@article {pmid41889817,
year = {2026},
author = {Lu, T and Dietz, ZK and Ericsson, AC and Picking, WD and Picking, WL},
title = {Eco-tank Housing Maintains Wild-Type Microbiota and Rewilds the Laboratory Mouse Gut Microbiome to Restore Natural Immune Tone.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.16.712136},
pmid = {41889817},
issn = {2692-8205},
abstract = {UNLABELLED: Laboratory mice housed under individually ventilated cage (IVC) conditions harbor simplified gut microbiota and immune phenotypes that diverge substantially from those shaped by environmental exposure, limiting translational relevance. To reintroduce controlled ecological complexity while maintaining biosafety and reproducibility, we developed the Eco-tank, a pathogen-monitored semi-natural housing system incorporating environmental substrates and dietary diversity. Longitudinal 16S rRNA sequencing revealed that even wild-caught Mus musculus rapidly lose microbial richness and predicted metabolic breadth under IVC housing. Eco-tank conditions stabilized diversity and preserved elements of wild-associated community structure during extended captivity. In parallel, standardized C57BL/6 mice housed in Eco-tanks underwent rewilding-like restructuring, with increased richness and community shifts toward a wild-associated configuration. Functional inference analyses indicated expansion of predicted pathways linked to short-chain fatty acid production, amino acid metabolism, and environmental substrate utilization. Eco-tank housing enhanced baseline resistance to pulmonary Pseudomonas aeruginosa (Pa) infection without compromising vaccine-induced protection, indicating that restoration of environmental microbial signals does not impair adaptive immunity. Together, these findings identify housing ecology as a dominant determinant of microbiome structure and functional potential. The Eco-tank provides a scalable and tractable framework for integrating environmental microbial complexity into laboratory models to better align preclinical immunology with ecologically conditioned immune systems.

IMPORTANCE: Laboratory mice are foundational models for immunology, yet their specific pathogen-free rearing and housing environments impose ecological constraints that reshape the gut microbiome and immune tone. This study introduces a scalable, pathogen-monitored Eco-tank system that restores environmental microbial complexity while preserving experimental control. By demonstrating that housing ecology reshapes microbiome functional potential and modulates baseline immune resistance without compromising vaccine responsiveness, this work highlights environmental context as a critical experimental variable in preclinical immunology and offers a tractable framework for improving translational relevance.},
}

@article {pmid41889844,
year = {2026},
author = {Brache-Smith, DM and Sogin, EM and Badillo, J and Maeda, S},
title = {Identification of bacterial candidates that promote the growth of the seagrass Zostera marina.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.19.712741},
pmid = {41889844},
issn = {2692-8205},
abstract = {BACKGROUND: Globally, seagrass ecosystems are threatened by anthropogenic activities that are leading to increased levels of eutrophication, coastal pollution and thermal conditions. Consequently, there is a growing need to develop new approaches that work to mitigate these stressors and enhance restoration efforts in seagrass meadows. One promising strategy is to identify, isolate and characterize microbial consortia that are likely to support seagrass productivity. However, our current understanding of key microbial functions that support plant growth in marine systems is limited. Based on evidence from terrestrial plant-microbe systems, seagrass-associated bacteria are expected to provide the plant with nitrogen and phosphorus resources while detoxifying sulfur and producing phytohormones. Here, we sequenced 61 bacterial cultures isolated from the rhizosphere, rhizoplane, and endosphere of the seagrass, Zostera marina to identify a consortium of six putative plant growth promoting (PGP) candidates.

RESULTS: Our cultivation approach using plant-based media allowed us to isolate 201 bacteria from Z. marina, which reflected 18% of the total microbial diversity of the starting inoculum. Genomic and phenotypic analyses of the 61-sequenced pure-cultures revealed that most of the sequenced taxa were able to mobilize nitrogen primarily through catabolic pathways, including denitrification (51%), dissimilatory nitrate reduction to ammonia (71%), and C-N bond cleavage (83%). Six of the isolates, which represent new lineages of Agarivorans, coded for the nitrogenase gene cassette. Additionally, 52% of the genomes had genes for sulfur and/or thiosulfate oxidation, 88.5% for phosphorus solubilization, and 60.5% for IAA production. Genomic analysis also revealed that some pathways, including denitrification and dissimilatory nitrite to ammonia DNRA, required cross-species cooperation as no one taxa contained all the genes needed to complete these metabolic pathways. Based on draft genome models and results from phenotypic assays, isolates Streptomyces sp. (Iso23 and Iso384), Mesobacillus sp (Iso127), Roseibuim sp. (Iso195), Peribacillus sp. (Iso49), and Agarivorans sp. (Iso311) represent a minimal microbial community that is likely to promote seagrass growth and enhance restoration efforts.

CONCLUSION: Our work provides a detailed genomic and phenotypic analysis of bacteria isolated from Zostera marina and identifies a minimal microbial community with complementary PGP traits. Isolating, identifying and characterizing bacteria that promote seagrass growth is critical towards enhancing restoration efforts of seagrass meadows.},
}

@article {pmid41889866,
year = {2026},
author = {Van Camp, AG and Park, J and Ozcelik, E and Eskiocak, O and Ozler, KA and Papciak, K and Subhash, S and Alwaseem, H and Ergin, I and Chung, C and Shah, V and Yueh, B and Fein, MR and Durmaz, C and Mozsary, C and Kilic, E and Garipcan, A and Damle, N and Najjar, D and Nelson, TM and Ryon, KA and Butler, DJ and Patel, CJ and Thaiss, CA and Birsoy, K and Mason, CE and Meydan, C and Tierney, BT and Beyaz, S},
title = {Diverse high-fat diets drive multi-omic reprogramming that persists after dietary reversal.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.17.708620},
pmid = {41889866},
issn = {2692-8205},
abstract = {Dietary fat composition modulates host physiology and the gut microbiome, but the long-term effects of specific fat sources and the extent to which these changes resolve after dietary reversal remain incompletely defined. Here, we present a longitudinal multi-omic resource of mice maintained for one year on a purified control diet, seven high-fat diets differing in predominant fat source, or reversal regimens in which animals were switched from high-fat to control diet after 4 or 9 months. We further incorporated two cohorts with distinct pre-existing microbiome configurations to determine how baseline community structure shapes diet-induced remodeling of the gut microbiome ecosystem. By integrating longitudinal phenotyping, fecal metagenomics, fecal metabolomics, plasma metabolomics and lipidomics, and intestinal single-cell RNA sequencing, we defined the shared and dietary fat-specific responses across host and microbiome compartments. Baseline microbiome composition strongly influenced microbial responses to diet, indicating that pre-existing community structure is a major determinant of dietary ecosystem remodeling. Although many altered features shifted toward baseline after dietary reversal, only approximately half of diet-associated microbial changes recovered within the study window. A subset of taxa exhibited persistent alterations, including sustained depletion of Lactobacillus johnsonii and Bifidobacterium pseudolongum and sustained enrichment of Alistipes finegoldii , consistent with a "microbiome memory" of prior high-fat diet exposure. This memory effect is mirrored in the host, by sustained suppression of major histocompatibility complex class II (MHC-II) gene expression in intestinal epithelial cells after dietary reversal. These findings indicate that dietary fats leave a lasting imprint on the host-microbiome interactome that survives dietary intervention. Together, these data establish a resource for defining how dietary fat source, baseline microbiome composition, and dietary history shape host-microbiome states. The entire resource is available online as an RShiny app.},
}

@article {pmid41889867,
year = {2026},
author = {Barua, A and Cong, F and Bao, H and Deng, WM},
title = {Tumor-induced species-specific dysbiosis drives renal innate immunity and nephrogenic ascites.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.10.710910},
pmid = {41889867},
issn = {2692-8205},
abstract = {Ascites is a life-threatening complication of advanced malignancies, yet how tumors disrupt systemic fluid homeostasis remains poorly understood. Here, using a Drosophila tumor allograft model that recapitulates key features of cancer-associated ascites, we identify a tumor-microbiome-renal axis that controls host fluid balance. Tumor-bearing hosts develop severe abdominal fluid accumulation accompanied by marked expansion and systemic dissemination of the gut commensal Acetobacter aceti . Tumor-induced bacterial dissemination activates innate immune signaling in the Malpighian tubules, the insect renal tubules, leading to uric acid accumulation, nephrolithiasis, and progressive ascites. Selective elimination of A. aceti , or renal-tubule-specific suppression of IMD/NF-κB signaling, abolishes these pathological changes. Conversely, mono-association of axenic hosts with A. aceti is sufficient to recapitulate the ascites phenotype through IMD pathway activation. Together, these findings demonstrate that tumors can remotely induce nephrogenic pathology through species-specific microbiome-dependent immune activation, establishing a mechanistic link between cancer progression and systemic fluid imbalance.},
}

@article {pmid41889965,
year = {2026},
author = {Landau, LJB and Jain, S and Griffin, N and Saikia, A and Kramer, JM and Knox, S and Ruhl, S and Gokcumen, O},
title = {Gene Expansion and Regulatory Rewiring Shape Sex-Biased Evolution of the Mouse Submandibular Gland Secretome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.18.712472},
pmid = {41889965},
issn = {2692-8205},
abstract = {Mammalian saliva plays essential roles in digestion, immunity, and host-microbiome interactions, yet its protein composition varies across species and sexes. The evolutionary mechanisms underlying this molecular diversity remain poorly understood. Here, we compared mouse and human salivary gland secretomes at genomic, transcriptomic, and proteomic levels to understand how saliva composition evolves. We performed RNA-seq analysis of the major mouse salivary glands (parotid, submandibular, and sublingual), liver and pancreas from both sexes, compared them with reanalyzed previously published human salivary gland transcriptomes, and integrated them with proteome data of mouse and human whole saliva. We found that evolution of gene expression in mouse salivary glands is driven by rapid gene turnover and sexual dimorphism. In the submandibular and sublingual glands, respectively, 68% and 73% of expression from genes encoding secreted proteins derives from lineage-specific genes that lack one-to-one human orthologs. Mouse submandibular gland shows striking sexual dimorphism, with 1537 tissue specific sex-biased genes, five times higher than in the liver, a classic model of sex-biased expression. These genes cluster in regions shaped by recent gene duplication, such as the kallikrein gene cluster, a mouse-specific expansion that accounts for ∼16.4% of male-biased submandibular expression. Our analyses suggest that this bias arises through regulatory changes that are expanded by gene duplication, including the spread of a testosterone-associated regulatory motif and the expansion of a shared chromatin domain that promotes coordinated gene regulation. Our results reveal how lineage-specific gene duplication and regulatory rewiring drive rapid, sex-specific evolution of the mammalian salivary gland secretome.},
}

@article {pmid41890109,
year = {2026},
author = {Stincone, P and Braun, LM and Bağcı, C and Navarro-Diaz, M and Pérez-Lorente, AI and Farrell, SP and Gómez-Pérez, D and Bode, J and Steuer-Lodd, K and Mahmoudi, M and Chaudhry, V and Romero, D and Aron, AT and Ziemert, N and Molina-Santiago, C and Kemen, EM and Petras, D},
title = {Cooperative siderophore use stabilizes a protective leaf microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.18.712463},
pmid = {41890109},
issn = {2692-8205},
abstract = {Plant-associated microbial communities provide crucial protection against pathogens. Specialized metabolites play key roles in plant-microbe and microbe-microbe interactions and, ultimately, in plant health; however, the molecular mechanisms underlying their plant-protecting properties remain largely unknown. Nutrient deficiency (e.g., iron) on leaf surfaces creates intense competition among microbes, driving both antagonism and cooperation. Using a gnotobiotic Arabidopsis thaliana model and a synthetic leaf microbial community, we show that community stability and plant protection depend on cooperative siderophore exchange between the basidiomycete yeast Rhodotorula kratochvilovae and commensal Pseudomonas species. Removal of Pseudomonas caused a strong shift in the community metabolome and accumulation of the yeast siderophore rhodotorulic acid (RA). RA selectively promoted the growth of commensal Pseudomonas via TonB-dependent transporters, which are absent in pathogenic Pseudomonas strains. Inactivation of these transporter genes abolished RA uptake, destabilized the synthetic community, and eliminated protection against Pseudomonas syringae infection. RA and Rhodotorula also induced host iron-deficiency and jasmonate-related defense metabolites, linking microbial cooperation to plant stress responses. These findings reveal that microbial siderophore exchange acts as a key mechanism that maintains stability in the phyllosphere microbiome. Rather than solely promoting competition, iron-binding compounds can serve as cooperative currencies that align microbial fitness with host protection.},
}

@article {pmid41890193,
year = {2026},
author = {Zhu, B and Qu, S and Li, J and Deng, W and Shen, WJ and Chen, J},
title = {The mechanisms underlying COVID-19 induced insulin resistance: a narrative review.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1781679},
pmid = {41890193},
issn = {1664-2392},
mesh = {Humans ; *Insulin Resistance/physiology ; *COVID-19/complications/metabolism ; SARS-CoV-2 ; Gastrointestinal Microbiome ; Diabetes Mellitus/etiology/metabolism ; },
abstract = {The COVID-19 pandemic, caused by SARS-CoV-2, has resulted in a significant increase in insulin resistance and new-onset diabetes among recovered individuals. This review examines the multifactorial mechanisms underlying these metabolic complications, including activation of the immune system and inflammatory cascades, lifestyle changes, nutritional deficiencies, imbalances in amino acid metabolism, alterations in ketogenesis, disruptions in the gut microbiome, psychological impacts, and COVID-19 vaccines. We discuss how these factors collectively contribute to insulin resistance, particularly in the context of COVID-19, and highlight potential therapeutic strategies, such as dietary interventions and ACE2 activators, that may mitigate these effects. Our analysis underscores the need for targeted approaches to prevent and treat insulin resistance in post-COVID-19 patients, emphasizing the importance of understanding the pandemic's long-term metabolic consequences.},
}

Humans
*Insulin Resistance/physiology
*COVID-19/complications/metabolism
SARS-CoV-2
Gastrointestinal Microbiome
Diabetes Mellitus/etiology/metabolism

@article {pmid41890637,
year = {2026},
author = {Fujita-Jimbo, E and Kawahara, G and Momoi, T},
title = {Foxp2 mutations and abnormal brain and gastrointestinal development: insights from animal models of speech-language and autism spectrum disorders.},
journal = {Frontiers in neuroanatomy},
volume = {20},
number = {},
pages = {1783101},
pmid = {41890637},
issn = {1662-5129},
abstract = {Autism spectrum disorder (ASD) and speech and language disorder (SLD) are distinct neurodevelopmental conditions, yet both share overlapping communication impairments. Forkhead box P2 (FOXP2), a key transcription factor involved in speech and language development, harbors pathogenic mutations such as R553H, which cause SLD and have been suggested to contribute to aspects of ASD-related phenotypes. This review synthesizes insights from animal models to explore the molecular mechanisms by which Foxp2 mutations disrupt the development of the cerebral cortex, thalamus, and enteric nervous system. We highlight findings from heterozygous Foxp2 mutants and discuss severe phenotypes observed in homozygous Foxp2 mutants (Foxp2[R552H/R552H] and Foxp2[R552H/R552H]/mCherry-Tg mice), including profound ultrasonic vocalization deficits, brain malformations, and early lethality. Notably, these mice exhibit gastrointestinal abnormalities involving the epithelium, smooth muscle, and enteric nervous system, which are linked to impaired autoregulation and interference with Wnt signaling during development. Such observations underscore the relevance of the brain-gut-microbiome axis and Hirschsprung-like pathology in neurodevelopmental disorders. Finally, this review discusses future directions using gene-editing approaches in non-mammalian models-zebra finches, zebrafish, and Drosophila-to dissect neural networks underlying intellectual disability and communication deficits. Collectively, these studies provide a framework for understanding FOXP2-related molecular mechanisms in the pathogenesis of ASD and SLD.},
}

@article {pmid41890703,
year = {2026},
author = {Li, X and Liu, F and Zhu, Y and Shi, H},
title = {Gut Microbiota, Insulin Resistance, and Alzheimer's Disease: A Narrative Review of Mechanistic Links and Therapeutic Perspectives.},
journal = {International journal of general medicine},
volume = {19},
number = {},
pages = {593664},
pmid = {41890703},
issn = {1178-7074},
abstract = {Alzheimer's disease (AD) is increasingly regarded as a "neurometabolic syndrome" wherein systemic insulin resistance exacerbates cerebral glucose hypometabolism, tau hyperphosphorylation, and neuroinflammation. We hypothesize that gut microbiota dysbiosis produces metabolites that are associated with peripheral insulin sensitivity, potentially contributing to disruptions in cerebral insulin signaling and an increased risk of AD. We conducted integrated search of PubMed, Web of Science, and Scopus to synthesize evidence showing: (i) consistent taxonomic shifts in AD, highlighting reduced Firmicutes and increased Proteobacteria and Bacteroidetes, depletion of Ruminococcaceae and enrichment of Blautia and Bilophila; (ii) functional consequences of dysbiosis, leading to lower short-chain fatty acids, altered secondary bile‑acid signaling, elevated lipopolysaccharide and trimethylamine‑N‑oxide, and perturbed tryptophan catabolism; (iii) these microbial metabolites compromising gut and blood-brain barrier integrity, thereby triggering chronic inflammation, potentially modulating the PI3K‑Akt‑GSK‑3β pathway, and linking peripheral insulin resistance to cerebral dysfunction; and (iv) a translational discussion of therapeutic strategies that target both microbiota and insulin pathways, including dietary modulation, probiotics and prebiotics, fecal microbiota transplantation, intranasal insulin, metformin, and metabolite-based agents, show promise. This review uniquely integrates taxonomic, functional, and therapeutic literature to propose a mechanistic microbiota-insulin resistance-AD axis and highlights the need for longitudinal and interventional trials.},
}

@article {pmid41890730,
year = {2026},
author = {Yanamadala, Y and Gokulan, K and Karn, K and Sutherland, V and Cunny, H and Santos, JH and Davis, K and Khare, S},
title = {Gestational and lactational exposure to HIV tri-combination therapy induces sex- and dose-dependent changes in inflammatory cytokine profiles, intestinal permeability, and villi morphology in adult rat offspring.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1668334},
pmid = {41890730},
issn = {1664-3224},
mesh = {Animals ; Female ; Pregnancy ; *Cytokines/metabolism ; Male ; Rats ; Permeability ; *Intestinal Mucosa/drug effects/metabolism/pathology/immunology ; *Prenatal Exposure Delayed Effects/immunology ; Lactation ; *HIV Infections/drug therapy/immunology ; *Anti-HIV Agents/adverse effects ; Lamivudine/adverse effects ; Sex Factors ; Piperazines ; Inflammation Mediators/metabolism ; Intestinal Barrier Function ; },
abstract = {INTRODUCTION: Gestational antiretroviral therapy (ART) has significantly reduced the risk of vertical transmission of HIV, but concerns linger about its long-term effects on the fetal immune system and intestinal health. Our previous work has demonstrated dose-dependent changes in the fecal and mucosa-associated microbiome of adult rat offspring perinatally exposed to TC-ART (tri-combination ART: dolutegravir, abacavir, and lamivudine). These changes may either be driven by alterations in immune system and intestinal barrier integrity or potentially impact them.

METHODS: In this study, we further investigated the long-term effects of perinatal TC-ART exposure on intestinal permeability, cytokine profiles, and intestinal mucosa morphology.

RESULTS: We observed statistically significant sex-dependent differences, with male offspring exhibiting reduced weight gain, a dichotomous response between low and high dose for inflammatory cytokines [interleukin-5 (IL-5), IL-7, and IL-12], differential regulation for the mRNA expression of intestinal permeability-related genes (21 downregulated), and disrupted villous architecture, while females showed dose-dependent decreases in inflammatory cytokines [IL-17, IL-5, and macrophage colony-stimulating factor (M-CSF)]. In females, while some intestinal permeability genes were downregulated, the upregulation of other permeability genes suggests a compensatory mechanism to maintain the intestinal barrier function, indicating an overall milder response to TC-ART.

