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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

CLINICALTRIALS: gov.},
}

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

@article {pmid42840662,
year = {2026},
author = {Chen, R and Xu, D and Li, Y and Yang, J},
title = {Gut mucosal microbiota and local intervertebral disc immunity: candidate circulating-cytokine-independent pathways informed by Mendelian randomization evidence.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1938023},
pmid = {42840662},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Intervertebral Disc/immunology/metabolism ; *Cytokines/immunology/metabolism/blood ; Mendelian Randomization Analysis ; *Intervertebral Disc Degeneration/immunology/microbiology ; Immunity, Mucosal ; Animals ; },
abstract = {Chronic low back pain secondary to intervertebral disc degeneration (IVDD) is the leading cause of disability across all musculoskeletal disorders worldwide. For decades, gut-disc crosstalk research has been framed almost exclusively by a systemic inflammatory paradigm, in which circulating pro-inflammatory cytokines (e.g., TNF-α, IL-1β) act as obligate mediators linking gut microbial dysbiosis to intervertebral disc degeneration. However, multi-cohort two-sample Mendelian randomization (MR) analyses have not identified significant mediation by the circulating inflammatory factors tested to date, exposing a gap in current mechanistic frameworks. A null indirect effect indicates that the measured mediators did not statistically explain the exposure-outcome association; it does not exclude a contribution from untested systemic pathways. Two core protective commensal taxa, Akkermansia muciniphila (Akk) and Eubacterium coprostanoligenes, have been genetically validated to reduce IVDD risk, yet their beneficial effects cannot be explained by systemic immune activation. Focusing on mucosal immunology and tissue-localized immune homeostasis, this review integrates human genetic data, in vitro nucleus pulposus experiments, in vivo bacterial extracellular vesicle (EV) evidence, and clinical endplate microbiome profiles to delineate three candidate gut mucosa-derived immune regulatory axes that are not explained by the circulating cytokines measured to date: (1) microbe-derived soluble metabolites-which are themselves circulating mediators-reshape local disc metabolic and immune responses via epigenetic modulation and receptor signaling; (2) EVs secreted by A. muciniphila act as cross-barrier immune messengers targeting the avascular disc tissue; (3) gut bacterial fragments translocate across damaged endplate barriers to trigger site-specific immune remodeling without elevating systemic inflammatory markers. This three-pathway framework offers one possible reconciliation of the null mediation findings from MR studies with the collapse of intrinsic disc immune privilege. Each proposed axis remains incompletely validated, and the available evidence does not establish that they operate independently of untested systemic immune pathways. We further summarize methodological limitations of gut-spine microbiome research and outline mucosa-targeted microbial immunotherapies for chronic low back pain. Collectively, this framework helps shift the field away from over-reliance on systemic inflammation as the sole mechanistic explanation for IVDD pathogenesis.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Intervertebral Disc/immunology/metabolism
*Cytokines/immunology/metabolism/blood
Mendelian Randomization Analysis
*Intervertebral Disc Degeneration/immunology/microbiology
Immunity, Mucosal
Animals

@article {pmid42840755,
year = {2026},
author = {Liu, X and Huang, S and Liu, JQ and Wang, SN and Pang, TX and Wang, QF},
title = {The gut microbiota-inflammageing axis in cardiometabolic health of older adults and dietary intervention strategies.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1931405},
pmid = {42840755},
issn = {2296-861X},
abstract = {Rapid global population ageing is accelerating the burden of cardiometabolic disease, and inflammageing-the chronic, low-grade, sterile inflammation that accompanies advancing age-has emerged as a shared pathological substrate linking cardiovascular disease, metabolic syndrome, and type 2 diabetes mellitus in older adults. Increasing evidence identifies the gut microbiota as an upstream driver of this process, forming a modifiable feedback loop with the intestinal barrier, the immune system, and cardiometabolic homeostasis. With advancing age, beneficial taxa such as Bifidobacterium and Faecalibacterium prausnitzii decline in abundance, whereas pro-inflammatory taxa expand; this dysbiosis compromises tight-junction integrity, producing the "leaky gut" phenotype and permitting translocation of lipopolysaccharide and other pathogen-associated molecular patterns into the portal circulation. The resulting metabolic endotoxaemia activates TLR4/NF-κB signalling and sustains systemic elevations of IL-6, TNF-α, and IL-1β, which converge on insulin resistance, endothelial dysfunction, oxidative stress, and vascular injury. Microbiota-derived metabolites further shape this trajectory: trimethylamine-N-oxide (TMAO) has been implicated in the acceleration of atherosclerosis, foam-cell formation, and platelet reactivity-largely on the basis of rodent studies and observational human data-whereas short-chain fatty acids reinforce barrier function and induce regulatory T cells. This review systematically synthesises current mechanistic and clinical evidence on the gut microbiota-inflammageing axis and its contribution to cardiometabolic deterioration during ageing, and critically appraises dietary intervention strategies as the most direct and actionable entry point into this feedback loop. The Mediterranean, Green-Mediterranean, and plant-based dietary patterns, together with intermittent fasting, have been shown to remodel the gut microbiota, reduce systemic inflammatory tone, and improve cardiometabolic risk profiles. Key dietary components-fibre-derived short-chain fatty acids, polyphenols and their microbial metabolites, omega-3 polyunsaturated fatty acids together with specialised pro-resolving mediators, and age-appropriate protein intake-act through distinct but converging molecular mechanisms to preserve barrier integrity, restore immunometabolic balance, and support healthy vascular ageing. Emerging translational approaches, including precision nutrition guided by individual microbiome profiles, next-generation probiotics, prebiotics and postbiotics, and small-molecule inhibitors targeting TMAO biosynthesis, are also examined, alongside their current translational limitations-including the absence of standardised microbiome analytical pipelines, strain-specific heterogeneity of probiotic effects, and the lack of formal recommendations in current cardiovascular and diabetes guidelines. Safety considerations relevant to frail older adults-such as hypoglycaemia risk during intermittent fasting, bleeding risk with high-dose omega-3 supplementation, and rare bacteraemia associated with probiotic use in immunocompromised individuals-are also highlighted. Research gaps such as scarce long-term follow-up, under-representation of non-Western populations, and heterogeneity across ageing stages are discussed. By integrating mechanistic insight with translational evidence, this review provides a theoretical foundation for the development of individualised nutritional strategies aimed at extending cardiometabolic healthspan in older adults.},
}

@article {pmid42840760,
year = {2026},
author = {Shi, L and Wang, P and Wu, B and Huang, C},
title = {The Plasticene Paradigm: Microplastics, Gut Dysbiosis, and Food Allergy - A Critical Commentary.},
journal = {Journal of asthma and allergy},
volume = {19},
number = {},
pages = {625708},
pmid = {42840760},
issn = {1178-6965},
abstract = {BACKGROUND: The increasing prevalence of food allergy (FA) in industrialized regions cannot be fully explained by traditional hygiene and biodiversity frameworks, suggesting the involvement of new environmental triggers. Microplastics (MPs), which are dietary contaminants now consistently found in human biological samples, have been proposed as a potential threat to gut-immune balance. However, direct evidence for this link in humans is still lacking.

MAIN BODY: This commentary critically examines and advances the "Plasticene Paradigm", which hypothesizes that dietary MP exposure disrupts the beneficial relationship between the host and its microbiota, thereby promoting the development of FA through microbiota-dependent mechanisms. The central mechanism proposed involves MP-induced dysbiosis, characterized by a reduction in short-chain fatty acid (SCFA) -producing bacteria. This reduction subsequently impairs the differentiation of regulatory T cells (Tregs), disrupts the balance between Th2 and Treg cells, and compromises the integrity of the intestinal barrier. While studies involving fecal microbiota transplantation in animal models offer causal evidence under experimental conditions, this evidence primarily comes from studies using supraphysiological doses of pristine polymers (mg/kg/day range). These doses exceed mass-based estimates of human daily intake (μg/kg/day range) by several orders of magnitude, although direct quantitative comparison is complicated by the use of heterogeneous exposure metrics (mass-based vs particle-count-based) across different estimation approaches. This significant difference in dosage fundamentally limits the applicability of these findings to human exposure levels found in the environment. We identify four obstacles to translating these findings: dose relevance, exposure complexity, challenges in model extrapolation, and analytical constraints. These barriers currently prevent drawing definitive conclusions about human risk.

CONCLUSION: The current evidence, which is predominantly preclinical, is constrained by issues of dose relevance, exposure complexity, and gaps in model extrapolation, with human data largely showing only associations. We propose a three-pronged research agenda: (I) establishing prospective birth cohorts with specific biomonitoring for polymers; (II) conducting mechanistic studies using environmentally relevant MP mixtures in FA models; and (III) developing microbiome-targeted interventions as needed. This framework aims to transform the Plasticene Paradigm from a hypothesis-driven mechanistic narrative into one supported by a stronger evidence base. This evidence may ultimately inform public health policy, food safety regulations, and precise prevention strategies for FA in an era of widespread plastic contamination.},
}

@article {pmid42840869,
year = {2026},
author = {Wang, H and Tang, Q and Hu, J and Li, J and Huang, Q},
title = {Exposure-shaped immunometabolic networks in chronic liver disease: translating multi-omics and artificial intelligence into preventive biomarkers.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1866951},
pmid = {42840869},
issn = {1664-3224},
mesh = {Humans ; Multiomics ; Biomarkers/metabolism ; *Liver Diseases/metabolism/etiology/immunology/prevention & control ; Chronic Disease ; Animals ; *Environmental Exposure/adverse effects ; *Artificial Intelligence ; Metabolomics ; },
abstract = {Chronic liver disease develops through sustained interactions among metabolic stress, environmental exposure, immune activation, and tissue remodeling. These processes are often studied as separate domains, yet in patients they converge within the same hepatic microenvironment and help explain why disease trajectories vary even within the same diagnostic category. Exposure science has sharpened attention to diet, alcohol, pollutants, chemical mixtures, gut-derived signals, sleep and circadian disruption, and other behavioral determinants of liver injury. At the same time, multi-omics approaches now capture complementary dimensions of disease biology, including genetic susceptibility, epigenetic memory, inflammatory transcriptional programs, proteomic signaling, metabolic rewiring, microbiome composition, and spatially restricted cell states. The central challenge is no longer simply to generate more data, but to connect these layers into clinically useful markers of progression. In this review, we discuss chronic liver disease as a set of exposure-shaped immunometabolic network states that extend across steatosis, inflammation, fibrosis, cirrhosis, and hepatocellular transformation. We summarize how major exposure domains feed into shared pathogenic hubs, how immune and metabolic circuits sustain injury, and how genomics, epigenomics, transcriptomics, proteomics, metabolomics, microbiome profiling, and single-cell or spatial methods can reveal biologically coherent biomarker candidates. We also examine how machine learning, deep learning, network-based modeling, and causal-inference strategies may support risk stratification and progression forecasting when used with attention to interpretability, cohort structure, and external validation. A prevention-oriented biomarker framework should identify transition-prone states early enough to guide monitoring, referral, treatment selection, or lifestyle intervention. Such translation will require better exposure assessment, longitudinal sampling, assay standardization, and transportable models tested across real-world populations.},
}

Humans
Multiomics
Biomarkers/metabolism
*Liver Diseases/metabolism/etiology/immunology/prevention & control
Chronic Disease
Animals
*Environmental Exposure/adverse effects
*Artificial Intelligence
Metabolomics

@article {pmid42840879,
year = {2026},
author = {Cheng, J and Zhang, X and Zhou, J and Liu, L and Feng, J and Zhao, L},
title = {Periodontitis and Parkinson's disease: a narrative review of associations, proposed mechanisms, and clinical considerations.},
journal = {Frontiers in oral health},
volume = {7},
number = {},
pages = {1926663},
pmid = {42840879},
issn = {2673-4842},
abstract = {Periodontitis is a common chronic inflammatory disease, and oral health problems are frequent in people with Parkinson's disease (PD). Observational studies consistently indicate poorer periodontal status in PD, but evidence that periodontitis increases the incidence or progression of PD is inconsistent and does not establish causality. This narrative review summarizes current evidence on epidemiological associations, biologically plausible mechanisms, and dental management considerations. Human data support an association between PD and greater periodontal disease burden, plausibly related to motor impairment, reduced self-care capacity, salivary dysfunction, and altered oral microbial ecology. By contrast, proposed pathways from periodontitis to PD, including systemic inflammation, blood-brain barrier disruption, microbial products, and the oral-gut-brain axis, are supported mainly by preclinical, indirect, or low-level human evidence and should be regarded as hypotheses rather than established mechanisms. Observational reports of lower PD incidence among individuals receiving dental scaling do not demonstrate a preventive effect of periodontal treatment. In clinical practice, periodontal care should therefore be justified by established oral-health needs and individualized for PD-related motor, swallowing, cognitive, medication, and device-related considerations, rather than presented as a strategy to prevent or modify PD. Better longitudinal studies and interventional trials are needed to clarify temporality, mechanisms, and any neurological effects of periodontal treatment.},
}

@article {pmid42840927,
year = {2026},
author = {Melchiorri, S and Castagliuolo, I},
title = {Microbiota-derived metabolic priming of CAR-T cell fitness: a translational framework for next-generation cell therapy.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1953443},
pmid = {42840927},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology/drug effects ; Animals ; *Receptors, Chimeric Antigen/immunology/metabolism ; *Immunotherapy, Adoptive/methods/adverse effects ; *T-Lymphocytes/immunology/metabolism ; Metabolome ; Metabolomics ; },
abstract = {Chimeric antigen receptor T-cell (CAR-T) therapy has transformed the treatment of hematologic malignancies, yet durable responses remain inconsistent and clinically significant toxicities persist. Emerging evidence identifies the gut microbiota as an extratumoral determinant of CAR-T efficacy, persistence, and toxicity. However, taxonomic signatures associated with clinical outcomes show limited reproducibility and are influenced by antibiotics, geography, diet, and methodological heterogeneity. Building on prior reviews addressing microbiome-CAR-T associations and CAR-T-cell immunometabolism separately, here we synthesize clinical, translational, and preclinical evidence into an integrated, metabolome-centered framework spanning the full CAR-T treatment and manufacturing trajectory. Broad-spectrum antibiotic exposure disrupts microbial metabolic output, depleting short-chain fatty acids, indole derivatives, and other bioactive metabolites, and has been associated with inferior clinical outcomes in several cohorts, although these associations are heterogeneous and may be confounded by baseline disease severity, systemic inflammation, and infection-related factors. Experimental studies further indicate that butyrate, valerate, inosine, indoles, and succinate modulate mitochondrial fitness, memory differentiation, epigenetic programming, cytotoxicity, and exhaustion through interconnected metabolic and receptor-mediated pathways. We propose that the gut microbiota acts as a distributed metabolic organ whose collective output shapes CAR-T-cell fitness and therapeutic response. This framework supports the development of metabolite-based biomarkers and therapeutic strategies, including microbiota-conscious antibiotic stewardship, ecosystem restoration, dietary or metabolite-based interventions, and ex vivo metabolic conditioning during CAR-T manufacturing. Shifting from descriptive microbiome profiling to functional metabolomics may improve both prediction and optimization of CAR-T therapy.},
}

Humans
*Gastrointestinal Microbiome/immunology/drug effects
Animals
*Receptors, Chimeric Antigen/immunology/metabolism
*Immunotherapy, Adoptive/methods/adverse effects
*T-Lymphocytes/immunology/metabolism
Metabolome
Metabolomics

@article {pmid42840990,
year = {2026},
author = {Mahajan, GB},
title = {Gut microbiome modulation by diet and lifestyle in kidney stone disease and autism spectrum disorder: emerging mechanisms and translational prospects.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1901989},
pmid = {42840990},
issn = {2813-4338},
abstract = {BACKGROUND: The gut microbiome occupies a central position in mediating the physiological consequences of diet, lifestyle, and physical activity. While this interplay is broadly recognized, its mechanistic consequences in two clinically underserved conditions-urolithiasis (kidney stone disease) and autism spectrum disorder (ASD)-remain poorly explained. Both conditions share convergent pathophysiology rooted in metabolic dysregulation, impaired epithelial barrier function, immune dysregulation, and altered microbial metabolite profiles, all of which are modifiable through dietary and behavioral interventions.

METHODS: This minireview synthesizes current evidence from clinical, epidemiological, and mechanistic studies to evaluate the bidirectional relationship between gut microbial ecology and disease pathogenesis in urolithiasis and ASD, with emphasis on dietary compounds, fermented foods, probiotics, and lifestyle behaviors as modulatory factors.

