

@article {pmid42905214,
year = {2026},
author = {Luo, S and Huang, L and Hou, E and Liu, S and Li, Y and Xiao, S and Wang, Y and Wang, Y and Zong, X},
title = {Weaning stress reprograms immune translation through GC biased codon usage in piglets with gut microbiota dysbiosis.},
journal = {Science China. Life sciences},
volume = {},
number = {},
pages = {},
pmid = {42905214},
issn = {1869-1889},
abstract = {Weaning stress constitutes a critical early-life challenge that disrupts immune homeostasis and reshapes gut microbiota composition. Here, we integrate ribosome profiling (Ribo-seq) and RNA sequencing (RNA-seq) to characterize transcriptional and translational responses in peripheral blood mononuclear cells (PBMCs) from healthy and weaning piglets. We show that weaning stress induces widespread translational reprogramming, with pronounced effects on immune genes, including significantly increased translation efficiency of key inflammatory mediators CD82, CCL25, and TNFSF13. These changes are accompanied by distinct shifts in codon usage patterns, with genes exhibiting enhanced translation in the weaning group displaying enrichment of GC-ending codons (GC3), including those encoding leucine, glutamate, and lysine. Integrative analysis further suggests a coordinated relationship between translational remodeling and gut microbiota dysbiosis. Genera enriched in healthy piglets, including Romboutsia, Lactobacillus, and Turicibacter, were associated with AT-rich codon usage patterns, whereas genera expanded under weaning stress, such as Fusobacterium and Streptococcus, were linked to GC-enriched codon profiles, concomitant with increased GC3 content and codon adaptation index. Collectively, these findings identify a previously unrecognized association between microbiota composition and codon-usage-linked translational regulation during stress-induced immune responses, providing a framework for understanding microbiome-host interactions at the level of translational control.},
}

@article {pmid42905676,
year = {2026},
author = {Hu, A and Liu, J and Chen, P and Yang, K and Xu, F and Luo, G and Zhang, J and He, M},
title = {Correction: Gut microbiome is associated with stereotypic behavior of the giant panda (Ailuropoda melanoleuca).},
journal = {PloS one},
volume = {21},
number = {10},
pages = {e0361345},
pmid = {42905676},
issn = {1932-6203},
abstract = {[This corrects the article DOI: 10.1371/journal.pone.0357625.].},
}

@article {pmid42905697,
year = {2026},
author = {Teutenberg, L and Winter, NR and Usemann, P and Stein, F and Thomas-Odenthal, F and Flinkenflügel, K and Borgers, T and Meinert, S and Leehr, EJ and Grotegerd, D and Papenbrock, S and Teckentrup, S and Hildebrand, A and Wellms, S and Mahjoory, K and Konowski, M and Spanagel, J and Fehse, L and Heider, D and Andlauer, TFM and David, FS and Forstner, AJ and Schöppner, P and Renz, H and Bang, C and Franke, A and Witt, SH and Rietschel, M and Streit, F and Alexander, N and Jansen, A and Nenadic, I and Straube, B and Jamalabadi, H and Dannlowski, U and Hahn, T and Kircher, T},
title = {Multimodal Machine Learning-Based Prediction of Relapse in Major Depressive Disorder.},
journal = {JAMA psychiatry},
volume = {},
number = {},
pages = {},
pmid = {42905697},
issn = {2168-6238},
abstract = {IMPORTANCE: Early identification of patients at high risk of relapse is key to personalized preventive strategies in major depressive disorder (MDD). However, current predictive models do not adequately account for the multimodal factors contributing to MDD relapse and fail to provide clinically meaningful predictions.

OBJECTIVE: To predict relapse within 2 years in patients with MDD by using a comprehensive machine learning pipeline that integrates an unprecedented set of multimodal data.