DISCUSSION: These findings suggest that perinatal exposure to TC-ART may have differential impacts on intestinal health, with females exhibiting a more adaptive response compared to males, highlighting the need for sex-specific considerations in evaluating long-term effects of ART.},
}

Animals
Female
Pregnancy
*Cytokines/metabolism
Male
Rats
Permeability
*Intestinal Mucosa/drug effects/metabolism/pathology/immunology
*Prenatal Exposure Delayed Effects/immunology
Lactation
*HIV Infections/drug therapy/immunology
*Anti-HIV Agents/adverse effects
Lamivudine/adverse effects
Sex Factors
Piperazines
Inflammation Mediators/metabolism
Intestinal Barrier Function

@article {pmid41890754,
year = {2026},
author = {Song, Z and Han, X and Zhou, Z and Hua, H and Wang, F and Zhang, X and Wen, S},
title = {Comprehensive management of hematopoietic stem cell transplantation complications: from infection prevention to immune microenvironment reconstruction.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1740067},
pmid = {41890754},
issn = {1664-3224},
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/adverse effects ; *Graft vs Host Disease/etiology/prevention & control/therapy/immunology ; *Hepatic Veno-Occlusive Disease/etiology/prevention & control/therapy ; *Infections/etiology/therapy ; Gastrointestinal Microbiome ; Disease Management ; Transplantation Conditioning/adverse effects/methods ; Animals ; },
abstract = {This article systematically reviews the management of key complications in hematopoietic stem cell transplantation (HSCT), including infections, graft-versus-host disease (GVHD), and hepatic sinusoidal obstruction syndrome (VOD/SOS). It highlights the importance of optimizing conditioning regimens to reduce infection risk and discusses the role of novel antiviral agents like letermovir in transforming infection control. For GVHD, the pathogenesis involving effector and regulatory T-cell imbalances is analyzed, together with prevention strategies such as post-transplant cyclophosphamide with antithymocyte globulin and TCRαβ/CD19 depletion. Ruxolitinib is emphasized for steroid-refractory GVHD, and gut microbiota modulation is noted as a promising intervention. For VOD/SOS, early biomarker detection and defibrotide treatment are critical. The review also explores the impact of immune reconstitution on infection control, GVHD development, and relapse, and examines how emerging approaches, including single-cell sequencing, microbiome analysis, and artificial intelligence, can be applied in building whole-course risk management models. Future directions include developing intelligent platforms and personalized strategies to enhance long-term patient outcomes.},
}

Humans
*Hematopoietic Stem Cell Transplantation/adverse effects
*Graft vs Host Disease/etiology/prevention & control/therapy/immunology
*Hepatic Veno-Occlusive Disease/etiology/prevention & control/therapy
*Infections/etiology/therapy
Gastrointestinal Microbiome
Disease Management
Transplantation Conditioning/adverse effects/methods
Animals

@article {pmid41890921,
year = {2026},
author = {Calafate, C and Alpuim Costa, D and Campos, T and Ribeiro, PC and Martinho, F and Freitas, C and Botelho de Sousa, C and Negreiros, I and Canastra, A and Borralho, P and Pereira, AG and Marçal, C and Ribeiro, R and Sousa, JG and Dinis, C and Chaleira, R and Calha, R and Rocha, JC and Calhau, C and Moreira-Rosário, A and Faria, A},
title = {Assessing mental health, cognitive function and quality of life of breast cancer patients: exploring associations with gut microbiota in an observational and preliminary study.},
journal = {Frontiers in psychology},
volume = {17},
number = {},
pages = {1437697},
pmid = {41890921},
issn = {1664-1078},
abstract = {INTRODUCTION: Breast cancer patients face several physical and psychological problems, such as anxiety, depression, and cognitive dysfunction. The disease and treatments can also impact the microbiota, which is associated with cognitive and psychological issues and, consequently, affected quality-of-life (QoL). This study aimed to correlate the initial gut microbiota of newly diagnosed HR+ (Hormone Receptor)/HER2- breast cancer patients with their mental health, cognitive function, and QoL at baseline and after 3 months of neoadjuvant chemotherapy.

MATERIALS AND METHODS: This is a prospective, longitudinal, observational, exploratory study. Newly diagnosed HR+/HER2- breast cancer patients undergoing neoadjuvant chemotherapy were recruited upon diagnosis. At baseline (before neoadjuvant chemotherapy), general and lifestyle information, adherence to the Mediterranean diet, biochemical analysis, gut microbiota profile, the European Organization for Research and Treatment of Cancer Quality-of-Life Questionnaire Core-30 (EORTC QLQ-C30), the Montreal Cognitive Assessment (MoCA) and the Hospital Anxiety and Depression Scale (HADS), were collected. The EORTC QLQ-C30, MoCA, and HADS were repeated 3 months later.

RESULTS: From the 11 participants, most showed mild cognitive impairment at baseline, and there was no clear trend of improvement or deterioration at 3 months. Participants had borderline anxiety at baseline, which improved to a normal range, while depression remained stable. QoL declined for most women, with over 70% experiencing problems at 3 months. The association of these parameters with microbiota profile suggested that women with poorer cognitive function over time had lower Shannon index and microbial richness. Women with improved scores in the depression subscale of the HADS appear to have higher Shannon index and lower richness. Contrarily, Shannon index was lower and richness was higher for improved anxiety and global QoL scores. The results also suggest that changes in the abundance of various genera and phyla may be linked to the evolution of scores for the 3 questionnaires.

CONCLUSION: Our study suggests a link between the microbiota profile at diagnosis and the psychological symptoms that develop at 3 months of breast cancer treatment. These findings shed light on potential strategies for positively modulating the microbiota to help enhance the body's resilience, particularly mental health, throughout the disease and treatments.},
}

@article {pmid41890980,
year = {2026},
author = {Shi, Y and Sanderson, H and Chuan, J and Khan, IUH and Sunohara, M and Craiovan, E and Lapen, DR and Diarra, M and Chen, W},
title = {Dual-platform metagenomic surveillance distinguishes pathogen and resistome hotspots across agricultural and mixed-use watersheds.},
journal = {One health (Amsterdam, Netherlands)},
volume = {22},
number = {},
pages = {101384},
pmid = {41890980},
issn = {2352-7714},
abstract = {Freshwater systems embedded in agricultural landscapes serve as dynamic reservoirs and conduits for fecal-associated microbes, zoonotic pathogens, and antimicrobial resistance (ARG) and virulence factor (VF) genes. Yet factors that govern their densities and diversity remain a research challenge. From 2016 to 2021, we conducted a longitudinal water surveillance in an agriculturally dominated river basin in eastern Ontario, Canada; characterizing fecal-associated bacterial communities using 16S rRNA gene amplicon and shotgun metagenomic sequencing. Agricultural drainage ditches consistently harbored higher fecal-associated bacterial diversity with pronounced seasonal shifts; i.e., higher levels during larger flow periods in spring and fall. Elevated discharge was associated with enrichment of genera containing zoonotic or opportunistic pathogens, such as those in Pseudomonas, Sphingomonas, and Massilia. Conditionally rare taxa (CRTs), although typically low in abundance, accounted for ∼12.6% of all pathogen-associated genera and disproportionately contributed to community turnover, highlighting their role as transient reservoirs of microbial risk. Shotgun metagenomics detected 27 ARGs, primarily at mixed-use sites, and 14 VFs, mainly in agricultural ditches. Clinically relevant β-lactamase genes (e.g., oxa, imp, sme) co-occurred with metal-resistance operons, a pattern suggestive of possible co-selection, although selective agents were not directly measured. Although the prevalence of ARG and VF was low (<5% of samples), their ecological context indicates potential transmission pathways. Limited overlap in ARGs between short-read and metagenome-assembled genome (MAG)-based profiling reflects their complementary strength: gene-level sensitivity versus host-resolved analysis. Together, these findings demonstrate the utility of integrated amplicon and shotgun metagenomic surveillance for proactive One Health risk assessment in agricultural watersheds.},
}

@article {pmid41891018,
year = {2026},
author = {Basso, M and Hildebrand, F and Winder, C and Baker, DJ and Manders, R and Barberis, M and Gibbons, SM and Cohen Kadosh, K},
title = {Anxiety associated with dietary intake and gut microbiome features in a cross-sectional cohort of sub-clinically anxious young women.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.18.26348688},
pmid = {41891018},
abstract = {Background Emerging evidence highlights the gut-brain axis as a key pathway linking diet and anxiety, yet the key determinants remain unclear. Most studies have focused on single components of diet and rarely integrate long- and short-term intake. Furthermore, prior gut-brain work has focused on microbiome composition, while functional features remain underexplored. In this study, we investigated associations between long- and short-term dietary intake, gut microbiome composition and functions, and anxiety in a subclinical cohort of 46 females (18-24 years) from the United Kingdom. Results Long-term diet quality was assessed using the Healthy Eating Index (HEI-2020) derived from a food frequency questionnaire, stratifying participants into lower and higher diet quality clusters. Short-term dietary intake was assessed via 24-hour recalls. Shotgun metagenomics of stool samples was used to assess differences in alpha and beta diversity indices, species abundances, and bacterial pathways putatively metabolizing gut-brain-axis-relevant molecules. Anxiety was measured using the State-Trait Anxiety Inventory (state subscale STAI-s). Regression models identified diet quality (HEI cluster) as the primary dietary feature of anxiety variation. The presence of Ruminococcus gnavus and Flavonifractor plautii and the abundances of Bilophila wadsworthia and Bacteroides thetaiotaomicron were positively associated with anxiety. The presence of Feacalibacterium prausnitzii and greater abundances of butyrate, propionate, and GABA synthesis pathways were inversely associated with anxiety. Non-linear models revealed a U-shaped relationship between inositol synthesis and STAI-s. Finally, we found that habitual diet quality may modulate anxiety-related responses to short-term dietary variation. Conclusions These findings reveal widespread links between long-term diet quality, microbiota composition and function, and anxiety symptoms. These results point towards several promising targets for prebiotic, probiotic, postbiotic, and dietary interventions aimed at reducing anxiety.},
}

@article {pmid41891123,
year = {2026},
author = {Jara, J and Alba, C and Fernández, L and Orozco Fernández, R and López Carrasco, A and Brunel García, I and Vilches Jiménez, JC and Buño-Soto, A and Regidor, PA and Gutiérrez, R and Lázcoz, B and Rodríguez, JM and Orgaz, B},
title = {Probiotic supplementation improves quality of life and modulates oestradiol in women with endometriosis: a randomised double-blind pilot trial.},
journal = {The European journal of contraception & reproductive health care : the official journal of the European Society of Contraception},
volume = {},
number = {},
pages = {1-15},
doi = {10.1080/13625187.2026.2644896},
pmid = {41891123},
issn = {1473-0782},
abstract = {OBJECTIVE: Endometriosis is a chronic, oestrogen-dependent inflammatory disorder affecting up to 10% of reproductive-age women, associated with pelvic pain, infertility, and reduced quality of life. Emerging evidence implicates the vaginal microbiome and oestrogen metabolism in its pathogenesis. This study aimed to evaluate the potential therapeutic role of the oral administration of Ligilactobacillus salivarius CECT 30632, a probiotic with demonstrated ability to metabolise oestrogens in vitro, to improve the quality of life in women with endometriosis.

MATERIAL AND METHODS: We conducted a pilot, randomised, double-blind, placebo-controlled clinical trial assessing its effects, alongside standard dienogest treatment, in 37 women with endometriosis. Outcomes included changes in the vaginal microbiota composition (16S rRNA sequencing), in the immunological markers, in serum oestradiol levels, and in the quality-of-life of participants assessed with the EHP-30 questionnaire.

RESULTS: Vaginal microbial diversity remained unchanged between groups; however, ∼20% of participants exhibited individualised microbiota shifts, including transitions to Lactobacillus-dominated profiles. In the immunological markers, the IL-10 levels decreased in 65% of probiotic supplemented participants (p = 0.042). Serum oestradiol levels were significantly reduced (∼50%) in the probiotic group (p = 0.013). The probiotic supplementation was associated with significant improvements in pain, emotional well-being, and perceived self-control (p < 0.05).

CONCLUSIONS: Daily oral intake of L. salivarius CECT 30632 was associated with changes in circulating oestradiol levels and improvements in the quality of life in women with endometriosis. These preliminary findings support further powered trials to confirm efficacy and clarify underlying mechanisms.},
}

@article {pmid41891189,
year = {2026},
author = {Jiménez-Padilla, Y and Sinclair, BJ},
title = {Gut yeasts accelerate chill coma recovery in Drosophila melanogaster.},
journal = {The Journal of experimental biology},
volume = {},
number = {},
pages = {},
doi = {10.1242/jeb.251533},
pmid = {41891189},
issn = {1477-9145},
support = {//Queen Elizabeth Scholars/ ; //Natural Sciences and Engineering Research Council of Canada/ ; },
abstract = {The role of microbial symbionts in host stress tolerance remains underexplored. Gut microbiome studies in Drosophila melanogaster have largely focused on bacteria, whereas yeasts have been assumed to provide nutrition rather than engage in true symbiosis. We explored the effect of gut yeasts on chill coma recovery time (CCRT, a proxy for cold tolerance) and its yeast species-specificity and dependence on live yeast cells. We generated flies with distinct gut microbiota conditions: axenic (microbe-free), with their native microbiota (derived from the microbes associated with flies conventionally reared in our colony), or gnotobiotic flies mono-associated with either live or heat-killed yeasts (Saccharomyces cerevisiae - not normally associated with Drosophila guts, and three species previously isolated from wild flies - Lachancea kluyveri, Pichia kluyveri, or P. nakasei). We quantified yeast abundance, sex differences in yeast ingestion, and measured CCRT after exposure to 0 °C for 8 hours. Female axenic flies recovered 42% more slowly than those with their native microbiota, but this delay was fully rescued by live L. kluyveri, P. kluyveri, or P. nakasei, not by S. cerevisiae or dead yeasts. The effect was rapid (occurs within 48 h), sex-specific (restricted to females), and appeared to be dose-dependent. We also confirmed that yeasts in the gut are alive, facilitating a true (albeit transient) symbiotic interaction. Our findings show that yeast symbionts may contribute to natural variation in thermal tolerance and may broadly impact host phenotypes. Excluding yeasts or assuming a solely nutritional role risks overlooking key symbiotic interactions that have profound functional consequences.},
}

@article {pmid41891399,
year = {2026},
author = {Elsheikh, M and Ibrahim, MA and Fares, S and Bhongade, M and Adhem, K and Ramirez-Morales, XI and Kaseb, AO and Petrosino, J and Hassan, MM and Jalal, PK},
title = {Influence of Gut Microbiota on Response to Immune Check Point Inhibitors in MASLD Patients With HCC: Unraveling the Connection.},
journal = {Cancer medicine},
volume = {15},
number = {4},
pages = {e71738},
doi = {10.1002/cam4.71738},
pmid = {41891399},
issn = {2045-7634},
support = {R21CA293626/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; *Gastrointestinal Microbiome/immunology/drug effects ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; *Liver Neoplasms/drug therapy/immunology/microbiology/complications ; *Carcinoma, Hepatocellular/drug therapy/immunology/microbiology/complications ; Dysbiosis/microbiology ; Drug Resistance, Neoplasm ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; },
abstract = {Immune checkpoint inhibitors (ICIs) have emerged as a promising treatment for various cancers, including advanced hepatocellular carcinoma (HCC). However, a significant proportion of patients with HCC, particularly those with metabolic dysfunction-associated liver disease (MASLD), exhibit resistance to ICI therapy. Studies have revealed that the presence of specific gut bacteria, such as Akkermansia, Bifidobacterium, and Lachnoclostridium, is associated with improved outcomes with ICI-treated HCC patients. Conversely, the overgrowth of bacteria like Enterobacteriaceae is linked to resistance to therapy. This review investigates the role of gut microbiota in shaping immune checkpoint inhibitor responses in MASLD-related hepatocellular carcinoma, focusing on how dysbiosis may contribute to ICI resistance and exploring microbiome modulation strategies, such as fecal microbiota transplantation and probiotics, aiming to optimize therapeutic outcomes.},
}

Humans
*Gastrointestinal Microbiome/immunology/drug effects
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
*Liver Neoplasms/drug therapy/immunology/microbiology/complications
*Carcinoma, Hepatocellular/drug therapy/immunology/microbiology/complications
Dysbiosis/microbiology
Drug Resistance, Neoplasm
Fecal Microbiota Transplantation
Probiotics/therapeutic use

@article {pmid41891724,
year = {2026},
author = {Goerlich, K and Mitchell, AP},
title = {Impact of Candida albicans NDT80 and UME6 on biofilm formation and fluconazole susceptibility.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0001426},
doi = {10.1128/msphere.00014-26},
pmid = {41891724},
issn = {2379-5042},
abstract = {The microbiome-associated fungus Candida albicans is an opportunistic pathogen. Virulence traits include its ability to produce biofilm, a surface-associated growth form that persists on mucosae and implanted medical devices. C. albicans clinical isolates vary in ability to produce biofilm and the constituent filamentous cell types. Here, we focus on two transcription factors that promote filamentation and biofilm formation, Ndt80 and Ume6. We address two questions. First, how variable is the impact of Ndt80 among C. albicans strains? Second, what is the genetic interaction between NDT80 and UME6? We find that Ndt80 is required for filamentation and biofilm formation in five clinical isolates in addition to the reference strain SC5314, where Ndt80 function has been well established. RNA-sequencing (RNA-seq) data indicate that UME6 RNA levels are reduced in an ndt80Δ/Δ mutant, possibly a result of altered RME1 and WOR1 expression, both of which control UME6. Increased expression of UME6 in ndt80Δ/Δ mutants of three strain backgrounds restores filamentation and biofilm formation, though RNA-seq assays indicate that it does not suppress the overall ndt80Δ/Δ gene expression defect. Ndt80 has an additional role in promoting tolerance to the antifungal drug fluconazole, an inhibitor of ergosterol synthesis. This ndt80Δ/Δ phenotype varies considerably among clinical isolates. In three strains tested, increased expression of UME6 in ndt80Δ/Δ mutants enhances their susceptibility to fluconazole. Therefore, our results show an unexpected relationship between Ume6 expression and azole drug sensitivity. To our knowledge, Ume6 has previously been understood to function only in filamentation, biofilm formation, and related processes.IMPORTANCEOur focus is the fungal pathogen Candida albicans. Two traits, biofilm/hypha formation and azole resistance, are major drivers of its infection ability. We examine the roles of two biofilm transcriptional regulators, Ndt80 and Ume6, in several C. albicans clinical isolates. Prior studies in one strain background (SC5314) indicated that Ndt80 controls both biofilm/hypha formation and azole drug susceptibility and that Ume6 controls biofilm/hypha formation. The four new findings here are that (i) Ndt80 effects on fluconazole sensitivity vary considerably with strain background; (ii) Ndt80 is required for filamentation and biofilm formation in multiple clinical isolates; (iii) the Ndt80 target Ume6 contributes to Ndt80 control of filamentation and biofilm formation in multiple clinical isolates; and (iv) Ume6 influences fluconazole vulnerability, the first Ume6 function to our knowledge that is unrelated to filamentation.},
}

@article {pmid41891974,
year = {2026},
author = {Zhang, H and Li, D and Zhu, L and Yan, H and Yang, L and Yang, X and Zhou, Y},
title = {Multi‑omics and their integration in psoriasis research (Review).},
journal = {Molecular medicine reports},
volume = {33},
number = {5},
pages = {},
doi = {10.3892/mmr.2026.13852},
pmid = {41891974},
issn = {1791-3004},
mesh = {Humans ; *Psoriasis/genetics/metabolism/microbiology/pathology ; *Genomics/methods ; Metabolomics/methods ; Epigenomics/methods ; Proteomics/methods ; Biomarkers ; Epigenesis, Genetic ; Genome-Wide Association Study ; Genetic Predisposition to Disease ; Transcriptome ; Animals ; Microbiota ; Multiomics ; },
abstract = {Psoriasis is a chronic, immune‑mediated skin disorder characterized by keratinocyte hyperproliferation, inflammatory infiltrates and systemic comorbidities. While genetic predisposition and immune dysregulation are established contributors, recent advancements in high‑throughput omics technologies have provided deeper insights into the molecular complexity of psoriasis. The present review synthesized findings from various omics layers, genomics, epigenomics, transcriptomics, proteomics, metabolomics and microbiomics, to elucidate their roles in psoriasis pathogenesis. Large‑scale genome‑wide association studies have identified both common and region‑specific susceptibility loci. Epigenetic factors and transcription factors regulate psoriasis‑related genes by modulating chromatin accessibility, DNA methylation, non‑coding RNAs and direct gene activation/inactivation, thereby reshaping the transcriptome. Genetic and epigenetic influences also drive significant alterations in the proteome and metabolome, both in the skin and plasma, shedding light on disease mechanisms and offering potential for biomarker discovery. While microbiome research in psoriasis remains in its early stages, shifts in skin and gut microbial communities have been observed, suggesting their involvement in disease pathogenesis. Together, the multi‑layered insights underscore the future potential of integrated systems approaches to unravel disease mechanisms and support the discovery of clinically actionable biomarkers and therapeutic targets, paving the way for more precise diagnosis and targeted therapeutic development in psoriasis.},
}

Humans
*Psoriasis/genetics/metabolism/microbiology/pathology
*Genomics/methods
Metabolomics/methods
Epigenomics/methods
Proteomics/methods
Biomarkers
Epigenesis, Genetic
Genome-Wide Association Study
Genetic Predisposition to Disease
Transcriptome
Animals
Microbiota
Multiomics