RESULTS: In urolithiasis, evidence implicates reduced abundance of oxalate-degrading taxa (notably Oxalobacter formigenes), dysbiotic short-chain fatty acid (SCFA) profiles, and urinary microbiome perturbations in stone formation and recurrence. In ASD, microbial alterations in gastrointestinal-symptomatic individuals converge on reduced butyrate-producing taxa, elevated pro-inflammatory species, and altered serotonin and gamma-aminobutyric acid (GABA) biosynthetic pathways.

CONCLUSION: Dietary interventions-particularly high-fiber regimens, polyphenol-rich foods, fermented products, and targeted probiotic formulations-show mechanistic plausibility for microbiome restoration in both conditions. However, clinical translation is constrained by methodological heterogeneity, confounding lifestyle variables, and a paucity of longitudinal, mechanistically anchored trials. We outline a research agenda prioritizing standardized multi-omics, paired gut-urine sampling protocols, and rigorously controlled dietary interventions to bridge this gap.},
}

@article {pmid42840992,
year = {2026},
author = {Liao, Y and Shi, Y and Pang, X and Yang, Y and Chen, X and Tang, Z and Xie, P and Cao, X},
title = {From local lesion to multisystem disease: integrated crosstalk among the gut microbiota, immune system, and host metabolism in endometriosis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1924352},
pmid = {42840992},
issn = {1664-3224},
mesh = {Humans ; *Endometriosis/metabolism/immunology/microbiology/etiology ; Female ; *Gastrointestinal Microbiome/immunology ; Animals ; *Immune System/metabolism/immunology ; Dysbiosis/immunology ; Estrogens/metabolism ; Immunity, Innate ; *Host Microbial Interactions/immunology ; },
abstract = {Endometriosis (EMs) is a common estrogen-dependent inflammatory disease characterized by pelvic pain and infertility. Despite its substantial clinical burden, its etiology and pathogenesis remain incompletely resolved, and current management continues to be constrained by delayed diagnosis, limited therapeutic efficacy, and frequent disease recurrence. Growing evidence indicates that EMs is not merely a localized gynecological disorder but a disease state with multisystem pathophysiological features, a condition defined by crosstalk among the gut microbiota, the immune system, and host metabolism. This review synthesizes current evidence to establish a systems biology framework in which gut dysbiosis, immune dysfunction, and metabolic reprogramming are integrated as interconnected drivers of disease initiation, progression, and persistence. We first examine alterations in gut microbial composition and function, including estrogen metabolism dysregulation, expansion of opportunistic pathogens, and impaired intestinal barrier integrity, and discuss how these changes influence estrogen homeostasis, inflammatory signaling, and host-microbe interactions. We then explore how aberrations in innate and adaptive immunity promote immune evasion, chronic inflammation, angiogenesis, and ectopic lesion survival. Furthermore, we highlight the multifaceted remodeling of carbohydrate, lipid, and amino acid metabolism, and its link to cell proliferation and the immunosuppressive microenvironment. Particular emphasis is placed on the bidirectional interplay among microbial metabolites, immunometabolic signaling, oxidative stress, and tricarboxylic acid cycle (TCA) intermediates, all of which coalesce into a self-reinforcing pathological network. By integrating these domains, This review advances a unifying "microbiome-immune-metabolic" framework to elucidate the multisystem pathophysiological features of EMs, aiming to inspire the discovery of non-invasive biomarkers and the development of precision therapeutic strategies that target microbial, immune, and metabolic pathways.},
}

Humans
*Endometriosis/metabolism/immunology/microbiology/etiology
Female
*Gastrointestinal Microbiome/immunology
Animals
*Immune System/metabolism/immunology
Dysbiosis/immunology
Estrogens/metabolism
Immunity, Innate
*Host Microbial Interactions/immunology

@article {pmid42841011,
year = {2026},
author = {Chen, M and Wang, Y and Zhang, S and Li, S and Zhi, M and Liang, L and Yang, K and He, X and Xu, M and Yuan, L},
title = {Engineering synthetic microbial communities for soil restoration: from rational design to multi-scale biogeochemical applications.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1939240},
pmid = {42841011},
issn = {1664-302X},
abstract = {Soil degradation caused by intensive land use, pollution, and climate stress threatens food production and ecosystem function. Single-strain inoculants often perform inconsistently because they do not persist or compete well in resident soil microbiomes. Synthetic microbial communities (SynComs) combine complementary microbial functions in defined consortia. Their performance, however, depends on community composition and environmental context. Multi-omics, high-throughput screening, and artificial intelligence (AI) can reduce the number of strain combinations that need to be tested. Yet the roles of AI and other computational approaches are often described imprecisely. We distinguish four roles: direct AI design, AI-assisted candidate discovery, model-guided design, and prediction-only analysis. This framework links computational methods to the experimental steps needed to construct and validate soil SynComs. We examine applications in nutrient acquisition, carbon cycling, pollutant remediation, disease suppression, and tolerance to drought and salinity. Direct AI design has so far been demonstrated only in a few controlled plant systems and soil microcosms. In most studies, machine learning (ML) is used earlier in the workflow to identify candidates, while cultivation, functional assays, and interaction tests determine the final community composition. To bridge this gap, we propose a staged design-build-test-learn (DBTL) framework, which links model evaluation and community reconstruction with testing in non-sterile soil, strain tracking, safety assessment, and field validation. AI can narrow the experimental search space, but empirical validation remains essential to establish causality, persistence, and transferability across soils and hosts.},
}

@article {pmid42841118,
year = {2026},
author = {Xia, JY and Komanduri, S and Keswani, RN and Rodrigues, TR and Sinha, J and Rengarajan, A and Moy, BM and Gruber, SF and Chen, YJ and Hepler, C and Prindle, A and Aadam, AA},
title = {Biliary Microbiome Dysbiosis Is Associated with Susceptibility to Post-ERCP Pancreatitis.},
journal = {Endoscopy international open},
volume = {14},
number = {},
pages = {a29496689},
pmid = {42841118},
issn = {2364-3722},
abstract = {Background & Aims Pancreatitis remains the most common adverse event following endoscopic retrograde cholangiopancreatography (ERCP), yet current risk stratification relies primarily on clinical and procedural factors. The present study aims to examine bile-based microbiome signatures as a potential link between nonprocedure patient-level risk factor for pancreatitis susceptibility after ERCP. Methods We performed analysis for rates of post-ERCP pancreatitis of a prospective single center cohort of patients undergoing ERCP (n = 148) with bile collected at the time of the procedure. Microbial profiling was performed using 16S rRNA sequencing. Alpha diversity, beta diversity, differential abundance analyses, and metabolic pathway analysis were evaluated between patients with and without post-ERCP pancreatitis (PEP). Results Patients with PEP demonstrated significantly reduced biliary microbial diversity and distinct composition compared with those without pancreatitis. Differential abundance analysis identified multiple depleted genera in the PEP group. Functional profiling revealed broad reductions in microbial metabolic pathways associated with PEP predominantly involving biosynthetic and central metabolic functions. ROC curve analysis demonstrated that differentially abundant bile microbes can discriminate patients with PEP from those without pancreatitis. Discussion Patients who develop PEP harbor a distinct and functionally depleted biliary microbiome. These findings parallel prior observations of gut dysbiosis in acute pancreatitis and suggest that the biliary microbiome may represent a biologic pathway associated with PEP susceptibility.},
}

@article {pmid42841227,
year = {2026},
author = {Wernike, C and Häder, A and Reisser, Y and Garakani, K and Hornung, F and Le Saux, CJ and Deinhardt-Emmer, S},
title = {Age-Associated Gut Microbiota Dysbiosis Impairs Antiviral Defense During Influenza Virus Infection and Identifies Acetate as a Protective Mediator in Senescent Human Lung Cells.},
journal = {Aging cell},
volume = {25},
number = {10},
pages = {e70750},
doi = {10.1111/acel.70750},
pmid = {42841227},
issn = {1474-9726},
support = {13N15466//BMFTR/ ; 13N15704//BMFTR/ ; 13N15745//BMFTR/ ; //Else Kröner-Fresenius-Stiftung/ ; },
mesh = {Humans ; Animals ; *Lung/virology/pathology ; *Acetates/pharmacology/metabolism ; Mice ; *Gastrointestinal Microbiome ; *Dysbiosis ; *Cellular Senescence/drug effects ; *Influenza A virus ; *Influenza, Human/virology ; *Orthomyxoviridae Infections/immunology ; *Aging ; Mice, Inbred C57BL ; Fatty Acids, Volatile ; },
abstract = {Aging is associated with profound alterations in gut microbiota composition and function, including reduced production of short-chain fatty acids (SCFAs), yet it remains unclear whether these age-related microbial changes directly contribute to impaired antiviral defense during influenza A virus (IAV) infection. To address this question, we first characterized age-associated alterations of the gut microbiome and SCFA-related metabolic potential in a murine model of IAV infection. We then used a complementary human senescent lung fibroblast model to determine whether acetate, a major microbiota-derived SCFA, directly modulates antiviral responses in aging-associated lung cells. In old mice, IAV infection was associated with marked microbiota dysbiosis, including reduced abundance of SCFA-producing commensals such as Akkermansia muciniphila and Faecalibaculum rodentium, accompanied by decreased expression of microbial pathways involved in carbohydrate fermentation and acetate production. These findings suggested impaired microbiota-derived metabolic support of antiviral immunity during aging. Based on these observations, mechanistic studies in senescent human lung fibroblasts demonstrated that acetate supplementation significantly reduced viral replication and inflammatory responses. These protective effects were associated with FFAR2/FFAR3 signaling and enhanced histone H3 acetylation, indicating metabolic and epigenetic modulation of the antiviral response. Together, our findings establish a translational link between aging-associated gut microbiota dysfunction and impaired antiviral defense by combining a murine model of aging and influenza infection with mechanistic validation in human senescent lung cells. They identify acetate as a potential mediator of the gut-lung axis and support microbiota-targeted interventions to reduce influenza severity in older individuals.},
}

Humans
Animals
*Lung/virology/pathology
*Acetates/pharmacology/metabolism
Mice
*Gastrointestinal Microbiome
*Dysbiosis
*Cellular Senescence/drug effects
*Influenza A virus
*Influenza, Human/virology
*Orthomyxoviridae Infections/immunology
*Aging
Mice, Inbred C57BL
Fatty Acids, Volatile

@article {pmid42841278,
year = {2026},
author = {Soumya, V and Kiranmayi, P and Indraneela, T and Chandrika, G and Akhileshwar, N},
title = {Integrated nanopore profiling of fungal and bacterial endophytes reveals microbiome reorganization in Catharanthus roseus under heavy metal stress.},
journal = {International journal of phytoremediation},
volume = {},
number = {},
pages = {1-12},
doi = {10.1080/15226514.2026.2740721},
pmid = {42841278},
issn = {1549-7879},
abstract = {Endophytes play a crucial role in plant adaptation to environmental stress; however, their coordinated responses to heavy metal contamination remain insufficiently understood, particularly in medicinal plants. This study investigated the influence of metal-contaminated soils on the composition and structuring of endophytic communities associated with Catharanthus roseus, a pharmaceutically significant species. Plants were cultivated for 12 months in contaminated soil collected from an industrial site, Hindustan Shipyard Limited (Visakhapatnam, India), and in uncontaminated control soil from the GITAM garden. Surface-sterilized leaf and root tissues were subjected to culture-independent microbial profiling. Fungal endophytes were characterized using internal transcribed spacer (ITS) amplicon sequencing, while bacterial communities were analyzed through 16S rRNA gene sequencing using the Oxford Nanopore platform. Sequencing data were processed through established bioinformatic pipelines, with taxonomic classification performed against the UNITE and Greengenes databases. The results revealed pronounced tissue- and site-specific shifts in endophytic community composition, with root tissues exhibiting greater microbial diversity than leaves. Communities from contaminated soils displayed reduced overall diversity but selective enrichment of stress-tolerant and metal-adapted taxa, indicating strong environmental filtering. These findings demonstrate that heavy metal-stress drives restructuring of endophytic assemblages and highlight the potential of native endophytes in microbe-assisted phytoremediation and sustainable management of metal-contaminated soils.},
}

@article {pmid42841281,
year = {2026},
author = {Luo, W and Wang, B and Ma, H and Li, H},
title = {Decoupling Community Complexity From Efficacy: A Meta-Analysis of Synthetic Microbial Communities for Plant Stress Resilience.},
journal = {Plant, cell & environment},
volume = {},
number = {},
pages = {},
doi = {10.1111/pce.70965},
pmid = {42841281},
issn = {1365-3040},
support = {32402670//National Natural Science Foundation of China/ ; 2025BEH04037//Ningxia Key Research and Development Project/ ; 2024AAC03141//Ningxia Natural Science Foundation/ ; CXXM2026015//Graduate Innovation Project of Ningxia University/ ; },
abstract = {Drought, salinity, pollution and nutrient deficiency substantially impair plant growth by disrupting water balance, ion homoeostasis, redox regulation and metabolism. Synthetic microbial communities (SynComs) represent a frontier in microbiome engineering, theoretically offering superior stability over single-strain inoculants through functional redundancy. However, the design rules governing their efficacy - specifically the trade-off between community complexity and phenotypic output - remain empirically unresolved. This meta-analysis evaluated how synthetic microbial communities (SynComs) affect plant growth and stress-related physiological responses under different stress conditions and examined whether their efficacy was associated with community complexity or specific microbial functional traits. Data from 34 studies (433 independent comparisons) were collected. Then, the natural log response ratios (lnRR) of plant morphological and physiological traits were calculated. A random-effects model was used to estimate global effect sizes and quantify between-study heterogeneity. Plant performance was significantly enhanced following SynComs inoculation, evidenced by a 111.93% increase in total biomass (mean lnRR = 0.751). The highest efficacy was observed under biotic stress (total plant dry weight +191.57%) and pollution (underground dry weight +154.23%), with biomass accumulation being more pronounced in belowground traits than in aboveground components. Physiologically, this growth promotion was associated with the alleviation of oxidative stress in plants, as manifested by the significant upregulation of antioxidant enzymes (CAT + 47.09%, POD + 41.55%, and SOD + 44.71%) and a concurrent reduction in lipid peroxidation. Furthermore, the weighted meta-analysis revealed that single-genus communities significantly outperformed multi-genus communities in the present dataset (p = 0.004). However, efficacy was entirely decoupled from community richness, measured as strain number (R[2] = 0.000, p = 0.490). These findings suggest that greater taxonomic breadth or higher strain richness was not necessarily associated with improved SynCom performance. Rather, efficacy appeared to be driven by specific microbial functional traits (such as IAA production and phosphorus solubilisation). We propose that the rational design of SynComs should prioritise strain function over community size to maximise agricultural sustainability and reduce metabolic burden.},
}

@article {pmid42841305,
year = {2026},
author = {Li, S and Ren, K and Yang, X and Zhao, Q and Huang, H},
title = {Gut microbiota alterations associated with dietary inflammation and sarcopenia in humans and aged mice: insights from integrated metabolomic analysis.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d6fo03587f},
pmid = {42841305},
issn = {2042-650X},
abstract = {Objective: To investigate the association between the dietary inflammatory index (DII) and sarcopenia risk in older adults and identify cross-species microbial signatures linking dietary inflammatory burden with muscle phenotypes. Methods: A total of 1048 older adults were enrolled, and multivariable logistic regression models were applied to evaluate the association between the DII and sarcopenia risk. A sub-cohort of representative participants (n = 86) underwent fecal 16S rRNA gene sequencing. In parallel, a 10-week pro-inflammatory dietary intervention in naturally aged mice was conducted, followed by gut microbiome and skeletal muscle untargeted metabolomic profiling. Cross-species microbial signatures were identified by integrating human and mouse microbiome data. Results: Higher DII scores were associated with a greater prevalence of sarcopenia (OR = 1.305, 95% CI: 1.128-1.509). No significant difference in gut microbial α-diversity was observed between participants with and without sarcopenia, whereas β-diversity differed significantly between the two groups (p = 0.005). In aged mice, pro-inflammatory dietary intervention reduced grip strength and lean body mass and altered gut microbiota composition and skeletal muscle metabolic profiles. Group-by-time interaction effects for forelimb and all-limb grip strength remained significant after FDR correction (q < 0.05). Metabolomic changes were mainly enriched in lipid and amino acid metabolism pathways. Cross-species integration identified conserved microbial signatures, including the Family XIII AD3011 group, Akkermansia, and Fusobacterium. Conclusions: Higher dietary inflammatory burden is associated with increased sarcopenia risk and impaired muscle function in older adults. Gut microbiota alterations and skeletal muscle metabolic remodeling may contribute to this association. The identified cross-species microbial signatures provide potential targets for future mechanistic studies and nutritional interventions.},
}

