@article {pmid42926212,
year = {2026},
author = {Alizadeh, M and Siaton, BC and Hudhud, D and von Rosenvinge, EC and Cross, RK and Ravel, J},
title = {The intestinal microbiome in inflammatory bowel disease and spondyloarthritides.},
journal = {Communications medicine},
volume = {6},
number = {1},
pages = {},
pmid = {42926212},
issn = {2730-664X},
abstract = {Extraintestinal manifestations (EIMs) of inflammatory bowel disease (IBD) can affect any organ system, ranging in presentation, frequency, and severity; the most common EIM is IBD-associated arthritis (IAA), an inflammatory arthritis affecting both axial and peripheral joints. IAA is a form of seronegative spondyloarthritis (SpA), which includes multiple arthritides, and those with IAA are also likelier to have other clinical features observed in those with SpA without IBD, such as increased rates of uveitis, psoriasis, and HLA-B27 positivity. These overlapping features are not limited to clinical disease features; the microbiome has been heavily implicated in the development of both IBD and SpA and is associated with non-SpA EIMs. In this review, we offer an overview of several bacterial taxa and associated metabolites that have been identified as differentially abundant in both IBD and SpA, both in stool and mucosal assessment, and how these taxa are associated with differences in intestinal permeability and immune profiles. We also describe how the overlapping dysbiotic microbiome and associated metabolome in IBD, EIMs of IBD, and SpA may differentially modulate the immune system, thus contributing to the shared underlying etiopathogenesis of these diseases. Further work is needed to characterize causal, mechanistic relationships beyond pure computationally identified associations, and apply these findings towards targeted therapeutic intervention and personalized medicine in IBD.},
}

@article {pmid42926290,
year = {2027},
author = {Mishra, AA and Poulides, N and Morrill, AC and Gan, S and Nguyen, G and Mollergren, MA and Zarek, CM and Koh, AY},
title = {Unbiased Microbiome and Metabolomic Profiling of Fecal Samples from Patients with Melanoma.},
journal = {Methods in molecular biology (Clifton, N.J.)},
volume = {3089},
number = {},
pages = {441-457},
pmid = {42926290},
issn = {1940-6029},
mesh = {*Melanoma/microbiology/metabolism ; Humans ; *Feces/microbiology ; *Metabolomics/methods ; *Metabolome ; *Gastrointestinal Microbiome ; Multiomics ; Animals ; Computational Biology/methods ; },
abstract = {Gut microbiota influence and modulate host immune responses. In preclinical cancer models, mice lacking gut microbiota have a markedly diminished response to immune checkpoint inhibitor therapy. Further, in melanoma patients, specific commensal gut microbiota have been associated with a positive clinical response to immunotherapy. In order to study the gut microbiome and metabolome, we have developed methods for fecal sample collection and processing, microbiome and metabolome profiling, and bioinformatic analysis. This protocol will be a useful tool for interrogating the taxonomic composition and functional output of a melanoma patient's gut microbiome.},
}

*Melanoma/microbiology/metabolism
Humans
*Feces/microbiology
*Metabolomics/methods
*Metabolome
*Gastrointestinal Microbiome
Multiomics
Animals
Computational Biology/methods

@article {pmid42926319,
year = {2026},
author = {Jacobson, R and Garza, T and Pimiento, J and Dineen, S and Mullinax, J and Mishra, S and Maurin, M and Soundararajan, R and Nywening, T and Karachristos, A and Yadav, H and Yeatman, T and Fleming, J},
title = {Western-style high fat, low fiber diet causes progression of colorectal peritoneal metastases in mice.},
journal = {JPEN. Journal of parenteral and enteral nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1002/jpen.70156},
pmid = {42926319},
issn = {1941-2444},
support = {//ASPEN Rhoads Research Foundation/ ; //Sean Dineen-consulting from Oncoinvent. John Mullinax-Moffitt Cancer Center has licensed Intellectual Property (IP) related to the proliferation and expansion of tumor infiltrating lymphocytes (TILs) to Iovance Biotherapeutics. Dr Mullinax (JEM) is an inventor on such Intellectual Property. JEM has participated in sponsored research agreements with Iovance Biotherapeutics, Intellia Therapeutics, and SQZ Biotech. JEM has received research support from the following entities: NIH-NCI (K08CA252642), Ocala Royal Dames, and V Foundation. Dr Mullinax has received ad hoc consulting fees from Merit Medical, Lyell Immunopharma and Iovance Biotherapeutics/ ; },
abstract = {BACKGROUND: Multimodality (physical, dietary, psychological) prehabilitation is associated with a disease-free survival advantage after colorectal cancer surgery; however, the underlying mechanism is unknown. We measured the effects of a western-style diet on gut dysbiosis, antitumor immunity, and cancer progression in a surgical mouse model of metastatic colorectal cancer and attempted to mitigate its effects with isolated dietary prehabilitation.

METHODS: Before surgery and tumor induction, mice were given either a western-style diet for 6 weeks, chow for 6 weeks, or 4 weeks of a western-style diet followed by 2 weeks of chow. Expelled stool was collected for analysis of the fecal microbiome. Four weeks after surgery, tumors were quantified and collected for analysis with an immunofluorescence panel.

RESULTS: The western-style diet was obesogenic. Fecal microbiome analysis illustrated that the western diet induced a severe and lasting dysbiosis as measured by alpha diversity metrics, pathogenic overgrowth and Firmicutes to Bacteroidetes ratio, which was partially rescued by prehabilitation. Mice fed the western diet demonstrated increased tumor bulk and decreased intratumoral immune cell infiltrate compared with chow-fed mice. prehabilitation rescued the intratumoral immune effects, but not tumor bulk.

CONCLUSION: An obesogenic, no fiber western-style diet increased gut dysbiosis and tumor bulk while decreasing antitumor immunity in our mouse model, which was partially rescued by prehabilitation. Microbiome-targeted prehabilitation for colorectal cancer surgery is a promising paradigm and further translational research is warranted.},
}

@article {pmid42926358,
year = {2026},
author = {Ruan, J and Ma, Y and Zhang, K and Wu, B and Xu, T and Wang, X and Duan, C and Xu, S and Xu, J and Yu, X and Wang, H and Chen, R and Cheng, Y and Zheng, Z and He, D and Sun, D and Luo, C},
title = {Probiotic Extracellular Vesicles Enable Oral Alendronate Therapy for Glucocorticoid-Induced Osteoporosis.},
journal = {Advanced healthcare materials},
volume = {},
number = {},
pages = {},
doi = {10.1002/adhm.71884},
pmid = {42926358},
issn = {2192-2659},
support = {2025HY1399//Zhejiang Provincial Health Commission/ ; 2024K076//Quzhou Municipal Bureau of Science and Technology/ ; 2025ZY01039//Central Government Funds for Guiding Local Scientific and Technological Development/ ; SHPY2025010//Wenzhou University/ ; },
abstract = {Glucocorticoid-induced osteoporosis (GIOP) involves impaired bone remodeling, intestinal dysbiosis, and immune imbalance, which together limit the long-term benefit of conventional oral bisphosphonate therapy. Here, we report LpEVs@ALN, a probiotic extracellular vesicle-based oral nanoplatform constructed by loading alendronate (ALN) into Lacticaseibacillus paracasei-derived extracellular vesicles. LpEVs@ALN maintains vesicle integrity and epithelial compatibility, improves ALN retention under acidic exposure, and enables sustained ALN release at intestinal pH conditions. In dexamethasone-suppressed BMSCs, LpEVs@ALN enhances osteogenic differentiation, as evidenced by increased ALP activity and matrix mineralization. In zebrafish GIOP models, LpEVs@ALN improves cranial mineralization, new bone formation, scale regeneration, and locomotor/shoaling performance; accompanied by reduced inflammatory tone, improved ALP/RANKL-associated bone turnover readouts, and rebalanced oxidative-stress indices. Microbiome profiling shows recovery of richness/diversity and reduced Proteobacteria dominance, while scale RNA-seq reveals broad reversal of glucocorticoid-driven dysregulation toward pro-osteogenic and anti-inflammatory programs. Integrated correlation analysis further linked microbial remodeling with systemic and skeletal responses, suggesting involvement of the gut-immune-bone axis. Collectively, LpEVs@ALN alleviates GIOP by combining ALN-mediated bone protection with probiotic extracellular vesicle-associated regulation of intestinal and systemic homeostasis, highlighting its potential as an oral therapeutic strategy for GIOP.},
}

@article {pmid42926400,
year = {2026},
author = {Roginski, AC and Godazgar, M and Salgado, CL and Lahiri, G and Woodrow, C and H McDermott, T and Costa Lima, BG and Rodriguez-Castano, GP and Voth-Gaeddert, LE and Borges da Silva, H and Dietrich, MO and Mana, MD and Florsheim, EB},
title = {Cholera toxin remodels intestinal immunity and suppresses systemic metabolism.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.09.29.755509},
pmid = {42926400},
issn = {2692-8205},
abstract = {Cholera toxin (CTx) is a potent enterotoxin and widely used mucosal adjuvant, yet the acute host response to CTx itself, in the absence of a co-administered antigen, remains vague. In this study, we integrated physiological and metabolic phenotyping with intestinal transcriptomics, epithelial imaging, immune profiling, hepatic gene-expression analysis, and paired microbiome profiling to characterize the response to a single oral CTx exposure in mice. Within 24 h, CTx remodeled immune-cell composition in both epithelial and lamina propria compartments, with responses shaped by sex and genetic background. Recurrent changes included increased epithelial group 3 innate lymphoid cells, reduced lamina propria RORγt+ regulatory T cells, and decreased epithelial ILC1/NK cells in males of both strains. CTx also increased villus DCLK1+ tuft cells and reduced MUC2 immunoreactivity. Jejunal transcriptomics revealed induction of inflammatory defense, glycolytic, autophagy, and lipid-utilization programs together with suppression of proliferative and mitochondrial programs, consistent with coordinated stress adaptation. These local changes were accompanied by rapid restructuring of the fecal microbial community and by systemic hypometabolism, despite markedly different hypothermic responses across strains. CTx also elicited a selective hepatic stress and metabolic program, including conserved suppression of Cyp7a1 across sexes and strains. Together, these findings show that CTx alone rapidly reorganizes the intestinal immune, epithelial, metabolic, and microbial environment while suppressing whole-body metabolism. This work provides an integrated framework for understanding the acute host response to CTx and for interpreting its widespread use as a mucosal adjuvant.},
}

@article {pmid42926460,
year = {2026},
author = {Cremer, J},
title = {Quantifying the Resource Landscape That Shapes the Human Gut Microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.10.01.756135},
pmid = {42926460},
issn = {2692-8205},
abstract = {The microbial ecosystem in the human gut is fundamentally shaped by the resources it receives. Yet, while quantitative information is available for many individual resource fluxes, a comprehensive description of the overall resource landscape is lacking. Here, I systematically integrate physiological measurements and food composition data to map diet and digestion to the fluxes of more than 30 major resources entering the human large intestine, including carbohydrates, proteins, mucus, bile acids, ions, and electron acceptors. Applying this reconstruction across dietary variation in the U.S. population and analyzing the resulting influxes of biomass-forming elements, I find that microbial growth is carbon-limited for most individuals, whereas phosphorus is limiting for a subset; nitrogen, by contrast, is not limiting once host-derived urea recycling is accounted for. Resource supply also determines whether microbial auxotrophies impose physiological constraints. While amino acid dependencies can often be satisfied by protein-derived influx, characterized dietary cobamide influx is insufficient to account for the fecal cobamide pool, pointing to a much greater contribution from microbial production. Together, these results provide a quantitative resource landscape for the human gut, defining physiological constraints on microbial growth and providing a basis for predictive models of microbiome function and its impact on the host.},
}

@article {pmid42926479,
year = {2026},
author = {Norton, GJ and Dudek, AM and Gerner, RR and Guo, C and Castillo, V and Argueta, FA and Beebout, CJ and Kamyabi, G and Drushell, J and Walker, GT and Hsu, CY and Bessho, S and Nuccio, SP and Chu, H and Zengler, K and Nolan, EM and Raffatellu, M},
title = {Targeting catecholate siderophore systems enables precision depletion of gut enterobacteria during colitis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.10.02.756324},
pmid = {42926479},
issn = {2692-8205},
abstract = {Adherent-invasive Escherichia coli (AIEC) is frequently isolated from the dysbiotic gut microbiome in inflammatory bowel disease and is implicated in disease progression, highlighting its potential as a therapeutic target. Here we show that iron acquisition is essential for AIEC colonization of the inflamed gut. Mechanistically, four catecholate siderophore receptors act redundantly to support AIEC growth under iron-limited conditions and during colitis. Immunization of colitis-prone Il10 [-/-] mice against catecholate siderophores reduced intestinal AIEC colonization, particularly its association with the mucosa, while largely preserving overall gut microbiome composition. Longitudinal metagenomic profiling identified immunization-associated shifts in Akkermansiaceae and Lactobacillaceae , and experiments in gnotobiotic Il10 [-/-] mice demonstrated that Limosilactobacillus reuteri , a member of the Lactobacillaceae , limited AIEC colonization, whereas Akkermansiaceae exacerbated disease. Our findings establish catecholate siderophore-mediated iron acquisition as a therapeutic target in AIEC and provide proof-of-principle that virulence-targeted immunization can selectively antagonize a disease-associated bacterium while preserving the gut microbiota.},
}

@article {pmid42926485,
year = {2026},
author = {Suh, Y and Wang, H and Li, L and Gu, H and Johnson-Martinez, J and Magis, AT and Gibbons, SM and Cui, JY},
title = {The microbial soy metabolite S-equol mitigates cadmium neurotoxicity in mice.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.10.01.756095},
pmid = {42926485},
issn = {2692-8205},
abstract = {Environmental exposures are major but understudied determinants of chronic disease. Cadmium is a pervasive toxic metal encountered through diet and tobacco smoke that has been associated with cognitive impairment and Alzheimer's disease mortality, yet strategies to mitigate its neurotoxicity remain limited. S-equol is a gut microbial metabolite of soy daidzein that crosses the blood brain barrier and preferentially activates estrogen receptor beta. Here, we show that cadmium disrupts an axis linking the equol producing gut bacterium Adlercreutzia equolifaciens to circulating S-equol and hippocampal estrogen receptor expression in mice, that S-equol attenuates cadmium-induced cytotoxicity and restores neuronal, glutamatergic and synaptic transcriptional programs in mouse neural progenitor cells, and that circulating S-equol in older humans is lower in apolipoprotein E4 carriers and covaries with body mass index, identifying S-equol as a microbiome-derived, host-modulated candidate countermeasure against cadmium neurotoxicity.},
}

@article {pmid42926492,
year = {2026},
author = {Staley, S and Cooper, C and Oxendine, S and Williams, J and Armstrong, A and Wilson, K},
title = {Sex-Dependent Microbiome-Metabolome Remodeling Associated with Bacteroides acidifaciens Modulation of Acute Respiratory Distress Syndrome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.10.05.756742},
pmid = {42926492},
issn = {2692-8205},
abstract = {UNLABELLED: Acute respiratory distress syndrome (ARDS) is a severe lung disorder influenced by the interplay between the intestinal microbiome, host metabolism, and immune function. We previously found that Bacteroides acidifaciens (BA) has opposing effects on staphylococcal enterotoxin B (SEB)-induced ARDS, worsening the condition in female mice while alleviating it in males. This study aimed to examine whether these outcomes are linked to sex-dependent changes in the intestinal microbiome and gut-lung metabolome. C3H/HeJ mice of both sexes were orally colonized with Bacteroides acidifaciens before SEB exposure. Stool and bronchoalveolar lavage fluid (BALF) were collected for analysis using 16S rRNA sequencing and untargeted liquid chromatography mass spectrometry metabolomics. Our findings revealed distinct sex-dependent metabolic and microbial responses. In females, disease exacerbation correlated with elevated lipid mediators (leukotriene B4, 13-oxoODE, and 13S-HODE) alongside shifts in bile acid and redox metabolism. The intestinal microbiome showed changes in Bacteroides, Akkermansia, and Lachnospiraceae. Conversely, males showed a protective phenotype characterized by increased butyrate and alterations in sphingolipid, amino acid, redox, and nucleotide pathways. Integrated analyses identified sex-associated microbial communities and metabolomic profiles, highlighting distinct patterns of lipid and redox associations in females versus sphingolipid and short-chain fatty acid patterns in males. These results suggest that host sex influences how a commensal bacterium affects inflammatory lung injury and point to pathways for future research.