@article {pmid41892210,
year = {2026},
author = {Liang, X and Li, X and Mi, N and Wu, Y and Wu, J and Chen, H and Liu, D},
title = {Early-Life Diarrhea Disrupts Antioxidant-Immune Homeostasis and Gut Microbiota in Suckling Calves.},
journal = {Biology},
volume = {15},
number = {6},
pages = {},
doi = {10.3390/biology15060450},
pmid = {41892210},
issn = {2079-7737},
support = {YLXKZX-NND-012//First-class Disciplines of Inner Mongolia Scientific Research Special Program/ ; 2023-JSGG-5//National Center of Technology Innovation for Dairy/ ; BR22-11-17//Basic Scientific Research Business Project of Universities directly under the Inner Mongolia Au-tonomous Region/ ; 2024LHMS03054//nner Mongolia Natural Science Foundation Project/ ; },
abstract = {Calf diarrhea is a common early-life disorder that adversely affects growth, oxidative balance, immune function, and intestinal microbiota, thereby compromising health and production performance. This study systematically investigates the effects of naturally occurring diarrhea in 7-day-old suckling calves on oxidative stress, immune responses, intestinal barrier integrity, and gut microbiota structure and function. Fecal scores, serum antioxidant and immune indices, and intestinal permeability markers were measured, and fecal samples were subjected to metagenomic sequencing. Diarrhea-affected calves exhibited higher fecal scores, increased oxidative stress indicated by reduced total antioxidant capacity, elevated lipid peroxidation, and altered antioxidant enzyme activities. Humoral immunity was impaired, inflammatory responses were dysregulated, and intestinal barrier function was disrupted. Gut microbial diversity declined, showing a depletion in health-associated taxa and the enrichment of opportunistic pathogens. Correlation analyses revealed that pathogenic bacteria abundance positively associated with diarrhea severity, oxidative stress, inflammation, and barrier disruption, while beneficial genera correlated with antioxidant and immune function. Functional profiling indicated a microbial shift from amino acid metabolism and antioxidant homeostasis toward carbohydrate and energy metabolism under diarrheic conditions. These findings highlight the pivotal role of gut microbiota dysbiosis in diarrhea pathogenesis and provide a foundation for developing microbiome-targeted interventions to improve calf health.},
}

@article {pmid41892267,
year = {2026},
author = {Tomuța, RA and Caltea, A and Ghitea, MC and Ghitea, EC and Gîtea, MF and Ghitea, TC and Banica, F},
title = {Physical Activity Is Associated with Gut Microbiome Features and Organic Acid Patterns in Adults Consuming Plant-Rich Diets: An Exploratory Cross-Sectional Study.},
journal = {Biology},
volume = {15},
number = {6},
pages = {},
doi = {10.3390/biology15060507},
pmid = {41892267},
issn = {2079-7737},
support = {410072//University of Oradea/ ; },
abstract = {BACKGROUND: Plant-rich dietary patterns are widely associated with metabolic and gastrointestinal health benefits. However, individuals consuming predominantly plant-based foods may also experience chronic low-dose exposure to dietary pesticide residues. At the same time, physical activity is recognized as an important lifestyle factor influencing metabolic health and gut microbiome composition. How microbiome features and microbiome-related metabolic profiles vary according to physical activity level in adults consuming plant-rich diets and reporting gastrointestinal symptoms remains insufficiently characterized.

OBJECTIVE: To explore associations between physical activity level, gut microbiome characteristics, and urinary organic acid patterns in adults consuming predominantly plant-rich diets and experiencing gastrointestinal symptoms, within a cohort characterized by comparable estimated dietary pesticide exposure used as a contextual dietary background variable.

METHODS: This cross-sectional observational study included 93 adults consuming ≥50% plant-based foods for at least six months and reporting persistent gastrointestinal symptoms. Participants were stratified according to physical activity level using WHO-based thresholds (<150 vs. ≥150 min/week of moderate-intensity activity). Stool microbiota were assessed using a targeted quantitative PCR panel, and microbial diversity was summarized using a laboratory-derived Shannon index. A voluntary subgroup (n = 50) underwent targeted urinary organic acid analysis (LC-MS/MS). Dietary pesticide exposure was indirectly estimated using national surveillance data combined with individual dietary records and was applied uniformly across groups. Analyses were primarily descriptive and exploratory; results are presented as associations.

RESULTS: Estimated dietary pesticide exposure did not differ between physical activity groups. Participants with lower physical activity were older and exhibited lower microbial diversity and a higher prevalence of reduced abundance in selected commensal taxa. Differences were observed in selected intermediary organic acid markers, while no statistically significant difference was found for the bile acid-related indicator. Several cross-domain correlations were identified between microbial features and metabolite patterns. However, given the cross-sectional design, age imbalance between groups, and subgroup-based metabolomic analyses, the findings should be interpreted as hypothesis-generating rather than indicative of independent effects of physical activity.

CONCLUSIONS: In adults consuming plant-rich diets and reporting gastrointestinal symptoms, physical activity level was associated with distinct microbiome and microbiome-related metabolic patterns under comparable estimated dietary pesticide exposure. These findings highlight the potential contribution of lifestyle factors to interindividual variability in gut microbial and metabolic profiles, while underscoring the need for age-adjusted, longitudinal, and biomarker-based studies to clarify directionality and mechanisms.},
}

@article {pmid41892298,
year = {2026},
author = {Prud'homme, GJ and Wang, Q},
title = {Antiaging Properties of the Klotho Protein.},
journal = {Cells},
volume = {15},
number = {6},
pages = {},
doi = {10.3390/cells15060507},
pmid = {41892298},
issn = {2073-4409},
support = {2-SRA-2018-497-A-B//Juvenile Diabetes Research Foundation International/ ; OG-3-13-4066//Diabetes Canada/ ; 81570518, 81630020, 82370814//National Science Foundation of China/ ; N/A//St. Michael's Hospital Foundation, Toronto, Canada/ ; N/A//Keenan Research Centre for Biomedical Science, Toronto, Canada/ ; },
mesh = {*Klotho Proteins/metabolism ; Humans ; *Aging/metabolism/genetics ; Animals ; *Glucuronidase/metabolism ; Inflammation/metabolism ; Cellular Senescence ; },
abstract = {Mice genetically deficient in α-Klotho (henceforth Klotho) display accelerated aging. The mechanisms are only partially understood. Here, we examine how these relate to the 12 hallmarks of aging consisting of chronic inflammation (inflammaging), as well as damaging changes to the genome (DNA damage), telomeres, epigenetic regulation, proteostasis, nutrient sensing, mitochondria, stem cells, intercellular communication, macroautophagy, microbiome and cell replication (senescence). Inflammation aggravates the other hallmarks. We report that Klotho counters the majority of these hallmarks. It ameliorates mitochondrial function and reduces reactive oxygen species (ROS), telomere attrition and cellular senescence. It protects against inflammation by inhibiting NF-κB and the NLRP3 inflammasome. This applies to inflammaging, several chronic inflammatory diseases, atherosclerosis, diabetes, and Alzheimer's disease. Klotho also counters some aging factors outside of these hallmarks. Low Klotho (often due to kidney disease) produces hyperphosphatemia, which injures cells (especially endothelial cells) and promotes aging. Another key action of Klotho is the mitigation of fibrosis in major organs (kidneys, heart, lungs and other), mainly through the inhibition of TGF-β and Wnt. Klotho also protects against muscle atrophy (sarcopenia)-a common feature of aging-and exhibits anti-cancer activity. We describe several factors that increase Klotho, and are potentially amenable to clinical therapy.},
}

*Klotho Proteins/metabolism
Humans
*Aging/metabolism/genetics
Animals
*Glucuronidase/metabolism
Inflammation/metabolism
Cellular Senescence

@article {pmid41892413,
year = {2026},
author = {Šuran, J and Pavlović, N and Božić, J and Kumrić, M and Vukojević, K and Filipović, N and Radić, B},
title = {IBS and SIBO: Gut Microbiota, Pathophysiology, and Non-Pharmacological Interventions.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {3},
pages = {},
doi = {10.3390/antibiotics15030251},
pmid = {41892413},
issn = {2079-6382},
abstract = {Irritable bowel syndrome (IBS) and small intestinal bacterial overgrowth (SIBO) share symptoms such as abdominal pain, bloating, and altered bowel habits. Both are linked to dysbiosis and gut-brain axis dysfunction. IBS is a multifactorial disorder characterized by abnormal motility, visceral hypersensitivity, low-grade inflammation, and alterations in the microbiota. In contrast, SIBO is defined by excessive bacterial colonization of the small intestine that can mimic or worsen IBS symptoms. Gut microbes and their metabolites influence motility, immune activation, barrier integrity, and gas production; methanogen overgrowth is associated with constipation-predominant presentations, while hydrogen- and hydrogen sulfide-related pathways may contribute to diarrhea and bloating. Because recurrent or empiric antibiotic use is common-particularly in suspected SIBO-yet carries risks of resistance, microbiome disruption, and relapse, there is a strong rationale to prioritize effective non-antibiotic strategies. Accordingly, this review synthesizes current evidence on IBS/SIBO pathophysiology and microbiota interactions. It evaluates non-pharmacological interventions including dietary approaches, probiotics/prebiotics, herbal therapies, and mind-body treatments (e.g., cognitive behavioral therapy and gut-directed hypnotherapy). We emphasize an integrative framework that supports symptom control and quality of life while helping reduce unnecessary antibiotic exposure.},
}

@article {pmid41892439,
year = {2026},
author = {Gomes-Gonçalves, S and Bento, JT and Moreira, G and Mourão, J and Cruz, R and Esteves, F and Baptista, AL and Pereira, MA and Caseiro, P and Carreira, P and Figueira, L and Mesquita, JR},
title = {Comprehensive Shotgun Metagenomic Profiling of Antibiotic Resistance Genes in Sheep and Goat Farming Environments.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {3},
pages = {},
doi = {10.3390/antibiotics15030277},
pmid = {41892439},
issn = {2079-6382},
support = {PRR-C05-i03-I-000190//RumiRes project-"Vigilância epidemiológica de resistências antimicrobianas e resíduos medicamentosos em Pequenos ruminantes da Região Centro"/ ; },
abstract = {BACKGROUND: Antimicrobial resistance (AMR) is a growing global health concern, driven in part by antibiotic use in animal production systems. Despite its relevance, the microbiome and resistome of small ruminant farm environments remain largely underexplored.

METHODS: In this study, shotgun metagenomics was applied to environmental samples from 46 sheep, goat and mixed-species farms across 14 municipalities in central Portugal.

RESULTS: Microbial profiling revealed a well-preserved microbiome with Pseudomonadota, Actinomycetota, Bacteroidota and Bacillota (syn. Proteobacteria, Actinobacteria, Bacteroidetes and Firmicutes respectively) as the most dominant phylum across different farm types. Regarding AMR, a total of 706 unique antimicrobial resistance genes (ARGs), covering 15 antibiotic classes, were detected. Tetracycline, aminoglycoside and macrolide resistance genes dominated across all samples, forming a conserved core resistome. While overall resistome profiles were broadly similar among farm types, significant differences were observed in specific ARG classes, such as pleuromutilin and fosfomycin.

CONCLUSIONS: These findings highlight small ruminant farm environments as potential reservoirs of clinically relevant ARGs, including WHO highest priority critically important antimicrobial (HPCIA) resistance genes for macrolides (mph(c), erm(f), erm(b)) and fluoroquinolones (qnrD1), as well as critically important antimicrobial (CIA) resistance genes for glycopeptides (vanR-SC, vanR-O) and aminoglycosides (str, aadA), supporting the need to incorporate these environments into surveillance strategies.},
}

@article {pmid41892455,
year = {2026},
author = {Dashti, AA and Vali, L and Walsh, F},
title = {Metagenomic Profiling of Soil Microbiomes and Resistomes in Arid Ecosystems of Kuwait.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {3},
pages = {},
doi = {10.3390/antibiotics15030294},
pmid = {41892455},
issn = {2079-6382},
support = {(RN01/15))//Kuwait University/ ; (code EASREF).//University of Gloucestershire/ ; },
abstract = {Background/Objective: This study addresses a significant knowledge gap in the literature concerning antibiotic resistance genes (ARGs) in arid soils by employing metagenomic approaches to characterise their diversity, using Kuwait as a model environment. Methods: Soil samples were collected from two agriculturally managed sites (K1 and K3) and one coastal unmanaged site (K2), representing distinct ecological conditions. Results: Taxonomic profiling revealed notable variation in microbial communities at both the phylum and genus levels. Alpha diversity analyses based on the Chao1 and Shannon indices indicated that agricultural soils exhibited greater microbial richness and diversity than the coastal soil. Beta diversity analysis further demonstrated substantial differences in microbial community composition among the sites. Consistent with previous soil microbiome studies, ARGs such as tetA, aac(3)-Ib, sul1, qep, muxB, mexW, mexB, and macB were detected across the sites. However, the identification of distinct clinically relevant resistance genes, including ugd, blaOXA-18, blaCMY-19, blaMOX-7, blaFOX-7, blaLRA-12, and novA, suggests the influence of site-specific or extreme selective pressures. Conclusions: Several of the detected ARGs appear to be rare or previously unreported in soil environments. Although the sample size is too small to support broad generalisations, the detection of ugd in soil is particularly noteworthy, suggesting that soils may serve as reservoirs of polymyxin resistance, potentially undermining the effectiveness of polymyxin antibiotics.},
}

@article {pmid41892571,
year = {2026},
author = {Munteanu, C and Prifti, E and Achim, L and Silaghi, CN and Mârza, SM},
title = {Next-Generation Hydrogels Integrating Natural Antioxidants and Microbiome Modulators for Improved Cancer Management.},
journal = {Gels (Basel, Switzerland)},
volume = {12},
number = {3},
pages = {},
doi = {10.3390/gels12030249},
pmid = {41892571},
issn = {2310-2861},
abstract = {Cancer remains a leading cause of death worldwide, and current treatments are often limited by toxicity and resistance. Emerging research highlights the crucial roles played by gut microbiome dysbiosis and oxidative stress in cancer development and treatment response. Through their antioxidant, anti-inflammatory, and immunomodulatory properties, natural antioxidants such as resveratrol, along with microbiome modulators like probiotics, prebiotics, and synbiotics, offer promising therapeutic benefits. However, issues such as low bioavailability, instability, and challenges related to targeted delivery hinder the clinical translation of these bioactive compounds. Next-generation hydrogels have emerged as adaptable platforms capable of delivering and protecting these agents in a site-specific and controlled manner. This review summarizes the design and synthesis of multifunctional hydrogels incorporating natural antioxidants and microbiome modulators for cancer therapy.},
}

@article {pmid41892593,
year = {2026},
author = {Krasenbrink, J and Chen, SC and Tanabe, TS and Sarikeçe, H and Meurs, P and Borusak, S and Samrat, R and Guan, G and Priemer, C and Osvatic, J and Séneca, J and Hausmann, B and Speth, DR and Selberherr, E and Wanek, W and Schleheck, D and Mussmann, M and Loy, A},
title = {Sulfoquinovose degradation by cow rumen microbiota.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag069},
pmid = {41892593},
issn = {1751-7370},
abstract = {Sulfoquinovose, a sulfonated sugar derived from the thylakoid membrane lipid sulfoquinovosyl diacylglycerol, is abundant in photosynthetic organisms and plays a key role in global sulfur cycling. Its degradation in nature is mediated by specialized bacteria, many of which rely on the enzyme sulfoquinovosidase (YihQ) to release sulfoquinovose from sulfoquinovosyl (diacyl)glycerol. Despite its ecological importance, the diversity and functional roles of sulfoquinovose-degrading microorganisms remain poorly characterized in natural environments. Here, we developed a yihQ-targeted amplicon sequencing approach to investigate the richness and distribution of SQ-degrading bacteria across selected environments. We revealed high richness of yihQ-containing microorganisms in the analyzed cow rumen samples, far exceeding that observed in human and mouse gut microbiomes, suggesting an important role of sulfoquinovose metabolism in ruminant digestion. Anoxic microcosm experiments with sulfoquinovose-amended rumen fluid revealed cooperative microbial degradation of sulfoquinovose to sulfide via isethionate cross-feeding. Amplicon sequencing and genome-resolved metagenomics and metatranscriptomics identified yet undescribed and uncultured sulfoquinovose-degrading taxa. Members of Caproiciproducens (Acutalibacteraceae), Candidatus Limivicinus (Oscillospiraceae), and Sphaerochaetaceae transcribed the isethionate-producing sulfo-transketolase pathway, whereas isethionate was likely respired by a Candidatus Mailhella bacterium (Desulfovibrionaceae). This study presents a functional gene-based assay for tracking environmental yihQ richness, highlights sulfoquinovose degradation as a central metabolic process in the cow rumen, describes previously unknown sulfoquinovose-metabolizing bacteria, and advances understanding of sulfur physiology in complex microbial communities.},
}

@article {pmid41892598,
year = {2026},
author = {Shah, RK and Lin, JJ and Makkapati, T and Berkowitz, AA and Greenwald, BD},
title = {The Effect of Traumatic Brain Injury on the Gastrointestinal System: A Comprehensive Review.},
journal = {Brain sciences},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/brainsci16030254},
pmid = {41892598},
issn = {2076-3425},
abstract = {BACKGROUND/OBJECTIVES: Traumatic brain injury (TBI) is a significant public health concern resulting in physical, cognitive, and behavioral impairments. Emerging evidence highlights a bidirectional relationship between brain injury and gut health, known as the brain-gut axis. This paper provides a comprehensive review of current literature exploring the relationship between TBI and various gastrointestinal (GI) pathologies, examining how brain injuries contribute to GI dysfunction and how gut health influences neurorecovery.

METHODS: A comprehensive search of peer-reviewed articles was conducted between March and June 2025 using databases including PubMed, Scopus, and Cochrane. Studies from 2010 onwards involving human subjects were screened. Search terms included combinations of "traumatic brain injury," "TBI," and "[gastrointestinal pathology]." Data regarding study design, population, GI outcomes, and proposed mechanisms were analyzed.

RESULTS: TBI triggers secondary injury cascades, including neuroinflammation, dysautonomia, and gut microbiome dysbiosis. The review identifies a wide spectrum of TBI-associated GI disorders, including dysphagia, esophageal disorders, gastric disorders, and intestinal disorders. Bowel dysfunction, manifesting as constipation or incontinence, is prevalent due to neurogenic factors and cognitive impairments. Additionally, metabolic dysregulation following TBI leads to malnutrition, hyperglycemia, and hypoglycemia, all of which impact morbidity.