@article {pmid42841513,
year = {2026},
author = {Chiu, YT and Lee, FJ and Kuo, CY and Yang, PC and Wong, JU and Liang, KS and Tseng, CH and Lin, JT and Wu, CY and Chang, CY},
title = {Longitudinal Shifts in Gut Microbiota After Cholecystectomy: A Point of No Return in Losing Lactobacillus Spp.},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.90057.2026},
pmid = {42841513},
issn = {1522-1547},
support = {NSTC 114-2314-B-030-008//National Science and Technology Council/ ; },
abstract = {Cholecystectomy alters bile acid dynamics and may influence gut microbiota composition. However, longitudinal data with preoperative baseline assessment remain limited, and existing evidence is largely based on cross-sectional studies with inconsistent findings. In this prospective cohort study, we aimed to characterize longitudinal changes in gut microbiota following cholecystectomy and explore their clinical relevance. Patients planning to undergo laparoscopic cholecystectomy were recruited and followed for 12 months. Stool samples were collected at baseline and at 1, 3, 6, and 12 months postoperatively. Microbiota composition was analyzed using 16S rRNA gene sequencing. Microbial diversity and differential abundance were evaluated using complementary statistical approaches, including longitudinal analyses accounting for repeated measurements. Clinical outcomes, including stool form and defecation frequency, were recorded. Twenty participants completed follow-up. Overall microbial diversity and community structure showed only modest changes over time. In contrast, differential abundance analyses consistently demonstrated an early postoperative reduction in the genus Lactobacillus, which remained relatively stable thereafter. Functional prediction suggested modest alterations in metabolic pathways without major disruption of global microbial function. No participants developed clinically significant post-cholecystectomy diarrhea. In conclusion, gut microbiota after cholecystectomy exhibited relatively modest overall changes but selective taxonomic alterations, particularly a persistent reduction in Lactobacillus. These findings suggest targeted microbial restructuring rather than global dysbiosis and may help explain the low incidence of post-cholecystectomy diarrhea.},
}

@article {pmid42841516,
year = {2026},
author = {Wu, D and Nie, MT and Lin, J and Liu, Y and Wang, Y and Chu, M and Zheng, L and Zhao, J},
title = {Rifaximin ameliorates memory impairment and Alzheimer's pathological changes in APP/PS1 mice associated with changes in the gut microbiome-bile acids-serum metabolites networks.},
journal = {British journal of pharmacology},
volume = {},
number = {},
pages = {},
doi = {10.1111/bph.70643},
pmid = {42841516},
issn = {1476-5381},
support = {2022MHPY02//Minhang Hospital of Fudan University/ ; 2025MHBJ03//Minhang Hospital of Fudan University/ ; MGWXK2023-04//Minhang Hospital of Fudan University/ ; 2024DR010//China University Industry-Academia-Research Innovation Fund/ ; },
abstract = {BACKGROUND AND PURPOSE: Modifying the brain-gut-microbiota axis has emerged as a promising therapeutic strategy against Alzheimer's disease (AD). Whether rifaximin, a non-absorbed and non-systemic antibiotic, can be applied to the treatment of AD remains unexplored. In this study, we investigated the effects of rifaximin using a APP/PS1 double-transgenic mouse model of AD.

EXPERIMENTAL APPROACH: Six-month-old male APP/PS1 mice were administered saline or rifaximin (100 mg·kg[-1]) via oral gavage for 2 months. Gut microbiota composition and metabolites were subsequently analysed to elucidate the underlying mechanisms of rifaximin in AD.

KEY RESULTS: Rifaximin modified gut microbiota composition, increasing abundance of Akkermansia muciniphila and Christensenellaceae, while decreasing abundance of Clostridia_UCG-014, Muribaculaceae, Lachnospiraceae, Turicibacter, Eubacterium_xylanophilum_group, Alistipes, Bacteroides_acidifaciens and Eubacterium_brachy groups. Furthermore, rifaximin alleviated memory impairment in APP/PS1 mice, decreased amyloid-β (Aβ) burden and secondary neuroinflammation and attenuated neuronal death and synaptic dysfunction. Metabolomic analysis revealed that rifaximin altered the profile of gut bile acids by decreasing the concentrations of primary (cholic acid and taurocholic acid) and secondary (taurodeoxycholic acid and taurolithocholic acid) bile acids. Additionally, rifaximin enhanced tryptophan metabolism, shown by increased serum 5-HT concentrations. Both microbial and metabolic shifts were closely correlated with gut microbiota composition.

CONCLUSIONS AND IMPLICATIONS: Our results showed that rifaximin alleviated spatial working and short-term recognition memory impairment and mitigated Alzheimer's-like pathological changes in APP/PS1 mice, effects accompanied by alterations in the gut microbiota-intestinal bile acid profile-serum metabolites network. Rifaximin could provide a new therapeutic approach to the treatment of AD.},
}

@article {pmid42841628,
year = {2026},
author = {Gao, M and Zeng, Q and Lam, K and Toro, M and Micallef, SA and Blaustein, RA},
title = {Microbiomes of soils and leafy vegetables in urban agriculture systems reflect crop management and local environmental conditions.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0155126},
doi = {10.1128/aem.01551-26},
pmid = {42841628},
issn = {1098-5336},
abstract = {Soil and plant microbiomes influence crop quality and preharvest food safety, yet these processes have been largely unexplored in urban agriculture environments. Here, we investigated how the microbiota of soil and leafy greens (e.g., kale, lettuce, chard, and cabbage) interact with site-specific management practices and environmental conditions across seven urban agriculture sites in the greater Washington, DC, area. Samples of leaf tissue (n = 92), rhizosphere soil (n = 92), and "native" or bulk soil (n = 39) were collected and analyzed with 16S rRNA gene and ITS2 genomic region amplicon sequencing. Microbial community composition varied significantly across sites for all sample types, as influenced by irrigation water source (i.e., municipal vs natural water), crop type, soil pH, soil moisture content, and climatic conditions (i.e., rainfall, temperature). Rhizosphere soils harbored the most bacterial taxa known to respond to organic inputs (e.g., Massilia and various members of Firmicutes and Verrucomicrobiota), whereas fungal networks dominated by saprotrophic members of Ascomycota were more stable in the bulk soils. Source-tracking analysis indicated that the phyllosphere microbiota, although variable and transient in composition, were largely derived from the rhizosphere soil. Notably, leafy greens at some sites were enriched with taxa associated with biocontrol potential (e.g., Lactobacillaceae). Moreover, machine learning models yielded strong performance in predicting specific production sites based on the bacterial communities in the rhizosphere and phyllosphere, suggesting possible microbiome-based applications for food traceability. Collectively, these findings demonstrate how local environments and crop management practices shape preharvest leafy green microbiomes in urban production.IMPORTANCEUrban farming and gardening are rapidly expanding to support local communities and enhance food security, yet these small-scale food systems are often established in uniquely developed landscapes and with resource-dependent operations. This study shows that complex site-specific factors influence the soil and leafy green microbiomes in urban agriculture systems. Our findings have important implications for future efforts in targeted farm management to enhance sustainable production and preharvest food safety.},
}

@article {pmid42841641,
year = {2026},
author = {Rubin, E and Felletti, M and Miller, TC and Bentlage, B and Vaz, DFB and Ord, TJ and Irisarri, I},
title = {Skin microbiome mirrors habitat divergence in amphibious combtooth blenny fish (Teleostei, Blenniidae).},
journal = {FEMS microbiology letters},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsle/fnag123},
pmid = {42841641},
issn = {1574-6968},
abstract = {Host-associated microbiomes play vital roles in species' ecology and evolution, yet little is known about their shift during the transition from aquatic to terrestrial habitats. We characterize the skin microbiomes of three combtooth blenny species (Blenniella paula, Praealticus labrovittatus, Alticus arnoldorum) that occupy distinct positions along the intertidal gradient-from fully subtidal to intertidal and supratidal environments. Using 16S rRNA sequencing, we compared skin-associated bacterial communities with those in seawater and substrate biofilms. The divergence between skin and substrate microbiomes parallels fishes' distribution along progressively higher intertidal zones. The supratidal A. arnoldorum had the most divergent microbiome, characterized by higher Gammaproteobacteria abundance and enrichment of epiphytic and mucus-associated taxa. Fish skins were enriched in 27 microbial orders that included genera commonly associated with fish (e.g., Vibrio, Alteromonas, Cetobacterium) but others rarely reported (e.g., Rubritalea, Granulosicoccus). Together, our findings suggest that variation in fish skin microbiomes parallels the ecological transition from subtidal (aquatic) to supratidal (terrestrial) habitats, although host and habitat effects could not be disentangled. We hypothesize that microbial symbionts may contribute to adaptations enabling amphibious lifestyles. This is the first study on fish microbiome variation across the intertidal gradient and offers a framework for predicting microbiome responses to environmental change.},
}

@article {pmid42841642,
year = {2026},
author = {Kain, T and Armstrong, E and Coburn, B},
title = {Peripheral microbial metabolites as indicators of gut microbiome disruption: systematic review and meta-analysis.},
journal = {mBio},
volume = {},
number = {},
pages = {e0192726},
doi = {10.1128/mbio.01927-26},
pmid = {42841642},
issn = {2150-7511},
abstract = {Gut microbiome disruption is often characterized by the loss of obligately anaerobic bacteria, which may lead to altered production of microbial metabolites that can be detected peripherally. The application of widely used sequencing-based microbiome analyses to clinical settings is limited by cost, turnaround time, and challenges with patients with very low stool output. Since some products of strictly bacterial metabolism are detectable in blood, peripheral metabolites may provide a rapid and scalable indicator of gut microbiome composition and function. We performed a systematic review and meta-analysis of studies reporting circulating microbial metabolites and gut microbiome composition to evaluate whether peripheral microbial metabolites could identify gut microbiome perturbation. Candidate metabolites were identified systematically across an independent set of studies reporting metabolite-microbiome associations, enabling the assessment of reproducibility across disease states and cohorts. We performed a meta-analysis of 19 human cohorts comprising 3,242 participants with paired blood metabolite and stool microbiome data. Anaerobe depletion (obligate anaerobe relative abundance <0.70) was associated with decreased plasma concentration of products of anaerobic microbial metabolism. Combinations of metabolites distinguished individuals with anaerobe-depleted microbiomes from those without. Circulating metabolite levels distinguished between cases and controls with similar performance as gut microbiome composition across a range of health/disease states and changed markedly within patients experiencing gut anaerobe depletion after antibiotic exposure. Circulating microbial metabolites are potentially informative indicators of gut microbiome disruption and may serve as a rapid and scalable method for patient stratification in clinical trials or acute care settings.IMPORTANCECirculating microbial metabolites represent a practical and scalable approach to detecting significant gut microbiome disruption, particularly the loss of obligate anaerobes. Our findings suggest that metabolites capture compositional consequences of microbiome collapse, with performance comparable to direct microbiome profiling in distinguishing disease states. Enabling diagnostic enrichment and real-time monitoring of microbiome injury (e.g., during antibiotic use or critical illness) has potential implications for both clinical care and research, including the selection of patients for investigation of microbiome-targeted therapies. With further validation, circulating metabolites could provide an accessible surrogate for gut microbiome composition in settings where sequencing is impractical.},
}

@article {pmid42841648,
year = {2026},
author = {Shen, Y and Dai, D and Han, H and Hao, Y and Yang, Z and Li, S},
title = {Dietary baicalin supplementation increases the milk unsaturated fatty acid proportion through modulating milk metabolism and the microbiome in dairy cows.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0083626},
doi = {10.1128/spectrum.00836-26},
pmid = {42841648},
issn = {2165-0497},
abstract = {The composition and characteristics of milk fatty acids, which play a pivotal role in nutrition, are profoundly influenced by the dietary components consumed by cows. Like other flavonoids, baicalin (BAI) may affect the proportion of milk fatty acids. This study evaluates the effect of dietary supplementation with BAI on milk microbiota and host metabolism to modulate milk fatty acid composition. Results indicated that dietary supplementation with BAI increased proportions of unsaturated fatty acids (UFAs) (e.g., C18:1n9c and C18:2n6c). BAI reshaped the milk microbiome, wherein enriched taxa such as Myroides were positively associated with increased milk UFA and altered milk metabolite profiles. Additionally, BAI regulated some metabolites (e.g., alpha-KG) in milk, which were linked to promoting the synthesis of UFA, and regulated host metabolism (e.g., primary bile acid biosynthesis) that enhanced UFA metabolism. Together, these findings demonstrate the great potential of BAI in effectively modifying the milk fatty acid profile to enhance its nutritional quality.IMPORTANCEMilk is a major source of dietary fat for humans, and increasing the proportion of unsaturated fatty acids (UFAs) in milk can improve its nutritional quality. This study demonstrates that dietary supplementation with baicalin, a natural flavonoid from Scutellaria baicalensis, effectively increases milk UFA content in dairy cows. The findings reveal that baicalin modulates milk fatty acid composition through reshaping the milk microbiome (e.g., enriching Myroides) and altering mammary and systemic metabolism. These results provide a novel, plant-based nutritional strategy for enhancing milk quality and offer mechanistic insights into the interplay between dietary bioactive compounds, mammary microbiota, and lipid metabolism in lactating dairy cows.},
}

@article {pmid42841652,
year = {2026},
author = {Voulgari-Kokota, A and Janson, E and Heikamp de Jong, I and Knol, J and van Elburg, R and van der Aa, NE and Hortensius, LM and Dudink, J and de Theije, CGM and Schipper, L and Kozior, M and van de Lagemaat, M and Groenendaal, F and van Bel, F and Wildt-Grootendorst, A and Drost-Verhoef, S and Hennink, A and Obihara, CC and van Hillegersberg-Schilder, JLAM and Dassel, CM and Oudshoorn, JH and Meijssen, CB and de Boer, IP and Illy, KE and Claessens, N and Viergever, MA and Isgum, I and Shetty, S and Wopereis, H and Benders, M and Belzer, C},
title = {Synbiotic supplementation leads to gut microbiome communities with functional capacity linked to better brain white matter development in preterm infants.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2743949},
doi = {10.1080/19490976.2026.2743949},
pmid = {42841652},
issn = {1949-0984},
mesh = {Humans ; Infant, Newborn ; *Infant, Premature/growth & development ; *White Matter/growth & development ; *Brain/growth & development ; *Gastrointestinal Microbiome ; *Synbiotics/administration & dosage ; Dietary Supplements ; Male ; Bifidobacterium breve ; Glutamine/administration & dosage ; Female ; Oligosaccharides/administration & dosage ; Neurodevelopment ; Magnetic Resonance Imaging ; Infant ; },
abstract = {Preterm birth, a major cause of brain injury, is often linked to dysregulated gut microbiome development. This association underscores microbial metabolic function as a modifiable target to support neurodevelopment. In this secondary analysis of data derived from a randomized controlled trial (Trial Registration: ISRCTN96620855), we tested whether daily nutritional supplementation with Bifidobacterium breve M-16V, short- and long-chain oligosaccharides, and L-glutamine could steer the gut microbiome of very and extremely preterm infants toward communities that support brain maturation. The gut microbiome was profiled with longitudinal shotgun metagenomics at nine time points during the intervention, which started at 48-72 h after birth and continued until 36 weeks postmenstrual age. Additionally, MRI scans were conducted when infants reached term-equivalent age to evaluate brain maturation. Supplementation promoted the early establishment of Bifidobacterium-rich communities in the test group, with enhanced capacity for amino acid biosynthesis and pyruvate fermentation towards acetate and lactate production. Integration of microbiome data with brain developmental markers post hoc showed that the same functions were markedly reduced in infants with delayed white-matter myelination. By integrating microbiome functional capacity profiling and evaluation of brain maturation via MRI, this study demonstrated that early microbial modulation could influence brain development, positioning the preterm gut microbiome as a clinically actionable target.},
}