This naturalistic longitudinal prognostic study used data from the Marburg-Münster Affective Disorders Cohort Study, with baseline assessments collected from October 2014 to May 2019 and follow-up approximately 2 years later, between October 2016 and June 2021. Data analysis was conducted between July 2024 and June 2026. The study was performed at 2 sites in Germany (Marburg and Münster), with participants recruited from psychiatric inpatient and outpatient departments and the general population. Patients meeting diagnostic criteria for current or lifetime MDD without history of neurological or severe somatic conditions were included.

EXPOSURE: Natural course of illness in patients with MDD.

MAIN OUTCOMES AND MEASURES: Balanced accuracy (BACC) for binary prediction of relapse vs no relapse during 2-year follow-up served as the primary outcome. Baseline features comprised 9 modalities including clinical and psychometric data, 4 structural and functional magnetic resonance imaging modalities, genetics, neurocognition, blood markers, and gut microbiome.

RESULTS: A total of 564 patients with a current or lifetime MDD diagnosis were included (367 female [65.1%]; mean [SD] age, 37.34 [13.38] years). A total of 270 patients relapsed during the 2-year follow-up, while 294 did not. Mean (SD) BACC for the prediction of relapse ranged from 47.21% (5.85%) to 64.43% (6.63%). The best-performing model was solely based on few clinical relapse risk factors, while multimodal data integration did not improve performance.

CONCLUSIONS AND RELEVANCE: In this prognostic study, the models achieved moderate accuracy, yet the results suggest limited scope for guiding individual-level clinical decision-making. Predictive performance was largely driven by established clinical risk factors, indicating limited incremental value of multimodal measures when assessed at a single time point. Future advances may instead benefit from dynamic modeling approaches that more closely align temporally evolving multimodal markers with longitudinal clinical outcomes.},
}

@article {pmid42905751,
year = {2026},
author = {Agbonifo, WO and Chimezie, J and Amoo, ZA and Chukwukaeme, C and Francis, HO and Awoleye, MO and Adedeji, TG},
title = {Dietary context and ethanol-related injury in preclinical models: A contemporary systematic review of predominantly obesogenic diets and liver outcomes.},
journal = {PloS one},
volume = {21},
number = {10},
pages = {e0352561},
pmid = {42905751},
issn = {1932-6203},
mesh = {Animals ; *Ethanol/adverse effects/toxicity ; *Liver/drug effects/metabolism/pathology ; Male ; Rats ; *Diet/adverse effects ; *Obesity ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Mice ; Humans ; },
abstract = {Diet composition is an important food-derived exposure that may influence alcohol-related tissue injury. However, evidence on how specific dietary contexts modify ethanol-induced injury and its underlying biological mechanisms in controlled preclinical models remains fragmented. This systematic review examined whether defined dietary patterns modify ethanol-related injury in controlled mammalian studies. Following PRISMA 2020, PubMed, Embase, and Scopus were searched for studies published from January 2021 to January 15, 2026. Eligible studies were controlled in vivo mammalian experiments comparing ethanol exposure under defined dietary patterns. Evidence was narratively synthesized by diet type, organ system, and mechanism; random-effects meta-analyses and prespecified interaction analyses were conducted when sufficiently comparable data were available. Twenty-seven studies met the inclusion criteria (24 mouse and three rat studies); 18 used male-only animals, most examined high-fat or Western-type diets, and liver outcomes predominated. Evidence for non-obesogenic diets was limited to one ketogenic-diet study. In acute high-fat-diet models, adding ethanol increased serum ALT (SMD 2.31, 95% CI 1.46-3.16), AST (SMD 1.18, 95% CI 0.54-1.81), and hepatic triglycerides (SMD 2.06, 95% CI 0.96-3.17). Acute interaction analysis identified dietary effect modification only for ALT (MD 74.56, 95% CI 59.03-90.10), while chronic analyses showed a negative interaction for hepatic triglycerides (MD -0.048, 95% CI -0.092 to -0.004; P = 0.03). Extrahepatic, microbiome, and multi-omics findings were sparse and heterogeneous. High-fat and Western-type diets generally exacerbated ethanol-induced hepatic injury, whereas evidence for other dietary patterns remains limited.},
}