CONCLUSIONS: The GI system is integrally connected to TBI recovery through immune modulation and nutrient absorption. Dysfunction within the brain-gut axis, specifically altered motility, permeability, and inflammation, contributes to secondary brain injury and impedes neurological outcomes. Clinical assessment of GI dysfunction should be integrated into routine TBI care. Therapeutic strategies, including early enteral nutrition, are essential to optimize recovery and reduce systemic inflammation.},
}

@article {pmid41892682,
year = {2026},
author = {Murgina, O and Stafeeva, K and Karaulova, S and Vostrikova, A and Kononova, S and Chursina, D and Pozdeeva, S and Makogonova, A and Burakova, I and Pogorelova, S and Morozova, P and Smirnova, Y and Syromyatnikov, M and Shutikov, V and Mikhailov, E and Gureev, A},
title = {Probiotic Bacillus subtilis, but Not a Lactobacillus spp., Ameliorates Cognitive Impairment in a Mouse Model of LPS and Zidovudine-Induced Neuroinflammation.},
journal = {Brain sciences},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/brainsci16030340},
pmid = {41892682},
issn = {2076-3425},
support = {FZGW-2024-0003//Mikhail Syromyatnikov/ ; },
abstract = {Background/Objectives: The gut-brain axis is increasingly recognized as a critical modulator of cognitive function. This study investigated the neurotoxic effects of combined exposure to bacterial lipopolysaccharide (LPS) and the antiretroviral drug zidovudine (ZDV) in a mouse model, and evaluated the protective potential of two probiotic interventions: Bacillus subtilis and a mixture of lactobacilli. Methods: Cognitive function was assessed using the Morris water maze (MWM). Gut microbiota composition was analyzed by 16S rRNA sequencing, and intestinal morphology was examined histologically. Gene expression of neuroinflammatory markers and mitophagy-related genes in brain tissue was quantified by RT-PCR. Plasma levels of cell-free mitochondrial DNA (cf-mtDNA) were measured as a marker of mitochondrial damage. Results: Combined LPS + ZDV exposure induced systemic inflammation, impaired spatial memory, damaged the intestinal mucosa, and caused dysbiosis characterized by an increase in pro-inflammatory Muribaculaceae. In the brain, LPS + ZDV significantly upregulated Tnfa expression, confirming neuroinflammation. Bacillus subtilis administration prevented cognitive deficits, maintained Tnfa at control levels, and significantly reduced Il1b and Il6 expression compared to the LPS + ZDV group. This was accompanied by activation of the PINK1/PTEN-dependent mitophagy pathway, prevention of cf-mtDNA release, and restoration of gut microbial diversity. In contrast, the Lactobacilli mixture not only failed to improve outcomes but was associated with exacerbated intestinal damage, more pronounced cognitive dysfunction, and no reduction in neuroinflammatory markers. Conclusions: Combined exposure to LPS and ZDV induces gut-brain axis dysfunction characterized by neuroinflammation, cognitive impairment, intestinal damage, and dysbiosis. Bacillus subtilis effectively preserves cognitive function through activation of PINK1/PTEN-dependent mitophagy and suppression of neuroinflammation, highlighting its potential as a therapeutic candidate for cognitive impairments associated with gut-brain axis dysfunction. The contrasting effects of the lactobacilli mixture underscore the critical importance of strain-specificity in probiotic interventions.},
}

@article {pmid41892691,
year = {2026},
author = {Li, L and Smardz, M and Soh, D and Marsh, PD and Hoare, A and Diaz, PI},
title = {Nutritional Pressure from Serum Amplifies Dysbiotic Features in an Oral Microbiome Synthetic Community.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag070},
pmid = {41892691},
issn = {1751-7370},
abstract = {Despite rapid advances in characterizing the human microbiome, the ecological pressures shaping its transitions from healthy to diseased states remain poorly resolved. This is particularly true for periodontitis, a slow-progressing chronic inflammatory disease associated with well-defined shifts in the subgingival microbiome. Here, we report the development of a complex synthetic community model of the subgingival microbiome, designed for systematic interrogation of ecological factors that drive community restructuring. The model includes 22 prevalent and abundant subgingival species maintained in mucin-rich medium under microaerophilic, continuous culture conditions, in a chemostat. Using this system, we interrogated the impact of serum, as a surrogate for the inflammatory exudate produced by the host in response to biofilm accumulation, on community structure and function. Through integrated 16S rRNA gene sequencing, metatranscriptomics, and metabolomics, we found that serum was not required for a community with a periodontitis-like configuration to establish, but its presence intensified features of dysbiosis. Serum increased total biomass, promoted polymicrobial aggregate formation, promoted nitrogen and protein metabolism thereby modifying the environmental pH towards alkalinity, and introduced nitrosative stress. Serum also modified the community metatranscriptome in ways that paralleled microbiome activities in human periodontitis. Serum, however, decreased community diversity by disproportionally conferring a competitive advantage to the pathogen Porphyromonas gingivalis. This synthetic community model has revealed serum as a key nutritional pressure that modulates subgingival microbiome ecology and may perpetuate dysbiosis.},
}

@article {pmid41892780,
year = {2026},
author = {Safi, S and Berro, D and Amram, J and Burden, D and Palazzolo, D and Cuadra, GA},
title = {Influence of E-Liquids and Oral Commensal Bacteria on the Growth of Porphyromonas gingivalis Planktonically and in Biofilms.},
journal = {Dentistry journal},
volume = {14},
number = {3},
pages = {},
doi = {10.3390/dj14030172},
pmid = {41892780},
issn = {2304-6767},
abstract = {Background: The increasing use of electronic cigarettes (ECIGs), especially among youth, has raised concerns about the impact of vaping on oral health. While ECIGs are often marketed as a safer alternative, the existing literature suggests that their use may have detrimental effects on the pulmonary and cardiovascular systems. The oral cavity is the first point of contact for ECIG aerosol, and new reports link vaping to the onset of periodontal disease. It is critical to understand the potential effects of vaping on the oral microbiome, which affects systemic health. This study investigates how flavored E-liquids and commensal bacteria influence the growth of Porphyromonas gingivalis, a periodontal pathobiont, under planktonic and biofilm conditions. Methods: P. gingivalis was grown planktonically in the presence of the supernatants of four streptococcal species (Streptococcus gordonii, Streptococcus intermedius, Streptococcus mitis, and Streptococcus oralis) and flavored E-liquids (tobacco, menthol, cinnamon, strawberry, and blueberry) under anaerobic conditions. Multispecies biofilms, including all the species mentioned above and Fusobacterium nucleatum, were also grown anaerobically and quantified by crystal violet assays, qPCR, and CFU counts. Results: Although E-liquids inhibit P. gingivalis growth under planktonic conditions, the presence of commensal supernatants partially mitigates this effect. However, P. gingivalis growth in multispecies biofilms is increased by E-liquid treatments. Conclusions: This study highlights the enhanced growth of P. gingivalis as part of an oral microbial community in the presence of E-liquids. These results suggest that E-liquid-induced alterations in multispecies biofilms may contribute to the observed dysbiosis in vapers and the associated risk of oral diseases.},
}

@article {pmid41892792,
year = {2026},
author = {Skutnik-Radziszewska, A and Lis, VE and Skutnik, A and Szulimowska, J and Zalewska, A},
title = {Changes in Salivary Biomarkers and Oral Immune Parameters in Patients with Psoriasis: A Systematic Review.},
journal = {Dentistry journal},
volume = {14},
number = {3},
pages = {},
doi = {10.3390/dj14030184},
pmid = {41892792},
issn = {2304-6767},
abstract = {Background: Psoriasis is a chronic immune-mediated inflammatory disease characterized by systemic inflammation and complex immune dysregulation that extends beyond the skin and may affect the oral environment. Increasing evidence suggests that saliva may serve as a non-invasive diagnostic medium reflecting both local and systemic pathological processes. This systematic review aimed to critically evaluate current evidence on salivary biomarkers in psoriasis, focusing on inflammatory mediators, oxidative stress parameters, immune-related factors, and oral microbiota alterations, and to assess their potential clinical and diagnostic relevance. Methods: A systematic literature search was performed according to PRISMA guidelines using PubMed, Scopus, and Web of Science databases, covering studies published between 1994 and October 2024. Original human studies evaluating salivary biomarkers in patients with psoriasis were included based on predefined PECOS criteria. Studies involving confounding inflammatory oral diseases without separate analysis were excluded. Eleven eligible studies were included in a qualitative synthesis. Results: The analyzed studies consistently demonstrated multidimensional alterations in salivary composition in psoriasis patients compared with healthy controls. Increased levels of pro-inflammatory cytokines (TNF-α, IFN-γ, IL-2) and reduced anti-inflammatory IL-10 indicated persistent immune activation. Elevated oxidative stress markers, including total oxidant status and oxidative stress index, supported the role of redox imbalance in disease pathogenesis. Alterations in innate immune components, such as salivary α-amylase, immunoglobulin A, and lysozyme, suggested impaired oral immune regulation. Moreover, emerging microbiome data revealed shifts toward pro-inflammatory bacterial taxa, including Prevotella and Porphyromonas. Some studies indicated that biologic therapy may modulate salivary biomarker profiles. Conclusions: Salivary biomarkers reflect systemic inflammatory and immunological alterations associated with psoriasis and represent promising non-invasive tools for disease monitoring and clinical assessment. Nevertheless, substantial methodological heterogeneity and limited sample sizes highlight the need for large-scale, standardized, and longitudinal studies to validate their diagnostic applicability.},
}

@article {pmid41892839,
year = {2026},
author = {Lista, AR and Ayala Mosqueda, CV and Palacios, R and García Mansilla, MJ and Rodríguez Sojo, MJ and Ho Plágaro, A and Garcia Garcia, J and Gálvez, J and Rodríguez Nogales, A and Ruiz Malagón, AJ and Rodríguez Sánchez, MJ},
title = {Modulation of Microbiome-Mitochondria Axis as a Novel Approach for Treatment of Obesity: A Scoping Review.},
journal = {Medical sciences (Basel, Switzerland)},
volume = {14},
number = {1},
pages = {},
doi = {10.3390/medsci14010124},
pmid = {41892839},
issn = {2076-3271},
support = {PI18/00826, PY20-01157, PI20/01447, B-CTS-664-UGR20, PI19/01058, PI24/02089 and JDC2022-049478-I, CD23/00117, IFI21/00030//Instituto de Salud Carlos III/ ; },
mesh = {Humans ; *Obesity/therapy/microbiology/metabolism ; *Gastrointestinal Microbiome/physiology ; *Mitochondria/metabolism ; Animals ; Probiotics/therapeutic use ; Energy Metabolism ; Fecal Microbiota Transplantation ; Prebiotics ; },
abstract = {Background: Obesity is a multifactorial, chronic disease characterised by excessive fat accumulation, low-grade inflammation, and metabolic dysfunction. Emerging evidence suggests that the gut microbiome-mitochondria axis may play a significant role in the pathophysiology of obesity, particularly in regulating energy metabolism, inflammatory responses, and mitochondrial function. However, most mechanistic insights into this axis derive from preclinical animal studies, while human evidence remains limited and largely associative. Mitochondrial dysfunction disrupts cellular energy balance, increases reactive oxygen species production, and may exacerbate gut dysbiosis, further contributing to metabolic disturbances. In addition, factors such as micronutrient deficiencies also play a relevant role in obesity development and progression. Objectives: This review aims to examine the bidirectional interactions between the gut microbiome and mitochondrial systems in obesity, with a focus on the underlying molecular mechanisms and their potential as therapeutic targets. Methods: Evidence from experimental models and clinical studies was analysed to evaluate how modulation of the microbiome-mitochondria axis through probiotics, prebiotics, dietary strategies, and faecal microbiota transplantation influences mitochondrial function, inflammation, and metabolic regulation. Results: Preclinical studies indicate that the gut microbiome modulates mitochondrial activity through the production of bioactive metabolites, including short-chain fatty acids, secondary bile acids, and tryptophan-derived compounds, which influence mitochondrial efficiency, lipid metabolism, and glucose regulation. Dysbiosis reduces these beneficial metabolites, impairing mitochondrial signalling and promoting adiposity and insulin resistance. Interventions targeting this axis have shown potential in restoring metabolic balance, improving mitochondrial function, and mitigating obesity-related complications such as hyperlipidaemia and glucose intolerance. Conclusions: Targeting the microbiome-mitochondria axis represents a promising therapeutic strategy for obesity, with the evidence based largely on preclinical findings. However, further well-designed human studies are required to clarify causality, optimise interventions, assess long-term safety and efficacy, and establish standardised clinical protocols for implementation.},
}

Humans
*Obesity/therapy/microbiology/metabolism
*Gastrointestinal Microbiome/physiology
*Mitochondria/metabolism
Animals
Probiotics/therapeutic use
Energy Metabolism
Fecal Microbiota Transplantation
Prebiotics

@article {pmid41893096,
year = {2026},
author = {Fan, J and Liu, S and Zhang, H and Jin, C and Wu, N},
title = {Dysbiosis of the Gut-Lung Axis and Its Immune Correlates During Pulmonary Cryptococcus neoformans Infection.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {12},
number = {3},
pages = {},
doi = {10.3390/jof12030163},
pmid = {41893096},
issn = {2309-608X},
support = {Grant No. 2023YFC2506004//National Key Research and Development Program of China/ ; },
abstract = {Cryptococcus neoformans is a major fungal pathogen responsible for life-threatening meningitis, especially in immunocompromised individuals. Although the gut-lung axis is known to regulate immune responses in respiratory infections, its role in cryptococcosis remains unclear. This study aimed to define the dynamic changes in the gut and lung microbiota and their relationship with host immunity during C. neoformans infection. Using a mouse model, we found that pulmonary infection induced significant dysbiosis in both the lung and gut microbiota, marked by decreased beneficial commensals and increased opportunistic pathogens. Integrated analysis showed these microbial shifts were closely associated with distinct immune responses: lung dysbiosis correlated with a strong IL-17-mediated pulmonary inflammatory response, while gut dysbiosis was linked to systemic immune activation in the spleen. Functional metagenomic prediction further revealed widespread disruption in microbial metabolic pathways, including energy metabolism and biosynthesis, in both sites. Importantly, a positive correlation was observed between lung and gut dysbiosis, indicating an interconnected gut-lung axis during cryptococcosis. These findings demonstrate that C. neoformans infection causes coordinated disruptions in microbiota and immunity across the gut-lung axis, underscoring the microbiome as a critical modulator of host response and suggesting potential avenues for microbiome-targeted therapies.},
}

@article {pmid41893120,
year = {2026},
author = {Wu, XH and Gu, QY and Ma, CY and Zhang, W and Dai, CC},
title = {Research Progress in Plant Beneficial Fungi-Mediated Alleviation of Drought Stress in Crops.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {12},
number = {3},
pages = {},
doi = {10.3390/jof12030188},
pmid = {41893120},
issn = {2309-608X},
abstract = {Climate change has emerged as a major global concern and has substantially intensified the occurrence of abiotic stresses in plants. Among the abiotic constraints limiting crop production, drought stress is regarded as one of the most severe and pervasive challenges. To this end, developing efficient and sustainable strategies to mitigate drought has become an urgent priority in agricultural research. Current approaches to improving drought tolerance mainly include optimizing irrigation management, applying chemical regulators, and breeding drought-resistant cultivars. However, these strategies often suffer from high input costs, limited durability of effects, potential environmental risks, or restricted regional applicability, making it difficult to achieve long-term and stable drought mitigation. In recent years, a growing body of evidence has indicated that rhizosphere microorganisms play pivotal regulatory roles in plant drought adaptation, with beneficial fungi being particularly important. Nonetheless, the key processes and mechanisms by which microbiomes mediate crop adaptation to drought need to be elucidated systematically. In this review, we synthesize recent advances in the field and, against the backdrop of increasingly severe global drought, summarize the major impacts of drought stress on crop growth and physiological processes. We further systematically synthesize the key mechanisms by which beneficial fungi alleviate drought stress in crops. Finally, we outline future research directions to deepen our understanding of rhizosphere-crop-microbe interaction networks and to provide a theoretical basis for developing beneficial fungus-centered microbial biofertilizers and microbiome-mediated strategies to enhance crop drought resilience.},
}

@article {pmid41893137,
year = {2026},
author = {Francis, DV and Kishorkumar, M and Ahmed, ZFR and Neumann, EG and Kurup, SS},
title = {Molecular Advances and Sustainable Strategies in Mushroom Production for Food Security: A Review.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {12},
number = {3},
pages = {},
doi = {10.3390/jof12030205},
pmid = {41893137},
issn = {2309-608X},
support = {21R097//ARIFSID/ ; },
abstract = {Mushrooms offer a promising solution for sustainable food production due to their nutritional value, low resource requirements, and ability to grow in diverse environments. As interest in mushrooms grows, it is important to understand where current research is focused and where key gaps remain. A bibliometric analysis of 776 research articles indexed in Web of Science revealed a strong emphasis on yield, substrate reuse, and enzymatic degradation, but limited attention to molecular approaches, climate adaptation, and studies from arid regions such as the Middle East. Building on these findings, this review explores the ecological diversity of mushrooms and their adaptations across tropical, temperate, boreal, and arid ecosystems. It discusses the role of mycorrhizal and microbial interactions in nutrient cycling and environmental resilience, including desert truffle symbioses. Key pathways and genetic regulation involved in lignin degradation are outlined, along with recent advancements in transcriptomics, proteomics, genomics, metabolomics, and metagenomics that support improved cultivation and bioactive compound production. The review also addresses sustainable practices, such as microbiome integration and resource recycling, to enhance mushroom farming. The aim is to bring together ecological insights and molecular strategies to support sustainable mushroom production, particularly in regions facing resource and climate challenges.},
}

@article {pmid41893303,
year = {2026},
author = {Wang, Y and Guo, X and Lu, J and Li, L and Tang, Y and Xiao, H and Li, S and Liu, W},
title = {Enhancement of Disease Resistance in Pengze Crucian Carp (Carassius auratus var. Pengze) by Carvacrol Through Modulation of Intestinal Microbiota and Serum Metabolism.},
journal = {Metabolites},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/metabo16030151},
pmid = {41893303},
issn = {2218-1989},
support = {JXSNKYJCRC202305//Jiangxi Academy of Agricultural Sciences/ ; 3246210059//National Natural Science Foundation of China/ ; CARS-45-42//China Agriculture Research System/ ; },
abstract = {Objectives: This study aimed to investigate the regulatory effects of dietary carvacrol on intestinal micro biota composition, serum metabolic profiles, and their association with increased resistance to Aeromonas hydrophila in Pengze crucian carp. Methods: Juvenile fish (5.63 ± 0.35 g) were randomly allocated into two experimental groups: a control group (CK) fed a basal diet and a treatment group (CA) supplemented with 600 mg/kg microencapsulated carvacrol. Following an 8-week feeding trial, nine specimens per group were sampled for venous blood and intestinal tract collection. Remaining individuals were subjected to a 12-h A. hydrophila challenge prior to identical sample collection. Results: Key findings revealed that carvacrol supplementation induced significant microbial modulations, notably reducing Firmicutes abundance while enhancing Cetobacterium populations by 33.25% compared to controls. Post-challenge analysis demonstrated marked declines in intestinal microbial diversity indices (Observed ASV, Chao1, ACE, and PD whole tree) in the CK group, whereas the CA group maintained stable microbial diversity. Pathogenic genera including Aeromonas, Shewanella, and Vibrio showed significant proliferation in challenged controls, contrasting with maintained microbial homeostasis in carvacrol-fed specimens. Serum metabolomic profiling identified the most significantly altered metabolic pathways associated with carvacrol administration: glycerophospholipid metabolism, linoleic acid metabolism, arachidonic acid metabolism, α-linolenic acid metabolism, GPI-anchor biosynthesis, and autophagy-animal pathways. Conclusions: Our results demonstrate that dietary carvacrol may reinforce intestinal microbial barrier function by optimizing beneficial microbial composition and reducing the proportion of pathogens, and modulate immune-related metabolic pathways critical for host defense, which might be involved in enhanced disease resistance.},
}

@article {pmid41893315,
year = {2026},
author = {Chen, Z and Jiang, S},
title = {Chemical Signaling and Metabolomic Crosstalk in Endophytic Fungi-Medicinal Plant Symbioses for Natural Product Discovery and Sustainable Bioproduction.},
journal = {Metabolites},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/metabo16030164},
pmid = {41893315},
issn = {2218-1989},
support = {K2025-001//Guiyang Kangyang University/ ; },
abstract = {Background: Medicinal plants function as complex holobionts, with their therapeutic potential significantly shaped by the associated microbiome, particularly endophytic fungi. These symbionts engage in a sophisticated "chemical signaling" with their hosts, acting as biotic elicitors that modulate plant secondary metabolism while simultaneously responding to host cues to activate their own cryptic biosynthetic gene clusters (BGCs). This review aims to critically summarize the multi-layered mechanisms driving this metabolic crosstalk and evaluate strategies to harness this symbiotic intelligence for natural product discovery. Methods: A systematic literature survey spanning the last decade was conducted across major databases. The search specifically targeted studies investigating endophytic fungi in medicinal plants, focusing on experimental designs for BGC activation, applications of spatial metabolomics (matrix-assisted laser desorption/ionization mass spectrometry imaging, MALDI-MSI), and the structural elucidation of novel bioactive natural products through co-culture or in planta models. Results: Our analysis reveals that host-derived chemical cues, such as specific root exudates and oxylipins, act as primary triggers to awaken silent fungal BGCs. We collated numerous recently discovered bioactive metabolites-including novel polyketides, highly rearranged terpenoids, and unique alkaloids-demonstrating their potent antimicrobial and cytotoxic properties. Furthermore, a critical evaluation of spatial metabolomics studies demonstrates that metabolic exchange is highly localized at the plant-fungus interface, providing contextual insights that traditional bulk tissue extraction fails to capture. Conclusions: This review bridges the gap between ecological understanding and synthetic biology applications. We conclude that translating the mechanisms of this "chemical signaling" into biotechnological strategies offers a sustainable pathway for the bioproduction of high-value pharmaceuticals, thereby reducing reliance on the wild harvesting of medicinal plants.},
}

@article {pmid41893325,
year = {2026},
author = {Han, G and Yuan, S and Yu, W},
title = {Obesity and Cancer: From Systemic Metabolic Reprogramming to Immunotherapy Paradox.},
journal = {Metabolites},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/metabo16030174},
pmid = {41893325},
issn = {2218-1989},
support = {2023YZ02//Yangtze University/ ; },
abstract = {With the global rise in overweight and obesity, excess adiposity has emerged as a modifiable carcinogenic exposure. Beyond energy surplus, obesity establishes a durable pro-tumorigenic baseline through endocrine-metabolic rewiring, chronic low-grade inflammation, and structural/mechanical remodeling of tissues, thereby shaping organ-specific microenvironments that favor malignant transformation and progression. This review integrates systemic metabolic and endocrine alterations with tumor microenvironmental physical barriers, immune reprogramming, and neuroimmune regulation to explain heterogeneity in cancer risk, progression, and treatment response. We propose a stratified assessment framework based on measurable indicators-body composition, inflammatory status, and treatment exposure-to support risk prediction, mechanistic validation, and the design of actionable experimental and clinical strategies.},
}