IMPORTANCE: ARDS is a fatal inflammatory response with high mortality and limited targeted therapies. Emerging evidence has pointed to the gut-lung axis as a source of inflammation that shapes pulmonary immune responses. Yet, how individual commensal bacteria influence this axis, and how biological sex alters both the microbiome and immune response remains poorly understood. Bacteroides acidifaciens , drives fundamentally different intestinal microbial and metabolic states in female and male mice during ARDS, and provides some evidence of how both can impact ARDS outcomes. Females develop an environment enriched in inflammatory lipid mediators, while males exhibit a metabolic profile associated with barrier support and reduced inflammation. These findings have implications for understanding sex-based differences in ARDS outcomes and for identifying microbiome-targeted therapeutic strategies.},
}

@article {pmid42926550,
year = {2026},
author = {Grossman, AS and S Souza, JG and Lei, L and Anochshenko, K and Xia, M and Wang, Y and Reyre, JL and Lowe, EC and He, X and Moynihan, PJ and Mougous, JD and Bor, B},
title = {Host Cell Wall Polysaccharides Modulate Nanosynbacteria Recognition and Attachment.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.10.06.756255},
pmid = {42926550},
issn = {2692-8205},
abstract = {UNLABELLED: Ultrasmall episymbiotic bacteria grow on the surface of their obligate bacterial hosts. These episymbionts have a restricted host range and likely rely on host-derived receptor molecules to identify and associate with cognate hosts. Nanosynbacteria from the oral microbiome, like Nanosynbacter lyticus , utilize a pair of distinct type 4 pili (T4P) for host surface interactions, T4P-1 and T4P-2. In this study we identify the adhesin components of both T4P, demonstrate that these adhesins localize to the cell wall of the cognate host Actinobacterium Schaalia odontolytica , and demonstrate that each adhesin binds distinct components of the host cell wall. The adhesin from the motility driving T4P-1, termed PilX1, showed a wide range of affinities in microarray screening and bound peptidoglycan directly, but could not bind purified cell wall polysaccharides (CWPS) from host surfaces. Conversely, the adhesin from T4P-2, termed PilX2, bound host-derived CWPS and preferentially bound episymbiont-naïve hosts over episymbiont-exposed hosts. Within the bacterial host we identified two CWPS biosynthesis pathways that altered adhesin binding and episymbiont susceptibility. Disruption of a rhamnose-CWPS pathway left hosts susceptible to episymbiont binding and disruption of a fucose remodeling pathway made hosts more resistant to episymbiont binding. Analyzing polysaccharide compositions revealed multiple CWPS, potentially including a rhamnose- and mannose-rich rhamnomannan. Consistent with this finding, exogenously added rhamnose and mannose were able to block binding by N. lyticus , supporting a role for these sugars in episymbiont defense. Our study reveals that Nanosynbacteria rely on the complex sugars that coat their host bacteria for recognition and attachment.

IMPORTANCE: Minisyncoccota is a diverse phylum of ultrasmall bacteria that live in many environments, including the human microbiome, but remain understudied because they can only grow on the surface of specific prokaryotic hosts. This lifestyle is called episymbiosis and little is known about how episymbionts recognize and attach to their specific hosts. We found that Nanosynbacter lyticus , a model Minisyncoccota episymbiont, uses a pair of pilus associated proteins to mediate recognition and adhesion to molecules within hosts' cell walls, including surface polysaccharides. Examining cell wall polysaccharide biosynthesis within the host revealed that changes in polysaccharide composition can increase or decrease susceptibility to episymbionts. These findings reveal distinct but overlapping adhesion roles for the two type 4 pili produced by N. lyticus , while also highlighting an important role for host surface sugars in influencing host-episymbiont compatibility.},
}

@article {pmid42926551,
year = {2026},
author = {Carley, L and Simha, A and Bass, E and Carmichael, A and Wagner, MR},
title = {Heritable variation in root bacterial microbiomes alters natural selection on host plants.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.10.07.757180},
pmid = {42926551},
issn = {2692-8205},
abstract = {Heritable variation in microbiome compositions could theoretically evolve in response to selection acting on hosts, but empirical evidence of this is scarce. We tested for effects of allelic variation in Boechera stricta on microbiome composition and downstream consequences for host fitness. In the greenhouse, near-isogenic lines with contrasting phytochemistry alleles differentially conditioned soil microbiota in ways that changed the genotypes' relative fecundity. In the field, root microbiome differences mediated allelic effects on host fitness. Selection gradients on individual taxa and multivariate axes of root microbiome composition suggest that independent components of the bacterial community favor each allele, especially under drought. These results show that microbiota contribute to natural selection on a major-effect phytochemistry gene, empirically "closing the loop" between microbiome heritability and host trait evolution.},
}

@article {pmid42926564,
year = {2026},
author = {Khan, D and Kwambana-Adams, B and Tientcheu, PE and Thomas, SA and Espinoza, JL and John, G and Mamaghani, T and Ndow, PS and Kinteh, MA and Worwui, A and Otchere, ID and Mohammed, NI and Nicol, MP and Dupont, CL and Antonio, M},
title = {Upper respiratory tract bacterial microbiome features associated with Streptococcus pneumoniae colonisation and environmental factors among healthy older children in a rural setting in The Gambia.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.10.04.756419},
pmid = {42926564},
issn = {2692-8205},
abstract = {The upper respiratory tract (URT) microbiome plays a vital role in respiratory health, with older children (5-14 years old) serving as key reservoirs for the transmission of bacteria to younger individuals (< 5 years old). However, the URT microbiome in this age group remains poorly characterised, particularly in relation to colonisation by the pathobiont Streptococcus pneumoniae . To address this gap, we analysed URT samples collected over eight visits from 134 healthy children aged 5-14 years in The Gambia, using culture-dependent methods to detect S. pneumoniae and culture-independent 16S rRNA sequencing to characterise the microbiome in parallel. 16S rRNA sequencing identified Streptococcus and Prevotella as the dominant microbiome constituents. When integrating longitudinal sampling data, we observed temporal instability with frequent switches in microbiome profiles over time. URT samples colonised with S. pneumoniae were associated with increased abundance of Moraxella , Streptococcus and Haemophilus, whereas non-colonised URT samples were enriched with Granulicatella and Filifactor . S. pneumoniae colonisation was also associated with lower Shannon diversity compared with non-colonised samples. Age and season were the strongest determinants of microbiome composition; increasing age was associated with decreasing prevalence and abundance of taxa including Haemophilus and Moraxella , while gram-positive taxa were predominantly enriched in the dry season. These findings provide new insight into the URT microbiome of older children in The Gambia and highlight Granulicatella and Filifactor as potential contributors to colonisation resistance against S. pneumoniae .},
}

@article {pmid42926685,
year = {2026},
author = {Tossas, KY and Zhu, B and Tyc, KM and Rhodes, C and Strauss, JF and Serrano, MG and Buck, GA},
title = {HPV co-infection burden, vaginal microbiota restructuring, and host context are associated with Cervical precancer risk in a racially restricted observational cohort.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-11028378/v1},
pmid = {42926685},
issn = {2693-5015},
abstract = {Background High-risk human papillomavirus (HPV) infection is necessary for cervical carcinogenesis, but HPV detection alone does not distinguish transient infection from lesions at greatest risk of progression. We evaluated whether HPV burden, vaginal microbiota structure, and host-context variables jointly characterize cervical intraepithelial neoplasia grade 3 (CIN3) in a Black/African American and White analytic cohort from the Vaginal Microbiome Health Project (VaMHP), integrating L1-based HPV typing, 16S rRNA vaginal microbiota profiling, and linked clinical metadata. Results Among 1181 participants, 75 had CIN3. CIN3 was associated with HPV positivity (55/75, 73.3% vs 431/1106, 39.0%; odds ratio [OR] 4.31, 95% CI 2.55-7.29; Fisher exact p = 7.9 x 10^-9) and with multiple HPV infection among HPV-positive participants (35/55, 63.6% vs 176/431, 40.8%; OR 2.54, 95% CI 1.42-4.54; p = 0.0022). HPV communities in CIN3-positive samples showed higher Shannon diversity, greater observed strain richness, higher evenness, and significant beta-diversity separation. In vaginal microbiota analyses, alpha diversity did not differ by CIN3 status, but community composition did, and Lactobacillus crispatus was the only taxon depleted in CIN3 after multiple-testing correction. Race, age, and metronidazole exposure were central nodes in the host-factor network. In predictive modeling, a full integrated model combining metadata, HPV, and vaginal microbiota features (auROC = 0.745) outperformed both HPV + vaginal microbiota (auROC = 0.670) and HPV-only (auROC = 0.440) models. Conclusions CIN3 in this cohort was associated with coordinated shifts in virologic burden, vaginal community structure, and host social-clinical context. The results support a structure-function interpretation in which loss of Lactobacillus crispatus-dominant states and enrichment of dysbiosis-associated communities define a host-microbiome context that is more permissive to HPV persistence and precancer. These findings move beyond descriptive omics by showing that microbiome and host-context features add nonredundant discriminatory signal beyond HPV-only models.},
}

@article {pmid42926836,
year = {2026},
author = {Guo, J and Tran, HTT and Cai, Q and Hoang, MV and Tran, TV and Shu, XO and Nguyen, SM},
title = {Rural-urban differences in gut microbiome among Vietnamese women.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.10.04.26364707},
pmid = {42926836},
abstract = {Gut microbiome plays an important role in human health. Urbanization has been suggested to alter the gut microbiome. We comprehensively evaluated differences in gut microbiome profiles of 76 urban and 81 rural female residents of Vietnam using shotgun metagenomic data. We evaluated rural-urban differences in gut microbial diversity, individual microbial taxa, and metabolic pathways. Rural residents had higher alpha and beta diversities in age-adjusted models (p<0.05). Additionally, significant rural-urban differences were observed for 35 microbial taxa in age-adjusted models (FDR<0.1). Rural residents had higher relative abundance of classes, orders, and families of FGB2982 and FGB38642 and strain SGB15332 of the species Faecalibacterium prausnitzii , whereas urban residents had higher relative abundances of species Bacteroides thetaiotaomicron, Coprobacter fastidiosus, Bilophila wadsworthia, Enterobacter cloacae, Enterobacter hormaechei, Klebsiella aerogenes , Dielma fastidiosa, and Holdemania massiliensis. Notably, these associations were attenuated after further adjustment for socioeconomic characteristics, lifestyle, dietary factors, and comorbidity (FDR>0.1). In the fully adjusted model, significant rural-urban differences were observed in the abundance of 17 microbial taxa, including Ruminococcus sp AF13 28 and Prevotella pectinovora, as well as in three metabolic pathways (FDR<0.1). This study suggests that urbanization-related factors may contribute to differences in the gut microbiome between urban and rural Vietnamese women.},
}

@article {pmid42926855,
year = {2026},
author = {Castillo-Vargas, E and Martin-Almeida, M and Bozack, AK and Garcia, EL and Martin-Gonzalez, E and González-Pérez, R and Hernández-Pérez, JM and Sardón-Prado, O and Poza-Guedes, P and Mederos-Luis, E and Corcuera-Elosegui, P and Sánchez-Machín, I and López-Fernández, L and Rifas-Shiman, SL and Hashimoto, S and Vijverberg, SJH and Neerincx, AH and Buntrock-Döpke, H and Gorenjak, M and Toncheva, AA and Harner, S and Brandstetter, S and Wolff, C and Potočnik, U and Kabesch, M and Kraneveld, AD and Villar, J and Hivert, MF and Oken, E and Gold, DR and Abdel-Aziz, MI and Maitland-van der Zee, AH and Cardenas, A and Lorenzo-Diaz, F and Pino-Yanes, M and Perez-Garcia, J},
title = {Epigenome-Wide Association Study of the Upper-Airway Microbiome Involved in Asthma Exacerbations.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.10.02.26364005},
pmid = {42926855},
abstract = {RATIONALE: The role of DNA methylation (DNAm) markers in the upper-airway microbiome related to asthma exacerbations despite inhaled corticosteroid (ICS) treatment is unexplored.

OBJECTIVES: To identify whole-blood DNAm markers associated with the upper-airway microbiome related to asthma exacerbations despite ICS treatment.

METHODS: We analyzed salivary, nasal, and pharyngeal microbiome in 242 asthma patients (GEMAS) for discovery. We tested associations between whole-blood DNAm at 703,505 CpGs and 21 exacerbation-related microbiome traits. Replication for the nasal microbiome was evaluated in 272 (Project Viva) and 66 (SysPharmPediA) children with and without asthma. We analyzed differentially methylated regions (DMRs), gene enrichment, associations with blood gene expression (RNA-seq, n=119), and DNAm predictors of plasma proteins.

MEASUREMENTS AND MAIN RESULTS: Whole-blood DNAm at 73 CpGs and 550 DMRs was associated with 17 exacerbation-related microbiome traits (false discovery rate [FDR]<0.05), including genes implicated in immune and inflammatory responses and the 17q12-q21 asthma locus ORMDL3 . Most CpGs were associated with Campylobacter (pharyngeal) and Leptotrichia (nasal) abundance. Ten DNAm markers were replicated (p <0.05), including the corticosteroid insensitivity-related gene PTPRR associated with nasal bacterial richness. Enrichment analyses identified genes related to diabetes, obesity, smoking, TGF-β, MAPK, and Wnt signaling and regulated by trichostatin A, NF-κB, and the glucocorticoid receptor (FDR<0.05). The CpG cg18994033, associated with pharyngeal Tannerella , was associated with ITM2C whole-blood expression. Nine DNAm-predicted plasma proteins involved in inflammation, tissue remodeling, and TGF-β signaling were associated with seven exacerbation-related microbiome traits, including Streptococcus and Selenomonas .