Animals
*Ethanol/adverse effects/toxicity
*Liver/drug effects/metabolism/pathology
Male
Rats
*Diet/adverse effects
*Obesity
Diet, High-Fat/adverse effects
Disease Models, Animal
Mice
Humans

@article {pmid42905905,
year = {2026},
author = {Liu, J and Garcia-Guevara, F and Macnaughtan, J and Jin, Y and Ferret-Miñana, A and Clasen, F and Yuen, N and Maset, RG and Ramón-Azcón, J and Kerbert, AJC and Portlock, T and Martinez, J and Habtesion, A and Phillips, A and De Chiara, F and Ingavle, G and Baldwin, T and Jimenez, C and Zaccherini, G and Husi, K and Rodriguez-Gandia, M and Cordero-Sanchez, P and Soeda, J and Oben, JA and Church, K and Li, JV and Jalan, A and Juanola, A and Sola, E and Eaton, S and Morgan, C and Avery, T and Kowalski, M and Green, D and Gander, A and Edwards, LA and Cox, IJ and Cortez-Pinto, H and Wiest, R and Durand, F and Caraceni, P and Elosua, R and Vila, J and Pavesi, M and Arroyo, V and Davies, N and Mookerjee, RP and Sandeman, S and Mehta, G and Marchesi, JR and Albillos, A and Rohn, JL and Andreola, F and Shoaie, S and Jalan, R},
title = {Impact of YAQ001 on the Gut Microbiome, Permeability and Markers of Systemic Inflammation in Patients With Cirrhosis.},
journal = {Liver international : official journal of the International Association for the Study of the Liver},
volume = {46},
number = {11},
pages = {},
pmid = {42905905},
issn = {1478-3231},
support = {634579//Rajiv Jalan/ ; 82570690//Jinxia Liu/ ; },
mesh = {Humans ; *Liver Cirrhosis/drug therapy/microbiology ; Female ; Biomarkers/blood ; Middle Aged ; Biofilms/drug effects ; Male ; *Gastrointestinal Microbiome/drug effects ; Permeability/drug effects ; Double-Blind Method ; Klebsiella pneumoniae/drug effects ; Inflammation ; Intestinal Barrier Function ; Adult ; },
abstract = {BACKGROUND & AIMS: YAQ001 is a novel, non-absorbable, gut-restricted, multiporous, carbon bead adsorbent. Pre-clinical studies and a clinical trial suggested its therapeutic potential and safety in patients with cirrhosis. This substudy aimed to explore the effects of YAQ001 on the gut microbiome and their exploratory association with biomarkers of gut permeability and systemic inflammation.

METHODS: Twenty-eight-patients with cirrhosis were randomized (double-blind) to receive YAQ001 (4 g once daily) or placebo. Gut microbiome and biomarkers of inflammation and gut permeability were assessed at baseline, after 4 and 12 weeks. Changes in biomarkers and relationship with microbiome composition and gene profiling were assessed. The effect of YAQ001 on Klebsiella pneumoniae biofilms was assessed in vitro.

RESULTS: Overall alpha and beta diversity remained unaltered. YAQ001 increased the abundance of bacteria associated with improved gut health such as Adlercreutzia equolifaciens, a bacterium commonly depleted in liver disease, and decreased the abundance of bacteria associated with infections and poor outcomes such as Klebsiella pneumonia, and Streptococcus mutans. YAQ001 impacted positively on virulence factors such as siderophores, fimbriae structures, and lipopolysaccharides that are associated with inflammation and invasion. Antibiotic resistance genes decreased significantly in the YAQ001 group. These changes were associated with a reduction in markers of gut permeability and systemic inflammation. YAQ001 prevented K. pneumoniae biofilms in vitro.