@article {pmid41893329,
year = {2026},
author = {Casadevall, C and Enríquez-Rodríguez, CJ and Eliassaf, A and Castro-Acosta, A and Faner, R and López-Campos, JL and Monsó, E and Pascual-Guàrdia, S and Camps-Ubach, R and Cosío, BG and Agustí, A and Shalev, O and Gea, J and On Behalf Of The Biomepoc Group, },
title = {Sex-Specific Plasma Metabolomic Signatures in COPD Reveal Creatine, Purine/Urate, and Bile-Acid Axes.},
journal = {Metabolites},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/metabo16030178},
pmid = {41893329},
issn = {2218-1989},
support = {PI21/00785//Instituto de Salud Carlos III (ISCIII) and the European Union/ ; PI25/01093//Instituto de Salud Carlos III (ISCIII) and the European Union/ ; M-BAE BA22/00009)//Instituto de Salud Carlos III (ISCIII) and the European Union/ ; PFIS, ref. FI22/00003//Instituto de Salud Carlos III (ISCIII) and the European Union/ ; Research Grant 2020//SEPAR/ ; Research Grant 2024//FUCAP/ ; },
abstract = {Metabolomic studies in COPD reveal systemic metabolic perturbations, yet sex is often treated as a covariate rather than a biological driver. We aimed to identify plasma metabolites differentiating COPD from controls and to define sex-specific metabolic signatures in both groups. Methods: In this controlled observational study (BIOMEPOC cohort), untargeted plasma metabolomics was performed by LC-MS/MS. Differential abundance was tested across four contrasts (COPD vs. controls; men vs. women within controls; men vs. women within COPD; sex-by-disease interaction) with a false discovery rate (FDR) correction. Because smoking history differed between COPD and controls, a post hoc ever-smokers analysis was conducted. Results: COPD differed from controls in nine metabolites (all decreased): DL-stachydrine, 3-methyl-L-histidine, fructose, pipecolinic and nipecotic acids, 5-nitro-o-toluidine, conjugated linoleic acid, aminoadipate, and creatinine. This pattern is compatible with metabolic depletion, remodeling, and/or altered flux across multiple compartments rather than simple substrate deficiency, spanning muscle-related pools, amino acid handling, carbohydrate-associated metabolism, and exposome-linked inputs. In ever-smokers, results were directionally consistent, with five metabolites remaining nominally significant. Among controls, five metabolites were higher in men after FDR correction (PABA, cis-4-hydroxy-D-proline, N-acetylasparagine, deoxycarnitine, and creatinine), consistent with physiological sex dimorphism in energy pathways, connective-tissue remodeling, and diet/microbiome-related metabolism. Within COPD, six metabolites differed by sex after FDR correction, defining three axes: creatine energy buffering (men: higher GAA/creatinine, lower creatine), purine/urate handling (men: higher urate), and conjugated bile acids (men: higher GCDCA), implicating muscle bioenergetics, redox/inflammatory tone, and gut-liver crosstalk. Conclusions: Plasma metabolomics identifies a pattern compatible with systemic remodeling in COPD and sex-associated divergences in creatine, purine/urate, and bile-acid pathways, supporting a sex-influenced view of systemic COPD heterogeneity and highlighting targets for mechanistic validation.},
}

@article {pmid41893350,
year = {2026},
author = {Muroya, S and Ojima, K and Banno, A and Nagai, H and Kakibuchi, K and Higuchi, T and Sakamoto, S and Matsukawa, K},
title = {Dietary Citrus Peel Supplementation Enhances Hepatic Energy Metabolism, Muscle 9-HODE Generation and Isoleucine Catabolism in Beef Cattle.},
journal = {Metabolites},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/metabo16030201},
pmid = {41893350},
issn = {2218-1989},
support = {2021-21//Japan Racing Association/ ; 25K02159//Japan Society for the Promotion of Science/ ; },
abstract = {BACKGROUND: Citrus components potentially suppress adipogenic differentiation and lipid accumulation, and exhibit anti-inflammatory and antioxidant effects. We hypothesized that the bioactive compounds in Citrus junos Sieb ex Tanaka (yuzu) fruit peel can alter the systemic metabolism and productivity of beef cattle.

METHODS: Japanese Brown (JBR) steers were fed with a diet supplemented with 2.5% yuzu peel during the last month of the finishing period. To investigate the effect of dietary yuzu supplementation (DYS) on beef and liver metabolism, we explored the metabolomic profiles of longissimus thoracis (LT, loin) muscle at 14 d postmortem using capillary electrophoresis (CE-TOF/MS) and high-performance liquid chromatography time-of-flight mass spectrometry (LC-TOF/MS).

RESULTS: The DYS treatment enhanced the beef fat score compared to that recorded in beef in the no-DYS (None) group (p = 0.050); however, the other carcass quality traits were not significantly different between the DYS and None groups. CE-TOF/MS and LC-TOF/MS revealed 242 and 107 annotated peaks, respectively, for the LT muscle. DYS significantly increased 9(S)-hydroxyoctadecadienoic acid (9-HODE, a beef flavor precursor), cyclo(-Leu-Pro), spermidine, asymmetric dimethylarginine, and 7α-hydroxycholesterol levels and reduced 2-ethylhydracrylic acid (2-EHAA), γ-tocopherol, coenzyme Q10 (CoQ10), sphingomyelin(d18:1/16:0), Cys-Gly, Tyr-Arg, and palmitoylcarnitine levels in postmortem LT muscle (p < 0.050). Concomitantly, in the fresh liver, DYS increased acetyl-CoA, 6-phosphogluconic acid, S-methylglutathione, ATP, ribulose 5-phosphate, and ADP levels and suppressed the content of thiamine, Ala-Ala, riboflavin, and ascorbate 2-sulfate (p < 0.050).

CONCLUSION: Collectively, yuzu ingredients activated ATP production in the liver through the elevation of hepatic energy metabolism primarily in the citrate cycle and β-oxidation, and potentially altered muscle metabolism, including linoleic acid oxidation, FAD-mediated electron transport chain, and isoleucine catabolism, as demonstrated in the reduced accumulation of 2-EHAA and CoQ10 in DYS beef. Moreover, DYS likely affects the gut microbiome by enhancing the production of cyclo(-Leu-Pro), an antimicrobial dipeptide.},
}

@article {pmid41893361,
year = {2026},
author = {Zhang, Q and Jin, Z},
title = {Gut Microbiota-Bile Acid Axis in Type 2 Diabetes-Associated Gallbladder Diseases: Mechanisms and Therapeutic Potential.},
journal = {Metabolites},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/metabo16030212},
pmid = {41893361},
issn = {2218-1989},
support = {No. SH2025042//Zhenjiang Key R&D Program-Social Development Track/ ; },
abstract = {Gallbladder diseases spanning cholelithiasis, cholecystitis, and gallbladder cancer represent a clinically heterogeneous continuum in which type 2 diabetes mellitus (T2DM) acts as a key metabolic modifier. Conventional models centered on bile supersaturation alone do not sufficiently account for the persistent inflammation and inter-individual variability frequently observed in practice. Here, we synthesize emerging evidence implicating the gut microbiota-bile acid (BA) axis as an integrative mechanism linking metabolic dysregulation, barrier dysfunction, and biliary pathobiology in the diabetic host. Hyperglycemia and insulin resistance, together with impaired mucosal resilience, are associated with shifts in microbial community structure and BA-transforming functions (e.g., bile salt hydrolase and 7α-dehydroxylation), favoring a more hydrophobic BA pool. These changes may disrupt BA receptor signaling, including FXR-FGF15/19 and TGR5-related pathways, thereby amplifying metabolic inflammation, promoting lithogenic bile formation, and impairing gallbladder motility. In parallel, barrier vulnerability may facilitate microbial translocation and LPS-driven immune activation, reinforcing a feed-forward loop that supports the gallstone-inflammation-carcinogenesis trajectory. Translationally, microbiome- and BA-oriented strategies (dietary patterns, bile acid therapeutics, and targeted microbiome modulation) are promising adjuncts, yet precision management should explicitly consider medication- and weight loss-related confounding-particularly with incretin-based therapies-to optimize biliary outcomes across disease stages.},
}

@article {pmid41893403,
year = {2026},
author = {Westerström, P and Bivand, JM and Kommedal, Ø and Ehrnström, B and Andreassen, JS and Afset, JE},
title = {Odontogenic Brain Abscess in a Hereditary Haemorrhagic Telangiectasia (HHT) Patient: Case Report with a Comprehensive Literature Review.},
journal = {Tropical medicine and infectious disease},
volume = {11},
number = {3},
pages = {},
pmid = {41893403},
issn = {2414-6366},
abstract = {BACKGROUND: Recent diagnostic methods have enabled the detection of often culture-negative pathogens, including anaerobic bacteria from the oral cavity. Characterising the microbial diversity and co-occurrence of bacteria in such infections is important for understanding the molecular pathophysiology in odontogenic brain abscesses.

CASE PRESENTATION: We describe a case of polymicrobial odontogenic brain abscess in a 59-year-old man of Vietnamese ethnicity with a documented increased risk of brain abscess due to Hereditary Haemorrhagic Telangiectasia (HHT). The microbiological diagnostic work-up included conventional culture, matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS), targeted 16S rDNA analysis using three broad-range group-specific PCR (polymerase chain reaction) assays and next-generation sequencing (NGS). A literature review was conducted, including database searches for each identified microorganism. Twelve anaerobic bacterial species were detected, among which Treponema medium, Capnocytophaga HMT-323 and Candidatus Saccharibacteria oral taxon 488 have not previously been reported in brain abscesses. In addition, we identified the extremely rare pathogens Arachnia propionica and Capnocytophaga ochracea.

CONCLUSION: This is the first report of Ca. Saccharibacteria oral taxon 488 in a clinical sample and the first detection of any species from this phylum in a brain abscess, co-detected with A. propionica, consistent with its obligate epibiotic lifestyle. Our findings broaden the known microbial diversity associated with odontogenic brain abscesses and underscore the value of 16S rDNA NGS in characterising polymicrobial infections, particularly when fastidious or uncultivable organisms are involved.},
}

@article {pmid41893554,
year = {2026},
author = {Lin, Q and Wu, X and Li, L and Peng, T and Zou, X and Li, G and Wang, J and Tang, X and Yue, X and Guo, C and Li, P},
title = {Impact of Aspergillus flavus Infection on the Rhizosphere Bacterial Microbiota of Peanut (Arachis hypogaea L.).},
journal = {Toxins},
volume = {18},
number = {3},
pages = {},
pmid = {41893554},
issn = {2072-6651},
support = {2024JH2/102600162; 2025JH2/101800102;2023JH1/10200002//Liaoning Provincial Department of Science and Technology/ ; 2023BS0803;2025JCX1002;2025QN2614;2025XKJS8531//Liaoning Academy of Agricultural Sciences/ ; 2023BBA002//Hubei Province Major Science and Technology Special Project/ ; SWDSJC2023002//Key Laboratory of Oilseeds Processing，Ministry of Agriculture and Rural Affairs, China/ ; 20254032//Agricultural Product Quality and Safety Risk Assessment Project of the Ministry of Agriculture and Rural Affairs/ ; },
mesh = {*Arachis/microbiology/growth & development ; *Aspergillus flavus ; *Rhizosphere ; *Microbiota ; *Bacteria/genetics/classification/growth & development ; Soil Microbiology ; Plant Roots/microbiology/growth & development ; *Plant Diseases/microbiology ; Phylogeny ; },
abstract = {This study investigated the effects of inoculating peanuts with two Aspergillus flavus strains (Aspergillus flavus CGMCC 3.4408 and A. flavus LNZW 23) on plant growth and the rhizosphere bacterial community. Infection significantly inhibited peanut growth. By 60 days post-inoculation (dpi), plant height in inoculated groups (CGMCC 3.4408, 26.4 cm; LNZW 23, 25.5 cm) was significantly lower than in the non-inoculated control (CK, 32.3 cm), with concomitant significant reductions in shoot and root biomass. Analysis of rhizosphere microbiota revealed that early infection (7 dpi) reduced bacterial species richness and phylogenetic diversity. Beta diversity analysis (PCoA) confirmed a significant divergence in microbial community structure between inoculated and control groups over time, with a statistically significant difference also observed between the two inoculated strains (p = 0.016). In terms of community composition, Proteobacteria, Acidobacteriota, and Actinobacteria were the three dominant phyla. At the genus level, infection altered the relative abundance of key taxa; genera such as KD4-96, Vicinamibacteraceae, and RB41 decreased at 7 dpi, while Sphingomonas remained relatively stable. By 60 dpi, community dominance increased, marked by rising abundances of Actinobacteria and Proteobacteria. In conclusion, A. flavus infection not only suppresses peanut growth but also persistently alters its rhizosphere microbial community, with effects demonstrating both time-dependency and strain-specificity.},
}

*Arachis/microbiology/growth & development
*Aspergillus flavus
*Rhizosphere
*Microbiota
*Bacteria/genetics/classification/growth & development
Soil Microbiology
Plant Roots/microbiology/growth & development
*Plant Diseases/microbiology
Phylogeny

@article {pmid41893658,
year = {2026},
author = {Lisjak, A and Correa Lopes, B and Pilla, R and Nemec, A and Lampreht Tratar, U and Suchodolski, JS and Tozon, N},
title = {Assessment of Fecal Microbiota in Healthy Dogs and Dogs with Cutaneous Mast Cell Tumors Treated with Electrochemotherapy Combined with Gene Electrotransfer of IL-12.},
journal = {Veterinary sciences},
volume = {13},
number = {3},
pages = {},
pmid = {41893658},
issn = {2306-7381},
support = {P3-0428, P4-0053, P3-0003, and J4-2546//The Slovenian Research and Innovation Agency/ ; The microbiome research at the Gastrointestinal Laboratory at Texas A&M University is in part funded through Purina PetCare Research Excellence Fund//Purina PetCare Research Excellence Fund/ ; },
abstract = {Cancer is a major health concern, with its incidence rate continuing to increase. There is growing interest in the microbiota and its role in carcinogenesis, as it significantly influences physiological and pathological processes. Various aspects of the microbiome have been shown to have both anti-tumor and pro-tumor effects. Advances in techniques such as high-throughput DNA sequencing have greatly improved our understanding of microbial populations in the human and canine gut. We aimed to (1) characterize the intestinal microbiota of healthy dogs and dogs with cutaneous mast cell tumors (MCTs), (2) assess changes in the intestinal microbiota of dogs undergoing electrochemotherapy (ECT) combined with gene electrotransfer (GET) of the IL-12 plasmid (IL-12), and (3) explore possible associations with the expression of immune markers Programmed cell death protein 1 (PD-1), Programmed death-ligand 1 (PD-L1), and Granzyme B (GZMB) in MCT tissue. Stool samples were collected from healthy dogs (n = 24) and dogs with MCTs (n = 24) before and after ECT and IL-12 GET. DNA was extracted from the samples, and shallow shotgun sequencing was performed. Immunohistochemistry was performed on the tumors to assess the expression of PD-1, PD-L1, and GZMB. The dysbiosis index, alpha diversity, and beta diversity did not differ between groups. Regarding microbial composition, Bifidobacterium animalis, Corynebacterium variabile, Lactobacillus johnsonii, Pediococcus pentosaceus, Streptococcus anginosus, Streptococcus equinus, Streptococcus intermedius, Clostridium thermobutyricum, Megasphaera elsdenii, and Anaerobiospirillum sp. were found in lower relative abundance in feces of dogs with MCTs, while Bacteroides togonis, Lactobacillus amylolyticus, Prevotella sp. CAG:279, and Megamonas hypermegale were more abundant compared to healthy dogs. Our study provides further insight into the composition of the gut microbiota in dogs with MCTs, where ECT and IL-12 GET did not lead to major shifts. We were unable to establish any association between the expression of immune markers and the microbiota.},
}

@article {pmid41893724,
year = {2026},
author = {Qiu, Q and Gong, T and Du, L and Li, W and Hu, Y and Li, D and Zhou, C and Liu, W},
title = {Comparative Analysis of Microbial Community Structure and Function in the Gut of South China Tigers Under Different Dietary Treatments.},
journal = {Veterinary sciences},
volume = {13},
number = {3},
pages = {},
pmid = {41893724},
issn = {2306-7381},
support = {2110499//Diagnosis and Treatment of Genetic Diseases and Training for Stereotypic Behaviors in South China Tigers at Changsha Ecological Zoo/ ; 2110499//Artificial breeding of Reeves's pheasant (Syrmaticus reevesii) at Changsha Ecological Zoo/ ; },
abstract = {The gut microbiota is a crucial component of a tiger's health and plays a significant role in adapting to changes in food and the environment. Although extensive studies have been carried out on the gut microbiota of tigers, investigating the responses of gut microbial composition and function to preadaptation to wild predation patterns under captive conditions is particularly significant for South China tigers, given that it is the only tiger subspecies existing solely in captive settings at present. Here, we performed shotgun metagenomic sequencing for a comprehensive analysis of the gut microbiota of South China tigers assigned to two dietary groups (live prey group, LP group; frozen meat group, FM group), thereby generating abundant valuable data for this endangered subspecies. The results indicated that the core intestinal microbial composition was similar between the two dietary groups. Differential analysis revealed associations between dietary treatments and microbial abundance in the intestines of South China tigers. Functional gene analysis revealed that the LP group exhibited upregulation of genes and pathways related to antimicrobial resistance, bacterial infection-related disease, cell motility and proliferation, while the FM group displayed efficient energy metabolism. A total of 1251 antibiotic resistance genes (ARGs) were identified in the gut microbiome of South China tigers. The core resistome mainly included resistance to peptides, glycopeptides, tetracyclines, fluoroquinolones, and macrolides. In addition, the differences in ARGs between the LP group and FM group may be related to a broader range of animal tissues of live prey and the processing conditions of frozen meat. In summary, although feeding live prey did not change the core framework of the gut microbiota in South China tigers, it was associated with differences in microbial abundance, metabolic pathways, and antibiotic resistance gene profiles.},
}

@article {pmid41894063,
year = {2026},
author = {Romero, JDJR and Barko, P and Suchodolski, JS and Williams, DA and Ganz, HH and Gal, A},
title = {Serum metabolomics of diabetic dogs treated with daily administration of a commercially available lyophilized feces preparation.},
journal = {Veterinary research communications},
volume = {50},
number = {3},
pages = {},
pmid = {41894063},
issn = {1573-7446},
support = {Vera Arvilla Traxler Fund//University of Illinois at Urbana-Champaign Companion Animal Research Grant Program/ ; },
}

@article {pmid41894083,
year = {2026},
author = {Li, Y and Jiang, M and Pang, J and Ma, C and Zhang, H and Yin, F and Jia, Y and Zou, X and Zuo, T and Zhang, H},
title = {High-altitude exposure remodels the gut microbiota: health and disease.},
journal = {MedScience},
volume = {},
number = {},
pages = {},
pmid = {41894083},
issn = {3091-4981},
abstract = {With the increasing number of individuals travelling to or residing in high-altitude regions, understanding the physiological and pathological consequences of such environments has become increasingly important. High-altitude exposure poses significant challenges to human health, primarily due to hypobaric hypoxia, which triggers a cascade of responses, including energy deficiency, oxidative stress, and inflammation. One of the critical consequences is the disruption of the gut barrier, which facilitates the translocation of the gut microbiota and further exacerbates local and systemic inflammation. Notably, the gut microbiota, a dynamic environmental sensor, undergoes significant remodelling in high-altitude environments. The modified production of microbial metabolites such as bile acids influences gut homeostasis as well as glucose and lipid metabolism, and ultimately contributes to individual variability in high-altitude acclimatization. These changes have been implicated in the pathogenesis of altitude-related illnesses such as acute and chronic mountain sickness, as well as in metabolic and gastrointestinal disorders such as diabetes, obesity, irritable bowel syndrome, colorectal cancer, cholelithiasis, and osteoporosis. Preliminary explorations have demonstrated the therapeutic potential of microbiome-based interventions such as faecal microbiota transplantation in acute and chronic mountain sickness. Further research into gut microbiota modulation may provide applicable options for promoting high-altitude acclimatization and preventing high-altitude illness.},
}

@article {pmid41894116,
year = {2026},
author = {Luo, S and Dang, Y and Chen, HD and Peng, J and Li, L},
title = {Community heterogeneity scaling of gut microbiomes across Chinese ethnicities and lifestyles appears invariant.},
journal = {International microbiology : the official journal of the Spanish Society for Microbiology},
volume = {},
number = {},
pages = {},
pmid = {41894116},
issn = {1618-1905},
}