CONCLUSIONS: Whole-blood DNAm markers implicated in inflammation, immunity, and asthma comorbidities were associated with the upper-airway microbiome linked to asthma exacerbations.},
}

@article {pmid42926938,
year = {2026},
author = {Vatanen, T and Kreuze, K and Björkgren, L and Turkington, C and Nezam-Abadi, N and Seymour, S and Shkoporov, A and Hill, C and Friman, V and Knip, M},
title = {Maternal transmission and limited virulent phage replication shape early infant gut virome maturation.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-11232673/v1},
pmid = {42926938},
issn = {2693-5015},
abstract = {Early life gut microbiome dynamics are increasingly recognized as important determinants of microbiome maturation, yet the ecological dynamics of its associated bacteriophages remain poorly resolved. Here, we performed bulk and virus like particle (VLP)-enriched metagenomic sequencing and fecal metabolomic profiling of longitudinal fecal samples from 32 mother-infant dyads, incorporating an exogenous phage spike in to enable absolute quantification of viral loads. Our results show that early infant gut phageome is defined by a profound lack of virulent phage genome copies while temperate phages remain relatively stable, challenging previous assumptions. We further identified extensive maternal sharedness of mainly virulent phages predicted to infect Bacteroidaceae, which could explain recovery of virulent phage absolute abundances. Virulent phage concentrations were further associated with several fecal metabolites including primary bile acids. These findings revise the current model of infant phageome assembly highlighting the underappreciated role of virulent phages.},
}

@article {pmid42926952,
year = {2026},
author = {Ferro, LE and Anyaso-Samuel, S and Yano, Y and Hua, X and Wan, Y and Chang, VC and Dagnall, CL and Jones, K and Hicks, BD and Hutchinson, A and Liao, LM and Huang, WY and Freedman, ND and Beane Freeman, LE and Sandler, DP and Abnet, CC and Shi, J and Sinha, R and Loftfield, E and Vogtmann, E},
title = {Associations between commonly consumed beverages and the oral microbiome in three US cohort studies.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.10.07.26364990},
pmid = {42926952},
abstract = {Multiple external factors shape human microbial communities. Beverages represent particularly frequent dietary exposures that may impact oral microbiome composition. We examined associations of coffee, tea, alcohol, sugar-sweetened beverages, artificially-sweetened beverages, and fruit juice consumption with the oral microbiome in three large cohort studies (n=5,598). Beverage consumption was assessed by food frequency questionnaire and categorized as non-consumers and tertiles of intake among consumers, except fruit juice, which was categorized into quartiles. DNA from oral wash specimens was sequenced (16S rRNA, V4 region). Associations with alpha and beta diversity and individual genera were assessed using multivariable linear, logistic, count-based regression models and weighted permutation-based models accounting for multiple comparisons in genus-level analyses. Only alcoholic beverage consumption was associated with all alpha diversity metrics; the highest tertile of alcohol drinking was associated with 10.18 (95% CI: 5.56, 14.80) greater observed amplicon sequence variants vs. non-consumers. All beverages accounted for 4.06% of variability in beta diversity (unweighted UniFrac); in univariable models, alcoholic beverages had the largest R[2] among individual beverages (0.86%) and accounted for the majority (25/28, 89.3%) of genus-level associations, mostly with beer and liquor. For example, high alcoholic beverage intake (T3 vs. non-consumers) was associated with 2.25 and 2.17 times the odds of having Megasphaera and Peptostreptococcus , respectively, and 23% lower abundance of Lautropia . Alcoholic beverage consumption was strongly associated with oral microbes, including taxa linked to poor oral health; these findings suggest that alcohol-associated differences in the oral microbiome may have implications for oral and systemic health.},
}

@article {pmid42927053,
year = {2026},
author = {Lundholm, KR and Satterfield, BC and Banks, S and Liu, PY and Kombala, CJ and Hurtado-Alvarado, G and Greer, AJ and Muck, RA and Layton, MA and Du, D and Gaddameedhi, S and Van Dongen, HPA},
title = {Biological Mechanisms Underlying the Adverse Health Consequences of Human Circadian Misalignment from Night Shift Work.},
journal = {Current sleep medicine reports},
volume = {12},
number = {1},
pages = {51},
pmid = {42927053},
issn = {2198-6401},
abstract = {PURPOSE OF REVIEW: The waking and working times of night shift workers are displaced relative to the natural light/dark cycle, putting behavioral patterns in misalignment with the circadian regulation of biological processes. This state of circadian misalignment constitutes a circadian health problem, with widespread negative consequences for metabolic, cardiovascular, and mental health, as well as elevated risk of cancer. Scientific advances over the past decade have shed light on key aspects of the underlying biological mechanisms. With a focus on recent human studies, this paper reviews novel insights into what drives the adverse health consequences of circadian misalignment due to night shift work.

RECENT FINDINGS: Misalignment between the central circadian pacemaker and externally driven behavioral patterns during night shift work produces a rapid uncoupling of peripheral rhythms, reflected in the cargo of exosomes and other signaling mechanisms, and causes conflict between central and peripheral regulatory mechanisms. This endogenous internal desynchrony has been shown to be linked to shifted meal timing and, in part, may be mediated by the gut microbiome. Endogenous internal desynchrony leads to insulin resistance - a manifestation of metabolic dysfunction. It perturbs the cardiometabolic and immune systems, and also erodes mental health. At the cellular level, mistimed DNA repair mechanisms leave residual DNA damage after exposure to a night shift schedule - which, over time, may result in genomic instability and ultimately carcinogenesis.

SUMMARY: A systems biology perspective serves to elucidate how the effects of endogenous circadian disruption from night shift work increase the risk of acute and chronic illnesses. Internal desynchrony, endogenous in nature, is a common underlying cause. Time-restricted eating may help to address metabolic dysfunction due to night shift work; countermeasures for other negative health outcomes, including cancer and mental health disorders, remain to be developed.},
}

@article {pmid42927080,
year = {2026},
author = {Sun, G and Guo, T and Lang, W and Peng, F and Jiang, X and Chen, J},
title = {Global research trends and emerging hotspots in probiotics and children's neurodevelopment: a bibliometric and visualized analysis (1998-2026, partial year).},
journal = {3 Biotech},
volume = {16},
number = {11},
pages = {473},
pmid = {42927080},
issn = {2190-572X},
abstract = {UNLABELLED: Research on the role of probiotics in children's neurodevelopment has expanded rapidly, yet a quantitative synthesis of this interdisciplinary field is lacking. This study aimed to map global research trends, identify key contributors, and reveal emerging hotspots in the field of probiotics and children's neurodevelopment through bibliometric and visualized analysis. Publications indexed in the Web of Science Core Collection from 1998 to 2026 (partial year, search conducted on 21 May 2026) were retrieved using a predefined search strategy combining terms related to probiotics, children, and neurodevelopment. After screening and deduplication, 1,684 documents were included. Bibliometric indicators, including annual publication trends, productive authors and journals, keyword co-occurrence networks, temporal trends in keyword frequency, and the top 15 most frequently cited references, were analyzed using the bibliometrix R package, igraph, ggplot2, and wordcloud. Common keyword synonyms were merged prior to network construction. Annual publication output increased steadily from 1998 to 2015 and accelerated sharply after 2020, reaching a peak in 2025. The most frequent publication venues included Nutrients and Frontiers in Microbiology. Keyword co-occurrence analysis revealed a core network centered on Gut Microbiota, Autism Spectrum Disorder, Probiotics, and Gut-Brain Axis, with ADHD emerging as a distinct and increasingly prominent node in the 2020-2026 period. Temporal trends in keyword frequency indicated a shift from broad descriptive associations toward more specialized terms such as Dysbiosis, Fecal Microbiota Transplantation, Neuroinflammation, and Metabolomics. Highly cited documents and the top 15 most frequently cited references were anchored by seminal works on the gut-brain axis and microbiome-behavior relationships, forming a stable intellectual base. This study provides a comprehensive overview of the research landscape in probiotics and children's neurodevelopment. The field is shifting from observational studies toward mechanism-oriented and interventional research, with ADHD and multi-omics approaches representing important emerging directions. As a single-database analysis, these findings should be interpreted with caution, and future studies should integrate additional databases to validate and extend them. Translational implications include stratifying patients by neurodevelopmental diagnosis and microbial profile, and testing mechanism-guided probiotic or synbiotic formulations in future trials. These findings offer useful guidance for researchers seeking to understand the structure of the field and identify promising areas for future investigation.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at https://doi.org/10.1007/s13205-026-05105-2.},
}

@article {pmid42927177,
year = {2026},
author = {Khoshaba, E and Huang, X and Cheek, C and Naqib, A and Shaikh, MW and Abdel-Mohsen, M and Mahdavinia, M and Rasmussen, HE and Keshavarzian, A and Bishehsari, F},
title = {Circadian misalignment associates with inflammation, gut barrier, and microbiome composition in humans with obesity.},
journal = {iScience},
volume = {29},
number = {11},
pages = {117892},
pmid = {42927177},
issn = {2589-0042},
abstract = {Circadian disruption has been linked to metabolic syndrome, but the biological links between circadian phenotypes and metabolic inflammation in humans remain incompletely characterized. We analyzed 87 adults with obesity from a randomized clinical trial to examine whether gut microbiome features and intestinal permeability relate to circadian misalignment and metabolic inflammation. Circadian phenotype was assessed using chronotype and meal timing, metabolic inflammation through a composite score of multiple biological measures, and gut permeability using sugar absorption testing. Late chronotype was associated with greater metabolic syndrome burden, while circadian misalignment was associated with increased gut permeability and inflammation, an association stronger among participants with higher permeability. These patterns co-occurred with lower abundance of short-chain fatty acid-associated bacteria, and intervention-related changes in permeability corresponded with changes in these taxa. These findings link circadian phenotypes with gut barrier and microbial features relevant to metabolic risk in obesity.},
}

@article {pmid42927796,
year = {2026},
author = {Yang, H and Shyong, O and Wu, L and Marcet, E and Dillon, B and Dillon, J and Marzialo, D and Krysiewicz-Bell, A and Popeo, L and Jamali, S and Schrodel, G and Davis, A and Shi, A and Cairns, DM and Power, LH and Kaplan, DL and McKee, A and Daneshvar, D and Vinacur, M and Pier, GB and Zafonte, R and Whalen, MJ and Cywes-Bentley, C},
title = {Persistent microbial-derived material accumulates after brain injury and associates with chronic neuroinflammation.},
journal = {Brain, behavior, and immunity},
volume = {},
number = {},
pages = {107082},
doi = {10.1016/j.bbi.2026.107082},
pmid = {42927796},
issn = {1090-2139},
abstract = {OBJECTIVE: Traumatic brain injury (TBI) is associated with chronic neurodegenerative sequelae, including chronic traumatic encephalopathy (CTE), but mechanisms sustaining long-term neuroinflammation in the injured brain remain unclear. Persistent, poorly cleared biological material has been proposed as a driver of chronic inflammation. This study tested whether microbial-derived material is present in CTE and experimental brain injury, and whether reducing such material is associated with improved outcomes.

METHODS: Post-mortem brain tissue from individuals with CTE and controls was analyzed for the microbial polysaccharide poly-N-acetyl-glucosamine (PNAG) and phosphorylated tau (pTau). Mice were subjected to single and repetitive closed head injury (CHI), with assessment of brain PNAG and tau accumulation, behavior, and neuropathology. Purified PNAG was administered intracerebrally to evaluate biological effects. Passive antibody treatment and active vaccination targeting PNAG were used to determine whether reducing brain PNAG altered outcomes after CHI.

RESULTS: PNAG accumulated in human CTE brains in a disease stage-dependent manner and colocalized with pTau. In mice, PNAG rapidly accumulated across multiple brain regions after CHI and remained elevated at two weeks. Intracerebral administration of purified PNAG induced physiological and behavioral deficits that differed by sex, whereas a lower dose produced no detectable behavioral deficits. Passive anti-PNAG antibody treatment reduced brain PNAG with limited functional benefit, whereas active vaccination in adolescence and early adulthood reduced brain PNAG accumulation and IBA1 immunoreactivity, was associated with lower pTau accumulation, and improved long-term motor outcomes one year after repetitive CHI.

CONCLUSIONS: Persistent microbial-derived material is detectable in human CTE and experimental TBI. Reduction of PNAG-associated microbial-derived material is associated with attenuation of chronic neuroinflammation, pathological tau accumulation, and improved long-term neurological outcomes, supporting a model in which persistent microbial-derived material may contribute to chronic post-traumatic neuroinflammation.},
}

@article {pmid42927859,
year = {2026},
author = {Das, R and Varshni, K and Mohanty, M and Chakraborty, U and Sekar, A and Mishra, P and Dash, R and Jain, M and Das, G and Ramadass, B},
title = {The Gut-Spine Axis in Lumbar Intervertebral Disc Degeneration: Microbial and Inflammatory Signatures.},
journal = {The spine journal : official journal of the North American Spine Society},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.spinee.2026.10.016},
pmid = {42927859},
issn = {1878-1632},
abstract = {BACKGROUND CONTEXT: Intervertebral disc degeneration (IDD) is commonly found in patients with chronic low back pain. Traditionally viewed as a biomechanical failure, emerging evidence implicates systemic inflammation in IDD pathogenesis. The proposed "gut-spine axis," in which gut dysbiosis may promote inflammation and, potentially, disc colonization, represents a paradigm shift. To bridge gaps in human data, we present the first multi-compartment (gut-blood-disc) study profiling paired microbiomes alongside systemic inflammatory biomarkers.

PURPOSE: To investigate the role of the gut-spine axis in intervertebral disc degeneration (IDD) by characterizing gut microbiome dysbiosis, its association with systemic inflammation, and the presence of distinct microbial signatures in degenerated disc tissue.

STUDY DESIGN/SETTING: Prospective clinical case-control study conducted at a tertiary care center.

PATIENT SAMPLE: Twenty adult patients (aged 18-65 years) undergoing surgical discectomy for symptomatic lumbar IDD (Pfirrmann grade ≥3) and twenty age-matched healthy controls without low back pain or radiographic evidence of IDD.

OUTCOME MEASURES: Primary outcomes included gut and disc microbial diversity (alpha diversity indices: Shannon, Simpson, observed genera; beta diversity: Bray Curtis dissimilarity), genus level relative abundance of key microbial organisms, and systemic inflammatory status assessed using the neutrophil-to-lymphocyte ratio (NLR). Secondary outcomes included associations between microbial organisms and systemic inflammation.

METHODS: We prospectively analyzed patients undergoing lumbar IDD surgery alongside matched healthy controls. Paired fecal and surgically excised disc samples underwent 16S rRNA sequencing. Systemic inflammation was quantified via the peripheral neutrophil-to-lymphocyte ratio (NLR). We evaluated alpha- and beta-diversity and employed linear regression to assess functional associations between microbial abundance and NLR RESULTS: Patients with symptomatic IDD exhibited significant gut dysbiosis, including elevated Streptococcus and a 7-fold enrichment of Collinsella (10% in IDD vs. 1.5% in controls). Fecal Acinetobacter positively correlated with systemic inflammation (NLR; R²=0.326, p=0.009), whereas beneficial Dorea negatively correlated (R²=0.230, p=0.032). Locally, degenerated discs harbored a unique, low-diversity microbiome (Simpson index p=0.038) dominated by the facultative anaerobes Acinetobacter and Stenotrophomonas (32% relative abundance vs. <1% in gut). Beta-diversity confirmed disc and gut communities are statistically distinct (PERMANOVA R²=0.451, p=0.001), a pattern more consistent with compartment-specific microbial communities than with surgical contamination.