CONCLUSION: YAQ001 was associated with favourable compositional shifts and trends towards reduced virulence-related gene signatures in the gut microbiome, alongside trends towards improved inflammatory biomarkers. The in vitro anti-biofilm effect of YAQ001 warrants further mechanistic investigation. The findings position YAQ001 as a potential microbiome therapeutic.},
}

Humans
*Liver Cirrhosis/drug therapy/microbiology
Female
Biomarkers/blood
Middle Aged
Biofilms/drug effects
Male
*Gastrointestinal Microbiome/drug effects
Permeability/drug effects
Double-Blind Method
Klebsiella pneumoniae/drug effects
Inflammation
Intestinal Barrier Function
Adult

@article {pmid42905964,
year = {2026},
author = {Hong, Z and Luo, J and Xie, Z and Chen, J and Zheng, S and Li-Gao, R and Deng, K and Wang, Y and Zhang, X and Fang, G and Zhang, Z},
title = {Microbial Imprints of Gestational Diabetes Mellitus: Longitudinal Shifts in Breast Milk, Areola Skin, and Infant Gut.},
journal = {Maternal & child nutrition},
volume = {22},
number = {4},
pages = {},
pmid = {42905964},
issn = {1740-8709},
support = {2025A04J5389//Science and Technology Program of Guangzhou/ ; 2022A1515011161//Natural Science Foundation of Guangdong Province/ ; CNS-HPNK-2021-91//Chinese Nutrition Society/ ; //JPI HDHL NUTRIMMUNE DIYUFOOD project/ ; },
mesh = {Humans ; Female ; *Milk, Human/microbiology ; *Diabetes, Gestational/microbiology ; Pregnancy ; Feces/microbiology ; Infant ; Adult ; Longitudinal Studies ; Infant, Newborn ; Skin Microbiome ; RNA, Ribosomal, 16S ; Microbiota ; *Skin/microbiology ; *Gastrointestinal Microbiome ; },
abstract = {Gestational diabetes mellitus (GDM) has been associated with alterations in maternal and infant gut microbiota. However, it remains unclear whether these associations extend to other maternal-infant microbial niches and persist during early infancy. This study aimed to characterise longitudinal associations between GDM and microbiota across human milk, areolar skin, and infant faecal niches during early life. We followed 104 mother-infant pairs (52 GDM and 52 controls) from delivery through 6 months postpartum. Human milk, areolar skin, and infant faecal samples were collected at 1, 4, and 6 months postpartum and profiled using 16S rRNA gene sequencing. Longitudinal associations were evaluated using mixed-effects models, permutational multivariate analysis of variance, and Spearman correlation. GDM was associated with differences in maternal and infant microbiota across all three niches. Reduced alpha diversity was observed in areolar skin, whereas significant GDM-by-time interactions were identified in human milk and infant faecal microbiota. Beta-diversity analyses revealed persistent differences in microbial community composition. At the genus level, GDM was associated with enrichment of Staphylococcus and temporal changes in Stenotrophomonas in human milk, decreases in Rothia in areolar skin, and an increase in Staphylococcus in infant faeces. Significant associations were also observed between several GDM-related maternal taxa and corresponding infant faecal taxa. In conclusion, GDM was associated with persistent and niche-specific microbial differences across interconnected maternal-infant microbial niches during early life. These findings provide new insights into maternal-infant microbiota in the context of GDM and support future mechanistic investigations.},
}

Humans
Female
*Milk, Human/microbiology
*Diabetes, Gestational/microbiology
Pregnancy
Feces/microbiology
Infant
Adult
Longitudinal Studies
Infant, Newborn
Skin Microbiome
RNA, Ribosomal, 16S
Microbiota
*Skin/microbiology
*Gastrointestinal Microbiome