@article {pmid41894142,
year = {2026},
author = {Sun, B and Zhao, C and Chen, X and Yang, B and Cui, W and Zhang, J and Hou, X and Yan, X and Ni, Q and Cheng, P and Chen, K},
title = {Fucoxanthin: A Comprehensive Review on Digestion, Biotransformation, Microbiome Interaction, and Targeted Delivery.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c12697},
pmid = {41894142},
issn = {1520-5118},
abstract = {Fucoxanthin, a marine carotenoid with diverse bioactivities, has attracted increasing attention for its health-promoting potential. However, its gastrointestinal fate and targeted delivery remain insufficiently understood, limiting its translation into effective applications. This review summarizes current knowledge on fucoxanthin's digestion, biotransformation, tissue distribution, interactions with the gut microbiota, and different delivery systems. In vivo, fucoxanthin is hydrolyzed to fucoxanthinol in the intestine and further converted to amarouciaxanthin A in the liver, undergoing subsequent dehydrogenation, isomerization, and esterification before distribution into plasma, liver, adipose tissue, and heart. Additionally, fucoxanthin modulates gut microbial composition through a duplibiotic effect, linking its metabolism to host-microbiota interactions. Lipid-, polysaccharide-, and protein-based delivery systems have been developed due to low oral bioavailability; these are also compared and summarized. Together, this review provides a theoretical framework for the rational design of functional foods and therapeutic applications of fucoxanthin.},
}

@article {pmid41894324,
year = {2026},
author = {Thompson, J and Connors, BM and Zavala, VM and Venturelli, OS},
title = {Physics-constrained neural ordinary differential equation models to discover and predict microbial community dynamics.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {13},
pages = {e2517661123},
doi = {10.1073/pnas.2517661123},
pmid = {41894324},
issn = {1091-6490},
support = {HR00112530072//DOD | ARPA | Defense Sciences Office, DARPA (DSO)/ ; R01EB030340//HHS | National Institutes of Health (NIH)/ ; HR00112320001//DOD | ARPA | Defense Sciences Office, DARPA (DSO)/ ; CBET-2315963//National Science Foundation (NSF)/ ; },
mesh = {Machine Learning ; *Microbiota/physiology ; *Neural Networks, Computer ; *Models, Biological ; Ecosystem ; },
abstract = {Microbial communities play essential roles in shaping ecosystem functions and predictive modeling frameworks are crucial for understanding, controlling, and harnessing their properties. Competition and cross-feeding of metabolites drives microbiome dynamics and functions. Existing mechanistic models that capture metabolite-mediated interactions in microbial communities have limited flexibility due to rigid assumptions. While machine learning models provide flexibility, they require large datasets, are challenging to interpret, and can overfit to experimental noise. To overcome these limitations, we develop a physics-constrained machine learning model, which we call the neural species mediator (NSM), that combines a mechanistic model of metabolite dynamics with a machine learning component. The NSM outperforms mechanistic or machine learning components on in vitro experimental datasets and provides insights into direct biological interactions. In summary, carefully embedding a neural network into a mechanistic model of microbial community dynamics improves prediction performance and interpretability compared to its constituent mechanistic or machine learning components.},
}

Machine Learning
*Microbiota/physiology
*Neural Networks, Computer
*Models, Biological
Ecosystem

@article {pmid41894325,
year = {2026},
author = {Russ, D and Saha, C and Paul, K and Zheng, Z and Law, TF and Anguita-Maeso, M and Lundberg, DS and Fitzpatrick, CR and Dangl, JL},
title = {Specialization of independently acquired flagellar FliC proteins in plant-associated Sphingomonas balances swimming and immunogenicity.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {13},
pages = {e2535583123},
doi = {10.1073/pnas.2535583123},
pmid = {41894325},
issn = {1091-6490},
support = {ALTF 743-2019//European Molecular Biology Organization (EMBO)/ ; 2021.0102//Knut och Alice Wallenbergs Stiftelse (kawforskning)/ ; 532852-2019//Natural Sciences and Engineering Research Council of Canada (NSERC)/ ; IOS-2416244//NSF (NSF)/ ; },
mesh = {*Flagellin/genetics/immunology/metabolism ; *Sphingomonas/genetics/immunology/physiology ; *Flagella/immunology/genetics/metabolism ; *Bacterial Proteins/genetics/immunology/metabolism ; },
abstract = {Plants monitor their environment for microbial invaders using pattern-recognition receptors that detect microbe-associated molecular patterns (MAMPs). Flagellin, the main component of bacterial flagellum, contains the flg22 epitope recognized by the plant immune receptor FLS2. Immune recognition can create an evolutionary conflict, requiring bacteria to balance flagellar function and immune evasion. Here, we show that plant-associated Sphingomonas resolve this constraint by partitioning two flagellar functions, motility and colonization, across two divergent and independently acquired flagellin genes. Comparative genomics revealed widespread coexistence of FliC proteins expressing either an immunogenic variant (FliC-H) or a nonimmunogenic variant (FliC-L). The nonimmunogenic FliC-L is necessary and sufficient for full directional swimming, whereas FliC-H is dispensable for swimming, but sufficient for full attachment and colonization. Flagellin expression patterns mirror these functions. Thus, FLS2 recognizes the flagellar variant required for colonization rather than motility, potentially restricting colonizing bacteria from entering internal leaf and root tissues.},
}

*Flagellin/genetics/immunology/metabolism
*Sphingomonas/genetics/immunology/physiology
*Flagella/immunology/genetics/metabolism
*Bacterial Proteins/genetics/immunology/metabolism

@article {pmid41894949,
year = {2026},
author = {Brem, AK and Khan, Z and Radermacher, J and Georgiadis, K and Lazarou, I and Grammatikopoulou, M and Pickering, E and Mitterreiter, J and Aakre, JA and Ashton, NJ and Baquero, M and Beser-Robles, M and Braboszcz, C and Brandt, S and Brown, J and Cacciamani, F and Campill, S and Collins, C and Deshpande, P and Diaz, A and Durrleman, S and Engelborghs, S and Ferré-González, L and Frisoni, GB and Gjestsen, MT and Gove, D and Honigberg, L and Huang, B and Hudak, A and Kaushik, S and Letoha, T and Marquardt, G and Mendes, AJ and Müllenborn, M and Paletta, L and de Barros, NP and Pszeida, M and Vik-Mo, AO and Rostamipour, H and Perneczky, R and Rauchmann, BS and Russegger, S and Schirmer, T and Shadmaan, A and Solana, AB and Soria-Frisch, A and Tegethoff, P and Ribbens, A and De Witte, S and van der Giezen, M and Nikolopoulos, S and Corbett, A and Fröhlich, H and Aarsland, D and , },
title = {Screening for Alzheimer's disease in the community using an AI-driven screening platform: design of the PREDICTOM study.},
journal = {The journal of prevention of Alzheimer's disease},
volume = {13},
number = {5},
pages = {100545},
doi = {10.1016/j.tjpad.2026.100545},
pmid = {41894949},
issn = {2426-0266},
abstract = {BACKGROUND: Recent developments in physiological, imaging and digital biomarkers combined with the approval of new disease-modifying drugs against Alzheimer's disease (AD) and diagnostic blood tests provide an opportunity to shift the first diagnostic steps to the home-setting. While these novel biomarkers enable scalable screening and earlier detection and treatment of AD, they require an evaluation of their accuracy, feasibility, and safety in primary care and the community setting.

OBJECTIVES: The aim of PREDICTOM is to develop and test the accuracy of an artificial intelligence (AI) driven screening platform for the risk assessment and early detection of AD to extend the clinical pathway to home-based screening using established and novel biomarkers.

DESIGN/SETTING: PREDICTOM is a European (Norway, UK, Belgium, France, Switzerland, Germany, Spain) observational, prospective cohort study using a cloud-based platform that stores a digitalised journey for each participant and provides a collection of artificial-intelligence (AI) algorithms and tools for risk assessment and early diagnosis and prognosis.

PARTICIPANTS: Cohort 1 consists of 4000 adults aged 50 years or older at risk of developing AD. Cohort 2 consists of 615 participants selected from Cohort 1 based on estimates indicating high (N = 415) or low (N = 200) risk of AD. Data from existing cohorts will guide the analytic strategy of the study.

MEASUREMENTS: Cohort 1 will undergo home-based assessments (Level 1), Cohort 2 will undergo in-clinic assessments (Levels 2 and 3). Level 1 includes at-home screening, collecting digital and physiological data (questionnaires, cognition, hearing, eye-tracking) and biofluids (capillary blood via finger-stick and saliva) for biomarker analysis. Level 2 comprises a more complex biomarker collection, most of which can be completed in primary care, including EEG, MRI, venous blood, microbiome from stool, cognition, hearing, and eye-tracking. Level 3 includes a diagnostic evaluation to confirm or rule out AD pathology using established biomarkers (cerebrospinal fluid, or amyloid PET).

CONCLUSIONS: PREDICTOM will develop AI-driven algorithms for the early detection of AD using biomarkers that can be collected at home or in the community care setting, and evaluate their integration into a well-defined and comprehensive clinical pathway.},
}

@article {pmid41895098,
year = {2026},
author = {Ninham, B and Battye, M and Carlin, M},
title = {Gut, brain and the Glycocalyx: A portrait of Parkinsons disease.},
journal = {Advances in colloid and interface science},
volume = {353},
number = {},
pages = {103880},
doi = {10.1016/j.cis.2026.103880},
pmid = {41895098},
issn = {1873-3727},
abstract = {Parkinson's disease (PD) has generated extensive data without a unifying mechanism. Although growing evidence implicates the gut microbiome in PD pathogenesis, the gut-brain connection remains unresolved. While the nature of such interactions remains elusive, increasingly it is the glycocalyx, a nanoscale structural network lining endothelial surfaces that is emerging as a key linkage to disease mechanisms. We propose the endothelial surface layer-glycocalyx (ESL-GC) complex as the missing mechanistic interface. Within this framework, microbiome dysbiosis, disruption of ESL-GC structure and function, potassium dysregulation, other specific ion effects, and reactive gas nanobubbles act together as foundational contributors to PD pathology. This model reframes PD from a primarily dopamine-centred neurodegenerative disorder to an interface-based systems disorder and offers a coherent basis for integrating previously conflicting findings.},
}

@article {pmid41895157,
year = {2026},
author = {Žukauskaitė, K and Rauduvytė, K and Baušys, A and Horvath, A and Poškus, T and Stadlbauer, V},
title = {Surgery and the Gastrointestinal Microbiome in Cancer: Bidirectional Impacts and Therapeutic Opportunities - a Narrative Review.},
journal = {Surgical oncology},
volume = {66},
number = {},
pages = {102411},
doi = {10.1016/j.suronc.2026.102411},
pmid = {41895157},
issn = {1879-3320},
abstract = {Gastrointestinal cancers rank among the most common malignancies globally, and although surgical resection remains the cornerstone of curative therapy, it is associated with considerable postoperative morbidity and mortality. Emerging evidence suggests that the gut microbiome is a critical determinant in the pathogenesis of postoperative complications, including surgical site infections, anastomotic leakage, and postoperative ileus. Microbiome-targeted interventions - including probiotics, prebiotics, and synbiotics - have shown promise in modulating microbial communities and supporting postoperative recovery; however, clinical efficacy remains inconsistent, and standardized perioperative protocols are yet to be established. This review summarizes current evidence on the interactions between gastrointestinal cancer surgery and the perioperative gut microbiome, emphasizing opportunities to harness microbiome-targeted interventions to reduce complications and enhance recovery.},
}

@article {pmid41895258,
year = {2026},
author = {Reilly, ER and Charron-Lamoureux, V and Mannochio-Russo, H and Morgan, EW and Boyle, NR and Koo, I and Coudriet, E and Hao, F and Mohanty, I and Perdew, GH and Dorrestein, PC and Patterson, AD},
title = {Systemic rhythmicity of host and bacterial bile acid amidates in the mouse.},
journal = {Cell systems},
volume = {},
number = {},
pages = {101541},
doi = {10.1016/j.cels.2026.101541},
pmid = {41895258},
issn = {2405-4720},
abstract = {Bacterial bile acid amidates (BBAAs) represent an emerging class of host-microbe co-metabolites formed when gut bacteria conjugate bile acids with amino acids beyond taurine and glycine. Although these conjugates have been shown to modulate immune signaling and epithelial integrity, their spatial and temporal distribution across host tissues remains poorly understood. Here, we profiled 690 samples from time-restricted-fed mice, spanning 14 organs, digestive tract contents, and biofluids, to map the temporal dynamics of BBAAs. We identified widespread and tissue-specific oscillations of BBAAs, with the greatest temporal synchronization observed in the ileal contents and progressively diminished rhythmicity in the periphery. Amidates with hydrophilic or hydrophobic side chains remained relatively constant, while aromatic conjugates exhibited the most substantial variation. These findings reveal that BBAAs are temporally and spatially distributed throughout the body, supporting a model in which microbes encode systemic signals through the timing and structure of their metabolites.},
}

@article {pmid41895287,
year = {2026},
author = {Gubatan, J and Sojwal, RS and Ye, J and Boye, TL and Hoang, JN and Fardeen, T and Temby, M and Rubin, SJS and Spencer, SP and Kotagiri, P and Rogalla, S and Rosen, MJ and Nielsen, OH and Boyd, S and Sonnenburg, J and Sinha, SR},
title = {Multi-omics reveal vitamin D regulation of immune-gut microbiome interactions and tolerogenic pathways in inflammatory bowel disease.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102703},
doi = {10.1016/j.xcrm.2026.102703},
pmid = {41895287},
issn = {2666-3791},
abstract = {Loss of immune tolerance to the gut microbiome plays a pathogenic role in inflammatory bowel disease (IBD). How dietary factors alter host immune-gut microbiome interactions in IBD is unclear. Here, we apply multi-omics (immunoglobulin A or G and 16S rRNA sequencing [IgA-seq, IgG-seq], blood single-cell RNA sequencing [scRNA-seq], and immune repertoire sequencing) to investigate the effects of 12 weeks of vitamin D on host immune microbe interactions in patients with IBD. Vitamin D treatment associates with decreased disease activity and inflammatory markers and increased IgA-bound and decreased IgG-bound gut microbiota. Vitamin D alters the profiles of IgA-bound (increased Lachnospiraceae, Blautia) and IgG-bound (decreased Proteobacteria, Enterococcaceae) gut bacteria. Vitamin D increases B cell activating factor (BAFF) signaling between plasmacytoid dendritic cells and B cells, alters BCR and TCR clonotypes that associate with Ig-bound gut microbiota, and increases α4β7+ B and T regulatory cells. Our results demonstrate that vitamin D promotes immune tolerance to gut microbiota in patients with IBD. Clinical trial is registered under NCT04828031.},
}

@article {pmid41895322,
year = {2026},
author = {Sykes, BE and Lutzoni, F and Renwick, A and Oita, S and Skarha, SM and Arnold, AE},
title = {Fungal endophytes of an endangered tree vary with stress and microenvironment in an ex situ conservation nursery.},
journal = {American journal of botany},
volume = {},
number = {},
pages = {e70181},
doi = {10.1002/ajb2.70181},
pmid = {41895322},
issn = {1537-2197},
support = {DEB-1541496//National Science Foundation/ ; },
abstract = {PREMISE: Plants in ex situ conservation nurseries acquire diverse fungal associates that may be moved among nurseries or into the wild during outplanting, including fungal endophytes that contribute to a broad range of functions and occur in leaves, sometimes alongside pathogens. To improve understanding of fungal symbionts in a plant of high conservation concern, we characterized foliar fungal endophytes of Torreya taxifolia, one of the world's most threatened conifers, in an ex situ conservation nursery.

METHODS: We used culture-based and culture-free approaches to characterize fungal endophytes in leaves of T. taxifolia over 2 years and evaluated how endophytes varied spatially and as a function of environmental, plant-specific, and edaphic factors. We also contrasted them with fungi in other plants (local species and species cultivated at a regional scale) and with soil fungi.

RESULTS: Culture-free methods revealed species-rich and phylogenetically diverse foliar fungal endophytes of T. taxifolia that vary spatially, reflecting symbiont acquisition from nearby plants, environmental factors, and plant stress. Endophyte community composition is subject to both stochasticity and temporal turnover and differs markedly from fungal communities in soils and other plants in the area.

CONCLUSIONS: Our study provides novel insights into factors that can shape fungal endophyte communities for a critically endangered tree species. In addition to identifying local determinants of endophytic symbioses, our work illustrates that plants in conservation nurseries host rich foliar fungal communities of potential importance in plant germplasm protection.},
}

@article {pmid41895330,
year = {2026},
author = {Siddiqui, R and Khan, NA},
title = {Towards Digital Periodontology in Space Medicine.},
journal = {Aerospace medicine and human performance},
volume = {97},
number = {4},
pages = {300-302},
doi = {10.3357/AMHP.6830.2026},
pmid = {41895330},
issn = {2375-6322},
mesh = {Humans ; *Aerospace Medicine ; *Space Flight ; Astronauts ; Microbiota ; *Periodontics ; Computer Simulation ; Weightlessness ; Periodontal Diseases ; },
abstract = {During spaceflight, microgravity, radiation, and altered immune function can disrupt balance, increasing susceptibility to both oral and systemic inflammation. We propose a periodontal digital twin, a computational model that integrates oral microbiome, immune, and metabolic data to simulate individual health in real time. The proposed framework conceptualizes a data-driven model linking multiomic and physiological inputs from astronauts to personalized simulations of oral ecosystem dynamics. By continuously updating with new biological and environmental data, the digital twin can predict early deviations from homeostasis. A periodontal digital twin could function as an early warning system for immune dysregulation and microbial imbalance during long-duration missions, supporting targeted preventive or therapeutic interventions. Beyond its application to astronaut health, this approach provides a new lens to study host-microbe coadaptation and establishes a foundation for precision and predictive healthcare in both terrestrial and extraterrestrial contexts. Siddiqui R, Khan NA. Towards digital periodontology in space medicine. Aerosp Med Hum Perform. 2026; 97(4):300-302.},
}

Humans
*Aerospace Medicine
*Space Flight
Astronauts
Microbiota
*Periodontics
Computer Simulation
Weightlessness
Periodontal Diseases

@article {pmid41895350,
year = {2026},
author = {S, SK and Jadhav, P and Paul, A and Kumar, R and Paul, D and Bose, S},
title = {Understanding gut microbiota dysbiosis as a plausible link between Obstructive Sleep Apnea (OSA), viral infections, and lifestyle diseases.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {108466},
doi = {10.1016/j.micpath.2026.108466},
pmid = {41895350},
issn = {1096-1208},
abstract = {Obstructive sleep apnea (OSA) is a multifactorial disorder which is influenced by intermittent hypoxia, sleep fragmentation, and systemic inflammation. Recent evidence suggests that lifestyle diseases and viral infections further exacerbate OSA severity through common inflammatory and metabolic pathways. Parallelly, gut dysbiosis has gained recognition as a key mediator which links respiratory, metabolic, and infectious disease processes via the gut-lung axis. This review explores the convergent role of gut microbial dysbiosis across OSA, lifestyle-associated comorbidities such as obesity, diabetes, and cardiovascular disease and viral infections including respiratory syncytial virus (RSV), influenza, dengue, Human Immunodeficiency Virus (HIV), and SARS-CoV-2. Across these conditions, a recurring pattern of reduced beneficial commensals (e.g., Bifidobacterium, Faecalibacterium prausnitzii, Roseburia, Akkermansia muciniphila) and a noted increase of pro-inflammatory taxa (e.g., Escherichia, Streptococcus, Enterobacteriaceae) has been observed. It contributes to epithelial barrier breakdown, endotoxemia, metabolic dysfunction, and immune dysregulation. In OSA patients, intermittent hypoxia is observed that causes gut barrier impairment and microbial translocation, thus amplifying systemic inflammation. Similarly, viral infections reshape the gut ecology, bringing adverse effects to host immunity and respiratory outcomes. The review highlights upon the therapeutic potentials of prebiotics and probiotics supplementation for modulating gut dysbiosis. It discusses the role of these therapeutic interventions in improving metabolic homeostasis, reducing inflammation, and potentially mitigating OSA-related complications. Collectively, this analysis highlights gut dysbiosis as a plausible unifying mechanism connecting lifestyle diseases, viral infections, and OSA, presenting a compelling avenue for integrated, microbiome-targeted interventions.},
}

@article {pmid41895366,
year = {2026},
author = {Fehér, B and Amorim das Vírgens, IP and Bakony, M and Tóth, E and Solymosi, O and Ütő, E and Kói, T and Hegyi, P and Váncsa, S and Ács, N and Can, G and Gupta, N and Biju, J and Melczer, Z},
title = {Cervicovaginal detection of genital mycoplasmas is associated with preterm birth and low birth weight: a systematic review and multivariate meta-analysis of adverse pregnancy outcomes.},
journal = {American journal of obstetrics and gynecology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajog.2026.03.008},
pmid = {41895366},
issn = {1097-6868},
abstract = {OBJECTIVE: Genital mycoplasmas (Mycoplasma genitalium, Mycoplasma hominis and Ureaplasma species) are highly prevalent in women of reproductive age worldwide. The relevance of cervicovaginal detection in pregnancy remains controversial. This study aimed to assess their associations with adverse pregnancy outcomes.