CONCLUSIONS: This study provides preliminary evidence for a potential functional gut-spine axis in symptomatic lumbar IDD. We show that IDD is associated with a pro-inflammatory gut dysbiosis that correlates with systemic inflammation. Furthermore, the identification of a unique, pathobiont-enriched microbiome within the degenerated disc challenges the view of IDD as a sterile condition. These findings suggest that IDD may have a systemic component, and point to microbiome-targeted diagnostics and therapeutics as potential avenues for future intervention.},
}

@article {pmid42927865,
year = {2026},
author = {Chung, S and Kim, JH and Nam, YD and Lim, MY},
title = {Gut microbiome-mediated associations between dietary intake and type 2 diabetes in a Korean population.},
journal = {Diabetes research and clinical practice},
volume = {},
number = {},
pages = {113626},
doi = {10.1016/j.diabres.2026.113626},
pmid = {42927865},
issn = {1872-8227},
abstract = {AIMS: Type 2 diabetes (T2D) is influenced by multiple risk factors, including dietary intake, which may affect disease risk through interactions with the gut microbiome. This study sought to identify microbial features that mediate these associations in a Korean population.

METHODS: Data from 1,347 participants aged 30-64 years were analyzed. Dietary intake was assessed using a food frequency questionnaire, and gut microbiome profiles were generated by 16S rRNA gene amplicon sequencing of the V3-V4 region. MaAsLin2 and mediation analyses were then performed.

RESULTS: Forty-eight amplicon sequence variants (ASVs) were associated with T2D. Lachnospira ASV054, Romboutsia B ASV190, and Clostridium T ASV104 were inversely associated with T2D and statistically mediated the associations of bread, starchy food, and kimchi intake with T2D, respectively (q < 0.001). Clostridium T ASV104 also exhibited indirect effects opposite to the direct effects of rice cake and ultra-processed food (UPF) intake on T2D (q < 0.05), suggesting suppressive effects.

CONCLUSIONS: Several gut microbial features inversely associated with T2D partially mediated diet-T2D associations and exhibited suppressive effects for rice cake and UPF intake. These findings suggest that the gut microbiome may play an important role in mediating associations between dietary intake and T2D.},
}

@article {pmid42928081,
year = {2026},
author = {McCabe, LR},
title = {Rethinking the Gut-Bone Axis: Diet, the Gut Ecosystem, and Skeletal Health.},
journal = {Current osteoporosis reports},
volume = {24},
number = {1},
pages = {},
pmid = {42928081},
issn = {1544-2241},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Bone and Bones/metabolism ; *Diet ; *Osteoporosis/metabolism/microbiology ; Animals ; Intestinal Barrier Function ; Probiotics/therapeutic use ; },
abstract = {PURPOSE OF REVIEW: The gut-bone field has expanded beyond its initial focus on the gut microbiota to include microbial metabolism, epithelial barrier integrity, immune and endocrine signaling, and host-microbial interactions. This review uses a functional gut ecosystem framework to integrate these mechanisms and examine how diet and other exposures influence skeletal health.

RECENT FINDINGS: No consistent microbial signature of osteoporosis has emerged across populations or experimental models. Instead, recent studies indicate that skeletal responses are associated with functional outputs of the gut ecosystem, including nutrient bioavailability, microbial co-metabolic products, barrier integrity, and host sensing. Gut-derived signals may act directly on bone or be further processed by the host. Diverse interventions, including whole foods, probiotics, postbiotics, and targeted therapies, can converge on these functions. Bone responds to the integrated biological signals generated by the gut ecosystem rather than microbial composition alone. Defining these functions and individual responder phenotypes may provide new approaches for preserving skeletal health.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Bone and Bones/metabolism
*Diet
*Osteoporosis/metabolism/microbiology
Animals
Intestinal Barrier Function
Probiotics/therapeutic use

@article {pmid42928377,
year = {2026},
author = {Wang, W and Huang, C and Liu, C},
title = {Community Assembly Mechanisms Facilitate Understanding of Microbial Responses to Habitat Transition along a Spatial Environmental Continuum in Alpine Plateaus.},
journal = {Microbial ecology},
volume = {89},
number = {1},
pages = {},
pmid = {42928377},
issn = {1432-184X},
mesh = {*Soil Microbiology ; *Microbiota ; *Bacteria/classification/genetics/isolation & purification ; *Ecosystem ; Grassland ; Wetlands ; Biodiversity ; Soil/chemistry ; },
abstract = {While soil microorganisms mediate important ecosystem functions, their community assembly mechanisms along a spatially connected environmental continuum remain elusive. Here, we profiled the taxonomic and functional characteristics of soil microbiomes across three independent wetland-grassland-bareland continua on the Pamir Plateau. Along this spatial environmental continuum, microbial diversity, network complexity, and network stability decreased significantly towards barelands. Null model analyses revealed a pronounced shift in community assembly within barelands, characterized by increased heterogeneous selection and dispersal limitation. This assembly shift, potentially associated with water limitation and salt stress, may contribute to the diminished diversity and network robustness. Notably, predicted soil microbial functional potential peaked in grasslands, likely reflecting enhanced plant-soil feedbacks. By linking community properties to predicted functionality, we demonstrated that microbial diversity, rather than network complexity, was more strongly associated with variation in predicted soil microbial functional potential. Ultimately, these findings provide a mechanistic understanding of microbial community assembly and functional transition in sensitive alpine ecosystems.},
}

*Soil Microbiology
*Microbiota
*Bacteria/classification/genetics/isolation & purification
*Ecosystem
Grassland
Wetlands
Biodiversity
Soil/chemistry

@article {pmid42928381,
year = {2026},
author = {Carrera-Bastos, P and Plaza-Florido, A and Pérez-Prieto, I and Radom-Aizik, S and Franceschi, C and Rodríguez-López, C and Serra-Rexach, JA and Emanuele, E and Lucia, A},
title = {Cardiovascular resilience in centenarians.},
journal = {Nature reviews. Cardiology},
volume = {},
number = {},
pages = {},
pmid = {42928381},
issn = {1759-5010},
abstract = {Centenarians - individuals aged ≥100 years - provide a unique human model for understanding resilience to cardiovascular ageing. Although cardiovascular and metabolic diseases, including hypertension, heart failure, atrial fibrillation and chronic kidney disease, are common in centenarians, their onset is typically delayed relative to that in individuals aged 80-100 years. Centenarians characteristically have structural changes in the heart and vessels, including concentric left ventricular remodelling, increased myocardial stiffness and vascular ageing, but often without the expected burden of myocardial infarction or overt heart failure. Their cardiometabolic profile is generally favourable, marked by preserved insulin sensitivity in cohorts with a low prevalence of diabetes mellitus, mid-range lipid levels and a low prevalence of obesity. Centenarians also have a distinctive inflammatory and gastrointestinal phenotype, characterized by chronic low-grade inflammation with elevated anti-inflammatory signalling, a gut microbiome that more closely resembles that of younger adults, and preserved intestinal barrier integrity. Genetically and epigenetically, exceptional longevity reflects highly polygenic contributions, selective maintenance of genomic stability and markedly younger epigenetic age compared with chronological age. In this Review, we summarize data on the cardiovascular system among centenarians by framing observations of longevity as a composite of delayed pathology, adaptive compensation and survivorship selection. Understanding the biological, behavioural and environmental mechanisms underlying cardiovascular resilience in extreme longevity might inform strategies to extend cardiovascular healthspan across all ages.},
}

@article {pmid42928559,
year = {2026},
author = {Zhu, N and Zhao, P and Liu, X and Leng, F and Guo, X and Yang, Z and Zhou, J and Wang, X and Luo, W and Gao, D and Luo, M and Wang, Y},
title = {Root rot suppression by synthetic microbiota is associated with rhizosphere bacterial shifts and amino acid metabolism.},
journal = {Journal of experimental botany},
volume = {},
number = {},
pages = {},
doi = {10.1093/jxb/erag521},
pmid = {42928559},
issn = {1460-2431},
abstract = {Root rot caused by Fusarium oxysporum (F. oxysporum) severely constrains Codonopsis pilosula (C. pilosula) production. Indigenous culturable bacteria associated with C. pilosula were screened for antifungal activity, plant growth-promoting traits, and interstrain compatibility, and two defined three-member synthetic microbial communities, SCI and SCII, were constructed. Both SynComs alleviated root rot, with SCI showing stronger overall performance and a biocontrol efficacy of 57.8%, together with improved root growth and photosynthetic performance. Rhizosphere bacterial profiling was integrated with rhizosphere metabolite profiling and root tissue metabolomics. SynCom treatment was associated with limited changes in overall bacterial diversity but variation in specific rhizosphere taxa. In roots, pathway-enrichment patterns shifted from sulfur metabolism and oxidative stress-related processes under pathogen stress toward amino acid-related metabolism after SynCom treatment, accompanied by treatment-associated variation in medicinally relevant metabolite features. Associations between metabolic changes and potentially beneficial bacteria indicated coordinated variation between host metabolism and rhizosphere bacterial composition. In vitro assays further showed that L-valine elicited chemotactic and growth responses in a representative Sphingomonas isolate. Collectively, SynCom-mediated root rot suppression was associated with constituent-strain antagonism, plant recovery, rhizosphere bacterial shifts, and amino acid-related metabolic variation.},
}

@article {pmid42929408,
year = {2027},
author = {Zhao, R and Song, X and Qin, M and Fan, B and Niu, S and Zheng, D and Liu, J and Qi, J and Wang, P and Sun, J and Bai, F and Bai, W},
title = {Exploring the association of quercetin with liver fibrosis through network pharmacology and 16S rRNA gene sequencing.},
journal = {Pakistan journal of pharmaceutical sciences},
volume = {40},
number = {1},
pages = {357-371},
doi = {10.36721/PJPS/2026.40.16003.1},
pmid = {42929408},
issn = {3105-9686},
mesh = {Animals ; *Quercetin/pharmacology ; Male ; Rats, Sprague-Dawley ; *RNA, Ribosomal, 16S/genetics ; *Liver Cirrhosis/drug therapy/pathology/microbiology/chemically induced ; Carbon Tetrachloride ; *Gastrointestinal Microbiome/drug effects/genetics ; Network Pharmacology ; Rats ; Liver/pathology/drug effects ; Protein Interaction Maps/drug effects ; },
abstract = {BACKGROUND: Liver fibrosis is a chronic wound healing process of liver injury and gut-liver axis dysregulation has been recently identified as an important contributor to liver fibrosis progression. Quercetin has been reported to have anti-inflammatory activity and microbiota-modulating effects. However, the potential targets of quercetin remain unclear, as does the relationship between quercetin-associated targets and changes in the gut microbiota in liver fibrosis.

OBJECTIVES: The purpose of this study was to use network pharmacology to predict potential targets of quercetin associated with liver fibrosis and to explore changes in gut microbiota following treatment with quercetin using a CCl4-induced rat model.

METHODS: Eighteen male Sprague-Dawley rats were randomized into CON group, MOD group and QR group (n = 6 per group). Liver fibrosis was induced by weekly subcutaneous injection of carbon tetrachloride (CCl4) for eight weeks. Oral gavage of quercetin (50 mg/kg/day) was performed in QR group. Histopathological changes were assessed by hematoxylin-eosin staining, Masson staining and Ishak scoring. Potential targets of quercetin were screened using network pharmacology, followed by protein-protein interaction (PPI) network construction and Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Cecal microbiota composition was determined by 16S rRNA gene sequencing. Parametric or non-parametric tests were used accordingly, including one-way ANOVA or Kruskal-Wallis test.

RESULTS: Histopathology revealed significant liver injury and fibrosis in the MOD group relative to the CON group. The QR group showed lower Ishak fibrosis scores and milder histopathological features compared with the MOD group. Network pharmacology analysis identified UBC, UBE2I, RBX1, PSMB7 and UBA1 as hub targets, with KEGG pathways of interest including the TNF signaling pathway, p53 signaling pathway, Toll-like receptor signaling pathway and ubiquitin-mediated proteolysis. Alpha diversity of the cecal microbiota differed significantly among groups, whereas beta diversity did not. Relative abundance of Proteobacteria decreased and Firmicutes increased in the QR group relative to the MOD group. Taxa enrichment analysis identified enrichment of Muribaculaceae and Ligilactobacillus in the QR group.

CONCLUSION: Histopathology and microbiome analyses indicated that quercetin intervention was associated with altered liver histopathological features and shifts in gut microbiota composition in rats with CCl4-induced liver fibrosis. Network pharmacology predicted several hub targets and pathways potentially linked to these observations. As the present analyses are purely correlational and lack mechanistic validation at the molecular level, no causal relationships are implied between the predicted targets/pathways and the observed histological or microbiome changes. These findings should be regarded as hypothesis-generating and warrant further validation studies.},
}

Animals
*Quercetin/pharmacology
Male
Rats, Sprague-Dawley
*RNA, Ribosomal, 16S/genetics
*Liver Cirrhosis/drug therapy/pathology/microbiology/chemically induced
Carbon Tetrachloride
*Gastrointestinal Microbiome/drug effects/genetics
Network Pharmacology
Rats
Liver/pathology/drug effects
Protein Interaction Maps/drug effects

@article {pmid42929450,
year = {2026},
author = {Lau, WS and Swords, CM and Thairu, MW and Hidalgo, N and Tatar, R and Rahrig, H and Wilson-Mendenhall, CD and Grupe, DW and Goldman, RI and Vack, NJ and Ferguson, C and Valdivia, G and Sankaran, K and Frye, C and Dahl, CJ and Lewis, R and Higgins, ET and Garza, M and Jiwani, Z and Hirshberg, MJ and Bernstein, A and Converse, E and Dimidjian, S and Ward, EC and Miller, GE and McDade, TW and Picard, RW and Handelsman, J and Rosenkranz, MA and Abercrombie, HC and Davidson, RJ and Goldberg, SB},
title = {Incorporating Objective Behavioral and Biological Measures in a Large-Scale Decentralized Mobile Health Trial for Depression: Randomized Controlled Trial.},
journal = {JMIR mental health},
volume = {13},
number = {},
pages = {e92589},
doi = {10.2196/92589},
pmid = {42929450},
issn = {2368-7959},
mesh = {Humans ; Female ; *Depression/therapy ; Male ; Adult ; Middle Aged ; Telemedicine ; Digital Health ; *Mobile Applications ; Feasibility Studies ; Surveys and Questionnaires ; },
abstract = {BACKGROUND: Decentralized (ie, fully remote) clinical trials (DCTs) offer a scalable and ecologically valid approach to evaluating digital mental health interventions (DMHIs). Yet, incorporating objective measures of well-being within DCTs poses novel methodological and feasibility challenges that can limit the rigor and precision of data collection in the field.

OBJECTIVE: We recently conducted the Behavior, Biology, and Well-being (BeWell) Study, a large-scale, 3-arm randomized DCT evaluating the Healthy Minds Program app (Humin)-a self-guided DMHI that includes didactic well-being information and meditation components. The current paper's objective is to describe the methodological approach to collecting and processing a multimodal battery of psychological (questionnaires and structured clinical interview), biological (blood and stool assays), and behavioral (stimulus-elicited affect [SEA] task, video log, and Mnemonic Similarity Task [MST]) measures, longitudinally across baseline, the 4-week intervention period, and 17-week follow-up. Secondarily, we evaluate its feasibility.

METHODS: The BeWell Study methodology is described. Descriptive statistics characterized recruitment and retention, as well as data completion and data quality. Binary logistic regressions evaluated whether recruitment sources, demographics, and depression severity predicted measure completion and data quality.