@article {pmid42906553,
year = {2026},
author = {Warmbrunn, MV and Tosti, V and Biswas, RK and Bertozzi, B and Cagigas, ML and Veronese, N and Spelta, F and Piccio, L and Head, RD and Rodrigues, RR and Early, DS and Zhou, Y and Trinchieri, G and Fiorito, G and Fontana, L},
title = {Weight loss during intermittent fasting, not Mediterranean diet quality alone, is associated with lower inflammation: A randomized controlled trial.},
journal = {Cell metabolism},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmet.2026.09.017},
pmid = {42906553},
issn = {1932-7420},
abstract = {Whether the anti-inflammatory effects of a Mediterranean diet reflect diet quality itself or accompanying weight loss is unclear. In a 16-week randomized controlled-feeding trial, 53 adults (77% female; mean age 54.7 years) with metabolic risk factors received a fully provided Mediterranean diet or their habitual western diet for 8 weeks, then added twice-weekly fasting days for a further 8 weeks. The primary outcome, high-sensitivity C-reactive protein, did not change during the diet-only phase despite clear dietary separation. After fasting began, C-reactive protein fell in the Mediterranean-diet group relative to controls, alongside greater weight loss, improved insulin sensitivity, and lower blood pressure; lipid improvements had already emerged during the diet-only phase. Multi-omic analyses showed parallel reductions in inflammatory signaling, with gut microbiome composition largely stable. Thus, diet quality alone does not lower inflammation over 8 weeks; negative energy balance and weight loss during fasting appear to be the stronger drivers. This study was registered at ClinicalTrials.gov (NCT02148458).},
}

@article {pmid42906824,
year = {2026},
author = {Liu, S and Feng, YW and Zhu, C},
title = {From aseptic ideal to microbial community balance: The shift in gut microbiota management models for hematopoietic stem cell transplant patients.},
journal = {Transplant immunology},
volume = {},
number = {},
pages = {102470},
doi = {10.1016/j.trim.2026.102470},
pmid = {42906824},
issn = {1878-5492},
abstract = {In the clinical practice of hematopoietic stem cell transplantation (HSCT), we find ourselves in a thought-provoking paradox. On one hand, hematologists strive to create an sterility paradigm for patients through systemic drug baths before admission, prophylactic use of broad-spectrum antibiotics during the conditioning phase, and sterile diets during transplantation. The core goal of these strategies is to minimize the risk of infection for patients. However, from a microbiological perspective, a completely different picture emerges; the gut microbiota is a virtual organ that co-evolved with the host and possesses critical metabolic and immune regulatory functions. Microbiologists point out that indiscriminate antibiotic clearing strategies, while attempting to eradicate a few pathogens, also destroy the diversity and ecological functions of the microbiota necessary for maintaining gut homeostasis, leading to the collapse of intestinal barrier, disruption of intestinal epithelial energy metabolism, and loss of immune regulatory signals. Increasing evidence suggests that this pursuit of aseptic ideal, particularly the extensive suppression of the gut microbiome by broad-spectrum antibiotics, may be opening another Pandora's box: severe gut dysbiosis, which is not only associated with unexplained fever and diarrhea but may also affect the overall reconstruction and regulation of the patient's immune system, thus correlating with the occurrence and development of challenging complications such as graft-versus-host disease (GVHD). The divergence of views between hematologists and microbiologists highlights a core cognitive conflict in contemporary HSCT management: are we treating a patient, or are we regulating a superorganism composed of human cells and symbiotic microorganisms? This comment aims to analyze this contradiction based on existing evidence and advocate for a more refined and ecologically-oriented new model of clinical management.},
}

@article {pmid42907037,
year = {2026},
author = {Liu, X and Wang, H and Chen, Z and Fang, X and Xu, Y and Feng, K and Ding, L and Wang, S and Blennow, A and Fang, JK and Chen, S and Zhong, Y},
title = {Reframing starch innovation for food security, sustainability, and metabolic health: From crop design to precision nutrition.},
journal = {Carbohydrate polymers},
volume = {392},
number = {},
pages = {125912},
doi = {10.1016/j.carbpol.2026.125912},
pmid = {42907037},
issn = {1879-1344},
mesh = {*Starch/chemistry/metabolism ; *Crops, Agricultural/metabolism/genetics/chemistry ; *Food Security ; Humans ; },
abstract = {Starch remains the caloric backbone of global diets, yet its long-term security is challenged by climate instability, dependence on a few staple crops, unsustainable processing practices, and the growing burden of diet-related metabolic diseases. Although major advances have been made in starch genetics, crop management, processing, and nutritional design, these developments are often discussed in isolation. This review adopts an integrated food-system perspective that follows starch from production to consumption and emphasizes how decisions across the value chain jointly shape functionality, resource efficiency, and metabolic outcomes. We synthesize progress in four interconnected areas: (i) genetic and agronomic strategies to improve starch yield, quality, and stress tolerance; (ii) diversification, preservation, and circular valorization of starch resources; (iii) structural and processing approaches for resistant starch and glycemic control; and (iv) emerging technologies including synthetic biology, artificial intelligence (AI), plant-microbiome engineering, and starch-based intelligent materials. We also identify key translational bottlenecks, including limited structure-to-function prediction, scale-up constraints, and regulatory and equity issues surrounding next-generation starch technologies. By integrating plant biotechnology, food engineering and nutritional physiology, this review provides a framework for developing resilient, sustainable, and health-oriented food systems.},
}