DATA SOURCES: We conducted a systematic review and meta-analysis of observational studies published up to February 1, 2026, in Medline, Embase, and the Cochrane Library.

STUDY ELIGIBILITY CRITERIA: Eligible studies reported the presence of any genital mycoplasmas and at least one adverse pregnancy outcome.

Four reviewers independently selected studies and extracted data. Pooled odds ratios and mean differences with 95% confidence intervals were calculated. Univariate and subgroup analyses were performed for primary and secondary outcomes, and multivariate analysis for preterm birth. Sensitivity analyses restricted to cohort studies and cervicovaginal sampling were conducted.

RESULTS: Of 11,957 records, 156 studies were included in meta-analysis. In sensitivity analyses excluding amniotic fluid and placental specimens, significant associations with spontaneous preterm birth and low birth weight remained for cervicovaginal samples. Cervicovaginal detection of Ureaplasma parvum was significantly associated with preterm birth (OR 1.63; CI: 1.36-1.96). For Ureaplasma species, first-trimester detection showed stronger associations compared to second-trimester positivity (p = 0.044). Cervicovaginal Ureaplasma detection was also associated with low birth weight (OR 1.56; CI: 1.33-1.83) and small for gestational age (OR 1.47; CI: 1.19-1.80). Mycoplasma hominis showed significant associations with both preterm birth (aOR 1.75; CI: 1.21-2.53) and low birth weight (OR 1.81; CI: 1.51-2.16) when detected in cervicovaginal samples.

CONCLUSION: Associations between genital mycoplasmas and adverse pregnancy outcomes are not limited to intraamniotic presence but are also observed with cervicovaginal detection. Given the observational nature of the available data and residual confounding, these associations should be interpreted cautiously and do not support routine screening or treatment. Cervicovaginal detection should be interpreted within the broader context of the vaginal microbial environment rather than as evidence of an isolated pathogenic effect.},
}

@article {pmid41895406,
year = {2026},
author = {Tain, YL and Hsu, CN},
title = {Developmental Origins and Environmental Determinants of Cardiovascular-Kidney-Metabolic Syndrome: A Pediatric Precision Prevention Perspective.},
journal = {Biomedical journal},
volume = {},
number = {},
pages = {100970},
doi = {10.1016/j.bj.2026.100970},
pmid = {41895406},
issn = {2320-2890},
abstract = {Cardiovascular-Kidney-Metabolic Syndrome (CKMS), formally defined by the American Heart Association in 2023, emphasizes the interconnections among chronic kidney disease, cardiovascular disease, obesity, and diabetes. Although CKMS typically manifests in adulthood, accumulating evidence indicates that vulnerability is established early in life through developmental programming shaped by maternal, perinatal, and early-childhood exposures. This review summarizes the developmental origins, environmental determinants, and mechanistic pathways of CKMS, with a particular emphasis on kidney programming and pediatric precision prevention. Recent nationally representative data indicate that CKMS risk-stage (stage ≥1) affects approximately 90% of U.S. adults and 40% of adolescents, highlighting the extensive population burden long before overt clinical disease develops, yet kidney health remains underrecognized within cardiometabolic risk assessment. In children, early metabolic disruption, excess adiposity, and subclinical cardiovascular dysfunction interact with structural or developmental renal vulnerability to accelerate CKD progression and amplify lifelong risk. Evidence from the Developmental Origins of Health and Disease framework demonstrates that maternal malnutrition, metabolic disease, toxicant exposures, preterm birth, and perinatal complications permanently alter nephron endowment, vascular function, and metabolic regulation. Animal studies reveal convergent mechanisms-including oxidative stress, aberrant renin-angiotensin activity, epigenetic modifications, gut microbiota dysbiosis, and sex-specific responses-that predispose offspring to CKMS and highlight targets for early-life reprogramming. Prevention should begin with maternal health and the first 1000 days, incorporating nutritional and lifestyle interventions, early screening for obesity, hypertension, and dyslipidemia, and emerging microbiome- or antioxidant-targeted therapies. Advances in multi-omics, digital health, and AI-enabled monitoring facilitate early risk stratification and precision prevention, although pediatric-specific guidelines remain limited. Viewed through a life-course lens, CKMS represents a gradual, self-reinforcing process rooted in developmental programming and environmental exposures. Integrating maternal and pediatric interventions within a life-course precision prevention framework provides a roadmap to disrupt disease trajectories, reduce intergenerational risk, and promote lifelong cardiovascular, kidney, and metabolic health.},
}

@article {pmid41895437,
year = {2026},
author = {Rinanda, T and Riani, C and Artarini, A and Sasongko, L},
title = {Exploring the role of gut methanogenic archaea in childhood stunting in Aceh Province, Indonesia.},
journal = {Anaerobe},
volume = {},
number = {},
pages = {103040},
doi = {10.1016/j.anaerobe.2026.103040},
pmid = {41895437},
issn = {1095-8274},
abstract = {BACKGROUND: Emerging evidence highlights the critical role of gut microbiota in childhood growth; however, the contribution of methanogenic archaea remains underexplored. In this study, we investigated the involvement of gut methanogens in linear growth impairment by analyzing their abundance, diversity, methanogenesis, and interactions with bacterial short-chain fatty acids (SCFAs) and glucagon-like peptide-1 (GLP-1) levels in stunted versus normal children.

METHODS: This case-control study included 42 children aged 24-59 months from Pidie, Aceh, Indonesia. Gut archaea were profiled through 16S rDNA amplicon sequencing, and mcrA gene expression was measured using quantitative Polymerase Chain Reaction. SCFAs were analyzed using gas chromatography-mass spectrometry, and GLP-1 levels were quantified using immunoassay. The microbial co-occurrence networks were also assessed.

RESULTS: Archaeal 16S rDNA amplicon sequencing revealed a lower abundance of Methanobacteriaceae, particularly Methanobrevibacter, in stunted children, although their presence contributed to greater microbial diversity. Reduced mcrA gene expression in stunted children indicates a decrease in methanogenesis. Although not statistically significant, mcrA gene expression positively correlated with height, SCFA concentrations, and GLP-1 levels. Microbial network analysis revealed a lower density of microbial networks, indicating reduced stability and resilience in stunted children, with Methanobrevibacter playing a substantial role. Notably, Methanobrevibacter exhibited a positive association with Elusimicrobium, a rare human-associated microbe, and a negative correlation with Lachnospiraceae in normal children, indicating unique microbial interactions that may influence metabolic health.

CONCLUSION: Methanogens, particularly Methanobrevibacter, may play a crucial role in shaping gut microbial ecology and supporting metabolic pathways relevant to linear growth during early childhood.},
}

@article {pmid41895499,
year = {2026},
author = {Kim, DH and Byeon, E and Jeong, H and Kim, MS and Yoon, C and Maszczyk, P and Hu, M and Wang, M and Wang, Y and Yang, Z and Lee, JS},
title = {Gut microbiome disruption impairs arsenic biotransformation and exacerbates toxicity in the water flea Daphnia magna.},
journal = {Comparative biochemistry and physiology. Toxicology & pharmacology : CBP},
volume = {},
number = {},
pages = {110522},
doi = {10.1016/j.cbpc.2026.110522},
pmid = {41895499},
issn = {1532-0456},
abstract = {Arsenic risk in waters depends on chemical speciation, yet studies on host-associated microbiota to the in vivo detoxification mechanisms remain unclear. We exposed Daphnia magna for 21 days to inorganic arsenic at 2 mg/L with/without a broad-spectrum antibiotic cocktail that disrupts the gut microbiome. We assessed life-history traits, whole-body arsenic species by HPLC coupled to ICP-MS, and gut community composition by 16S rRNA gene sequencing with LEfSe and PICRUSt2 analyses. Both Arsenic and antibiotics alone impaired growth and reproduction, while co-exposure produced the strongest effects. Microbiome disruption increased total arsenic burden (~14%) and shifted speciation away from detoxified end-products. Formation of arsenobetaine decreased by an order of magnitude, whereas dimethylarsinic acid approximately doubled. Under arsenic exposure alone, core taxa such as Aeromonas proliferated, accompanied by enrichment of predicted arsenic reductases and methyltransferases. Antibiotic treatment eliminated these taxa, favored Streptococcus, Methylophilus, and Veillonella, and suppressed predicted arsenic-processing functions. These results demonstrate that an intact Daphnia gut microbiome facilitates conversion of inorganic arsenic to less toxic organoarsenicals and mitigates toxicity. Microbiome integrity emerges as a practical control on arsenic fate and hazard in freshwater zooplankton, relevant to risk assessment under antibiotic co-contamination.},
}

@article {pmid41895971,
year = {2026},
author = {Silva, FA and Cabral, L and de Assis, BBT and Ferreira, DP and Egea, MB and Pimentel, TC and Magnani, M},
title = {Microbiota of foods: a comprehensive review of diversity and potential implications.},
journal = {Food research international (Ottawa, Ont.)},
volume = {232},
number = {},
pages = {118899},
doi = {10.1016/j.foodres.2026.118899},
pmid = {41895971},
issn = {1873-7145},
mesh = {*Food Microbiology ; *Fermented Foods/microbiology ; *Microbiota ; Fermentation ; Metagenomics ; Humans ; Metabolomics ; Bacteria/classification/genetics ; RNA, Ribosomal, 16S/genetics ; Biodiversity ; },
abstract = {Microbial communities play a central role in food ecosystems. Fermented foods, in particular, host complex and dynamic microbiomes that are shaped by raw materials, fermentation substrates, processing environments, and regional production practices. This review provides an in-depth analysis of microbial diversity in various spontaneously fermented food products, including beverages, dairy products, and ethnic and other traditional food products. It highlights how microbial composition evolves throughout fermentation and how specific microorganisms contribute to the safety and sensory profiles of the final products. The field has undergone a methodological transformation, moving from classical culture-based methods to advanced omics technologies. Culture-independent approaches such as metataxonomics, metagenomics, metatranscriptomics, metaproteomics, and metabolomics enable a more comprehensive characterization of microbial communities, providing insights not only into their taxonomic composition but also into their functional roles. Despite increasing interest in metagenomics and metatranscriptomics, metataxonomic high-throughput sequencing, particularly 16S rRNA and ITS gene analyses, remains the most widely used technique due to its lower cost and accessibility. However, it provides limited resolution at the species level and cannot distinguish between live and dead cells. Microbiome characterization using omics has practical implications for the food industry, including the identification of microbial signatures in artisanal foods and the improvement of understanding fermentation processes. Our manuscript emphasizes a broad comparative overview of microbial diversity across multiple categories of fermented foods and integrates this with a methodological perspective on omics approaches used to characterize these communities. Findings outline the main methodological approaches, sequencing platforms, primer sets, and bioinformatic tools used in studies, as well as the current limitations and future directions in the field. Integrative multi-omics strategies are expected to significantly enhance food safety, quality, traceability, and functionality across diverse food systems.},
}

*Food Microbiology
*Fermented Foods/microbiology
*Microbiota
Fermentation
Metagenomics
Humans
Metabolomics
Bacteria/classification/genetics
RNA, Ribosomal, 16S/genetics
Biodiversity

@article {pmid41895972,
year = {2026},
author = {Yu, J and Qiang, H and Hoffmann, TG and Mahajan, P and Chaiwong, S and An, X},
title = {From bruise to breakdown: Multi-omics of transport-induced deterioration in apples.},
journal = {Food research international (Ottawa, Ont.)},
volume = {232},
number = {},
pages = {118900},
doi = {10.1016/j.foodres.2026.118900},
pmid = {41895972},
issn = {1873-7145},
mesh = {*Malus/microbiology/metabolism/chemistry ; *Fruit/microbiology/chemistry/metabolism ; Cell Wall/metabolism ; *Metabolomics/methods ; *Stress, Mechanical ; Lipid Peroxidation ; Polysaccharides/metabolism ; Pectins/metabolism ; Microbiota ; Multiomics ; },
abstract = {Mechanical damage during express transportation is a major driver of postharvest quality deterioration in fresh produce. In this study, we integrated physiological and biochemical assays with microscopic observations and multi-omics approaches to comprehensively characterize the consequences of transportation-induced mechanical stress in Fuji apples. Structural analyses revealed that mechanical injury caused immediate disruption of cell wall architecture, including polysaccharide depolymerization and increased exposure of functional groups. Microscopic and FTIR analyses confirmed that mechanical stress caused cell wall collapse, polysaccharide network depolymerization, and increased exposure of functional groups. Biochemical assays further demonstrated that damage markedly accelerated cell wall disassembly, as reflected by a 140.91% increase in pectin solubilization and a 91.24% rise in cellulase activity, while also intensifying lipid peroxidation (52.71% increase in MDA content) and enzymatic browning (93.20% increase in PPO activity). Non-targeted metabolomics revealed extensive metabolic reprogramming, including the accumulation of stress-related phenolics, inhibition of tryptophan metabolism, and disruption of lipid-derived signaling pathways. Moreover, mechanical stress profoundly reshaped the apple fruit's epiphytic microbiome, shifting the community structure from protective Bacillus-dominated populations to spoilage-associated Metchnikowia yeasts with strong pectinolytic capacity. By linking macroscopic phenotypes with molecular and microbial signatures, this work provides mechanistic insight into how postharvest mechanical impact accelerates deterioration in apples and offers a scientific foundation for developing targeted intervention strategies in transport-intensive supply chains.},
}

*Malus/microbiology/metabolism/chemistry
*Fruit/microbiology/chemistry/metabolism
Cell Wall/metabolism
*Metabolomics/methods
*Stress, Mechanical
Lipid Peroxidation
Polysaccharides/metabolism
Pectins/metabolism
Microbiota
Multiomics

@article {pmid41895994,
year = {2026},
author = {Çelik, MN and Dazıroğlu, MEÇ and Pınar, BA and Nanì, MF and Romano, B and Ağagündüz, D and Capasso, R},
title = {Microbiome crosstalk and nutrition: the interplay between gut microbiota-organ axis and dietary factors.},
journal = {Food research international (Ottawa, Ont.)},
volume = {232},
number = {},
pages = {118945},
doi = {10.1016/j.foodres.2026.118945},
pmid = {41895994},
issn = {1873-7145},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Diet ; Probiotics ; Animals ; Prebiotics ; *Nutritional Status ; Gastrointestinal Tract/microbiology ; },
abstract = {The gut microbiota (GM) is referred to as the central organ due to its dynamic and adaptable contact network with other organs through humoral, immunological, metabolic, endocrine, and neurological pathways. Recent studies have emphasized the concept of the "gut-organ axis", which shows that the effects of GM go beyond the gastrointestinal system (GIS) and encompass the reciprocal interactions between other organs. Communication along these axis occurs mainly through mediators such as short-chain fatty acids (SCFAs), microbial metabolites, neurotransmitters, cytokines, and hormonal signals. Therefore, imbalances in GM may surpass gut problems and be linked to diseases affecting the brain, liver, lungs, heart, mouth, skin, and many other organs. Understanding these reciprocal interactions can inform strategies for disease prevention and treatment. Emerging evidence suggests that interactions between the GM and other organ-specific metabolites it secretes are dynamic and influenced by various environmental and lifestyle factors, particularly diet. The gut and other organ microbiomes are maintained in balance with the help of nutritional supplements like probiotics, prebiotics, symbiotic, vitamins, omega-3 fatty acids, and dietary fiber. Consuming processed or red meat, high-fat, high-sugar, high-glycemic index foods, and excessive salt can upset this balance and raise the risk of systemic inflammation and disease. The purpose of this review is to examine the interactions between various organ-specific microbiomes in the human body, to elucidate the effects of these interactions on health, and to highlight how microbiome-targeted nutritional interventions can modulate these interactions, potentially affecting disease risk and overall metabolic homeostasis.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Diet
Probiotics
Animals
Prebiotics
*Nutritional Status
Gastrointestinal Tract/microbiology

@article {pmid41896037,
year = {2026},
author = {Shi, S and Bastías, DA and Wang, H and Faville, M and O'Callaghan, M},
title = {A roadmap for plant-microbiome breeding to enhance plant stress tolerance.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2026.02.012},
pmid = {41896037},
issn = {1878-4380},
abstract = {Plants constantly form associations with microorganisms, and some are vital for plant performance, especially under stress conditions. Although some microorganisms have been developed into commercial bioinoculant products, their associations with plants can be transient, and their efficacy is often inconsistent in the field. Here, we propose a framework and key research steps needed for plant breeders and microbiologists to work together to match plant genetics with compatible microbial inoculants. Recent studies have successfully identified plant genetic factors that play a role in the recruitment of beneficial microorganisms, and many associated technologies are ready for implementation towards this goal. This innovative and collaborative approach could provide novel, enduring plant-microbiome associations for environmental sustainability and food security under a changing climate.},
}

@article {pmid41896075,
year = {2026},
author = {Waymouth, VJ and Keynton, ACW and Brumley, DR and Ebert, B and Watt, M},
title = {Cell walls and their role in the plant root microbiome.},
journal = {Trends in plant science},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tplants.2026.02.005},
pmid = {41896075},
issn = {1878-4372},
abstract = {Plant roots form a microbiome that interacts at the cell wall extracellular matrix before entering the cell. The root primary and accessory walls present a dynamic, cell-type-dependent scaffold that microbes must navigate, using shared cellulose or contrasting chitin motifs and influencing plant gene responses that encode enzymes for cell wall biosynthesis and degradation. We propose that an interface evolves as microbes reach the root tip and interact with host polymers, potentially driving concurrent degradation of root and microbial cells. Knowledge gaps span diffusion, fluid flow, nutrient exchange, and the physics of microbial motion within the wall boundary. Advances in in situ imaging and mathematical modelling can help understand the dynamics of cell walls to design root microbiomes to function in agroecosystems.},
}

@article {pmid41896210,
year = {2026},
author = {Zhang, X and Cheng, HS and Zhan, X and Li, X and Huang, J and Liu, H and Chua, D and Wang, G and Li, X and Shi, Y and Wang, F and Xu, Z and Qu, J and Pethe, K and Li, G and Tan, NS and Mac Aogáin, M and Chotirmall, SH and Li, L},
title = {Single-bacterial cell insights into mechanisms of ceftriaxone resistance in Neisseria subflava.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-68621-y},
pmid = {41896210},
issn = {2041-1723},
support = {Grant No. 32470194//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {The contribution of airway pathobionts to chronic respiratory disease is increasingly recognized, yet the evolutionary processes that shift commensals to pathogens remain poorly understood. Here we investigate how antibiotic pressure drives adaptation in Neisseria subflava, a common airway commensal associated with bronchiectasis. Using serial passage under ceftriaxone exposure, we observe a >300-fold increase in resistance, accompanied by enhanced biofilm formation and genetic reprogramming. Whole-genome sequencing reveals recurrent mutations in the adhesin gene ataA, while single-cell transcriptomics identifies six functionally distinct clusters indicating adaptive programs in growth, metal homeostasis, oxidative stress, and cell-wall remodeling. Notably, biofilm integrity is maintained through compensatory upregulation of comP and bamE, which promotes phagocytic evasion and resistance in experimentally evolved strains and clinical isolates. Iron availability further stabilizes biofilm and modulates antibiotic tolerance, underscoring metal homeostasis as a contributory adaptive axis. Together, these findings reveal a multifaceted strategy by which N. subflava exploits antibiotic selection to transition towards pathogenicity. By integrating experimental evolution with single-cell resolution, we establish a framework for understanding the commensal-to-pathobiont transition, with broad implications for the airway microbiome and antimicrobial resistance in chronic respiratory disease.},
}

@article {pmid41896243,
year = {2026},
author = {He, Y and Peng, H and Li, L and Sheng, S and Wang, Q and Li, W and Lin, F and Yi, J},
title = {Valeric acid from oral microbiome suppresses esophageal cancer growth by disrupting eEF1A1 -mediated translational output.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-71209-1},
pmid = {41896243},
issn = {2041-1723},
abstract = {Dysbiosis of the oral microbiome has been associated with esophageal squamous cell carcinoma (ESCC), but how it impacts ESCC remains largely unknown. Surprisingly, we find that the oral microbiota derived from ESCC patients-not that from healthy controls-exhibits potent inhibitory and cytotoxic effects on ESCC cells. This anti-tumor effect is attributable to Veillonella, which is enriched in the ESCC-associated microbiota. Mechanistically, Veillonella produces valeric acid, which is transported into cells via MCT1 and inhibits the GTPase activity of eEF1A1, thereby suppressing protein translation. These findings identify valeric acid as a potential postbiotic for ESCC treatment and underscore the necessity of functional validation beyond observational and correlative studies.},
}