Humans
Infant, Newborn
*Infant, Premature/growth & development
*White Matter/growth & development
*Brain/growth & development
*Gastrointestinal Microbiome
*Synbiotics/administration & dosage
Dietary Supplements
Male
Bifidobacterium breve
Glutamine/administration & dosage
Female
Oligosaccharides/administration & dosage
Neurodevelopment
Magnetic Resonance Imaging
Infant

@article {pmid42841654,
year = {2026},
author = {Vargas-Albores, F and Garibay-Valdez, E and Guirado-Flores, JSO and Martínez-Córdova, LR and Méndez-Martínez, Y and Medina-Félix, D and Cortés-Jacinto, E and Martínez-Porchas, M},
title = {Beyond abundance: ecological and functional relevance of intestinal fungi in the fish gut microbiome.},
journal = {FEMS microbiology letters},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsle/fnag114},
pmid = {42841654},
issn = {1574-6968},
abstract = {Fish gut microbiome research primarily focuses on bacterial communities, while intestinal fungi are often treated as low-abundance background signals or environmental contaminants. Here, we argue that this asymmetry is no longer justified. Evidence from fish systems demonstrates recurrent gut-associated fungi, context-dependent assembly shaped by the host and environment, and multiple routes by which fungi influence host outcomes despite low read fractions. These include extracellular enzymatic activity, immune modulation, and cross-kingdom ecological interactions. Importantly, low fungal read fractions do not indicate low abundance or activity, as cross-kingdom sequencing comparisons are complicated by technical factors, including differential DNA extraction and host DNA contamination. Integrating fungi into conceptual models of the fish gut microbiome requires moving beyond abundance-based interpretations toward a framework grounded in ecological filtering, functional specialization, and redundancy.},
}

@article {pmid42841659,
year = {2026},
author = {Kovenskiy, A and Mukhanbetzhanov, N and Jarmukhanov, Z and Duisebayeva, A and Morenko, M and Kossumov, A and Chulenbayeva, L and Vinogradova, E and Popov, M and Kushugulova, A and Kozhakmetov, S},
title = {Escherichia coli-derived enterobactin is associated with delayed gut microbiome maturation in infants born to mothers with obesity.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0098626},
doi = {10.1128/msystems.00986-26},
pmid = {42841659},
issn = {2379-5077},
abstract = {Maternal obesity has been increasingly recognized as a factor influencing early-life microbiome development. However, its impact on the infant gut resistome and virulome remains insufficiently characterized. In this prospective longitudinal study, we investigated gut microbiome composition, antibiotic resistance genes (ARGs), and virulence factor profiles in infants born to mothers with obesity and normal weight during the first year of life. Shotgun metagenomic sequencing was performed on maternal and infant fecal samples collected at birth and at 1, 3, 6, and 12 months. Infants born to obese mothers exhibited delayed microbiome maturation characterized by early enrichment of Pseudomonadota, particularly Escherichia coli and Klebsiella pneumoniae, and reduced abundance of Bifidobacterium species. This compositional pattern was accompanied by a significantly higher ARG burden in early life, including enrichment of genes associated with antibiotic inactivation, efflux mechanisms, and β-lactam resistance. Although taxonomic differences between groups were no longer statistically detectable at the 12-month time point, where the sample size was smallest, functional disparities in the resistome persisted. Additionally, infants born to obese mothers demonstrated increased relative abundance of secretory virulence-associated genes and E. coli-derived enterobactin, suggesting enhanced iron-scavenging capacity and competitive potential of Enterobacteriaceae. Together, these findings suggest that maternal obesity is associated with altered early microbial ecological dynamics, promotes resistome expansion, and may delay transition toward a stable Bacteroidota- and Bacillota-dominated microbiome.IMPORTANCEThe first year of life is a critical window for gut microbiome development, during which early microbial disturbances may influence later health. This study shows that maternal obesity is associated not only with altered infant microbial succession but also with functional changes in the infant gut microbiome, including greater antibiotic resistance gene burden and enrichment of virulence-associated traits. The finding of increased Escherichia coli-derived enterobactin suggests that iron-scavenging mechanisms may help Enterobacteriaceae persist during early infancy and may contribute to delayed microbial maturation. By linking maternal obesity with infant microbiome development, resistome expansion, and virulence-related functions, this work provides new insight into how maternal metabolic status may shape early microbial ecology and potential microbiome-associated risks.},
}

@article {pmid42841727,
year = {2026},
author = {Wheeler, M and Bakkeren, E},
title = {Microbiome ecology and antibiotic treatment failure: resistance spread, microbial competition and community engineering.},
journal = {Microbial genomics},
volume = {12},
number = {10},
pages = {},
doi = {10.1099/mgen.0.001856},
pmid = {42841727},
issn = {2057-5858},
mesh = {*Microbiota/drug effects/genetics ; *Anti-Bacterial Agents/therapeutic use/pharmacology ; Gene Transfer, Horizontal ; Humans ; *Drug Resistance, Bacterial/genetics ; *Bacteria/drug effects/genetics ; *Microbial Interactions ; Treatment Failure ; *Drug Resistance, Microbial ; },
abstract = {The failure of antibiotic treatment is a growing concern, driven in large part by the rising incidence of antimicrobial resistance (AMR). Increasing evidence points to the importance of microbial competition in preventing the colonization of disease-causing pathogens and the spread of AMR. Crucially, the pathogens we target with antibiotics do not exist in isolation but instead compete and interact with the microbial communities that colonize the human body, microbiomes. Here, we therefore argue that the key to approaching the challenge of antibiotic treatment failure is understanding the strategies and mechanisms that microbes use to succeed in microbiomes. We discuss how microbial competition influences the colonization of pathogens and the spread of resistance via horizontal gene transfer. We then discuss how microbial competition may be used to synergize with antibiotic treatment or even replace it. Overall, we argue that studying microbial interactions offers a powerful approach to understanding and even mitigating antibiotic treatment failure.},
}

*Microbiota/drug effects/genetics
*Anti-Bacterial Agents/therapeutic use/pharmacology
Gene Transfer, Horizontal
Humans
*Drug Resistance, Bacterial/genetics
*Bacteria/drug effects/genetics
*Microbial Interactions
Treatment Failure
*Drug Resistance, Microbial

@article {pmid42842037,
year = {2026},
author = {Rocha, FI and Borsanelli, AC and de Oliveira, AP and Filho, CVS and Coelho, MRR and Schwab, S and Dos Santos, CM and Teixeira, WG and Cole, J and Howe, A and Dutra, IS and da Conceição Jesus, E},
title = {Soil-plant-animal properties and microbial reassembly distinguish cattle oral disease prevalence across converted Amazon pasture systems.},
journal = {Environmental geochemistry and health},
volume = {48},
number = {16},
pages = {},
pmid = {42842037},
issn = {1573-2983},
support = {AID-OAA-A-11-00012//United States Agency for International Development/ ; },
mesh = {Animals ; Brazil/epidemiology ; Cattle ; *Soil Microbiology ; *Soil/chemistry ; Prevalence ; *Cattle Diseases/epidemiology/microbiology ; Microbiota ; RNA, Ribosomal, 16S/genetics ; Bacteria/genetics/classification/isolation & purification ; *Periodontitis/epidemiology/veterinary/microbiology ; Biofilms ; },
abstract = {Forest-to-pasture conversion can alter soil properties, forage composition, and microbial communities, but whether these changes are associated with bovine periodontitis remains unclear. We compared eight pasture systems in the Western Brazilian Amazon classified by high or low herd-level prevalence of periodontal lesions. Soil physicochemical properties, forage composition, microbial communities in soil, forage, and bovine subgingival biofilms, and the relative abundance of the streptomycin biosynthesis gene strB1 were evaluated. Although the systems had similar deforestation histories, low-prevalence pastures had finer-textured soils, greater soil Cu and forage Zn, and greater representation of Bacilli and Gammaproteobacteria. High-prevalence pastures had sandier soils, greater soil C:N ratios, lower micronutrient availability, and greater representation of Actinobacteria and Bacteroidetes. Microbial communities differed between prevalence classes in all three compartments, with higher alpha and gamma diversity and more compartmentalized co-occurrence networks in high-prevalence systems. Tax4Fun predicted greater representation of pathways related to carbohydrate metabolism and glycan biosynthesis in these systems, while qPCR showed higher strB1 abundance normalized to bacterial 16S rRNA gene abundance in soil and forage. These concurrent differences in soil properties, forage composition, and microbial communities were associated with bovine periodontitis prevalence. They do not demonstrate microbial transfer or causality but support the hypothesis that soil and forage conditions may influence environmental exposures related to oral microbiome dysbiosis.},
}

Animals
Brazil/epidemiology
Cattle
*Soil Microbiology
*Soil/chemistry
Prevalence
*Cattle Diseases/epidemiology/microbiology
Microbiota
RNA, Ribosomal, 16S/genetics
Bacteria/genetics/classification/isolation & purification
*Periodontitis/epidemiology/veterinary/microbiology
Biofilms

@article {pmid42842161,
year = {2026},
author = {Jeyavelkumaran, R and Saravanan, MD and Keerthivasan, N},
title = {Next-generation probiotic platforms for food nutrition: integrating functional foods with advanced delivery technologies.},
journal = {Folia microbiologica},
volume = {},
number = {},
pages = {},
pmid = {42842161},
issn = {1874-9356},
abstract = {Functional microbial systems have emerged as promising components of next-generation food biotechnology due to their ability to improve gut microbiota balance, immune regulation, and metabolic health. However, conventional probiotic formulations often exhibit poor stability and limited gastrointestinal survivability during food processing and storage. This review discusses recent advances in probiotic delivery technologies, including encapsulation, nanoencapsulation, hydrogel systems, edible films, biofilms, and smart packaging approaches for enhanced microbial protection and controlled release. The roles of dairy-based, non-dairy, synbiotic, and fermented food matrices in supporting probiotic functionality are critically evaluated. Emerging trends such as AI-assisted food formulation, 3D food printing, precision nutrition, and sustainable packaging technologies are also highlighted. Despite significant technological progress, challenges related to scalability, regulatory standardization, and long-term microbial stability remain. Overall, advanced probiotic platforms offer substantial potential for developing precision-oriented, microbiome-driven functional food systems.},
}

@article {pmid42842295,
year = {2026},
author = {Lin, WY and Chang, YJ and Gill, T and Ching, J and Anderson, D and Creek, DJ and Ayub, Q and Rahman, S and Chong, CW},
title = {Association of microbial pathways predicted/inferred using 16S and shotgun metagenome with faecal metabolite abundances.},
journal = {Microbial genomics},
volume = {12},
number = {10},
pages = {},
doi = {10.1099/mgen.0.001855},
pmid = {42842295},
issn = {2057-5858},
mesh = {*Feces/microbiology/chemistry ; *RNA, Ribosomal, 16S/genetics ; *Metagenome ; *Metagenomics/methods ; Humans ; Metabolic Networks and Pathways/genetics ; *Gastrointestinal Microbiome/genetics ; Shotgun Sequencing ; *Bacteria/genetics/classification/metabolism ; Metabolome ; Liquid Chromatography-Mass Spectrometry ; },
abstract = {The gut microbiome is an essential metabolic organ influencing host health through metabolite production. While metabolite production levels can be directly measured by gas or liquid chromatography, they are commonly inferred from the abundance of metagenomic functional pathways. To evaluate the accuracy of these inferences, we established a single, manually curated metabolite-pathway/enzyme mapping list as a standardized biological reference. We then compared liquid chromatography-mass spectrometry (LC-MS)-based faecal metabolites with functional pathways/enzymes inferred from four approaches: 16S rRNA gene amplicons, reference-based shotgun, de novo assembly-based contigs and de novo assembly-based metagenome-assembled genomes (MAGs). Our results demonstrate that predictive accuracy is strongly metabolite-specific and method-dependent rather than a uniform characteristic of metagenomic data. While 16S (9.9%), ref-shotgun (14.2%) and de novo-contigs (5.5%) yielded only a small fraction of well-predicted metabolites, the de novo-MAGs approach significantly outperformed other approaches, achieving a 36.9% well-predicted rate for mapped metabolites. Notably, this approach provided the most robust functional-metabolite associations for indicators of gut health. In conclusion, while microbial functional potential does not always mirror metabolic reality, high-quality genomic binning via MAGs offers a significantly more robust framework for selective metabolite prediction.},
}

*Feces/microbiology/chemistry
*RNA, Ribosomal, 16S/genetics
*Metagenome
*Metagenomics/methods
Humans
Metabolic Networks and Pathways/genetics
*Gastrointestinal Microbiome/genetics
Shotgun Sequencing
*Bacteria/genetics/classification/metabolism
Metabolome
Liquid Chromatography-Mass Spectrometry

@article {pmid42842318,
year = {2026},
author = {Yu, B and Wang, C and Zhou, N and Yin, M},
title = {From Bacterial Infection to Emerging Microbiome Signals in Prostatitis: A Bibliometric Analysis, 1985-2026.},
journal = {American journal of men's health},
volume = {20},
number = {5},
pages = {15579883261495668},
doi = {10.1177/15579883261495668},
pmid = {42842318},
issn = {1557-9891},
mesh = {*Prostatitis/microbiology ; Humans ; Male ; *Bibliometrics ; *Microbiota ; *Bacterial Infections/microbiology ; },
abstract = {Prostatitis research has expanded from conventional bacterial infection models to microbiome approaches. This expansion has not resolved uncertainty about the scale of the newer literature or the visibility of clinical and methodological information in indexed fields. To quantify this expansion, this bibliometric analysis mapped publication patterns and assessed prespecified indexed-field indicators in the modern microbiome, gut microbiome, and Mendelian randomization (MR) subcorpora. The Web of Science Core Collection was searched on June 2, 2026. Eligible records were English-language Articles and Reviews with prostatitis or chronic pelvic pain syndrome in the title. The microbiology criterion required a related concept in the title, abstract, or author keywords. The analysis covered annual publication output, country-level publication output and co-authorship, cited-reference frequencies, author-keyword co-occurrence, and prespecified term-defined subcorpora. Among 755 eligible records, modern microbiome terms occurred in 71 (9.40%), gut microbiome terms in 40 (5.30%), and MR in 5 (0.66%). China and the United States led country-level publication output, whereas the strongest bilateral co-authorship links were Belgium-Italy and Canada-United States. Within the modern microbiome subcorpus, 46 records (64.8%) contained terms indicating a clinical phenotype, 46 (64.8%) named a specimen, and 38 (53.5%) mentioned a molecular microbiome method. Terms indicating a longitudinal or interventional design appeared in 16 records (22.5%), while no terms indicating independent or external validation appeared in the indexed fields. Microbiome work remains a recent but still small branch of prostatitis microbiology, and the findings support longitudinal designs, standardized sampling, and independent validation for clinically interpretable research.},
}

*Prostatitis/microbiology
Humans
Male
*Bibliometrics
*Microbiota
*Bacterial Infections/microbiology

@article {pmid42832260,
year = {2026},
author = {Song, X and Jia, S and Chen, L and Cao, C and Chen, Z and Hang, L and Jiang, H and Chen, Z},
title = {Deep-sea Microbial Dataset of the Antarctic Ocean (dsMDAO): A high-resolution deep-sea microbial dataset of the Antarctic Ocean reveals potential for taxonomic and functional diversity.},
journal = {Microbial genomics},
volume = {12},
number = {10},
pages = {},
pmid = {42832260},
issn = {2057-5858},
mesh = {Antarctic Regions ; *Seawater/microbiology ; *Bacteria/genetics/classification/isolation & purification/metabolism ; *Archaea/genetics/classification/isolation & purification ; Metagenome ; Phylogeny ; *Microbiota/genetics ; Geologic Sediments/microbiology ; Oceans and Seas ; Metagenomics ; Biodiversity ; },
abstract = {Antarctic deep-sea ecosystems harboured unique and metabolically versatile micro-organisms that sustained key biogeochemical processes under extreme polar conditions. However, the genomic diversity and ecological functions of these sedimentary or deep-sea microbial communities remained largely unexplored. Here, we constructed a comprehensive deep-sea microbial dataset of the Antarctic Ocean (dsMDAO) by integrating three newly sequenced Prydz Bay sediment metagenomes with 22 publicly available datasets (9 seawater and 13 sediment samples), spanning water depths of ~300-3500 m. Genome binning yielded 186 metagenome-assembled genomes spanning 19 phyla, including 175 bacteria and 11 archaea, a substantial proportion of which represent previously uncharacterized species. Meanwhile, reads mapping with the available standard Kraken2 database (k2_standard) enabled the expansion of species richness of the dsMDAO database. Furthermore, functional annotation revealed diverse metabolic and ecological potentials, including carbon, nitrogen and sulphur cycling, as well as secondary metabolite biosynthesis, virulence-associated defence and cold-adaptation mechanisms. Sediment microbiomes exhibited higher phylogenetic and functional diversity, enriched in Thaumarchaeota and Chloroflexi, whereas seawater communities were dominated by Proteobacteria with more competitive biosynthetic and interaction potentials. Co-occurrence analyses further indicated complex and competitive networks in seawater versus modular and cooperative assemblages in sediments, reflecting distinct ecological strategies. Collectively, dsMDAO provides the first genome-resolved dataset of Antarctic deep-sea microbiota, revealing the hidden taxonomic and functional diversity that underpins ecosystem resilience in polar oceans. This resource lays a foundation for future ecological, evolutionary and biotechnological exploration of Antarctic microbial dark matter.},
}