*Starch/chemistry/metabolism
*Crops, Agricultural/metabolism/genetics/chemistry
*Food Security
Humans

@article {pmid42907164,
year = {2026},
author = {Zeng, S and Chen, Y and Zhang, X and Wang, B},
title = {Ensuring independent external validation of GutIO.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2026-340844},
pmid = {42907164},
issn = {1468-3288},
}

@article {pmid42907181,
year = {2026},
author = {Venkatraman, A and Jacobs, K and Thibeault, SL},
title = {Comparison of Stress-Mediated Vocal Fold Epithelial Effects in Conventionally-Raised and Germ-Free Mice.},
journal = {The Laryngoscope},
volume = {},
number = {},
pages = {},
doi = {10.1002/lary.71008},
pmid = {42907181},
issn = {1531-4995},
support = {F32DC021367//NIH NIDCD/ ; R01DC012773//NIH NIDCD/ ; T32DC009401//NIH NIDCD/ ; R01DC004336//NIH NIDCD/ ; },
abstract = {INTRODUCTION: Up to 25% of patients with voice disorders report concurrent psychosocial stress, which has been shown to cause laryngeal microbiome dysbiosis. Microbiome dysbiosis underlies disease pathophysiology in other organs, leading to uncontrolled inflammation via epithelial barrier dysfunction. There is a need to delineate microbial versus nonmicrobial epithelial stress pathways in the vocal folds (VF) in order to clarify how psychosocial stress may contribute to VF epithelial disease.

METHODS: C57BL/6 conventionally-raised (CR) and germ-free (GF) adult mice were equally allocated to stressed and unstressed groups (n = 64, 32 per mouse-type/group, equal sexes). Stressed animals completed a validated restraint stress protocol. Following stress, larynges were collected. Outcomes of VF epithelial barrier dysfunction were compared across stressed, unstressed GF, and CR mice. Immunofluorescence/Immunohistochemistry determined protein expression of epithelial adherens junctions, mucins, and proliferation in mid-membranous VF tissue. Transmission electron microscopy assessed VF epithelial permeability.

RESULTS: Regardless of microbiota status, stressed animals had reduced protein expression of VF epithelial adherens junctions, mucins (MUC1, 4) and increased epithelial permeability. Presence of microbiota was associated with stress-induced increases epithelial proliferation, observed in CR, but not GF mice.

CONCLUSION: Presence of microbiota was associated with stress-induced increase in VF epithelial proliferation. This increased proliferation may represent an adaptive response to damaged cells to maintain epithelial integrity. Collectively, these findings provide a foundation for identifying VF epithelial targets that could be leveraged in probiotic-based therapies.