RESULTS: From June 1, 2022, through July 15, 2024, 52,052 individuals started the screening questionnaire. Of these, 2.22% (n=1156 participants; mean age 38.69, SD 12.14 years; women=75.50%; non-Hispanic White=68.88%) completed the screener, met eligibility criteria (including elevated depressive symptoms [Patient Health Questionnaire-9 [PHQ-9] score≥5]), completed baseline measures, were enrolled, and were randomized. Participants were recruited from Craigslist (694/1154, 60.14%), a US-based advertisement website, and university email messages (107/1154, 9.27%); participants were enrolled from every US state. Across the study, 84% (971/1156) of participants were retained (completed ≥1 measure at 17-week follow-up). Across time points, ≥81.40% (941/1156) of participants completed questionnaires and ≥75.17% (869/1156) completed biological samples. Of those completing questionnaires, ≥84.14% (796/946) completed SEA and video log tasks and ≥91.75% (868/946) completed the MST. Of completed assessments, high-quality or analyzable data rates across all time points were ≥97.89% (926/946) for questionnaires, ≥90.20% (773/857) for SEA, ≥84.60% (725/857) for video logs, ≥94.20% (1056/1121) for the MST, ≥98.84% (849/859) for dried blood spots, and ≥99.43% (865/870) for microbiome samples. Greater depressive symptoms at screening, but not age, predicted completion of baseline measures (odds ratios 0.96-0.99; P<.001). For enrolled participants, recruitment sources and baseline depressive symptoms were not predictive of data completion or quality. Older age and having a college degree predicted significantly higher rates of data completion across all data types (questionnaire, behavioral, and biological) at week 4 or week 17 follow-ups.

CONCLUSIONS: This methodological approach offers one model of incorporating objective measures of well-being into DCTs testing DMHIs. Implications and limitations of our approach are discussed.},
}

Humans
Female
*Depression/therapy
Male
Adult
Middle Aged
Telemedicine
Digital Health
*Mobile Applications
Feasibility Studies
Surveys and Questionnaires

@article {pmid42929529,
year = {2026},
author = {Chang, T-E and Lin, H-H and Luo, J-C and Chen, Y-F and Wang, Y-P and Lee, K-C and Lee, P-C and Lin, Y-T and Huang, H-C and Su, C-W and Huang, Y-H and Hou, M-C},
title = {Integrated microbiome and metabolomic profiling reveals alterations across the adenoma-colorectal cancer sequence.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0105926},
doi = {10.1128/spectrum.01059-26},
pmid = {42929529},
issn = {2165-0497},
abstract = {The incidence of colorectal cancer (CRC) has been increasing in Taiwan and is associated with multiple risk factors. Increasing evidence suggests that gut microbiota dysbiosis contributes to CRC development. This study aimed to characterize microbial and metabolic alterations across premalignant and malignant colorectal lesions and to identify potential microbiome-associated biomarkers. Individuals undergoing colonoscopy for screening or surveillance at Taipei Veterans General Hospital were enrolled. Gut microbial composition was analyzed using full-length 16S rRNA gene sequencing to achieve high-resolution taxonomic profiling. Predicted functional pathways were inferred from microbial communities, and targeted metabolomic profiling was performed to evaluate microbial metabolic outputs. A total of 122 individuals were included, comprising 62 healthy controls, 15 adenoma cases, and 45 CRC cases. Change in microbial composition and predicted functional pathways were observed across the control, adenoma, and CRC groups. Control-associated taxa were linked to carbohydrate fermentation and amino acid metabolism pathways, whereas CRC-associated taxa, particularly Fusobacterium, showed broad negative correlations with multiple biosynthetic pathways. Metabolomic analysis showed increased tauro-ursocholanic acid and reduced short-chain fatty acids (SCFAs) in CRC. CRC-associated bacteria were negatively correlated with SCFAs and positively correlated with several bile acid metabolites, including lithocholic acid, murocholic acid, tauro-ursocholanic acid, and taurohyocholic acid. Integrative analysis of full-length 16S rRNA sequencing, predicted functional pathways, and metabolomic profiling identified microbial and metabolic differences across the control, adenoma, and CRC groups. These findings are consistent with an association between gut microbial alterations and colorectal neoplasia and may inform future studies of microbial and metabolic biomarkers for CRC.IMPORTANCEColorectal cancer (CRC) develops through an adenoma-carcinoma sequence, yet the microbial and metabolic alterations accompanying this progression remain incompletely understood. In this study, we integrated full-length 16S rRNA gene sequencing with metabolomic profiling to characterize taxonomic, functional, and metabolic changes across healthy controls, adenoma, and CRC. Our results showed coordinated changes in microbial taxa, predicted metabolic pathways, and fecal metabolites across the control, adenoma, and CRC groups. Control-associated taxa were linked to pathways related to carbohydrate fermentation and amino acid metabolism, whereas CRC-associated taxa, particularly Fusobacterium, showed negative correlations with several biosynthetic pathways. In addition, CRC-associated taxa were associated with reduced short-chain fatty acids (SCFAs) and increased levels of certain bile acid-related metabolites. These findings suggest an association between microbiome-associated metabolic alterations and colorectal neoplasia and support further investigation of microbial and metabolic biomarkers.},
}

@article {pmid42929541,
year = {2026},
author = {Ngor, L and Palmer-Young, E and Vo, H and Alkhunder, A and Verma, V and McFrederick, QS},
title = {Nest ecology-associated impacts of wastewater on wild bee microbiomes.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0138126},
doi = {10.1128/aem.01381-26},
pmid = {42929541},
issn = {1098-5336},
abstract = {Anthropogenic pollution affects environments differently depending on proximity to the pollution source, exposure route, and species ecology. Thus, understanding an organism's ecological role and exposure route to contaminants is central to assessing pollution impact. Treated municipal wastewater releases contaminants into waterways and alters microbial communities. Plants absorb contaminants and expose animals through foraging and nest-building activities. Nesting ecology differences of ground and wood cavity-nesting bees offer insight into niche-specific susceptibility to pollution. We compared gut microbiomes of directly exposed soil-nesting Halictus ligatus and indirectly exposed wood-nesting Ceratina spp. upstream and downstream of wastewater. We collected bees, flowers, and soil and analyzed their bacterial microbiomes using 16S rRNA sequencing. The effect from wastewater explained a much larger proportion of the variance in the ground-nesting H. ligatus microbiome than wood cavity-nesting Ceratina adults, Ceratina larvae, and pollen provisions. Conversely, soil and flower microbiomes remained stable, indicating higher stability. These findings suggest that wastewater exposure leads to strong host-associated microbiome disruption, with ground-nesting bees most affected.IMPORTANCEBecause contaminants bind strongly to soil, ground-nesting bees near wastewater are likely most impacted, while wood cavity-nesting bees are likely less impacted since plant uptake of contaminants is species dependent. These results suggest that exposure routes drive contaminant susceptibility, with bee-associated microbes most vulnerable. Because bees are important pollinators and biodiversity contributors, these disruptions point to broader ecological risks in increasingly contaminated landscapes.},
}

@article {pmid42929808,
year = {2026},
author = {Agoni, L and Pericolini, E and Salvatore, S and Candiani, M and De Seta, F},
title = {The Vaginal Microbiome-Mitochondria Axis: Implications for Genital Tract Infections.},
journal = {Cells},
volume = {15},
number = {20},
pages = {},
doi = {10.3390/cells15201835},
pmid = {42929808},
issn = {2073-4409},
mesh = {Female ; Humans ; *Microbiota ; *Vagina/microbiology ; *Mitochondria/metabolism ; *Reproductive Tract Infections/microbiology/metabolism ; Animals ; Dysbiosis/microbiology ; },
abstract = {The vaginal microbiome influences epithelial and immune homeostasis through microbial metabolites, virulence factors, and other molecular signals, yet intracellular mechanisms translating microbial activity into host responses remain largely unexplored. Here, we propose the vaginal microbiome-mitochondria axis as a functional framework linking microbial activity to host-cell metabolism, redox signaling, immunity, and cell fate. We integrated evidence from vaginal microbiology, mitochondrial biology, mucosal immunology, and immunometabolism, distinguishing direct observations in the female genital tract from mechanistic evidence obtained in other host-microbe systems. Available evidence indicates that microbial products relevant to vaginal homeostasis and dysbiosis can modulate mitochondrial bioenergetics, reactive oxygen species generation and redox signaling, membrane potential, dynamics, and quality control pathways, while mitochondrial responses can influence epithelial integrity and antimicrobial and inflammatory functions. We further propose that the balance between mitochondrial adaptation and dysfunction may contribute to resolution or persistence of vaginal disorders and that incomplete mitochondrial recovery could contribute to an incomplete microbial ecosystem-host reset and recurrence. Although direct vaginal evidence remains limited, this framework identifies mitochondria as a potentially important functional interface between microbial ecology and host response and generates testable hypotheses for investigating whether mitochondrial homeostasis contributes to durable resolution of vaginal dysbiosis and infection.},
}

Female
Humans
*Microbiota
*Vagina/microbiology
*Mitochondria/metabolism
*Reproductive Tract Infections/microbiology/metabolism
Animals
Dysbiosis/microbiology

@article {pmid42929988,
year = {2026},
author = {Berikkhanov, Z and Resnina, K and Akulov, Z and Tarabrin, E and Shestakov, A and Razumovsky, V and Kotelnikov, A and Nikolaev, A and Ivanova, M and Nourmahal, S and Muraviev, S},
title = {Viral Signals in Acute Appendicitis: Direct Tissue Infection, Systemic Triggers, and the Unresolved Biology of Spontaneous Resolution.},
journal = {Diseases (Basel, Switzerland)},
volume = {14},
number = {10},
pages = {},
doi = {10.3390/diseases14100361},
pmid = {42929988},
issn = {2079-9721},
abstract = {BACKGROUND/OBJECTIVES: Acute appendicitis is readily recognised, but its initiating mechanisms remain uncertain. Viral findings are often interpreted without separating direct appendiceal infection, systemic host responses, clinical phenocopies, and virome effects. We examined the evidence for these scenarios and their possible relationship to spontaneous resolution.

METHODS: A structured narrative synthesis of 82 publications integrated tissue studies, clinical series, epidemiology, microbiome and virome research, natural history, and treatment outcomes.

RESULTS: Direct viral injury is documented in rare clinicopathological settings. Available tissue studies argue against frequent direct adenoviral infection. Systemic infection could provoke lymphoid activation, oedema, or early microvascular injury, but this causal sequence has not been demonstrated in humans. Clinical studies document resolution in selected uncomplicated cases, including recovery without antibiotics, without establishing a viral cause.

CONCLUSIONS: The framework separates observed findings from competing causal hypotheses. A viral prodrome is a candidate research variable whose independent diagnostic and prognostic value remains unestablished. Prospective studies must link infection chronology to local inflammation and subsequent outcomes before such information can guide treatment. Viral symptoms or positive tests cannot justify withholding indicated antibiotics or surgery.},
}

@article {pmid42930337,
year = {2026},
author = {Doyle, N and Kennedy, M and Mbandlwa, P and Linehan, K and Grimaud, G and Gillen, G and Smith, PE and Martinez, I and O'Donovan, M and Dillon, P and Hill, C and Ross, RP and Egan, M and Stanton, C},
title = {Bacteriocin-producing lactic acid bacteria as silage inoculants to reduce methane emissions in late lactation dairy cattle.},
journal = {The Journal of dairy research},
volume = {},
number = {},
pages = {1-18},
doi = {10.1017/S0022029926102702},
pmid = {42930337},
issn = {1469-7629},
abstract = {Enteric fermentation in ruminants is the largest agricultural source of methane (CH4) and contributes to global warming. Practical mitigation strategies are therefore needed for sustainable dairy production. This study evaluated a silage inoculant composed of bacteriocin-producing lactic acid bacteria (LAB) strains, Lactococcus lactis subsp. lactis SL242 and Lactiplantibacillus plantarum LP58 in late-lactation, spring-calving Holstein cows. Thirty cows were housed indoors and fed inoculated or control silage for 7 weeks. Daily milk yield and CH4 emissions were measured, milk composition was analysed weekly and body weight and body condition scores (BCSs) were recorded biweekly. Dry matter intake (DMI) was determined using the n-alkane technique in week 4 of the experimental period to allow the animals to be fully adapted to the experimental diets, with estimated LAB intake of ∼10[11] CFU/cow per day. Treatment had no effect on DMI (12.4 ± 0.34 kg/cow per day), concentrate intake (4.3 kg/cow per day), milk yield or BCSs. However, a significant treatment-by-week interaction was observed for milk composition, with transient increases in milk fat concentration and milk solids production in the LAB group during weeks 4 and 5. Rumen microbiota analysis (16S rRNA sequencing) revealed distinct beta diversity clustering between groups at weeks 4 and 7. No overall reduction in CH4 was observed, but emissions were numerically lower (5.8%) during weeks 4-7, with the greatest decrease (7.7%) at week 5 in the LAB group. These findings suggest that bacteriocin-producing LAB may transiently influence rumen microbial communities and reduce CH4 output. Further research is warranted to optimise delivery strategies and maximise their potential to support sustainable dairy production.},
}

@article {pmid42930383,
year = {2026},
author = {Talapaneni, S and Jamieson, L and Nath, S},
title = {Does Diabetes Influence the Microbiological Response to Non-Surgical Periodontal Therapy? A Systematic Review.},
journal = {Dentistry journal},
volume = {14},
number = {10},
pages = {},
doi = {10.3390/dj14100617},
pmid = {42930383},
issn = {2304-6767},
abstract = {Background/Objectives: The aim of this systematic review was to synthesise evidence on how non-surgical periodontal therapy (NSPT) alters the oral microbiota and periodontal parameters in patients with diabetes and periodontitis compared with non-diabetic patients with periodontitis. Methods: Electronic searches of MEDLINE/PubMed, Scopus, Embase, Ovid Emcare, JBI EBP, Web of Science, Dentistry and Oral Sciences Source, and grey literature sources were conducted from inception to March 2025. Eligible studies were clinical studies that included participants with diabetes and periodontitis, used NSPT as the primary intervention, and reported pre- and post-treatment oral microbiological and periodontal parameters as outcomes. The risk of bias was assessed using the Risk of Bias 2 (RoB 2) tool for randomised trials, and ROBINS-I for non-randomised studies and certainty of evidence was evaluated with GRADE. The review protocol was registered with PROSPERO (CRD420251005668). Results: Fourteen studies involving 374 participants with diabetes and 276 non-diabetic participants with periodontitis were eligible for inclusion. Thirteen studies used targeted methods restricted to pre-specified taxa, and one used 16S rRNA gene sequencing. In the targeted studies, NSPT was associated with reductions in periodontal pathogens, particularly Porphyromonas gingivalis, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans, which were found in both diabetic and non-diabetic groups, with small or no differences observed between the groups. There were improvements in probing depth, clinical attachment, bleeding on probing and plaque scores after NSPT in both groups, with no consistent between-group differences. In most studies, RoB 2 was rated "some concerns", and GRADE ranged from very low to moderate for microbiological and clinical outcomes. Conclusion: NSPT reduces selected periodontal pathogens and improves periodontal parameters in adults with periodontitis, with and without diabetes. Community-level microbiome evidence is limited to one small study, and the available data do not show whether diabetes modifies the microbiological response to NSPT.},
}