Antarctic Regions
*Seawater/microbiology
*Bacteria/genetics/classification/isolation & purification/metabolism
*Archaea/genetics/classification/isolation & purification
Metagenome
Phylogeny
*Microbiota/genetics
Geologic Sediments/microbiology
Oceans and Seas
Metagenomics
Biodiversity

@article {pmid42832270,
year = {2026},
author = {Almatrafi, R and Alqurainy, N and Hakami, M and Ajina, R and Alrabiah, S and Arafah, AM and Alotibi, RS and Aldriwesh, MG},
title = {Gut microbiome and healthy ageing: a systematic review of literature.},
journal = {Microbiology (Reading, England)},
volume = {172},
number = {10},
pages = {},
doi = {10.1099/mic.0.001779},
pmid = {42832270},
issn = {1465-2080},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Healthy Aging/physiology ; *Bacteria/classification/genetics/isolation & purification ; Metagenomics ; RNA, Ribosomal, 16S/genetics ; Aged ; Aging ; Centenarians ; Aged, 80 and over ; Longevity ; },
abstract = {The gut microbiome undergoes compositional and functional changes with ageing. However, microbial signatures specifically associated with healthy ageing, independent of age-related diseases, remain poorly defined. This systematic review aimed to identify compositional and functional features of the gut microbiome associated with healthy ageing. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, a systematic search was conducted using PubMed, Web of Science and ScienceDirect for studies published up to January 2026. The search strategy focused on gut microbiome, ageing and healthy terms. Risk of bias was assessed using the Newcastle-Ottawa Scale. Gut microbiome composition was reviewed across five predefined age groups, while the functional pathways were reviewed for older adults and centenarians. The included studies represented several regions, including recognized longevity hotspots, although geographic representation remained limited. Most studies used 16S rRNA gene sequencing (n=24; 58.5%), followed by shotgun metagenomics (n=13; 31.7%), both (n=3; 7.4%) or metaproteomics (n=1; 2.4%). Enrichment of specific taxa such as Akkermansia, Alistipes and Parabacteroides was consistently reported in centenarians, alongside distinct patterns in older adults and long-lived individuals. Functional profiling suggested differences in pathways related to amino acid catabolism, vitamin biosynthesis and pathways potentially linked to immune modulation, inflammatory processes and gut barrier support. This review provides the first structured synthesis of gut microbiome signatures associated with healthy ageing across the lifespan, highlighting consistent functional traits and the need for a wider geographic representation in future research. It supports standardized, multi-omics framework to identify robust biomarkers and potential microbiome-based interventions for promoting healthy ageing.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Healthy Aging/physiology
*Bacteria/classification/genetics/isolation & purification
Metagenomics
RNA, Ribosomal, 16S/genetics
Aged
Aging
Centenarians
Aged, 80 and over
Longevity

@article {pmid42832303,
year = {2026},
author = {Bosch, P and Lackner, A and Dreo, B and Fessler, J and Moazedi-Fürst, F and Husic, R and Séneca, J and Haidmayer, A and Stadlbauer, V and Muralikrishnan, AS and Thiel, J and Stradner, M},
title = {Efficacy and safety of probiotic supplementation in psoriatic arthritis - a randomized controlled trial.},
journal = {Rheumatology (Oxford, England)},
volume = {},
number = {},
pages = {},
doi = {10.1093/rheumatology/keag547},
pmid = {42832303},
issn = {1462-0332},
abstract = {OBJECTIVES: To evaluate the clinical efficacy and safety of a multispecies probiotic in patients with psoriatic arthritis (PsA) in moderate disease activity.

METHODS: In this single-centre, randomized, double-blind, placebo-controlled trial (RCT), 66 PsA patients with moderate disease activity (Psoriatic Arthritis Disease Activity Score [PASDAS] >3.2 to < 5.4) on stable immunomodulatory therapy were randomized 1:1 to receive either a multispecies (Lactobacillus, Bifidobacterium) probiotic or placebo for 12 weeks. The primary outcome was treatment response at week 12, defined as achieving low disease activity or remission (PASDAS ≤3.2) without treatment change. Secondary outcomes included gut permeability markers, immune cell and microbiome composition. Analyses were conducted per a modified intention-to-treat (only complete cases for primary outcome), with sensitivity analyses using multiple imputation, per-protocol datasets, and qPCR-based detection of the probiotic strains in stool (adherence).

RESULTS: Fifty-six participants were included in the main analysis. Thirteen (43%) participants in the probiotic group and 17 (65%) in the placebo group achieved the primary outcome (p = 0.167). The corresponding odds ratio was 0.4 (95% CI 0.13 to 1.18). Patient-reported pain and global assessment were the main PASDAS components improving over time, with no between-group differences. No differences were observed in secondary clinical outcomes, gut permeability markers (zonulin, calprotectin, alpha-1-antitrypsin), immune cell profiles, or stool microbiome composition between groups at week 12. No serious adverse events related to the study product were reported.

CONCLUSION: In this first RCT investigating probiotic supplementation in PsA, probiotic treatment did not show superiority over placebo in achieving treatment response, or altering gut microbiome, or permeability.},
}

@article {pmid42832344,
year = {2026},
author = {Simm, NM and Williams, GM and Fowler, S and Barlow, K and Carter, B and Talley, NJ and Keely, S and Duncanson, K and Hoedt, EC},
title = {Assessing diet-microbiome associations with linear models: variability across human studies.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2740905},
doi = {10.1080/19490976.2026.2740905},
pmid = {42832344},
issn = {1949-0984},
mesh = {Humans ; *Diet ; *Gastrointestinal Microbiome ; },
abstract = {Understanding and identifying relationships between dietary intake and the gastrointestinal microbiome can provide critical information for optimization of human health. However, methodological approaches largely differ and can impact research findings. Here we outline differences in reported diet-microbiome associations from a range of studies utilizing comparable statistical methods. From a subset of 25 studies using comparable methodology, only 3% of reported diet-microbe associations were common across more than one study. As such, we emphasize the inconsistencies of findings within the literature and wider implications of these differences.},
}

Humans
*Diet
*Gastrointestinal Microbiome

@article {pmid42832417,
year = {2026},
author = {L'Heureux, JE and Roelands, B and Wylie, L and Meeusen, R and Jones, AM and Vanhatalo, A},
title = {Oral microbiome signatures of ageing and cognitive function across distinct geographical cohorts.},
journal = {PloS one},
volume = {21},
number = {10},
pages = {e0359559},
pmid = {42832417},
issn = {1932-6203},
mesh = {Humans ; *Cognition/physiology ; *Aging/physiology ; *Microbiota ; Female ; Aged ; Male ; Saliva/microbiology ; RNA, Ribosomal, 16S/genetics ; *Mouth/microbiology ; United Kingdom ; Adult ; Belgium ; Nitrates/blood/metabolism ; Middle Aged ; Cohort Studies ; Young Adult ; Nitrites/blood ; },
abstract = {Declining cognitive function in older adults may be linked to reduced nitric oxide (NO) bioavailability, which is supported by oral nitrate-reducing bacteria. Oral microbiome community structure varies geographically, complicating understanding of microbiome-cognition relationships across populations. This study aimed to identify consistent associations between the oral microbiome and cognitive function across two geographically distinct cohorts from the UK and Belgium, and to explore age-related differences in NO biomarkers, cognitive performance, and microbiome composition using 16S rRNA sequencing. Sixty healthy participants (15 young and 15 older adults per location) completed a cognitive test battery, blood pressure measurements, plasma and saliva collection for nitrate and nitrite analysis, and a tongue swab for oral microbiome assessment. Despite geographical differences in oral microbiome composition (PERMANOVA P = 0.04), age-related microbial shifts were consistent across geographic cohorts, including enrichment of Treponema and Tannerella in older adults. Nitrate-reducing taxa such as Haemophilus parainfluenzae and Neisseria flavescens were consistently associated with cognitive performance measures in both cohorts (P < 0.05). In the UK, higher plasma [nitrate] was associated with improved Digit Symbol Substitution Test (DSST) accuracy (β = 19.2, P < 0.01) and reaction times (β = -3444 ms, P < 0.05), but poorer Emotion Recognition Task (ERT) accuracy (β = -5.219, P < 0.05), while UK plasma [nitrite] was associated with slower Balloon Analog Risk Task (BART; β = 2277 ms, P < 0.001) and ERT (β = 8577 ms, P < 0.05) reaction times. In Belgium, saliva [nitrate] was associated with slower Visual Object Learning Test (VOLT) reaction times (β = 202 ms, P < 0.05), while in the UK, saliva [nitrite] correlated with slower BART (β = 111 ms, P < 0.05) and LOT (β = 1888 ms, P < 0.01). Overall, geography emerged as a major driver of oral microbiome variation, yet consistent age-related microbial and cognitive associations were preserved across populations. These findings emphasise the need to account for geographic context in microbiome-health research. A better understanding of oral microbial patterns may help inform future mechanistic or interventional studies to promote cognitive health in ageing.},
}

Humans
*Cognition/physiology
*Aging/physiology
*Microbiota
Female
Aged
Male
Saliva/microbiology
RNA, Ribosomal, 16S/genetics
*Mouth/microbiology
United Kingdom
Adult
Belgium
Nitrates/blood/metabolism
Middle Aged
Cohort Studies
Young Adult
Nitrites/blood

@article {pmid42832459,
year = {2026},
author = {Ajebli, M and Hebi, M and Ousaaid, D and Akdad, M and Mankour, Z and Khouya, T and Moukafih, B and El Kartouti, A and Eddouks, M},
title = {Apigenin and Hypertension: A Review of Natural Sources, Pharmacodynamic and Pharmacokinetic Evidence.},
journal = {Pharmacology},
volume = {},
number = {},
pages = {1},
doi = {10.1159/pha/aejag005},
pmid = {42832459},
issn = {1423-0313},
abstract = {PURPOSE: This review aimed to synthesize recent evidence on the pharmacological effects of APG in the management of hypertension.

METHODS: A comprehensive literature search was conducted using PubMed, Scopus, Web of Science, and Google Scholar.

RESULTS: Pharmacokinetic studies reveal that APG exhibits poor oral bioavailability due to low solubility and extensive metabolism yet demonstrates wide tissue distribution and neuroprotective potential. It interacts with drug-metabolizing enzymes and transporters, influencing the pharmacokinetics of co-administered agents while maintaining a favorable safety profile at dietary levels. Preclinical evidence shows that APG lowers blood pressure by promoting vasodilation through TRPV4/NO pathways, attenuating oxidative stress and inflammation, and regulating genetic signaling to prevent vascular and cardiac remodeling. Toxicity studies confirm safety up to 5000 mg/kg, while additional findings highlight its beneficial modulation of gut microbiota.

CONCLUSION: APG emerges as a promising supplementary compound for hypertension management, combining vascular, molecular, and microbiome-mediated mechanisms with a strong safety margin.},
}

@article {pmid42832478,
year = {2026},
author = {Calzada, D and Martín-López, L and Carnés, J},
title = {Genetic and microbiomics approaches allow the monitoring of the growth of Dermatophagoides pteronyssinus cultures and their environmental influences.},
journal = {PloS one},
volume = {21},
number = {10},
pages = {e0359777},
pmid = {42832478},
issn = {1932-6203},
mesh = {Animals ; *Dermatophagoides pteronyssinus/growth & development/microbiology/genetics ; *Microbiota ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Dermatophagoides pteronyssinus is cultured in industrial facilities to produce allergen extracts for allergy diagnosis and therapeutic treatment. In these facilities, mite growth and production should be monitored, and exhaustive quality control is mandatory to harvest mites, reach optimal expansion, and avoid potential microbial contamination. In this study, we explored genetic approaches to monitor the growth of five independent D. pteronyssinus cultures. Microbiological studies were performed to characterise the evolution of microbial communities during culture. Finally, we designed a qRT-PCR application to quantify mite populations in the cultures. Our microbiome studies revealed the presence of non-pathogenic bacteria and the absence of Gram-negative bacteria. Despite the variability in microbiome genera at the beginning of the five cultures, the microbiome composition tended to be more homogeneous among the culture batches as mite growth progressed. Specifically, Staphylococcus sp., Virgibacillus sp., and Malassezia sp. appeared to be the most significant taxa involved in culture progression. In summary, we developed a specific method for quantifying and monitoring mite cultures, which could be used to establish an objective method for harvesting mites to manufacture standardised allergen extracts. Additionally, we provide a comprehensive description of the relationship between mites and their symbiotic microorganisms.},
}

Animals
*Dermatophagoides pteronyssinus/growth & development/microbiology/genetics
*Microbiota
RNA, Ribosomal, 16S/genetics

@article {pmid42832513,
year = {2026},
author = {Yuan, X and Arany, Á and Formanek, A and Moreau, Y and Lähdesmäki, H and Vatanen, T},
title = {LGTM: Gaussian process modulated neural topic modeling for longitudinal microbiome.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2741488},
doi = {10.1080/19490976.2026.2741488},
pmid = {42832513},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome ; Longitudinal Studies ; *Bacteria/classification/genetics/isolation & purification ; Models, Statistical ; Metagenome ; Normal Distribution ; },
abstract = {Longitudinal microbiome data are key to understanding the dynamics of microbial communities and their relationships with the host and environment. However, analysis of such data is challenging due to high dimensionality, compositionality, irregular sampling and temporal dependencies on external covariates. Existing analytical approaches typically address only subsets of these challenges, limiting their ability to yield biologically interpretable insights. We introduce LGTM, a probabilistic modeling framework that combines flexible non-linear longitudinal modeling with interpretable topic-based representations of the microbiome. LGTM simultaneously identifies microbial co-abundance patterns ("topics") and models how their proportions change over time and in relation to host and environmental covariates. Using multiple longitudinal human gut microbiome datasets, we demonstrate that LGTM identifies diverse microbial topics whose major patterns are reproducible across runs, while achieving competitive performance in imputation and forecasting tasks. A key strength of the framework is its interpretability: LGTM yields microbial topics with biologically interpretable taxonomic compositions and directly quantifies associations between covariates and microbial dynamics. LGTM is available at https://github.com/yuanx749/lgtm.},
}

Humans
*Gastrointestinal Microbiome
Longitudinal Studies
*Bacteria/classification/genetics/isolation & purification
Models, Statistical
Metagenome
Normal Distribution

@article {pmid42832545,
year = {2026},
author = {Souza, AK and Giroux, A and Zangirolamo, AF and Droher, RG and Bonato, FGC and Alfieri, A and Zamberlam, G and Seneda, MM and Costa, M},
title = {The impact of the estrous cycle on the vaginal microbiota of dairy cows.},
journal = {PloS one},
volume = {21},
number = {10},
pages = {e0359551},
pmid = {42832545},
issn = {1932-6203},
mesh = {Animals ; Female ; Cattle ; *Vagina/microbiology ; *Estrous Cycle/physiology ; *Microbiota/genetics ; Pregnancy ; RNA, Ribosomal, 16S/genetics ; },
abstract = {The present study investigated the vaginal microbiota of dairy cows throughout the estrous cycle and early gestation, under natural physiological conditions and without hormonal manipulation. Vaginal swabs were collected at estrus (D0), metestrus (D3), diestrus (D15), and Day 19 post-insemination (representing proestrus for non-pregnant cows or early gestation for pregnant cows). Pregnancy diagnosis was performed on day 31 post-insemination. Microbial characterization was performed using 16S rRNA gene sequencing, followed by analyses of alpha- and beta-diversity, community composition, and differential abundance. Overall, the vaginal microbiota exhibited high inter-individual variability and only subtle shifts across reproductive phases. Beta diversity analysis revealed modest but significant compositional rearrangements between estrus vs. proestrus (strictly within the non-pregnant cohort) and estrus vs. diestrus. Differential abundance testing identified two taxa enriched during pregnancy (Muribaculum and Hoministercoradaptatus), indicating potential microbial biomarkers associated with the gestational environment. These findings demonstrate that, in naturally cycling cows, physiological hormonal oscillations induce only mild microbial changes, whereas individual factors appear to play a dominant role in shaping the vaginal community. The work contributes to defining baseline microbial patterns in non-manipulated animals and highlights the importance of distinguishing natural variation from hormonally induced effects in reproductive microbiome research.},
}

Animals
Female
Cattle
*Vagina/microbiology
*Estrous Cycle/physiology
*Microbiota/genetics
Pregnancy
RNA, Ribosomal, 16S/genetics

@article {pmid42832647,
year = {2026},
author = {Hong, S and Kim, KW and Im, Y and Jang, J and Cheon, DH and Lee, EK and Han, YM and Park, JW and Lee, HJ and Park, H and Jo, SJ and Kim, D and Kang, HW and Im, JP and Kim, ES and Kim, JW and Kim, BG and Kim, JS and Koh, SJ},
title = {Enterotype-based stratification identifies clinically distinct microbial subtypes in inflammatory bowel disease.},
journal = {Inflammatory bowel diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/ibd/izag176},
pmid = {42832647},
issn = {1536-4844},
support = {//National Research Foundation of Korea/ ; RS-2023-00227939//Korean government (MSIT)/ ; NRF-2022R1F1A1076019//Korean government (MSIT)/ ; 26-2021-0060//Seoul National University Hospital Research Fund/ ; 04-2024-0370//Seoul National University Hospital Research Fund/ ; //Jeonbuk National University (2022)/ ; 2024-5//Korean Association for the Study of Intestinal Diseases/ ; 04-2025-0006//Seoul Metropolitan Government Seoul National University Boramae Medical Center/ ; },
abstract = {BACKGROUND: Inflammatory bowel diseases (IBDs) are heterogeneous disorders in which gut microbial dysbiosis may influence disease activity and clinical outcomes. However, it remains unclear whether microbiome-based stratification identifies clinically relevant IBD subtypes.