LEVEL OF EVIDENCE: N/A.},
}

@article {pmid42907250,
year = {2026},
author = {Krawczyk, AI and Duron, O and Hübschen, JM},
title = {Friend or foe? Functional roles of Ixodes ricinus microbes.},
journal = {Trends in parasitology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.pt.2026.09.018},
pmid = {42907250},
issn = {1471-5007},
abstract = {The tick Ixodes ricinus is a major vector of multiple pathogens in Europe, yet the functional roles of its microbial communities and their impact on disease risk remain largely unexplored. Here, we propose a framework linking microbial transmission mode and microbial function to their effects on I. ricinus. We argue that transmission mode shapes the evolutionary pressures on microbes and, therefore, the nature and stability of their interactions with ticks. Building on the apparent absence of a single obligate nutritional symbiont in I. ricinus, we further propose that complementary and functionally redundant microbial traits may be more important than individual microbial taxa. This perspective provides a basis for understanding how microbiome function may influence tick adaptation, resilience, and ultimately disease risk.},
}

@article {pmid42907311,
year = {2026},
author = {Clasen, F and Jin, Y and Brett, J and Garcia-Guevara, F and Ehrlich, SD and Shoaie, S},
title = {Microbial resistance from genotype to metabolic phenotype.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2026.09.009},
pmid = {42907311},
issn = {1878-4380},
abstract = {Antimicrobial resistance (AMR) poses an escalating global threat, yet surveillance and mechanistic understanding remain anchored in individual resistance genes, an approach that is inadequate for capturing the ecological, genomic, and metabolic complexity through which resistance emerges and spreads. In this opinion article, we argue that genome-scale metabolic models (GEMs) offer a principled framework for advancing AMR research beyond this gene-centric paradigm. Strain-resolved GEMs embed resistance determinants within metabolic networks, with the potential to generate quantitative, context-dependent phenotypic predictions, including minimum inhibitory concentrations and environment-conditional resistance, that sequence-based tools do not provide. Expanded GEM frameworks incorporating mobile genetic elements, horizontal gene transfer, and community-level interactions support ecology-aware resistance profiling. At the therapeutic level, whole-network modelling can identify metabolic vulnerabilities, synthetic lethal interactions, and microbiome-targeted strategies. Integrating GEMs with multiomics and data-driven approaches represents a critical step toward a mechanism-aware AMR platform connecting surveillance, diagnosis, and drug discovery.},
}

@article {pmid42907312,
year = {2026},
author = {Warsi, OM and Andersson, DI},
title = {Community context redirects evolutionary trajectories under stress.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2026.09.008},
pmid = {42907312},
issn = {1878-4380},
abstract = {Adaptation to abiotic stress is typically studied in single-species cultures, yet bacteria inhabit and evolve in multispecies communities where neighboring organisms reshape, for example, nutrient availability, redox state, and cellular physiology. We recently demonstrated that interspecies interactions can alter the fitness effects of antibiotic resistance mutations, and we suggest that this reflects a broader principle. Stress-response networks are extensively cross-regulated and draw upon a shared, finite pool of proteomic and energetic resources. Consequently, activation of one pathway constrains others, creating physiological trade-offs. Because microbial interactions routinely perturb the physiological inputs to these networks, they can systematically redirect evolutionary trajectories under abiotic stress. We discuss the evidence, limitations, and implications of this framework for predicting evolution and understanding microbiome stability.},
}