@article {pmid42930391,
year = {2026},
author = {Cannon, ML and Peldyak, J and Vigerust, DJ},
title = {The Oral-Gut Microbiome Axis: Microbial Transit, Ectopic Colonization, Systemic Associations, Salivaomics, and Clinical Control Points.},
journal = {Dentistry journal},
volume = {14},
number = {10},
pages = {},
doi = {10.3390/dj14100625},
pmid = {42930391},
issn = {2304-6767},
abstract = {The oral cavity is a continuous microbial source for the gastrointestinal tract. Adults swallow approximately 0.5-1.5 L of saliva each day, carrying a large and variable bacterial load. Gastric acidity removes most ingested organisms, but survival increases with food buffering, acid tolerance, mucin or biofilm protection, and proton-pump inhibitor use. Oral taxa are therefore repeatedly detected in stool, intestinal mucosa, and diseased tissues. The strongest mechanistic evidence concerns Fusobacterium nucleatum in colorectal cancer and Porphyromonas gingivalis in inflammatory and metabolic pathways, although detection alone does not prove stable colonization or causality. This narrative review summarizes microbial transit, key taxa, salivaomics, systemic associations, and practical oral control points. It also identifies clinical control points, including probiotics and polyols such as xylitol, as selective microbiome-modulating adjuncts at varying stages of evidence. The evidence suggests a strong clinical message: treat oral dysbiosis for established dental reasons, while paired oral and gut studies determine when downstream systemic benefits are achieved.},
}

@article {pmid42930403,
year = {2026},
author = {Schnutenhaus, S and Weinmann, M and Olms, C and Dreyhaupt, J and Rathke, A},
title = {Clinical and Microbiological Outcomes of Implant-Supported Hybrid Abutment Crowns in the Posterior Region as a Function of Restorative Material: Exploratory Results of a 36-Month Randomized Clinical Trial.},
journal = {Dentistry journal},
volume = {14},
number = {10},
pages = {},
doi = {10.3390/dj14100637},
pmid = {42930403},
issn = {2304-6767},
support = {CF41.506//Oral Reconstruction Foundation/ ; },
abstract = {Background: Hybrid abutment crowns combine a prefabricated titanium base with a custom, CAD/CAM-fabricated ceramic superstructure. Despite their increasing clinical use, only limited long-term in vivo data are available on how the restoration material influences clinical and microbiological outcomes. Objective: We investigated the clinical, radiographic, and microbiological outcomes of implant-supported hybrid abutment crowns in the posterior region over 36 months as a function of crown material. Methods: In a single-center, randomized, controlled clinical trial with blinded data analysis, 60 patients with a single-tooth gap in the posterior region received a Camlog iSy implant. Two implants were lost within the first four weeks, before prosthetic loading and randomization. The remaining 58 patients were randomized after stratification by sex and edentulous region to a polymer-infiltrated ceramic network hybrid ceramic (PICN; VITA Enamic, n = 28) or a lithium disilicate ceramic (LS2; IPS e.max CAD, n = 30). At 36 months, 57 patients (27 PICN, 30 LS2) were analyzed. The primary endpoint was implant survival; as no post-loading failure occurred, this was reported descriptively. Secondary endpoints were marginal bone level change (standardized intraoral radiographs, prosthetic baseline to 36 months), peri-implant probing depth (Florida Probe, baseline to 36 months; linear mixed-effects model), and the subgingival microbiome (micro-iDent plus, 6 and 36 months). Technical complications of this cohort have been reported separately 37. The trial was not powered to demonstrate equivalence, non-inferiority, or superiority. Results: The implant survival rate was 100%. Marginal bone resorption was low and stable. It did not differ significantly between crown materials (mesial mean difference 0.10 mm, 95% CI -0.11 to 0.31 mm; distal 0.15 mm, 95% CI -0.09 to 0.39 mm), nor by sex, jaw, implant length, diameter, or shoulder position. Probing depths remained low over 36 months without clinically relevant progression. The change in probing depth differed statistically between materials (mean difference 0.52 mm, 95% CI 0.12 to 0.92 mm; p = 0.012), but this difference was not considered clinically relevant. Microbiologically, most bacteria showed a stable to favorable course. For individual species (including Fusobacterium nucleatum, Campylobacter rectus, Eikenella corrodens, and Capnocytophaga spp.), deteriorations occurred more frequently, particularly in the LS2 group, without accompanying clinical or radiographic abnormalities. Conclusions: Within the limits of sample size and the 36-month follow-up, hybrid abutment crowns showed high peri-implant stability irrespective of crown material, with no clinically relevant differences between groups. This should not be interpreted as evidence of equivalence. When selecting materials, the higher technical complication rate in the PICN group reported separately for this cohort should also be considered.},
}

@article {pmid42930488,
year = {2026},
author = {Daviaud, C and Dominguez, H and Fernández, LG and Mourelle, ML and Baranger, K and Bridiau, N and Picot, L},
title = {Beyond Beauty: Microalgae and Cyanobacteria as Next-Generation Platforms for Functional Dermocosmetics, Cutaneous Delivery, and Skin Health.},
journal = {Marine drugs},
volume = {24},
number = {10},
pages = {},
doi = {10.3390/md24100359},
pmid = {42930488},
issn = {1660-3397},
support = {EAPA_0145/2024//Interreg Atlantic Area Programme through the European Regional Development Fund (ERDF), under the SMACC+ project, Sustainable Microalgae and Cyanobacteria-Based Bioactive Com-pounds for Cosmeceuticals and Nutraceuticals (project code: EAPA_0145/2024)./ ; },
mesh = {Humans ; *Cyanobacteria/chemistry/metabolism ; *Microalgae/chemistry/metabolism ; Animals ; *Skin/drug effects/metabolism ; Administration, Cutaneous ; Cosmetics ; },
abstract = {Microalgae and cyanobacteria are valuable sources of bioactive ingredients and innovative biological systems for skin applications. Their metabolites include exopolysaccharides (EPS), mycosporine-like amino acids (MAAs), carotenoids, phycobiliproteins, peptides and lipopeptides, polyunsaturated lipids, chlorophyll derivatives, and distinctive secondary metabolites such as scytonemin. Cyanobacteria additionally provide defined molecular candidates, including sacran, C-phycocyanin, MAAs, scytonemin-related compounds, and specialized peptide scaffolds. These compounds may support hydration and barrier function, photoprotection, control of oxidative stress and inflammation, pigmentation, antimicrobial and antibiofilm activity, extracellular-matrix preservation, and wound repair. This review examines major bioactive families, their sources and mechanisms, with particular emphasis on the strength of evidence supporting skin applications. Recent developments from 2024 to 2026 are highlighted, including microalgal extracellular vesicles (nanoalgosomes), photoactivated antimicrobial systems, photosynthetic hydrogels and microneedle patches, green extraction and biorefinery strategies, reconstructed human skin and skin-on-chip models, and artificial-intelligence-assisted formulation. Most reported effects remain supported mainly by biochemical, cellular, or preclinical evidence, whereas human validation is still limited. Translation will, therefore, depend on rigorous chemical standardization, effective cutaneous delivery, demonstrated stability and safety, scalable manufacturing, and validation in human-relevant models. Microalgae and cyanobacteria thus extend beyond conventional natural extracts toward next-generation dermocosmetic and cutaneous-delivery platforms.},
}

Humans
*Cyanobacteria/chemistry/metabolism
*Microalgae/chemistry/metabolism
Animals
*Skin/drug effects/metabolism
Administration, Cutaneous
Cosmetics

@article {pmid42930530,
year = {2026},
author = {López-Zambrano, R and García-García, J and López-Escánez, L and Vezza, T and Gbati, L and Palacios-López, R and Martin-Castaño, B and Vargas-Castillo, G and Martínez-Zaldivar, M and Caballero-Mateos, AM and García, F and Redondo-Cerezo, E and Fernández García, R and Fernández-Varón, E and Morón, R and Pischel, I and Suarez, CG and Rodríguez-Nogales, A and Rodríguez-Cabezas, ME and Gálvez, J},
title = {Thymus serpyllum Extract Improves Gastrointestinal Symptoms and Modulates Fecal Gut Microbiome Composition in a Multicenter, Randomized, Placebo-Controlled Clinical Trial.},
journal = {Medical sciences (Basel, Switzerland)},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/medsci14060611},
pmid = {42930530},
issn = {2076-3271},
support = {PI24/02089//Institute of Health Carlos III/ ; PID2022-143102-OBI00//Spanish Ministry of Economy and Competitiveness/ ; //Finzelberg GmbH & Co. KG/ ; },
mesh = {Humans ; Female ; *Thymus Plant/chemistry ; *Plant Extracts/pharmacology/therapeutic use ; *Feces/microbiology ; Male ; *Gastrointestinal Microbiome/drug effects ; Middle Aged ; *Gastrointestinal Diseases/drug therapy/microbiology ; Adult ; Quality of Life ; Double-Blind Method ; Aged ; },
abstract = {BACKGROUND/OBJECTIVES: Functional gastrointestinal discomfort is highly prevalent and affects up to 40% of the global population and remains challenging to manage due to its multifactorial nature. Usual interventions include dietary and lifestyle modifications, such as targeted phytochemical-based interventions. This multicenter, double-blind, randomized, placebo-controlled trial investigated the efficacy and exploratory microbiome-related effects of a standardized wild thyme extract (WThE) administered for 8 weeks on gastrointestinal symptoms, health-related quality of life, and fecal microbiome dynamics in adults without diagnosed organic gastrointestinal disease who reported gastrointestinal discomfort.

METHODS: A total of 178 adults without diagnosed organic gastrointestinal disease and with persistent gastrointestinal discomfort were randomized to WThE (n = 90) or placebo (n = 88); 131 participants had observed week-8 outcome data.

RESULTS: The analysis showed a greater reduction in overall gastrointestinal symptom burden with WThE than placebo, measured by the GSRS total score, with the largest exploratory domain-level differences observed in indigestion, constipation, and diarrhea-related symptoms. Improvements were also observed in health-related quality of life. At the microbiome level, no significant between-group differences were detected in α- or β-diversity; however, taxon-level analyses identified specific changes in fecal microbial composition, and predicted functional profiling suggested associated pathway-level differences. Moreover, the extract was well tolerated, with no product-related adverse events reported during the 8-week intervention.

CONCLUSIONS: Overall, WThE reduced self-reported gastrointestinal symptom burden and improved selected quality-of-life outcomes in adults with persistent gastrointestinal discomfort, supporting Thymus serpyllum as a safe and well-tolerated botanical intervention linked to favorable modulation of the fecal microbiome and enhanced gastrointestinal function.

CLINICALTRIALS: gov no: NCT06639126.},
}

Humans
Female
*Thymus Plant/chemistry
*Plant Extracts/pharmacology/therapeutic use
*Feces/microbiology
Male
*Gastrointestinal Microbiome/drug effects
Middle Aged
*Gastrointestinal Diseases/drug therapy/microbiology
Adult
Quality of Life
Double-Blind Method
Aged

@article {pmid42930540,
year = {2026},
author = {Meri Junior, AE and Batista, ECC and Meri, AD and Pereira, ACGC and Carlos, FM and Belo, VS and Gomes, AJPS and Sanches, C and Woo, S and Baldoni, AO and Gontijo, TS},
title = {Exploring Mechanisms and Therapeutic Strategies for Metformin Hydrochloride-Induced Diarrhea and Gastrointestinal Intolerance: A Bibliometric Analysis.},
journal = {Medical sciences (Basel, Switzerland)},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/medsci14060621},
pmid = {42930540},
issn = {2076-3271},
support = {//Federal University of São João del-Rei/ ; //Fundação de Amparo à Pesquisa do Estado de Minas Gerais/ ; 001//Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)/ ; 304131/2022-9//Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)/ ; },
mesh = {*Metformin/adverse effects ; Bibliometrics ; Humans ; *Diarrhea/chemically induced/therapy ; *Hypoglycemic Agents/adverse effects ; *Gastrointestinal Diseases/chemically induced ; },
abstract = {Background: Metformin hydrochloride (MET) gastrointestinal adverse effects (GAEs) are associated with intestinal accumulation, gut microbiota alterations, transporter saturation, and increased serotonin and lactate levels. This study mapped the scientific literature indexed in Web of Science (WoS) and Scopus, with MET-induced gastrointestinal intolerance and diarrhea as the primary research focus, concentrating on mechanisms and strategies to mitigate GAEs. Methods: This bibliometric analysis followed the PRISMA and PICO guidelines. WoS and Scopus were searched using terms derived from DeCS/MeSH descriptors. Two independent reviewers performed study selection. Data were analyzed using Bibliometrix (biblioshiny) in RStudio for performance analysis, scientific mapping, and collaboration networks. Results: A total of 6998 articles were identified, resulting in the inclusion of 153 studies (116 original articles and 37 reviews), distributed across 117 journals. The annual growth rate was 4.74%, with a peak in productivity between 2022 and 2025, and an average of 45.01 citations per document. GAEs constituted the most investigated area (28.1%), followed by molecular mechanisms (11.8%) and associated comorbidities (10.5%). The United States led scientific production (n = 37), followed by China (n = 18) and India (n = 17). Conclusions: Despite advances in understanding mechanisms, interventional studies and therapeutic strategies remain underrepresented. Strengthening international collaboration and participation from low- and middle-income countries is essential to develop more effective and equitable approaches.},
}

*Metformin/adverse effects
Bibliometrics
Humans
*Diarrhea/chemically induced/therapy
*Hypoglycemic Agents/adverse effects
*Gastrointestinal Diseases/chemically induced

@article {pmid42930557,
year = {2026},
author = {Meduri, GU and Torres, A},
title = {Homeostatic Correction During Severe Physiologic Stress: A Phase-Specific Model for GC-GRα-Coordinated Organism-Wide Adaptation.},
journal = {Medical sciences (Basel, Switzerland)},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/medsci14060638},
pmid = {42930557},
issn = {2076-3271},
mesh = {*Homeostasis ; Humans ; *Stress, Physiological/physiology ; *Adaptation, Physiological ; *Receptors, Glucocorticoid/metabolism ; Animals ; Signal Transduction ; Critical Illness ; *Models, Biological ; },
abstract = {Critical illness is increasingly recognized as a disorder of disrupted systemic homeostasis rather than simply a consequence of maladaptive systemic inflammation or isolated organ failure. Although researchers have extensively investigated adaptive biologic responses to severe physiologic stress, far less attention has been paid to the integrative mechanisms that coordinate these responses across multiple organ systems throughout the course of illness. This review synthesizes current evidence from systems biology, immunology, endocrinology, network physiology, and critical care to present a systems-level conceptual model of homeostatic correction that explains how coordinated adaptive biologic programs restore organismal homeostasis after severe physiologic stress. The model organizes these responses into three dynamic, partially overlapping phases: Priming, which establishes adaptive readiness and immediate survival responses; Modulatory, which limits excessive activation while preserving essential host-defense and physiologic functions; and Restorative, which promotes resolution, tissue repair, regenerative recovery, and the restoration of integrated organ-system function. In this model, glucocorticoid-glucocorticoid receptor alpha (GC-GRα) signaling serves as a central integrative regulator coordinating immune, neuroendocrine, metabolic, mitochondrial, vascular, epithelial, lymphatic, microbiome, and regenerative adaptive biologic programs through context-, tissue-, and phase-specific mechanisms. Rather than acting solely as an anti-inflammatory pathway, GC-GRα signaling functions as a dynamic, systems-level regulator coordinating adaptive capacity, inter-organ communication, disease tolerance, tissue protection, and recovery while preserving essential host-defense functions. The proposed model shifts the focus from isolated pathophysiologic abnormalities to understanding critical illness as a disorder of disrupted organism-wide adaptive coordination. It provides a biologically organized foundation for investigating adaptive capacity, identifying phase-specific biomarkers, and developing precision therapeutic strategies to restore homeostatic resilience across acute and chronic disease states.},
}