METHODS: We profiled the gut microbiome of a cohort comprising patients with IBD (n = 260), at-risk individuals (n = 166), and healthy control individuals (n = 57) using 16S rRNA gene amplicon sequencing. Unsupervised clustering was used to define gut microbial enterotypes. Associations with clinical characteristics and outcomes, including fecal calprotectin levels and medication step-up, were evaluated. Statistical and machine learning approaches were applied to identify enterotype-specific microbial signatures.

RESULTS: Four enterotypes were identified and labeled according to their most discriminative genera: Faecalibacterium and Blautia, Prevotella, Phocaeicola, and Bifidobacterium with reduced Faecalibacterium (Bif + Faec-low). Faecalibacterium and Blautia and Prevotella were enriched in healthy control individuals, Phocaeicola was enriched in at-risk individuals, and Bif + Faec-low was enriched in patients with IBD. The Bif + Faec-low enterotype was associated with lower body mass index, higher fecal calprotectin levels, and an increased risk of medication step-up (hazard ratio, 1.71; 95% confidence interval, 1.10-2.66). Microbial composition and network analyses identified distinct enterotype-specific taxa and hub genera, suggesting functional divergence among enterotypes.

CONCLUSIONS: Gut microbial enterotypes are associated with distinct clinical phenotypes and treatment escalation in IBD, and exhibit enterotype-specific microbial community structures and alterations across disease states. Enterotype-based stratification may provide a clinically relevant framework for assessing risk assessment and guiding personalized disease management.},
}

@article {pmid42832926,
year = {2026},
author = {Gu, QY and Wu, XH and Zhang, SY and Jiang, L and Song, LL and Li, XY and Sun, K and Zhang, W and Dai, CC},
title = {Root exudate-mediated interspecific interactions reshape the rhizosphere microbiome and promote the accumulation of bioactive compounds in Pinellia ternata.},
journal = {Microbiological research},
volume = {314},
number = {},
pages = {128746},
doi = {10.1016/j.micres.2026.128746},
pmid = {42832926},
issn = {1618-0623},
abstract = {Plant recognition and responses to neighbors are key mechanisms that regulate interspecific interactions. Although aboveground signaling via volatile organic compounds has received increasing attention, the role of soil-derived signals in belowground interactions remains poorly understood. In this study, a peanut (Arachis hypogaea L.)-Pinellia ternata (Thunb.) Makino intercropping system was used to investigate how root exudates regulate the recruitment of rhizosphere microbes to neighboring plants, with the aim of providing a theoretical basis for understanding how intercropping promotes plant growth. Intercropping with peanut significantly altered the rhizosphere microbial community structure of P. ternata and markedly enhanced the colonization of Sphingomonas spp. Inoculation experiments revealed that Sphingomonas sp. Y6 significantly increased both plant biomass and bioactive compounds of P. ternata. A belowground segregation experiment supported the role of root exudates as important mediators of interspecific interactions between peanut and P. ternata. Peanut-derived L-proline promoted the recruitment of Sphingomonas sp. Y6, increasing its rhizosphere colonization by 1.96-fold in the split-root experiment. Metabolomic profiling further indicated that exposure to peanut-derived signals was associated with increased accumulation of nucleoside compounds in P. ternata root exudates, which enhanced chemotaxis and biofilm formation by Sphingomonas sp. Y6. Overall, these findings identify a potentially important mechanism linking interspecific plant interactions, metabolite-mediated changes in root exudates, and rhizosphere microbial recruitment, ultimately contributing to increased bioactive compound accumulation in P. ternata, and provide new insights into optimizing plant-microbe interactions to enhance the accumulation of bioactive compounds in medicinal plants.},
}

@article {pmid42833212,
year = {2026},
author = {Vasquez, KS and Wong, DPGH and Kotaka, K and McKeithen-Mead, S and Pedro, MF and Brian Yu, F and Jain, S and Meng, X and Higginbottom, SK and DeFelice, BC and Neff, N and Bhatt, A and Tropini, C and Xavier, KB and Sonnenburg, JL and Good, BH and Huang, KC},
title = {Within-host evolution and transmission of a human gut symbiont across ecological scales.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.09.002},
pmid = {42833212},
issn = {1934-6069},
abstract = {Gut bacteria rapidly evolve in vivo, but their long-term success requires dispersal across hosts. Here, we quantify this interplay by tracking ∼70,000 genomically barcoded lineages of the commensal Bacteroides thetaiotaomicron (Bt) among co-housed mice. Adaptive mutations rapidly spread between hosts, overcoming colonization resistance imposed by resident Bt strains. Daily transmission rates varied >10-fold across hosts, but shared selection pressures drove predictable engraftment of specific lineages. Spatially resolved sampling within hosts revealed emergent preferences among adaptive lineages. The addition of a highly diverse community shifted the adaptive landscape without slowing the rate of evolution and reduced transmission while allowing specific mutants to engraft. Whole-genome sequencing uncovered diverse modes of adaptation involving complex carbohydrate metabolism. In vitro evolution across 29 carbon sources revealed variable overlap with in vivo selection pressures, potentially reflecting synergistic and antagonistic pleiotropies. These results illustrate how high-resolution lineage tracking enables quantification of commensal evolution across ecological scales.},
}

@article {pmid42833252,
year = {2026},
author = {van Vorstenbosch, R and Esenkova, EE and Jonkers, DMAE and Elizalde Vilalta, M and de Graaf, MCG and Keszthelyi, D and Pachen, D and van Schooten, FJJ and Mujagic, Z and Smolinska, A},
title = {Investigating the presence of microbiota-based phenotypes in Irritable Bowel Syndrome.},
journal = {Journal of breath research},
volume = {},
number = {},
pages = {},
doi = {10.1088/1752-7163/aeb043},
pmid = {42833252},
issn = {1752-7163},
abstract = {Irritable Bowel Syndrome (IBS) is heterogenous disorder of gut-brain interaction, with a key role for the dysregulated host-gut microbiota interplay. IBS subtyping is based only on symptoms of bowel habits, reflecting limited insight into underlying biological mechanisms. Aims: This study aimed to define microbiota-based IBS phenotypes and to compare these to traditional stool-based subtyping. Methods: The study utilised data from the Maastricht IBS cohort. Gut microbiota composition was analysed using shotgun metagenomic sequencing. Faecal volatile organic compounds (VOCs) were measured by gas chromatography mass spectrometry. Dietary intake and gastrointestinal and mental health symptoms were assessed using a food frequency questionnaire, the Dutch Healthy Diet-15 index, the Gastrointestinal Symptom Rating Scale, and Hospital Anxiety and Depression scores, respectively. Machine-learning approaches were applied to identify microbiota-based phenotypical clusters, which were compared with established Rome III subtypes, and associated with faecal VOCs, gastrointestinal symptom severity, diet and mental health. Results: 178 IBS patients and 134 healthy controls were included. Gut microbiota composition distinguished IBS patients from healthy controls with an AUCROC 0·8. This discriminatory profile was not associated with Rome III subtypes, while statistically significant associations were found with faecal VOCs profiles (i.e. R=0·67, p=4·46e-4) and symptom severity scores of abdominal pain (p=0·05), reflux (p=0·03), and diarrhoea (p=0·01) and depression (p<0·001). Dietary associations varied across clusters. Conclusion: These results suggest that gut microbiota profiling might provide a basis to define relevant IBS endotypes. Further exploration and validation efforts into this direction are needed using longitudinal studies to refine IBS patient stratification ultimately. .},
}

@article {pmid42833300,
year = {2026},
author = {Gan, C and Xiang, J and Liu, Y and Nie, S and Hu, Q and Yi, L and Liu, Y and Guo, X and Zou, J and Tang, Y and Cui, J and Xie, J},
title = {Nucleoside antitumor drugs: From molecular mechanisms and adaptive resistance to clinical translation.},
journal = {Biochemical pharmacology},
volume = {},
number = {},
pages = {118501},
doi = {10.1016/j.bcp.2026.118501},
pmid = {42833300},
issn = {1873-2968},
abstract = {Nucleoside-based anticancer drugs are still needed to treat solid tumours and blood cancers, but due to systemic toxicity and the emergence of resistance, they have performed poorly in clinical practice. These agents inhibit deoxyribonucleic acid (DNA) synthesis, disrupt ribonucleic acid (RNA) metabolism, or deplete nucleotide pools in the past. However, a large number of studies have also found that the pharmacological effects of these agents include replication stress, epigenetic modification, viral mimicry and immunogenic cell death , as well as direct damage to nucleic acids. At the same time, resistance to nucleoside-based therapy is now known to be a system-level adaptation phenomenon. This resistance network includes impaired nucleoside transport, altered kinase-dependent activation, increased catabolism by enzymes such as cytidine deaminase (CDA) and sterile alpha motif and histidine-aspartate domain-containing protein 1 (SAMHD1), compensatory DNA damage repair, immune suppression, and microbiome-mediated drug inactivation in the tumour ecosystem. We will introduce the molecular mechanisms and multi-level resistance networks of nucleoside-type anticancer drugs in this paper, and based on the obtained results, put forward new therapeutic strategies. Particular emphasis is placed on phosphoramidate prodrug (ProTide) technology, multivalent oligonucleotide prodrugs, nanocarrier-mediated delivery and mechanism-guided combination therapy. We will also introduce the new applications of antibody-based delivery systems for tumour-selective delivery. According to the tumour's biology and drug-metabolism properties, delivery science and biomarker-guided therapy can be employed to convert nucleoside-based therapy into a form of personalised medicine that overcomes adaptive resistance.},
}

@article {pmid42833450,
year = {2026},
author = {Hao, H and Tong, Z and Wang, Q and Xiao, T and Zhang, Y and Yue, Y and Zhao, Z and Zhang, J and Chen, H},
title = {Flavonoid-associated microbial defense and Cellvibrio sp. C74 pretreatment collectively enhance straw degradation by Stropharia rugosoannulata.},
journal = {Bioresource technology},
volume = {},
number = {},
pages = {136013},
doi = {10.1016/j.biortech.2026.136013},
pmid = {42833450},
issn = {1873-2976},
abstract = {Stropharia rugosoannulata efficiently utilizes straw in natural habitats, yet how it simultaneously defends against competing environmental microorganisms and degrades lignocellulose remains unclear. Here, transcriptomic, metabolomic, and microbiome analyses were integrated with flavonoid antibacterial assays and bacterial pretreatment experiments to characterize fungus-bacterium interactions during straw degradation. The flavonoid biosynthesis-related genes chi, fns, and fls were significantly upregulated during degradation, and the total flavonoid content reached 101.06 μg/g dry weight at the end of the process. Flavonoid accumulation was also significantly associated with specific bacterial taxa. At concentrations ≥ 25 μg/mL, both exogenous flavone and crude endogenous mycelial flavonoid extracts significantly inhibited Sphingomonas sp. S125, Cellvibrio sp. C74, and Sphingobacterium sp. S85, supporting a role for accumulated flavonoids in microbial defense. Conversely, pretreatment with Cellvibrio sp. C74 disrupted the straw surface and increased lignocellulolytic enzyme activities during subsequent fungal degradation, resulting in a 24.39 %-26.97 % increase in degradation efficiency relative to the sterilized-straw control. These findings extend the mechanistic understanding of straw degradation from fungal enzyme systems to fungus-bacterium interactions, revealing a dual mode of flavonoid-associated defense and Cellvibrio sp. C74-assisted degradation. Moreover, Cellvibrio sp. C74 represents a promising biological pretreatment agent for efficient straw bioconversion.},
}

@article {pmid42833452,
year = {2026},
author = {Julià, AL and Heintze, Q and Garcia, J and Gonzalez-Flo, E},
title = {Putative functional redundancy in cyanobacterial microbiomes allows stable bioplastic production despite shifts in dominant populations.},
journal = {Bioresource technology},
volume = {},
number = {},
pages = {136012},
doi = {10.1016/j.biortech.2026.136012},
pmid = {42833452},
issn = {1873-2976},
abstract = {This study investigates whether a single initial cyanobacterial microbiome, originating from a mixed community, retains its capacity for polyhydroxybutyrate (PHB) production under non-sterile long-term operation when subjected to cultivation conditions that promote different dominant cyanobacterial populations. Distinct selective pressures were applied in two photobioreactors: one subjected to high pH (>10) and nutrient limitation, which favored the dominance of Synechococcus sp., and one operating under controlled pH (8.0-8.25) and sufficient nutrient supplementation, which promoted the enrichment of Synechocystis sp. Despite these shifts in cyanobacterial population dominance, the microbiome retained the capacity to accumulate PHB over 31 days, indicating functional stability and potential functional redundancy within mixed cyanobacterial consortia. Differences in productivity between photobioreactors, with the Synechocystis sp.-dominated culture achieving a maximum PHB content of 36 %dcw compared to 17 %dcw in the Synechococcus sp.-dominated culture, were more likely associated with the distinct operational conditions imposed rather than with the dominant cyanobacterial population, though the contribution of population composition cannot be fully excluded. Daily acetate addition (100 mg·L[-1]) proved to be an effective supplementation strategy for sustaining PHB accumulation in both systems. These findings suggest that bioplastic production can be maintained despite changes in cyanobacterial population dominance within a shared microbiome, consistent with putative functional redundancy, and that operational parameters may be more decisive than species dominance in determining PHB productivity.},
}

@article {pmid42833601,
year = {2026},
author = {Cheng, Q and Hong, L and Hui, C and Xu, L and Liu, Y and Wang, F and Wang, Q and Ma, J and Lin, H},
title = {Phycosphere microbiome remodeling and Brevundimonas partnership establishment enhance microalgal nonylphenol tolerance.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2026.10.006},
pmid = {42833601},
issn = {2090-1224},
abstract = {INTRODUCTION: Microalgae are vital primary producers in aquatic ecosystems yet increasingly threatened by nonylphenol (NP), a common endocrine disruptor. Current ecotoxicological assessments, however, largely rely on single-species models, overlooking the role of the phycosphere microbiome in host stress adaptation.

METHODS: Here, using the NP-tolerant microalgae Dictyosphaerium sp. as a model holobiont, we integrated multi-omics, axenic algae-bacteria co-culture, physiological, and metabolic analyses to unravel how associated microbes contribute to microalgal NP fitness.