@article {pmid42907460,
year = {2026},
author = {Khatib, L and Oles, R and Hernández, AR and Myers, T and Zhao, J and Kumar, M and Laroya, A and Tolosa-Enguis, V and Matsunami, N and Suzuki, D and Chiba, N and Gilbert, KE and Das, P and Sanders, JG and Patel, L and Litwin, N and Nowinski, B and Birmingham, A and Farmer, S and Brennan, C and Bryant, M and Tribelhorn, C and Sanders-Bodai, K and Cowart, C and Nizet, O and Diaz, EA and Veiga, P and Shetty, SA and Knol, J and Lay, C and Koutnikova, H and Chaumont, S and Tap, J and Cotillard, A and Derrien, M and Laiola, M and González, A and Tovar, AR and Torres, N and Sanz, Y and Yamada, T and McDonald, D and Song, SJ and Bartko, A and Knight, R},
title = {Five-country analysis of geographic and dietary drivers of gut microbiome composition and genomic variation.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42907460},
issn = {2041-1723},
support = {T32 GM154642/GM/NIGMS NIH HHS/United States ; },
mesh = {Humans ; Mexico ; *Diet ; *Gastrointestinal Microbiome/genetics ; United States ; Japan ; Spain ; United Kingdom ; Metagenomics ; Geography ; Genetic Variation ; Female ; Bacteria/classification/genetics/isolation & purification ; Metagenome ; Male ; },
abstract = {Human diet and lifestyle vary widely across cultures, shaping global diversity in gut microbiome composition and function. However, comparable cross-population studies have been limited by methodological heterogeneity. The Human Diets and Microbiome Initiative (THDMI) integrates standardized recruitment, dietary assessment, and shotgun metagenomics across 1,976 participants from the United States, United Kingdom, Spain, Mexico, and Japan to disentangle biological from technical variation. We observed pronounced geographic differences in nutrient intake, food consumption, and microbial composition, with both shared and country-specific features linked to diet. Sparse canonical correlation and machine-learning analyses revealed that microbiome-diet associations were largely population-specific, with limited cross-country generalization. Strain-level analyses further uncovered significant genomic differentiation of gut microbes, consistent with localized dietary and ecological differences. Together, these results show that while core microbial responses to healthy eating exist, the structure and function of the human gut microbiome varies strongly with culture, geography, and long-term dietary practices.},
}

Humans
Mexico
*Diet
*Gastrointestinal Microbiome/genetics
United States
Japan
Spain
United Kingdom
Metagenomics
Geography
Genetic Variation
Female
Bacteria/classification/genetics/isolation & purification
Metagenome
Male

@article {pmid42907590,
year = {2026},
author = {Tysoe, O},
title = {Gut microbiome development could predict T1DM risk.},
journal = {Nature reviews. Endocrinology},
volume = {},
number = {},
pages = {},
pmid = {42907590},
issn = {1759-5037},
}

@article {pmid42907645,
year = {2026},
author = {Chiritoiu, GN and Chiritoiu-Butnaru, M and Porosencova, T and Porosencov, E and Uncuta, D and Istrati, D and Isvoranu, G and Petrescu, AJ and Munteanu, CVA},
title = {Mass Spectrometry-Based Oral Meta-Omics Analysis-What We Know and What We Don't.},
journal = {Advances in experimental medicine and biology},
volume = {1359},
number = {},
pages = {397-423},
pmid = {42907645},
issn = {0065-2598},
mesh = {Humans ; Multiomics/methods ; *Metabolomics/methods ; *Microbiota ; *Proteomics/methods ; *Mouth/microbiology ; *Mass Spectrometry/methods ; *Dental Caries/microbiology/metabolism/diagnosis ; *Periodontal Diseases/microbiology/metabolism/diagnosis ; },
abstract = {According to the World Health Organization, dental caries and periodontal disease are the most prevalent oral health conditions worldwide, usually linked with oral microbiome dysbiosis. It is assumed that oral microbiota alterations are also associated with immune challenges, beyond the oral cavity, thus having implications in the progression of various systemic diseases, but the mechanism by which the plaque biofilm microbiota contributes to the development of such diseases is not entirely clear. In this context, metaproteomics and mass spectrometry-based metabolomics can reveal essential information about such correlations, particularly by integration with other -omics technologies. It can extend the molecular analytical repertoire and provide a deeper understanding of the molecular mechanism, delivering disease-specific biomarkers with great potential for clinical application, mainly considering the recent technological innovations in the field. Here, we address some of the latest findings exploiting mass spectrometry in the pathological context of dysregulated oral microbiome, by describing essential principles and methodologies in the field of mass spectrometry-based multi-omics analysis. We emphasize critical aspects related to sample collection, preparation and analysis using liquid chromatography coupled with mass spectrometry, with a focus on some controversial key aspects related to the analysis workflow.},
}

Humans
Multiomics/methods
*Metabolomics/methods
*Microbiota
*Proteomics/methods
*Mouth/microbiology
*Mass Spectrometry/methods
*Dental Caries/microbiology/metabolism/diagnosis
*Periodontal Diseases/microbiology/metabolism/diagnosis