*Homeostasis
Humans
*Stress, Physiological/physiology
*Adaptation, Physiological
*Receptors, Glucocorticoid/metabolism
Animals
Signal Transduction
Critical Illness
*Models, Biological

@article {pmid42930581,
year = {2026},
author = {Wang, Y and Cheng, L and Wang, C and Wang, X and Li, J and Wang, Y and Gao, X and Luo, G},
title = {Re-Du-Ning Alleviates Airway-Intestinal Inflammation of COPD Rats by Regulating Glycerophospholipid Metabolism and Modulating Gut Microbiome.},
journal = {Medical sciences (Basel, Switzerland)},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/medsci14060662},
pmid = {42930581},
issn = {2076-3271},
support = {U21A20407//National Natural Science Foundation of China/ ; 2240STCZB2613//Ministry of Industry and Information Technology/ ; 82003957//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Pulmonary Disease, Chronic Obstructive/drug therapy/metabolism/microbiology ; *Glycerophospholipids/metabolism ; Rats ; *Gastrointestinal Microbiome/drug effects ; *Drugs, Chinese Herbal/pharmacology/therapeutic use ; Male ; Humans ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Rats, Sprague-Dawley ; },
abstract = {Background: Re-Du-Ning (RDN) is a traditional Chinese medicine (TCM) formulation composed of Lonicera japonica, Gardenia jasminoides, and Artemisia annua. Previous in vitro studies have demonstrated that RDN suppresses pro-inflammatory cytokine release in RAW264.7 macrophages and exhibits potential anti-COPD activity; however, its precise molecular mechanism remains elusive. Methods: A rat COPD model was established by combining cigarette smoke exposure and intratracheal instillation of lipopolysaccharide (LPS). Rats were intragastrically administered with gradient doses of RDN to evaluate its in vivo pharmacological efficacy. Untargeted metabolomics and 16S rRNA microbiome sequencing were performed to screen differential metabolites and gut bacterial genera following RDN intervention, followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis of core metabolic pathways. Further functional validations were conducted via antibiotic-mediated gut microbiota depletion, fecal microbiota transplantation (FMT), targeted glycerophospholipid supplementation, and human clinical cohort datasets from the Gene Expression Omnibus (GEO) to verify the central roles of gut microbiota and glycerophospholipid metabolism. Results: RDN intervention partially improved lung-function impairment and attenuated histopathological changes in the lung and colon in rats with COPD, while simultaneously reducing the levels of IL-1β, TNF-α, and IL-6 in serum, BALF, and feces. Mult-omics analysis further revealed that RDN partially restored glycerophospholipid metabolic profiles and reshaped gut microbiota composition, and a "host phenotype-metabolite-gut microbiota" network was constructed using correlation analysis. Finally, antibiotic depletion and faecal microbiota transplantation (FMT) experiments suggested that an intact gut microbiota is required for the full protective effect of RDN and that part of this effect is transferable by FMT; LPC (14:0) and LPC (16:0) can regulate cytokine release in BEAS-2B cells, and data from the GEO human cohort further validated the role of glycerophospholipid metabolism in COPD. Conclusions: RDN effectively alleviates symptoms in rats with COPD by regulating the gut microbiota and glycerophospholipid metabolism, providing a comprehensive and in-depth understanding of the multisystem regulatory network underlying COPD.},
}

Animals
*Pulmonary Disease, Chronic Obstructive/drug therapy/metabolism/microbiology
*Glycerophospholipids/metabolism
Rats
*Gastrointestinal Microbiome/drug effects
*Drugs, Chinese Herbal/pharmacology/therapeutic use
Male
Humans
Disease Models, Animal
Fecal Microbiota Transplantation
Rats, Sprague-Dawley

@article {pmid42930589,
year = {2026},
author = {Nassar, SA},
title = {From Dysbiosis to Symbiosis: Using the Gut Microbiome to Improve Cancer Outcomes.},
journal = {Medical sciences (Basel, Switzerland)},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/medsci14060669},
pmid = {42930589},
issn = {2076-3271},
support = {2025/03/37810//Prince Sattam Bin Abdulaziz University/ ; },
mesh = {Humans ; *Symbiosis ; *Dysbiosis/microbiology ; *Gastrointestinal Microbiome/physiology ; *Neoplasms/microbiology/therapy ; Animals ; },
abstract = {The gut microbiome has emerged as an important regulator of cancer biology, influencing carcinogenesis, treatment response, and therapy-related toxicity. This narrative review synthesizes current evidence on the mechanistic roles of the gut microbiota in gastrointestinal (GI) cancers and evaluates emerging microbiome-based strategies for improving cancer outcomes. Dysbiosis-characterized by altered microbial diversity, depletion of beneficial functions, and enrichment of disease-associated taxa-may contribute to tumorigenesis through interconnected mechanisms involving chronic inflammation, genotoxicity, metabolic dysregulation, epigenetic alterations, and immune evasion. Key cancer-associated bacteria, including Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis (ETBF), pks[+]Escherichia coli, and Helicobacter pylori, illustrate the mechanistic diversity of microbiota-associated carcinogenesis. Beyond cancer initiation, the gut microbiome can influence the efficacy and toxicity of anticancer therapies. In immunotherapy, specific microbial taxa and metabolites modulate antitumor immunity and immune checkpoint inhibitor (ICI) responses, while antibiotic-associated dysbiosis has been linked to poorer outcomes. In chemotherapy, microbial metabolism and microbiota-derived metabolites can alter drug efficacy and toxicity, including modulation of 5-fluorouracil (5-FU) activity. Microbiome-based biomarkers show promise for cancer detection and treatment prediction, with fecal microbial signatures, including F. nucleatum, potentially improving colorectal cancer (CRC) screening when incorporated into multimarker strategies. Therapeutic approaches aimed at restoring microbial symbiosis include fecal microbiota transplantation (FMT), which has shown preliminary potential to restore ICI responsiveness in treatment-refractory melanoma, and probiotic interventions, although clinical evidence remains limited. Emerging engineered microbial therapeutics, including tumor-targeting bacteria designed to deliver localized immunostimulatory payloads, are advancing toward clinical translation. Despite substantial progress, important challenges remain, including methodological heterogeneity, lack of standardized protocols, confounding factors, and unresolved safety concerns. Personalized strategies integrating microbial features with host characteristics and treatment context may ultimately enable more effective microbiome-based approaches to improve cancer outcomes.},
}

Humans
*Symbiosis
*Dysbiosis/microbiology
*Gastrointestinal Microbiome/physiology
*Neoplasms/microbiology/therapy
Animals

@article {pmid42930741,
year = {2026},
author = {Wang, H and Che, Y and Liu, H and Yu, X and Liu, B and Shu, F and Zhou, J and Wu, M},
title = {Arbuscular Mycorrhizal Fungi Inoculation Promotes Growth and Alleviates Fusarium tricinctum-Induced Growth Inhibition in Quercus variabilis Seedlings.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {12},
number = {10},
pages = {},
doi = {10.3390/jof12100776},
pmid = {42930741},
issn = {2309-608X},
support = {No. 42430702//National Natural Science Foundation of China/ ; },
abstract = {Quercus variabilis is a key species for reforestation in East Asia, yet the mechanisms by which arbuscular mycorrhizal fungi (AMF) influence seedling growth and responses to soil-borne fungal challenge remain incompletely understood. This study combined physiological and metagenomic approaches to address this gap. Among seven rhizosphere fungal isolates, Fusarium tricinctum (F15) exerted the strongest growth-inhibitory effect on Q. variabilis seedlings and was therefore selected for subsequent experiments. Inoculation with the AMF Rhizophagus intraradices significantly promoted seedling growth (p < 0.05), increasing root length by 4.94% relative to the uninoculated control and increasing ground diameter and aboveground fresh weight by 28.57% and 117.07%, respectively, relative to F15-treated seedlings. AMF inoculation also significantly altered substrate nutrient status (p < 0.05), particularly nitrogen, phosphorus, and potassium, and enhanced the activity of antioxidant enzymes, including peroxidase and catalase (p < 0.05). Metagenomic analysis revealed that AMF significantly reshaped rhizosphere microbial community composition and bacterial α-diversity (p < 0.05), enriching beneficial taxa such as Mesorhizobium. Functional profiling showed differences in predicted microbial functional profiles between AMF-inoculated and F15-treated groups. Together, these results indicate that AMF enhances seedling growth and mitigates the negative effects associated with F15 challenge, potentially through altered substrate nutrient dynamics, enhanced antioxidant capacity, and modulation of the rhizosphere microbial community.},
}

@article {pmid42930786,
year = {2026},
author = {Samalia, PD and Chen, SS and Lu, LM and Sims, JL and Lindsay, K and Niederer, RL},
title = {Lifestyle Modifiers of Non-Infectious Uveitis: A Narrative Review of Current Evidence and Future Directions.},
journal = {Journal of personalized medicine},
volume = {16},
number = {10},
pages = {},
doi = {10.3390/jpm16100511},
pmid = {42930786},
issn = {2075-4426},
abstract = {Background: Non-infectious uveitis is a leading cause of preventable visual impairment and arises from complex interactions between genetic susceptibility, environmental exposures, and immune dysregulation. Purpose: To review current evidence regarding modifiable lifestyle factors that may influence the development, severity, recurrence, and outcomes of uveitis. This narrative review used structured searches of MEDLINE, PubMed, Embase and the Cochrane Database of Systematic Reviews from database inception, last updated on 30 June 2026, supplemented by reference-list screening. Results: Diet, smoking, obesity, physical activity, sleep, psychological stress, alcohol consumption, and micronutrient status may affect uveitis through effects on systemic inflammation, Th1/Th17 immunity, regulatory T-cell function, oxidative stress, and the gut microbiome. Conclusions: Although the evidence remains limited and largely observational, lifestyle assessment may support personalized adjunctive care by considering the patient's uveitis phenotype, systemic comorbidities, treatment exposures and individual priorities. Lifestyle measures should support systemic health and shared decision-making without being presented as substitutes for established non-infectious uveitis treatment or as proven ocular disease-modifying interventions.},
}

@article {pmid42930862,
year = {2026},
author = {Mohamad, NAS and Puhendhiran, T and Sawai, S and Cheah, FK and Sudi, S and Lasimbang, H and Lee, PC},
title = {Biomaterials in Menstrual Cup Design: Challenges, Innovations and Future Perspectives.},
journal = {Journal of functional biomaterials},
volume = {17},
number = {10},
pages = {},
doi = {10.3390/jfb17100527},
pmid = {42930862},
issn = {2079-4983},
support = {IMAP012-2/2024.//Ministry of Higher Education/ ; IMAP012-2/2024.//Inno Therapeutics (M) Sdn. Bhd./ ; },
abstract = {Menstrual cups are an expanding alternative in menstrual hygiene management, positioned at the intersection of biomaterial science, women's health, and sustainability. Because these intravaginal devices are intended for prolonged, repeated mucosal contact, their safety, functionality, and user acceptance largely depend on material selection and engineering design. This review critically evaluates the biomaterials used in contemporary menstrual cup manufacturing, focusing on medical-grade silicone (MGS), thermoplastic elastomers (TPEs), and natural rubber and compares their physicochemical properties, mechanical behaviour, biocompatibility, sterilisation compatibility, and chemical safety. Beyond material comparison, we draw on clinical, microbiological, and post-market surveillance data to contextualise tissue response, vaginal microbiome stability, and rare but clinically significant adverse events such as toxic shock syndrome. We also examined emerging innovations, including surface and interface engineering, biodegradable elastomers and composite blends, and advances in manufacturing and design. We argue that menstrual cup development is best understood as a multidisciplinary biomaterials challenge integrating polymer chemistry, surface engineering, microbiological safety, regulatory science, and user-centred design. Realising safer, more functional and more sustainable cups will require rigorous biocompatibility testing, long-term studies, and transparent material characterisation.},
}

@article {pmid42931080,
year = {2026},
author = {Hudu, SA and Morad, EA and Alhazimi, GM and Othman, RQA and Elboraei, YAE and Jimoh, AO},
title = {Hidden Microbiome of Mining Environments: Implications for Occupational Health, Bioaerosol Exposure, and Antimicrobial Resistance.},
journal = {Journal of xenobiotics},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/jox16060194},
pmid = {42931080},
issn = {2039-4713},
support = {NBU-CRP-2026-3770.//Northern Border University/ ; },
abstract = {Mining environments are extreme subsurface ecosystems characterized by elevated concentrations of metals and minerals, limited light, and high particulate loads. Occupational health research in mining has traditionally emphasized physical and chemical hazards, whereas biological exposures remain less well-characterized. This narrative review synthesizes evidence on mining-associated microbial communities, bioaerosols, occupational exposure, respiratory health, and antimicrobial resistance (AMR). The literature search covered PubMed/MEDLINE, Scopus, and Web of Science from database inception through August 2026. Evidence from coal, uranium, metal mining, acid mine drainage, and mine dust environments indicates that geochemical conditions and mining activities shape microbial communities. Drilling, blasting, excavation, and ore transport can aerosolize microbial cells, spores, and dust-associated microbial components, creating plausible inhalation pathways. Metal-rich environments may also favor persistence and co-selection of metal- and antibiotic-resistance determinants within environmental microbial communities. Metagenomic sequencing and environmental DNA approaches have expanded detection of microbial diversity, functional genes, and environmental resistomes. However, environmental detection does not establish microbial viability, effective worker exposure, transmission, or disease causation. Future research should integrate standardized environmental and personal microbial exposure measurements with respirable dust and chemical monitoring, longitudinal occupational epidemiology, and functional validation of resistance determinants to determine the actual occupational-health significance of mining-associated microbiomes.},
}

@article {pmid42931155,
year = {2026},
author = {Nevins, A and Stansbury, N and Robinson, RD and Zhong, G},
title = {Microbial Dysbiosis, Infection, and Immunometabolic Signaling in Polyendocrine Metabolic Ovarian Syndrome (Formerly PCOS).},
journal = {Pathogens (Basel, Switzerland)},
volume = {15},
number = {10},
pages = {},
doi = {10.3390/pathogens15101003},
pmid = {42931155},
issn = {2076-0817},
mesh = {Humans ; Female ; *Dysbiosis ; *Polycystic Ovary Syndrome/metabolism/etiology/microbiology/immunology ; Animals ; Signal Transduction ; Gastrointestinal Microbiome ; },
abstract = {Polyendocrine metabolic ovarian syndrome (PMOS), recently proposed as a new name for polycystic ovary syndrome (PCOS), is a heterogeneous endocrine-metabolic disorder characterized by hyperandrogenism, ovulatory dysfunction, and variable ovarian morphology. Low-grade inflammation is common, but its initiating and sustaining factors differ among phenotypes. Microbial communities have emerged as potential modifiers of this inflammatory and metabolic environment. Human studies generally identify differences in gut microbial community structure between affected and unaffected women, although no universal taxonomic signature has been reproduced across regions, phenotypes, or analytic platforms. Mechanistic studies implicate altered intestinal barrier signaling, microbial metabolites, bile acid-interleukin-22 pathways, and immune-cell polarization; however, several influential pathways remain supported principally by animal models. Evidence for lower genital tract dysbiosis is more limited, and apparent associations may reflect hormonal state, menstrual irregularity, adiposity, medications, sexual exposures, or sampling methods. Evidence that specific infections cause PMOS/PCOS is sparse and inconsistent. Small serologic studies involving Chlamydia species and Helicobacter pylori do not establish temporality or causality. This review distinguishes dysbiosis from infection, evaluates human and experimental evidence, and proposes a bidirectional microbial-immune-metabolic-ovarian framework. A focused hypothesis involving interleukin-12-STAT4 signaling is also examined because it provides a specific, testable framework linking microbial or sterile inflammatory signaling to ovarian dysfunction. STAT4 can promote inflammatory T-helper-1 programs and granulosa-cell apoptosis in non-PCOS models, while estrogen can enhance STAT4 activation; nevertheless, direct human PMOS/PCOS evidence is currently absent, and the proposed pathway should not be interpreted as an established disease mechanism. Future studies require deep phenotyping, longitudinal multi-omics, compartment-specific sampling, standardized analysis, and mechanistic validation before microbiome-directed or immune-directed interventions can enter clinical care.},
}