RESULTS: Under environmentally relevant NP concentrations (10-900 µg/L), the holobiont sustained 20.3-91.3% higher biomass than axenic cultures. NP exposure reshaped the phycosphere community, enriching beneficial taxa. Among 16 bacterial isolates, Brevundimonas sp. D-1 exerted the strongest protective effect, boosting algal biomass by 39.9%. Mechanistically, D-1 significantly accelerated NP removal (P < 0.05), achieving a 28.8% increase within 4 days. Oxidative stress in NP-exposed algae was also markedly achieved, as reflected by 29.3% and 46.8% reductions in reactive oxygen species and malondialdehyde levels, respectively, alongside ultrastructural preservation and > 1.3-fold increases in photosynthetic pigment contents. Moreover, D-1 modulated extracellular polymeric substances, restraining their overproduction while enriching tyrosine- and tryptophan-like components to reinforce the interfacial barrier. Transcriptomic profiling further revealed downregulation of stress-defense genes (e.g., DNA repair and photoprotection) and restoration of growth-related pathways, including photosynthesis and energy metabolism.

CONCLUSION: Our findings establish a community-to-strain paradigm for phycosphere microbiome-mediated tolerance of microalgae to NP, deepen our understanding of inter-species cooperation, and provide a basis for designing tailored algae-bacteria consortia for bioremediation.},
}

@article {pmid42833737,
year = {2026},
author = {Fu, Y and Cannon, RD and Cheng, L and Li, KC and Ekambaram, M and Cooper, PR and Mei, ML},
title = {Smart peptide-based materials and their clinical application for caries management.},
journal = {Journal of the American Dental Association (1939)},
volume = {157},
number = {10},
pages = {1105-1117},
doi = {10.1016/j.adaj.2026.07.002},
pmid = {42833737},
issn = {1943-4723},
mesh = {Humans ; *Dental Caries/prevention & control/therapy/drug therapy ; Tooth Remineralization/methods ; Biofilms/drug effects ; *Peptides/therapeutic use ; *Antimicrobial Peptides/therapeutic use ; Biomimetic Materials/therapeutic use ; },
abstract = {BACKGROUND: Caries remains the most prevalent biofilm-mediated disease, requiring a shift toward minimally invasive, biologically driven management. Conventional therapies lack specificity and may disrupt microbial balance. Smart peptide-based materials provide a precision-guided strategy enabling the simultaneous targeting of cariogenic pathogens and promotion of biomimetic remineralization.

TYPES OF STUDIES REVIEWED: The authors examined the literature regarding the design principles, mechanisms of action, and translational potential of smart peptide-based anticaries systems, including antimicrobial, remineralizing, and environmentally responsive constructs, and clinical use in caries management.

RESULTS: Smart peptides are engineered to sense disease-associated cues such as acidic pH, specific cariogenic bacteria, or tooth-binding ability. Targeted antimicrobial peptides selectively inhibit cariogenic pathogens while preserving commensal microbiota. Remineralizing peptides guide biomimetic mineralization in early lesions. Multifunctional constructs that integrate these properties address both microbial dysbiosis and tissue demineralization. Although most systems remain preclinical, emerging in vivo and early clinical evidence support their feasibility and translational potential.

Smart peptide-based materials provide a precision-guided and minimally invasive approach for caries management. By means of integrating pathogen-targeted antimicrobial activity with biomimetic tissue repair and environmental responsiveness, these materials align closely with the principles of precision dentistry. Continued development and clinical validation may enable personalized, microbiome-sparing, and lesion-specific interventions in routine oral health care.},
}

Humans
*Dental Caries/prevention & control/therapy/drug therapy
Tooth Remineralization/methods
Biofilms/drug effects
*Peptides/therapeutic use
*Antimicrobial Peptides/therapeutic use
Biomimetic Materials/therapeutic use

@article {pmid42833816,
year = {2026},
author = {Das, R and Victor, C and Hatt, JK and Durán-Viseras, A and Konstantinidis, KT and Sinharoy, SS and Waller, L and Nalá, R and Levy, K and Freeman, MC and Jesser, KJ},
title = {Effect of diarrhea on early-life gut microbiome composition and subsequent infant growth in Beira, Mozambique: analysis of the PAASIM longitudinal birth cohort.},
journal = {The American journal of clinical nutrition},
volume = {124},
number = {4},
pages = {101464},
doi = {10.1016/j.ajcnut.2026.101464},
pmid = {42833816},
issn = {1938-3207},
mesh = {Humans ; Mozambique/epidemiology ; Infant ; Longitudinal Studies ; *Diarrhea/microbiology/epidemiology ; *Gastrointestinal Microbiome ; Female ; Male ; Birth Cohort ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; *Child Development ; Infant, Newborn ; Bacteria/classification/genetics/isolation & purification ; },
abstract = {BACKGROUND: The first year of life is a critical period for gut microbiome maturation; however, the interplay between diarrheal burden, microbial development, and growth in high-burden settings remains poorly understood.

OBJECTIVES: We leveraged longitudinal data from the Pesquisa Sobre o Acesso à Água e a Saúde Infantil em Moçambique (PAASIM) longitudinal birth cohort study in Beira, Mozambique, to test whether diarrhea is associated with gut microbiome characteristics and whether microbiome profiles relate to infant growth.

METHODS: Stool samples collected at 3, 6, 9 (n ∼150 at each time point), and 12 (n = 536) mo underwent 16S rRNA gene sequencing, with microbial diversity and taxonomic composition analyzed alongside monthly caregiver-reported diarrhea and anthropometric measurements.

RESULTS: Alpha diversity increased across infancy, and beta diversity shifted significantly with age, consistent with the ongoing maturation of the microbiome. Cumulative period prevalence of diarrhea from birth to 12 mo was not associated with microbial diversity or community composition at 12 mo. Higher alpha diversity at 3 mo was positively associated with length-for-age z-scores (LAZ) at 12 mo [β coefficient: 1.49; 95% confidence interval (CI): 0.33, 2.67], whereas higher diversity at 6 mo was inversely associated with LAZ at 12 mo (β: -2.85; 95% CI: -4.25, -1.45), showing age-dependent relationships with later linear growth. At 12 mo, we observed small beta-diversity differences between wasted and nonwasted (permutational multivariate analysis of variance, PERMANOVA R[2] = 0.05, P = 0.012) and between stunted and nonstunted children (R[2] = 0.05, P = 0.014). An exploratory longitudinal analysis revealed a positive association between Finegoldia abundance and wasting at 12 mo (β = 1.66; 95% CI: 0.83, 2.48), which met multiple-testing thresholds [false discovery rate = 0.19].

CONCLUSIONS: These findings suggest that early microbial trajectories, independent of cumulative diarrheal burden, may be linked to growth outcomes, warranting further research to identify potential microbiome-targeted interventions in the first year of life, a pivotal window for promotion of healthy growth in resource-limited settings.},
}

Humans
Mozambique/epidemiology
Infant
Longitudinal Studies
*Diarrhea/microbiology/epidemiology
*Gastrointestinal Microbiome
Female
Male
Birth Cohort
Feces/microbiology
RNA, Ribosomal, 16S/genetics
*Child Development
Infant, Newborn
Bacteria/classification/genetics/isolation & purification

@article {pmid42833873,
year = {2026},
author = {Haque, M and Lesker, TR and Rolle-Kampczyk, U and Segers, A and De Vos, WM and Molinaro, A and Basavanapura, T and Chen, Y and Backhaus, M and Mohamed, MR and Jiang, L and Salih, Q and Candels, L and Henricsson, M and Bielecka, A and Lang, S and Tacke, F and Hengstler, JG and Schneider, CV and Demir, M and Strowig, T and von Bergen, M and Schneider, KM and Trautwein, C},
title = {Microbiota-host genetic interactions modulate MASLD risk in PNPLA3[I148M] carriers via ceramides and are reversible by targeted microbial interventions.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2026-338178},
pmid = {42833873},
issn = {1468-3288},
abstract = {BACKGROUND: The factors that determine when genetic susceptibility to metabolic dysfunction-associated steatotic liver disease (MASLD) progresses to clinically significant liver injury remain incompletely understood.

OBJECTIVE: We investigated whether disruption of the intestinal host-microbiota interface acts as a contextual modifier that amplifies PNPLA3[I148M] -associated hepatic injury.

DESIGN: We used a dual-hit mouse model combining hepatic Pnpla3[I148M] -expression with Nlrp6-deficiency, a model of impaired intestinal mucosal homeostasis, under western-diet conditions. Multi-omics profiling, including metagenomics, metabolomics and transcriptomics, was integrated with analyses in human cohorts (Lifelines, Charité MASLD, Human Phenotype Project). Microbiota-dependent effects were examined using faecal microbiota transplantation (FMT), antibiotic-mediated depletion and targeted intervention with Akkermansia muciniphila or its membrane protein Amuc_1100.

RESULTS: In mice, the combination of Pnpla3[I148M] expression and impaired intestinal sensing synergistically exacerbated gut-barrier dysfunction and bacterial encroachment, accompanied by increased portal levels of microbiota-associated metabolites, including long-chain ceramides (Cer(d18:1/16:0), Cer(d18:1/18:0)) and bile acids. These changes were associated with hepatic mitochondrial stress and inflammatory responses. Human carriers with advanced MASLD displayed microbial and metabolic signatures consistent with increased gut-derived metabolic signalling. Restoration of eubiotic microbiota via FMT or Amuc_1100 treatment improved intestinal barrier integrity and attenuated hepatic lipid accumulation in experimental models.

CONCLUSION: These findings suggest that gut-derived signals resulting from a disrupted intestinal barrier may act as modifiers of PNPLA3[I148M] -clinical penetrance by amplifying downstream metabolic and inflammatory responses. By identifying these pathways linking environmental context to genetic susceptibility, this study highlights the host-microbiota interface as a potential target for strategies aimed at limiting MASLD progression in genetically at-risk individuals.},
}

@article {pmid42834054,
year = {2026},
author = {Wang, T and Ahmad, S and Santos de Lima Rosa, R and Binion, B and Fernandez-Materan, FV and Igbalaye, JO and Chung, D and Bushra, A and Perez, V and Biedak, MA and Tang, E and Barnick, B and Olukoya, D and Mbuvi, P and Dutta, D and Erdman, JW and Gaskins, HR and Yang, G and Irudayaraj, J and Bernardi, RC and Ridlon, JM},
title = {The urinary pathobiont Actinobaculum massiliense can generate androgens via the dirAB pathway.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42834054},
issn = {2041-1723},
support = {GM145920//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; CA287126//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; GM145965//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; MCB-2143787//National Science Foundation (NSF)/ ; },
mesh = {Humans ; Male ; *Androgens/biosynthesis/metabolism ; *Actinomycetaceae/metabolism/genetics/isolation & purification/enzymology ; Phylogeny ; *Bacterial Proteins/metabolism/genetics ; },
abstract = {While overlooked during the Human Microbiome Project, characterizing the urinary microbiota in health and disease is a new frontier in microbiome science. Recent studies have associated differential abundance of bacterial taxa including Propionimicrobium lymphophilum and Actinobaculum/Actinotignum spp. with prostate cancer. In this study, we collected urine from subjects before prostate biopsy and applied a Human Sterolbiome Discovery High-throughput (HSDH) assay to identify culturable urinary bacteria with the ability to generate androgens. Application of the HSDH Assay to urine samples led to the isolation of eight P. lymphophilum strains positive for cortisol side-chain cleavage (steroid-17,20-desmolase), 17β-HSDH activity, or both. In addition, we isolated three strains of Actinobaculum massiliense that carry the DHEA isomerase reductase (dir) genes. The dirA gene encodes a multifunctional 3β/17β-hydroxysteroid dehydrogenase/Δ[4,5]-isomerase and the dirB gene encodes a 17β-hydroxysteroid dehydrogenase isoform. Structural prediction and molecular dynamics reveal probable catalytic mechanisms based on the shared catalytic triad but distinct binding-pocket geometries of DirA and DirB, which enabled predictions of their respective reactions. Phylogenetic analysis of DirA and DirB revealed homologs in urinary tract commensals and in bacteria associated with steroid degradation in aquatic and terrestrial environments. Taken together, the development of the HSDH Assay and the identification of the dir pathway genes provide the methodological foundation and provide the molecular basis for advancing our understanding of the role of urinary tract bacteria in host endocrine physiology.},
}

Humans
Male
*Androgens/biosynthesis/metabolism
*Actinomycetaceae/metabolism/genetics/isolation & purification/enzymology
Phylogeny
*Bacterial Proteins/metabolism/genetics

@article {pmid42834084,
year = {2026},
author = {Peñarete-Acosta, D and Noe, P and Kellogg, T and Li, S and Radolf, JD and Hyams, JS and Jalili, S},
title = {Microphysiological models of human gastrointestinal diseases.},
journal = {Nature biomedical engineering},
volume = {},
number = {},
pages = {},
pmid = {42834084},
issn = {2157-846X},
support = {P30CA034196//U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)/ ; },
abstract = {Gastrointestinal (GI) diseases impose a growing global health burden, extending beyond localized pathology to disrupt systemic metabolism, immunity and cancer risk. Despite advances in conventional animal and cell models, critical mechanisms driving chronic inflammation, tumour initiation and host-microbiome dysregulation remain incompletely understood, limiting translational progress. Microphysiological systems, including organoids and organ-on-a-chip technologies, have transformed our ability to model human GI biology and pathology with increasing cellular, spatial and mechanical fidelity. Here we synthesize recent advances in organoid and organ-on-a-chip models of GI disease, highlighting their applications across inflammatory, infectious and neoplastic conditions throughout the GI tract. We integrate emerging engineering approaches with mechanistic and clinical insights, assessing how these systems advance disease modelling while identifying remaining gaps in complexity, translation and scalability. By bridging microengineering innovation with clinical gastroenterology, we outline how next-generation, human-relevant models can inform mechanistic discovery, guide targeted therapeutic development and support precision medicine in GI disease.},
}

@article {pmid42834089,
year = {2026},
author = {Jiang, J and Dai, DLY and Poulsen, CS and Tranæs, K and Wang, T and Petersen, C and Hoskinson, C and Moraes, TJ and Mandhane, PJ and Simons, E and Azad, MB and Subbarao, P and Chawes, B and Bønnelykke, K and Thorsen, J and Turvey, SE and Stokholm, J},
title = {Microbial-derived tryptophan metabolites in the infant gut associate with increased risk of asthma following cesarean section.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42834089},
issn = {2041-1723},
mesh = {Humans ; *Cesarean Section/adverse effects ; *Asthma/microbiology/etiology/metabolism/epidemiology ; *Tryptophan/metabolism ; Female ; Infant ; *Gastrointestinal Microbiome/physiology ; Feces/microbiology/chemistry ; Risk Factors ; Pregnancy ; Child, Preschool ; Male ; Birth Cohort ; Canada ; Metabolome ; },
abstract = {Delivery by cesarean section (CS) is a risk factor for childhood asthma and a strong determinant of the early-life gut microbiome. It has been reported that a CS-perturbed gut microbiome plays a mediating role in the association between CS and asthma risk. However, the underlying mechanisms remain unclear. Here, using deeply phenotyped participants in the Canadian birth cohort (CHILD), we characterized the CS microbial composition at 3 months and 1 year of age using machine learning models and described the perturbation using CS scores. The association between CS and the gut microbiota composition was more pronounced at 3 months (area under the curve (AUC) = 0.78) and attenuated at age 1 year (AUC = 0.60). An increased asthma risk at age 5 years was associated only with 1-year CS microbial scores (Odds ratio 1.41, P = 0.004; adjusted odds ratio 1.30, P = 0.034), consistent with our previous work. Extending this, we identified metabolic imbalances associated with 1-year CS microbial scores, marked by elevated tryptophan metabolites in the stool metabolome. These results replicate our previous findings about the mediating role of the 1-year CS microbial signature in the association between CS and asthma risk from the Danish COPSAC2010 cohort, and provide new insight into the underlying mechanism of host-microbe interaction following cesarean section.},
}

Humans
*Cesarean Section/adverse effects
*Asthma/microbiology/etiology/metabolism/epidemiology
*Tryptophan/metabolism
Female
Infant
*Gastrointestinal Microbiome/physiology
Feces/microbiology/chemistry
Risk Factors
Pregnancy
Child, Preschool
Male
Birth Cohort
Canada
Metabolome

@article {pmid42834167,
year = {2026},
author = {Hu, Y and Bode, J and Gómez-Pérez, D and Guerreiro, MA and Mari, A and Wang, K and Niemann, S and Mahmoudi, M and Kemen, A and Duran, P and Wacker, O and Straub, D and Nahnsen, S and Schwessinger, B and Roux, F and Alonso-Blanco, C and Ågren, J and Hacquard, S and Stukenbrock, EH and Kemen, E},
title = {Thiamine cross-feeding drives microbial coexistence in the leaf microbiome.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {42834167},
issn = {2058-5276},
support = {2016-05435, 2020-04434//Vetenskapsrådet (Swedish Research Council)/ ; TRR356//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; EXC 2124-390838134//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; },
abstract = {Microbiome homeostasis is crucial for host health and ecosystem function, yet the molecular and ecological mechanisms underlying community assembly and stability remain elusive. Here we uncover a conserved yeast-oomycete association that promotes their coexistence in the leaf microbiome. Using a continental-scale microbiome survey, we identified an asymmetric mutualistic interaction between two eukaryotic hub microbes: the yeast Dioszegia hungarica and the obligate oomycete Albugo laibachii. We show that Dioszegia facilitates Albugo colonization by supplying thiamine via a dedicated membrane permease, alleviating Albugo's auxotrophy. Genomic and transcriptomic analyses indicate that natural selection has acted on thiamine production in Dioszegia, shaping this metabolic complementation. In planta assays further suggest that Albugo presence supports Dioszegia persistence under glasshouse conditions. Our study illustrates how the evolution of nutrient cross-feeding mediates microbial coexistence and microbiome stability. Targeting microbial nutrient flows offers new strategies for engineering microbiomes and enhancing plant resilience in natural and agricultural systems.},
}

@article {pmid42834399,
year = {2026},
author = {Correa, F and Luise, D and Palumbo, F and Scicchitano, D and Rampelli, S and Molino, S and Panciroli, N and Candela, M and Garay-Mayol, B and Ávila-Gálvez, MÁ and González-Sarrías, A and Castagnetti, A and Trevisi, P},
title = {Chestnut-quebracho tannins shape the fecal metabolome of weaned pigs through microbiota-dependent urolithin production.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {42834399},
issn = {1674-9782},
support = {n.818290//Horizon 2020 Framework Programme/ ; },
abstract = {BACKGROUND: Chestnut and quebracho tannins may support gut health in weaned piglets, but their efficacy likely depends on farm environment and microbial capacity to convert tannins into bioactive metabolites. This study evaluated the effects of a blend of chestnut-derived hydrolysable tannins and quebracho-derived condensed tannins on growth performance, diarrhea occurrence, gut metagenome, and fecal metabolome in piglets reared under two commercial farm conditions. A total of 160 weaned piglets (initial body weight 6.53 ± 0.13 kg) were assigned to a 2 × 2 factorial design comprising 2 weaning units (W1 and W2) and 2 dietary treatments (control diet or control diet + 2 g/kg tannin blend; 40 piglets per treatment × farm). The trial lasted 76 d, with weighings at T0 (entry into weaning, median 28 d), T1 (d 35), T2 (d 49), and T3 (d 76). Fecal scores and samples were collected at T1, T2, and T3 for shotgun metagenomics (155 samples per time point) and untargeted metabolomics, and targeted urolithin quantification was performed in tannin-treated piglets at T1 and T2.

RESULTS: Tannin supplementation did not affect overall growth performance throughout the weaning phase, but reduced diarrhea occurrence at T2 in W2 (P = 0.032). Species-level beta diversity was consistently affected by treatment across time points (R[2]= 0.01-0.03; P < 0.01), whereas alpha diversity was mainly farm-driven during the early post-weaning phase. Linear discriminant analysis effect size identified farm-dependent taxonomic markers, including Escherichia coli in control pigs from W1 at T1 and Megasphaera elsdenii, Faecalibacterium prausnitzii, and Lactobacillus amylovorus in tannin-treated pigs at later time points. Untargeted metabolomics revealed treatment-related fecal signatures, with isourolithin A and urolithin B among the most discriminant metabolites in treated pigs, especially in W2. Targeted analysis identified 3 urolithin metabotypes (metabotype B in 50.0% of samples), with higher isourolithin A, urolithin B, and urolithin A in W2 than W1 at T2 (P < 0.01). Network integration identified candidate cooperative microbial consortia associated with urolithin production, including Ellagibacter isourolithinifaciens; these co-abundance associations are correlative and remain to be functionally validated.

CONCLUSIONS: Overall, chestnut-quebracho tannins were associated with a farm-dependent reduction in post-weaning diarrhea and modulated the gut ecosystem through microbiota-dependent polyphenol metabolism.},
}

@article {pmid42834458,
year = {2026},
author = {Liao, Y and Gui, Y and Li, T and Zhou, Q and Chen, X and Chen, Q},
title = {The Therapeutic Potential of Berberine in Treating Diabetes and Its Complications: Molecular Mechanisms and Future Perspectives.},
journal = {The American journal of Chinese medicine},
volume = {},
number = {},
pages = {1-34},
doi = {10.1142/S0192415X26500795},
pmid = {42834458},
issn = {1793-6853},
abstract = {Diabetes mellitus (DM), a chronic metabolic disorder characterized by persistent hyperglycemia, poses a significant global health burden. Berberine (BBR), a natural isoquinoline alkaloid derived from medicinal plants such as Coptidis Rhizoma, has shown therapeutic promise for DM and its complications. Preclinical and clinical studies have revealed that BBR exerts multi-target effects, including remodeling the gut microbiome, promoting insulin secretion, ameliorating insulin resistance, and inhibiting hepatic gluconeogenesis. Its protective mechanisms against diabetic complications, such as nephropathy, cardiomyopathy, and retinopathy, involve modulating key pathways like AMPK/SIRT1, PI3K/Akt, and TGF-[Formula: see text]/Smad, which attenuate oxidative stress, inflammation, and fibrosis. Despite its low oral bioavailability, a wide array of formulation strategies, including polymer nanocarriers, lipid-based nanocarriers, mixed micelles, and absorption enhancer, have improved systemic exposure in preclinical models, although clinical translation remains limited. This review synthesizes evidence from the past decade spanning preclinical mechanisms, randomized controlled trials, pharmacokinetics and nanoformulation strategies, concluding that BBR is a promising candidate for complementary therapy, although the supporting clinical evidence remains limited. Further studies are warranted to clarify its mechanisms, and optimize its delivery. In particular, larger and longer-term trials, along with systematic pharmacokinetic-pharmacodynamic studies of BBR and its metabolites, are needed to confirm its efficacy and long-term safety.},
}

@article {pmid42834635,
year = {2026},
author = {Limaye, S and Bhide, P and Kale, A and Bokey, N},
title = {SCFA Alterations in IBS Subtypes: Systematic Evidence and Future Prospects for Biomarker-Based Diagnosis in India.},
journal = {Journal of microbiology and biotechnology},
volume = {36},
number = {},
pages = {e2605029},
doi = {10.4014/jmb.2605.05029},
pmid = {42834635},
issn = {1738-8872},
mesh = {Humans ; *Biomarkers/analysis ; *Irritable Bowel Syndrome/diagnosis/classification/metabolism ; *Fatty Acids, Volatile/metabolism/analysis ; Feces/chemistry/microbiology ; India ; Butyrates/analysis ; Propionates/analysis/metabolism ; Acetates/analysis ; Gastrointestinal Microbiome ; },
abstract = {Irritable bowel syndrome (IBS) is a chronic disorder of gut-brain interaction characterized by abdominal pain and altered bowel habits. Short-chain fatty acids (SCFAs), microbial metabolites of dietary fiber, play key roles in gut physiology and have been implicated in IBS pathogenesis. Propionate, acetate, and butyrate are of particular interest as potential biomarkers for diagnosis and subtype differentiation. A systematic search of PubMed, Web of Science, and Embase identified studies reporting fecal SCFA concentrations in IBS patients versus healthy controls (HCs). Adult cohorts diagnosed by Rome criteria, case-control or randomized designs, and sufficient SCFA data for effect size calculation were included. Data were harmonized to mean ± SD and analyzed; pooled standardized mean differences (SMDs) with 95% confidence intervals (CI) were calculated, with subgroup analyses for IBS-D and IBS-C. Methodological quality was assessed using the Newcastle-Ottawa Scale (NOS). Eleven studies met inclusion criteria. Across all IBS cohorts, propionate was significantly elevated compared to HCs, while acetate and butyrate showed no differences. In IBS-D, propionate was consistently higher. In IBS-C, total SCFAs were significantly reduced, with negligible heterogeneity. Acetate, propionate, and butyrate remained non-significant, with moderate to substantial heterogeneity. NOS assessment indicated that most studies were of good quality, with one rated moderate. This meta-analysis highlights propionate elevation as a biomarker for IBS, particularly IBS-D, and reduced total SCFAs as a distinct metabolic signature in IBS-C. Variability in individual metabolites reflects dietary and methodological influences. The absence of Indian cohorts limits generalizability; future studies integrating SCFA profiling with microbiome analysis in Indian populations are needed to validate biomarker utility and support precision management of IBS.},
}

Humans
*Biomarkers/analysis
*Irritable Bowel Syndrome/diagnosis/classification/metabolism
*Fatty Acids, Volatile/metabolism/analysis
Feces/chemistry/microbiology
India
Butyrates/analysis
Propionates/analysis/metabolism
Acetates/analysis
Gastrointestinal Microbiome

@article {pmid42834636,
year = {2026},
author = {Grover, M},
title = {Maternal circadian rhythm writes immune fate in offspring.},
journal = {Journal of biosciences},
volume = {51},
number = {36},
pages = {},
doi = {10.1007/s12038-026-00608-9},
pmid = {42834636},
issn = {0973-7138},
mesh = {Animals ; *Circadian Rhythm/genetics/immunology ; *Caenorhabditis elegans/immunology/genetics/microbiology ; *Caenorhabditis elegans Proteins/genetics/immunology ; Female ; Pseudomonas aeruginosa/pathogenicity/immunology ; },
abstract = {An organism's environment is rarely constant. Light, temperature, humidity, food availability, and microbial exposure often fluctuate rhythmically, creating daily patterns that organisms must anticipate and respond to (Paranjpe and Sharma 2005; van der Linden et al. 2010; Thaiss et al. 2014). The ability of biological systems to align physiology with such environmental cycles has fascinated biologists for decades, and circadian regulation is now known to influence diverse processes, including metabolism, behaviour, development, immunity, and stress responses (Fagiani et al. 2022; Poole and Kitchen 2022). Whether environmental rhythms experienced by the mother can influence offspring physiology has only begun to be explored (Yao et al. 2025). In a recent study, Lalsiamthara et al. (2026) provide compelling evidence that infection vulnerability in offspring can be shaped by maternal circadian rhythms. Using Caenorhabditis elegans, the authors first asked whether genetically similar animals differ in a measurable pre-infection state that anticipates later infection outcomes. They focused on irg-5, a PMK-1/p38 MAPK-regulated infection-response reporter (Peterson et al. 2019), and found that animals with high basal irg-5 expression before infection were more susceptible to subsequent Pseudomonas aeruginosa PA14 challenge. Importantly, this high-irg-5 state was not simply a sign of generally poor health, because these animals did not show obvious differences in baseline lifespan, feeding, movement, or pathogen avoidance. The study then asked whether this pre-infection state could be influenced by maternal circadian rhythms. Mothers were exposed to alternating 12 h light/20 C and 12 h dark/15 C cycles, mimicking daily fluctuations that worms may experience in nature. This entrainment did not increase irg-5 expression in the mothers themselves; instead, it rhythmically altered the proportion of offspring entering the high basal irg-5 state. The transgenerational effect of this state was further supported by the observation that high-irg-5 mothers produced more high-irg-5 offspring than low-irg-5 mothers. Consistent with clock-associated regulation, knockdown of nhr-23, a C. elegans homolog of mammalian ROR clock genes (Hiroki and Yoshitane 2024), disrupted this rhythmic oscillation. Together, these experiments connect maternal environmental timing, offspring immune-marker heterogeneity, and infection vulnerability in a single framework. These observations raise mechanistic and evolutionary questions. Mechanistically, what maternal cues are transmitted to offspring: metabolites, small RNAs, chromatin-associated states, or nutrients, and how do they influence basal immune state? Evolutionarily, why might mothers generate heterogeneous offspring states, especially when the high-irg-5 state increases susceptibility to PA14 in this study? One possibility is that this state is not universally maladaptive. Caenorhabditis elegans inhabits transient microbe-rich substrates such as rotting vegetation and compost, where temperature, humidity, food availability, and microbial communities can fluctuate with daily cycles (Schulenburg and Felix 2017). In such habitats, rhythmic cues are not merely background variables; they may act as reliable signals of changing risk. Temperature cycles can influence worm development, movement, and feeding, while also altering microbial growth and community composition (Felix and Braendle 2010). Light exposure may be indirect in soil or rotting-fruit microenvironments, but together with temperature it can serve as a proxy for day-night transitions (van der Linden et al. 2010). Maternal entrainment to these cues could therefore allow offspring physiology to be adjusted in anticipation of conditions that are likely, but not guaranteed, to follow. A state that is costly against one pathogen may be beneficial under other microbial, thermal, or nutritional conditions. Maternal generation of heterogeneous offspring states could therefore resemble bet-hedging, spreading risk across uncertain environments rather than optimizing all progeny for a single challenge. In a self-fertilizing organism with limited genetic diversity, such non-genetic heterogeneity could increase the chance that at least some individuals are appropriately tuned to future conditions. This idea could be tested further by asking whether natural genetic variation or microbiome context modifies intergenerational circadian immune heterogeneity in C. elegans. Such modifiers are plausible since, in mice, the gut microbiome can influence host circadian gene expression and metabolic rhythms (Thaiss et al. 2014), while in humans, genetic variation has well-established effects on circadian timing and behaviour (Kalmbach et al. 2017). Wild C. elegans isolates and defined natural microbiota (Dirksen et al. 2020) would therefore provide useful context to ask about the general nature and ecological sensitivity of this phenomenon. Beyond circadian regulation of intergenerational immune heterogeneity, the study also raises an important point about how basal immune markers should be interpreted. The irg-5 result is counterintuitive because irg-5 is an established PMK-1-regulated infection-response gene (Peterson et al. 2019), yet animals with high basal irg-5 expression were more susceptible to PA14. This does not mean that immune activation is generally harmful, or that irg-5 alone defines immune status. Instead, the same immune-marker expression may have different implications before and after infection: pathogen-induced expression may participate in defence, whereas high basal expression may mark altered intestinal homeostasis, metabolic imbalance, low-grade stress-pathway activity, or marker-specific transcriptional regulation. Mechanistically, prior ChIP data support binding of UNC-62 (MacNeil et al. 2015), a conserved MEIS/homeobox transcription factor (Van Nostrand et al. 2013), near the irg-5 promoter, and the present study shows that loss of UNC-62 increases basal irg-5 expression in mothers through PMK-1 and ELT-2. Thus, basal irg-5 heterogeneity appears to be a regulated transcriptional state shaped by UNC-62-dependent control. More broadly, this adds to an emerging view in C. elegans immunity that conserved developmental regulators can be redeployed in differentiated tissues to tune adult immune defence (Drury et al. 2023; Liu et al. 2024). The broader relevance of this work lies in connecting two ideas that are often considered separately: circadian regulation of immunity and maternal shaping of offspring physiology. Mammalian studies have shown that immune function is strongly time-of-day dependent, and that disruption of circadian rhythms can alter inflammatory responses and susceptibility to infection (Curtis et al. 2014; Poole and Kitchen 2022). Separately, the maternal environment, for example, nutritional state during pregnancy and lactation, can shape offspring metabolic, developmental, and behavioural physiology (Yao et al. 2025). Lalsiamthara et al. (2026) bring these themes together in a genetically tractable organism by showing that maternal circadian rhythms can shape infection-relevant heterogeneity in the next generation. Although the molecular details may be partly conserved and partly organism- or context-specific, the conceptual message is broad: before the pathogen arrives, vulnerability may already carry the imprint of time, ancestry, and environment.},
}

Animals
*Circadian Rhythm/genetics/immunology
*Caenorhabditis elegans/immunology/genetics/microbiology
*Caenorhabditis elegans Proteins/genetics/immunology
Female
Pseudomonas aeruginosa/pathogenicity/immunology