Humans
Female
*Dysbiosis
*Polycystic Ovary Syndrome/metabolism/etiology/microbiology/immunology
Animals
Signal Transduction
Gastrointestinal Microbiome

@article {pmid42931221,
year = {2026},
author = {Mahalingam, SS and Cameron, CM and Richardson, B and Cameron, MJ and da Silva Paes, A and Pinto, A and Tamilselvan, B and Jayaraman, S and Jacobson, JM and Yendewa, G and Pandiyan, P},
title = {Polyamines and Epithelial Barrier Loss During HIV Infection.},
journal = {Pathogens (Basel, Switzerland)},
volume = {15},
number = {10},
pages = {},
doi = {10.3390/pathogens15101069},
pmid = {42931221},
issn = {2076-0817},
support = {/NH/NIH HHS/United States ; },
mesh = {Humans ; *Polyamines/metabolism ; *HIV Infections/metabolism/immunology/drug therapy/pathology/virology ; *Mouth Mucosa/metabolism/pathology/immunology ; Animals ; Epithelial Cells/metabolism ; },
abstract = {Despite effective antiretroviral therapy (ART), people with HIV (PWH) continue to experience chronic oral mucosal disease characterized by persistent T-cell inflammation, regulatory T cell (Treg) dysfunction, impaired CD8[+] tissue resident cell (TRM) immunity and microbial dysbiosis. Emerging evidence implicates dysregulated polyamine metabolism and mucosal T-cell dysfunction as key mediators of these pathological processes. However, the effects of polyamines on the oral mucosal epithelium remain largely unexplored. The paradoxical dose-dependent effects of polyamines on oral epithelial barrier integrity are critically discussed, and a unified mechanistic model is proposed. This paper also highlights single-cell transcriptomic data from our laboratory that implicates epithelial cell barrier dysfunction in PWH and offers a perspective on how it may worsen persistent inflammation even after combined anti-retroviral treatment. This hypothesis reports current knowledge on how HIV-induced polyamine overload and Fusobacterium-derived putrescine could drive oral epithelial barrier disruption through interconnected mechanisms involving oxidative stress, α6β4 integrin-laminin-332 signaling, HIF-1α stabilization, tight junction disorganization, and innate immune dysregulation. Finally, we outline key future research directions, including therapeutic targeting of polyamine oxidation to restore oral mucosal homeostasis in PWH.},
}

Humans
*Polyamines/metabolism
*HIV Infections/metabolism/immunology/drug therapy/pathology/virology
*Mouth Mucosa/metabolism/pathology/immunology
Animals
Epithelial Cells/metabolism

@article {pmid42931248,
year = {2026},
author = {Yu, YD and Park, DS and Han, MY},
title = {Long-Term Autoimmune Risk Following Pediatric Acute Pyelonephritis: A Nationwide Cohort Study.},
journal = {Pathogens (Basel, Switzerland)},
volume = {15},
number = {10},
pages = {},
doi = {10.3390/pathogens15101096},
pmid = {42931248},
issn = {2076-0817},
support = {HR22C1605//Ministry of Health and Welfare/ ; },
mesh = {Humans ; *Pyelonephritis/complications/epidemiology ; Female ; *Autoimmune Diseases/epidemiology/etiology ; Child ; Male ; Child, Preschool ; Retrospective Studies ; Republic of Korea/epidemiology ; Infant ; Hospitalization ; Adolescent ; Acute Disease ; Incidence ; Risk Factors ; Cohort Studies ; },
abstract = {INTRODUCTION: Acute pyelonephritis (APN) is a serious bacterial infection requiring hospitalization during childhood. This study investigated whether hospitalization for APN is associated with increased subsequent autoimmune disease risk.

METHODS: In this nationwide, population-based retrospective cohort study using the Korean National Health Insurance Service database, we included children born between 2002 and 2005. Children hospitalized for APN (identified by inpatient ICD-10 codes) were matched by birth year and sex to controls without APN. Clinical data including microbiological outcomes were unavailable. The primary outcome was incident autoimmune disease after a 1-year lag period.

RESULTS: The study included 31,856 children with APN and 318,560 matched controls. Autoimmune disease incidence was 98.35 and 59.91 per 10,000 person-years, respectively. APN was associated with increased risk, with heterogeneity across diseases; the strongest association was for IgA nephropathy (aHR 2.14; 95% CI 1.92-2.29). Risks were elevated for autoimmune thyroiditis, Behçet disease, and acute disseminated encephalomyelitis. Recurrent APN carried higher risk than a single episode.

CONCLUSIONS: Hospitalization for childhood APN was associated with increased autoimmune disease risk through early adolescence. The stronger association with recurrence suggests a dose-response relationship. However, exposure misclassification, unmeasured urinary tract anomalies, and antibiotic-related microbiome effects limit causal inference.},
}

Humans
*Pyelonephritis/complications/epidemiology
Female
*Autoimmune Diseases/epidemiology/etiology
Child
Male
Child, Preschool
Retrospective Studies
Republic of Korea/epidemiology
Infant
Hospitalization
Adolescent
Acute Disease
Incidence
Risk Factors
Cohort Studies

@article {pmid42925928,
year = {2026},
author = {Shao, Y and Wen, Z and Ye, C and Yang, M and Fuzzati, N and Zhang, B and Cavellec, C and Jiang, W and Li, L and Hao, Q and Shu, Q and Li, Y},
title = {Native AMF from wild Paeonia ostii enhance root development via PoCCD4-mediated hormone homeostasis and reshape rhizosphere microbiome assembly and function.},
journal = {Plant science : an international journal of experimental plant biology},
volume = {},
number = {},
pages = {113550},
doi = {10.1016/j.plantsci.2026.113550},
pmid = {42925928},
issn = {1873-2259},
abstract = {Arbuscular mycorrhizal fungi (AMF) play vital roles in plant growth and rhizosphere microbiome assembly. Tree peony (Paeonia sect. Moutan DC.) is an economically valuable perennial crop, yet the symbiotic mechanisms between it and native AMF remain poorly understood. In this study, we surveyed the rhizosphere AMF community of wild P. ostii from its native habitat, and isolated two dominant species: Funneliformis mosseae and Claroideoglomus etunicatum. Inoculation with these AMF significantly improved root development and leaf photosynthetic efficiency. Furthermore, the promotion involved a novel pathway whereby carotenoid cleavage dioxygenase 4 (PoCCD4) mediated strigolactone and abscisic acid homeostasis in P. ostii roots. Beyond direct effects on host plant growth, AMF inoculation fine-tuned rhizosphere microbiota composition, reinforcing host-driven assembly and favoring beneficial consortia without altering overall diversity. Correlation analyses revealed that the AMF-shaped microenvironment established a disease-suppressive network linked to soil nutrient dynamics and phytohormone profiles. This study elucidates the interaction mechanisms between native AMF and P. ostii, uncovers their co-adaptive relationships, and offers a scientific basis for developing AMF inoculants for sustainable tree peony cultivation.},
}

@article {pmid42925981,
year = {2026},
author = {Zaghloul, HAH and Xiao, Z and Huang, GH},
title = {Temporal dynamics of bacterial communities in Spodoptera exigua during Heliothis virescens ascovirus 3 h infection.},
journal = {Journal of invertebrate pathology},
volume = {},
number = {},
pages = {108775},
doi = {10.1016/j.jip.2026.108775},
pmid = {42925981},
issn = {1096-0805},
abstract = {Ascoviruses are insect viruses that cause chronic disease in infected hosts. The infection results in the partition of infected cells into multiple virion-containing vesicles, where viral replication continues for weeks before mortality. The vesicles accumulate in the hemolymph (equivalent to blood). The interaction among the virus, the host, and the microbiome during infection is poorly understood. Therefore, this study aimed to examine the temporal dynamics of whole-body bacterial communities in Spodoptera exigua larvae infected with Heliothis virescens ascovirus 3 h (HvAV-3 h) during early (12 hpi), late (48 hpi), and very late (96 hpi) viral replication stages. The 16S rRNA gene sequencing approach revealed that the HvAV-3 h-infected larvae encountered a decrease in the relative abundance of family Leuconostocaceae and genus Weissella and an increase in the relative abundance of family Acetobacteraceae and genus Acetobacter, when compared to the mock larvae. Moreover, the qPCR quantification demonstrated statistically significant decreases in the bacterial load during the late and very late stages of infection relative to the mock-infected larvae. In contrast, we detected statistically significant increases in the viral load with infection progress. We confirmed the presence of some of the identified bacterial genera, such as Bacillus sp. and Lactic Acid Bacteria (LAB), in uninfected S. exigua whole-body samples using a culture-based approach. Further research will be needed to identify the specific roles of the identified bacterial communities and to clarify the mechanisms that contribute to controlling the host bacterial load. Future studies should consider examining different host tissue microbial communities in this system given the HvAV-3 h wide tissue tropism.},
}

@article {pmid42926092,
year = {2026},
author = {Ruan, C and He, Y and Ran, N and Wang, Z},
title = {Time-resolved profiling reveals nonlinear dose-time trajectories of gut microbiota in PM2.5 and PFOS exposure models.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {129383},
doi = {10.1016/j.envpol.2026.129383},
pmid = {42926092},
issn = {1873-6424},
abstract = {The gut microbiota is a dynamic ecological system, yet environmental microbiome studies often provide only limited temporal resolution. We characterized gut microbial responses across multiple exposure levels and sampling stages in two independent but complementary mouse models of PM2.5 inhalation and perfluorooctane sulfonate (PFOS) drinking-water exposure. Time-resolved 16S rRNA gene sequencing, ecological analyses, PICRUSt2-based functional inference, and generalized additive models (GAMs) were integrated to examine temporal succession and nonlinear dose-time relationships. Under unexposed conditions, temporal microbial succession was evident in both models, highlighting the importance of accounting for background community dynamics. Within the PM2.5 model, community restructuring was most apparent during early-to-intermediate exposure stages, with prominent nonlinear trajectories in Lactobacillus, Prevotella, and the Firmicutes/Bacteroidetes ratio. In the PFOS model, microbial restructuring extended across a longer observation period and involved taxa including Akkermansia, Allobaculum, and UBA7173. PICRUSt2 suggested temporal and dose-associated variation in predicted pathways related to nitrogen metabolism, carbohydrate utilization, and fermentation, although these functions were not directly measured. GAMs identified stage-specific nonlinear response windows in both models. These findings highlight the importance of jointly considering dose and time in environmental microbiome studies and demonstrate the value of time-resolved modeling for detecting microbial response patterns that may be missed by endpoint analyses.},
}

@article {pmid42926093,
year = {2026},
author = {Li, X and Liu, H and Wu, J and Xi, C},
title = {Source Apportionment and Resistome Signatures of Community and Hospital Effluents in Urban Sewer Networks.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {129378},
doi = {10.1016/j.envpol.2026.129378},
pmid = {42926093},
issn = {1873-6424},
abstract = {Antibiotic resistance surveillance has traditionally focused on clinical settings, potentially overlooking broader microbial reservoirs in the community. Wastewater-based epidemiology (WBE) provides a powerful tool for capturing these population-level signals. This study aimed to identify source-specific resistome characteristics and estimate the relative compositional contributions of hospital and residential wastewater to the downstream wastewater treatment plant (WWTP). By integrating droplet digital polymerase chain reaction (ddPCR) with metagenomic sequencing, spatiotemporal dynamics across an urban sewer network were characterized. Bacterial 16S rRNA gene concentrations did not differ significantly between hospital and residential wastewater. Under the specified flow scenarios, hospital wastewater represented a small fraction of the estimated total influent volume. Bayesian source tracking further indicated that residential sources collectively accounted for nearly 80% of the inferred source contribution to the influent antibiotic resistance genes (ARGs) profile and 70.9% of the influent microbial community composition, whereas hospital wastewater accounted for only 5.5% of the inferred resistome contribution. These findings show that hospital wastewater contained clinically important resistance genes (e.g., blaKPC-2), whereas the sampled residential references accounted for the largest combined inferred contribution to the influent microbiome and resistome. Together, these results highlight the importance of incorporating community surveillance through wastewater-based approaches within the One Health framework.},
}

@article {pmid42926175,
year = {2026},
author = {Uribarri, J and Calvo, MS},
title = {Intestinal Phosphate Absorption and Phosphate Metabolism in Chronic Kidney Disease: Direct and Indirect Toxicity of Phosphate Additives in Ultra-processed Diets.},
journal = {Seminars in nephrology},
volume = {},
number = {},
pages = {151748},
doi = {10.1016/j.semnephrol.2026.151748},
pmid = {42926175},
issn = {1558-4488},
abstract = {In chronic kidney disease (CKD), intestinal phosphate absorption stays largely constant even as the kidneys lose the ability to excrete phosphate, creating a tendency toward positive phosphate balance. Rising fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH) keep serum phosphate near normal until advanced CKD, but these same adaptations can cause systemic harm long before overt hyperphosphatemia develops. Ultra-processed foods worsen this burden through phosphate additives (Pi-additives) used as preservatives, emulsifiers, stabilizers, leavening agents, and moisture retainers. These additives are absorbed more readily than natural food phosphate and are poorly captured by nutrient databases. Therefore, true phosphorus exposure is easily underestimated. This perspective outlines 2 pathways of harm. The direct pathway involves PTH and FGF23 activation, vascular and soft-tissue calcification, endothelial dysfunction, disordered bone remodeling, faster CKD progression, and cellular senescence-effects documented in CKD and possibly relevant even with preserved kidney function. The indirect pathway reflects that Pi-additives rarely occur alone: they accompany added sugars, non-nutritive sweeteners, nitrites, emulsifiers, and preservatives in ultra-processed foods, combinations that may drive gut dysbiosis, intestinal barrier dysfunction, oxidative stress, inflammation, and the formation of advanced glycation endproducts and other gut-derived toxins. We synthesize current understanding of phosphate homeostasis with mechanistic and epidemiologic evidence linking Pi-additives-alone and combined with other additives-to cardiovascular, skeletal, renal, and metabolic disease. Future research should move beyond single-additive safety testing toward evaluating additive mixtures, cumulative exposure, and food-matrix interactions. Better exposure assessment and transparent phosphorus labeling are essential to clarify the long-term health effects of these ubiquitous additives.},
}

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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