@article {pmid41896298,
year = {2026},
author = {Byonanebye, A and Khamis, FM and Mwangi, M and Namikoye, ES and Ajene, IJ and Akutse, KS},
title = {Temperature dependent immunological responses of Spoladea recurvalis exposed to entomopathogenic fungi.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-45475-4},
pmid = {41896298},
issn = {2045-2322},
support = {DPP-020/2022-2024//Biovision Foundation for Ecological Development/ ; },
}

@article {pmid41896360,
year = {2026},
author = {Yang, X and Tang, J and Lai, Z and Dong, Z and Liao, J and Guo, Y and Wang, Z},
title = {Comparative Analysis of Nasal and Cloacal Bacterial Communities in Three Sea Turtle Species under Rescue Center Conditions.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-026-02751-0},
pmid = {41896360},
issn = {1432-184X},
support = {No. 2021B1212110005//Science and Technology Infrastructure Project of Department of Science and Technology of Guangdong Province/ ; },
}

@article {pmid41896437,
year = {2026},
author = {Jin, H and Zhou, W and Ying, R},
title = {Impact of ileostomy reversal on gut microbiome and metabolome in rectal cancer: a review of mechanisms and clinical consequences.},
journal = {Langenbeck's archives of surgery},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00423-026-04031-4},
pmid = {41896437},
issn = {1435-2451},
support = {2024S00023//the Social Development Science and Technology Project of Wenling City, Zhejiang Province/ ; },
}

@article {pmid41896632,
year = {2026},
author = {Lei, J and Qi, J and Zhai, J and Chen, Z and Li, N and Zhang, Y and Yuan, Y and Sun, C},
title = {Dynamic gut responses to sepsis uncovered by multi-omics profiling in a rodent model.},
journal = {Communications biology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s42003-026-09940-0},
pmid = {41896632},
issn = {2399-3642},
support = {82470617//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {Sepsis reflects an immune dysregulation in response to infection, and the intestine functions as the largest immune organ in the human body. However, the multidimensional dynamic changes within the gut environment during the progression of sepsis remain incompletely understood. Here, we show the alterations in the gut over the course of pneumonia-induced sepsis through the analysis of cellular, microbial, metabolic, and protein profiles over time. We demonstrate that subsets of immune cells, including mononuclear phagocytes and T cells, undergo compositional and transcriptional shifts. Simultaneously, specific structural cells and mucus-producing cells exhibit adapted roles in antigen presentation and the regulation of intestinal homeostasis. Furthermore, we detail alterations in the gut microbiome composition, metabolite levels, and colonic protein expression, identifying shared fluctuation patterns across these biological dimensions. These findings outline the interactions among the gut microbiome, cellular activity, and immune responses, providing potential therapeutic targets for future sepsis management.},
}

@article {pmid41896639,
year = {2026},
author = {Puetz, LC and O Delmont, T and Mitchell, AL and Finn, RD and Zhang, G and Shepeleva, DV and Kharlamova, AV and Kukekova, AV and Trut, LN and Gilbert, MTP},
title = {Gut microbiome community structure correlates with different behavioral phenotypes in the Belyaev Farm-Fox Experiment.},
journal = {Communications biology},
volume = {9},
number = {1},
pages = {},
pmid = {41896639},
issn = {2399-3642},
support = {NIH R35 GM144276//U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS)/ ; RSF-21-44-04405//Russian Science Foundation (RSF)/ ; DNRF143 Center for Evolutionary Hologenomics//Danmarks Grundforskningsfond (Danish National Research Foundation)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Behavior, Animal ; *Foxes/microbiology/physiology ; Phenotype ; Domestication ; Male ; },
abstract = {Domestication represents one of the largest biological shifts of life on Earth, and for many animal species, behavioral selection is thought to facilitate early stages of the process. The gut microbiome of animals can respond to environmental changes and have diverse and powerful effects on host behavior. As such, we hypothesize that selection for tame behavior during early domestication, may have indirectly selected on certain gut microbiota that contribute to the behavioral plasticity necessary to adapt to the new social environment. Here, we explore the gut microbiome of foxes from the tame and aggressive strains of the "Russian-Farm-Fox-Experiment". Microbiota profiles reveal a significant depletion of bacteria in the tame fox population that have been associated with aggressive and fear-related behaviors in other mammals. Our metagenomic survey allows for the reconstruction of microbial pathways enriched in the gut of tame foxes, such as glutamate degradation, which converge with host genetic and physiological signals, revealing a potential role of functional host-microbiota interactions that could influence behaviors associated with domestication. Overall, by characterizing how compositional and functional potential of the gut microbiota and host behaviors co-vary during early animal domestication, we provide further insight into our mechanistic understanding of this adaptive, eco-evolutionary process.},
}

Animals
*Gastrointestinal Microbiome
*Behavior, Animal
*Foxes/microbiology/physiology
Phenotype
Domestication
Male

@article {pmid41896698,
year = {2026},
author = {Jung, S and Militsi, E and Huck, O},
title = {Oral Microbiome in Systemic Autoimmune Diseases: A Systematic Review.},
journal = {Oral diseases},
volume = {},
number = {},
pages = {},
doi = {10.1111/odi.70215},
pmid = {41896698},
issn = {1601-0825},
abstract = {OBJECTIVE: The oral cavity represents a key but underexplored interface between host immunity and microbial communities. The aim of this systematic review was to synthesize current literature on oral microbiota alterations in systemic autoimmune diseases.

METHODS: PubMed and Web of Science databases were searched for human studies published between January 2000 and April 2025. Eligible observational studies compared adults with diagnoses of systemic autoimmune diseases to controls and characterized oral microbiota diversity and/or composition using sequencing-based methods. Different oral habitats were analyzed (saliva, dental plaque, oral mucosa, gingival crevicular fluid).

RESULTS: 42 studies met inclusion criteria: 19 on rheumatoid arthritis, 18 on primary Sjögren's syndrome, 5 on systemic lupus erythematosus, and 1 on anti-neutrophil cytoplasmic autoantibody-associated vasculitis. 16S rRNA gene sequencing predominated and only 3 studies used shotgun metagenomics, among which one also profiled the oral virome. Across systemic autoimmune diseases, dysbiosis was characterized by enrichment of anaerobic genera (Prevotella, Veillonella) and depletion of commensals (Neisseria, Haemophilus), with distinct β-diversity separation from controls. Periodontal disease and reduced salivary secretion significantly modulated microbial communities but did not fully explain disease-associated alterations.

CONCLUSION: The oral microbiome exhibited shared dysbiotic signatures. However, methodological and clinical heterogeneity limited direct comparison between studies.},
}

@article {pmid41896724,
year = {2026},
author = {Connell, E and Sami, S and Khondoker, M and Minihane, AM and Pontifex, MG and Müller, M and McArthur, S and Le Gall, G and Vauzour, D},
title = {Circulatory dietary and gut-derived metabolites predict early cognitive decline.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2649487},
doi = {10.1080/19490976.2026.2649487},
pmid = {41896724},
issn = {1949-0984},
mesh = {Humans ; *Cognitive Dysfunction/microbiology/blood/metabolism/diagnosis ; Male ; *Gastrointestinal Microbiome ; Female ; Aged ; Middle Aged ; *Bacteria/metabolism/classification/genetics/isolation & purification ; Biomarkers/blood ; Dysbiosis/microbiology ; Diet ; Bile Acids and Salts/blood ; Methylamines/blood ; Aged, 80 and over ; Tryptophan/blood ; },
abstract = {INTRODUCTION: A key component of disease prevention is the identification of at-risk individuals. Microbial dysbiosis in the early stages of cognitive decline and Alzheimer's disease (AD) and can modulate the levels of microbe-derived metabolites (MDM), thought to contribute to neuroinflammation, blood‒brain barrier dysfunction, and neuronal degeneration. However, the precise role of MDM in this process, as well as their potential value as risk factors, remains poorly understood.

METHODS: Mass spectrometry platforms determined the serum concentration of 33 metabolites (13 tryptophan-related compounds, 15 bile acid compounds, 3 TMAO-related metabolites and 2 cresol metabolites) from cognitively healthy subjects, subjective cognitive impairment (SCI) participants and mild cognitive impairment (MCI) participants (n = 50 per group, matched for age, BMI and sex). Multiple linear regression and machine learning techniques were applied to identify a metabolite panel capable of classifying early cognitive decline. 16S rRNA amplicon sequencing was employed to identify bacterial taxa associated with these metabolic changes.

RESULTS: Multiple linear regression modelling, adjusted for sex, BMI, age, albumin (for its role in metabolite transport), liver and kidney function, and background diet, identified key neuroprotective metabolites, namely choline, 5-hydroxyindole acetic acid, and indole propionic acid (IPA), as lower in SCI and MCI individuals compared to healthy controls. In contrast, the cytotoxic metabolite, indoxyl sulfate, and kynurenic acid were elevated. A random forest algorithm with multiclass classification further validated these findings, highlighting six metabolites (indoxyl sulfate, choline, 5-hydroxyindole acetic acid, IPA, kynurenic acid, and kynurenine) as classifiers of early cognitive decline, achieving an area under the curve (AUC) of 0.79.

CONCLUSION: These findings suggest that MDM may serve as putative composite biomarkers of early cognitive decline, offering potential clinical relevance for metabolic risk stratification and supporting the future development of minimally invasive screening tools.},
}

Humans
*Cognitive Dysfunction/microbiology/blood/metabolism/diagnosis
Male
*Gastrointestinal Microbiome
Female
Aged
Middle Aged
*Bacteria/metabolism/classification/genetics/isolation & purification
Biomarkers/blood
Dysbiosis/microbiology
Diet
Bile Acids and Salts/blood
Methylamines/blood
Aged, 80 and over
Tryptophan/blood

@article {pmid41896753,
year = {2026},
author = {Lin, D and Li, Q and Suleiman, M and An, M and Zhu, Y},
title = {Microbiome and metabolomics analysis of different bryophytes under cadmium stress.},
journal = {BMC plant biology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12870-026-08651-2},
pmid = {41896753},
issn = {1471-2229},
support = {2022D01C678//Natural Science Foundation of Xinjiang/ ; },
}

@article {pmid41897048,
year = {2026},
author = {Pignataro, E and Brindisi, G and Gori, A and Colletti, G and Moraca, P and Cinicola, BL and Spalice, A and Anania, C and Zicari, AM},
title = {Pediatric Vernal Keratoconjunctivitis (VKC): Current State and Future Directions-A Narrative Review of Clinical Features, Diagnostic Strategies, and Emerging Therapies.},
journal = {Children (Basel, Switzerland)},
volume = {13},
number = {3},
pages = {},
doi = {10.3390/children13030335},
pmid = {41897048},
issn = {2227-9067},
abstract = {Vernal keratoconjunctivitis (VKC) represents far more than a typical allergic eye disease. It is a distinct and often underestimated chronic inflammatory condition that primarily affects children during critical stages of physical and emotional development. Though frequently grouped with seasonal allergic conjunctivitis, VKC differs significantly in its immunopathology, clinical presentation, and long-term implications. Its intense ocular symptoms and its potential for corneal damage and substantial psychosocial burden require, rather than symptom control, coordinated and multidisciplinary management. This narrative review explores VKC from every angle, with a particular focus on its implications for pediatric care. VKC, in fact, represents a genuine clinical challenge: as its symptoms can mimic milder forms of conjunctivitis, its course is often unpredictable, and its treatment requires balancing efficacy and safety in vulnerable age groups. We examined the immunological mechanisms that make it a model of localized Th2 inflammation, the diagnostic pitfalls that delay recognition, and the evolving treatment landscape, from conventional therapies like cyclosporine A and tacrolimus to innovative agents such as omalizumab and dupilumab. We also highlighted the role of emerging biomarkers, the influence of environmental and microbiome factors, and the urgent need for standardized care pathways. As research continues to expand our understanding, VKC is emerging as a prime example of how personalized medicine and translational science can intersect to address complex immune-mediated diseases in children. For the ones treating pediatric allergic disorders, VKC is no longer a rare curiosity: it is a clinical challenge worth understanding deeply.},
}

@article {pmid41897098,
year = {2026},
author = {Baghdadi, ZD},
title = {Equity or Two-Tier Care? Guardrails for Silver Diamine Fluoride and Delegated Early Childhood Caries Pathways.},
journal = {Children (Basel, Switzerland)},
volume = {13},
number = {3},
pages = {},
doi = {10.3390/children13030386},
pmid = {41897098},
issn = {2227-9067},
abstract = {Early childhood caries (ECC) is a complex, multifactorial disease shaped by biofilm ecology, host susceptibility, diet and behaviors, and structural determinants of health. Silver diamine fluoride (SDF) is an effective non-restorative option for arresting cavitated lesions in many settings and can support access when definitive care is delayed. However, translating short-horizon "arrest" outcomes into broad policy claims-that SDF-first, delegated pathways can substitute for dentist-led diagnosis and comprehensive rehabilitation-risks institutionalizing a two-tier standard of care for children facing the greatest access barriers. This perspective critically appraises evidence-to-implementation pathways for SDF and delegated ECC management, using risk-of-bias and reporting guidance as interpretive tools and drawing on pragmatic regimen trials, microbiome substudies, oral health-related quality of life (OHRQoL) analyses, and implementation work including the Canadian Caries Risk Assessment Tool (CCRAT) in primary care. We explicitly distinguish what studies demonstrate (e.g., feasibility and short-term arrest differences by reapplication interval) from what they do not establish (e.g., long-term tooth survival, pulpal outcomes, definitive treatment completion, and equity impacts). We propose practical guardrails that position SDF as interim management within a continuum of care: dentist-led diagnosis and escalation when pulpal risk is suspected; time-bound referral pathways with completion tracking; protocolized follow-up aligned with lesion/risk status; outcome sets that extend beyond "arrest" to include pain, function, OHRQoL, tooth survival, and equity stratification; and lesion-site sampling plus preregistered analyses when mechanistic claims are advanced.},
}

@article {pmid41897337,
year = {2026},
author = {Nawaz, S and Sugiura, T and Yusuf, I and Sultany, A},
title = {Gut-Heart Axis in HFpEF: The Emerging Role of Microbiome-Driven Inflammation and Endothelial Dysfunction.},
journal = {Biomolecules},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/biom16030401},
pmid = {41897337},
issn = {2218-273X},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Inflammation/microbiology/metabolism ; *Heart Failure/microbiology/physiopathology/metabolism ; Animals ; Dysbiosis/microbiology ; Stroke Volume ; *Endothelium, Vascular/physiopathology ; },
abstract = {Heart failure with preserved ejection fraction (HFpEF) represents the predominant form of heart failure, affecting over 50% of all heart failure patients with increasing prevalence in aging populations. Despite significant advances in cardiovascular medicine, HFpEF remains a complex clinical syndrome with poorly understood pathophysiology and limited treatment options. While most studies have traditionally focused on the renin-angiotensin-aldosterone system (RAAS) and other related mechanisms, emerging evidence has unveiled a critical bidirectional relationship between dysregulation of gut microbiota and HFpEF development. This phenomenon, mediated through microbiome-driven inflammation and endothelial dysfunction, introduces a novel concept and potential emerging conceptual framework in understanding HFpEF. This comprehensive review explores this novel gut-heart axis by synthesizing the latest evidence from original studies and clinical trials. We discuss novel mechanisms involving bacterial metabolites, including short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO), bile acids, and amino acid derivatives. We also examine how gut dysbiosis may contribute to systemic inflammation through lipopolysaccharide translocation, NLRP3 inflammasome activation, and endothelial dysfunction. Furthermore, clinical trials investigating microbiome-targeted interventions, including probiotics, fecal microbiota transplantation, metabolite supplementation, and precision medicine approaches, are critically evaluated for their therapeutic potential. This review provides a framework for hypothesis generation and future research directions about therapeutic strategies targeting the gut-heart axis in HFpEF management.},
}

Humans
*Gastrointestinal Microbiome
*Inflammation/microbiology/metabolism
*Heart Failure/microbiology/physiopathology/metabolism
Animals
Dysbiosis/microbiology
Stroke Volume
*Endothelium, Vascular/physiopathology

@article {pmid41897363,
year = {2026},
author = {Nuncio, ASP and Motovilov, K and Weed, M and Shah, S and Bazzi, S and Idnani, E and Lime, T and Sauceda, DC and Mangieri, RA and Maguire, C and Melamed, E},
title = {High-Dose Ethanol-Induced Immunosuppression Modulates Sex-Specific Disease Outcomes in a Murine Model of Multiple Sclerosis.},
journal = {Biomolecules},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/biom16030427},
pmid = {41897363},
issn = {2218-273X},
support = {K08 T26-1616-11/AA/NIAAA NIH HHS/United States ; NA//Homer Lindsey Bruce & Fred Murphy Jones Endowed Fellowship/ ; F31 AA032720/AA/NIAAA NIH HHS/United States ; 5T32 DA018926-18/DA/NIDA NIH HHS/United States ; NA//The University of Texas at Austin Graduate Continuing Fellowship/ ; U01 AA016651/AA/NIAAA NIH HHS/United States ; T32 AA007471/AA/NIAAA NIH HHS/United States ; },
mesh = {Animals ; *Ethanol/pharmacology/administration & dosage ; Male ; *Encephalomyelitis, Autoimmune, Experimental/immunology/drug therapy/pathology ; Mice ; *Multiple Sclerosis/immunology/drug therapy/pathology ; Female ; Disease Models, Animal ; Gastrointestinal Microbiome/drug effects ; Mice, Inbred C57BL ; T-Lymphocytes/immunology/drug effects ; Immunosuppression Therapy ; },
abstract = {Both epidemiological studies and prior work in animal models suggest that moderate-dose alcohol reduces disease severity across several autoimmune conditions, including multiple sclerosis (MS). However, the mechanisms underlying the potentially beneficial effects of alcohol and how these effects may change with alcohol dose in autoimmunity remain underexplored. In this study, we characterize the effects of chronic, high-dose ethanol consumption in experimental autoimmune encephalomyelitis (EAE), a murine model of MS, by examining EAE disease severity, gut microbial composition, and peripheral cell immunophenotypes. We found that high-dose ethanol-fed males exhibited a significant amelioration in peak EAE disease severity, in association with decreased T cell activation and B cell proportions. Concurrently, we observed proinflammatory shifts in gut microbiota and hepatic lipid accumulation. Our results suggest that high dose ethanol may benefit autoimmune neuroinflammation in EAE through immunosuppressive effects on adaptive immunity, however its toxic systemic effects preclude the use of alcohol as an immunomodulator in MS. Overall, our findings reveal a mechanistic basis for alcohol's beneficial properties in autoimmunity and could inform the development of more targeted disease modifying therapies that recapitulate these benefits without alcohol-associated toxicity.},
}

Animals
*Ethanol/pharmacology/administration & dosage
Male
*Encephalomyelitis, Autoimmune, Experimental/immunology/drug therapy/pathology
Mice
*Multiple Sclerosis/immunology/drug therapy/pathology
Female
Disease Models, Animal
Gastrointestinal Microbiome/drug effects
Mice, Inbred C57BL
T-Lymphocytes/immunology/drug effects
Immunosuppression Therapy

@article {pmid41897366,
year = {2026},
author = {van Steensel, MAM},
title = {The Evolving Microbial Paradigm in Acne.},
journal = {Biomolecules},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/biom16030430},
pmid = {41897366},
issn = {2218-273X},
support = {nil//ArrowBiome pte ltd/ ; },
mesh = {*Acne Vulgaris/microbiology/drug therapy/pathology ; Humans ; *Propionibacterium acnes/pathogenicity/drug effects ; Anti-Bacterial Agents/therapeutic use/pharmacology ; Sebum/metabolism ; Biofilms/drug effects/growth & development ; },
abstract = {This review discusses the microbiology of acne vulgaris, a chronic inflammatory condition of the pilosebaceous unit that affects most adolescents and can persist into adulthood. The current standard of care consists largely of antibacterial interventions, based on the traditional view of Cutibacterium acnes as a pathogen. Alternative treatments are suggested by the "comedo switch" hypothesis, which attributes acne to aberrant differentiation of LRIG1+ sebaceous progenitor cells. While there is strong evidence to support this idea, it does not explain the efficacy of antibacterial interventions. We propose a unified mechanism wherein C. acnes phylotype IA1 can act as a trigger for the comedo switch. Unlike commensal strains, phylotype IA1 has high lipase activity, hydrolyzing sebum triglycerides into free fatty acids, specifically palmitic acid. This metabolite stimulates LRIG1+ progenitors, inducing inflammation and initial comedo formation. The review discusses C. acnes phylotypes, emphasizing known virulence factors of IA1, such as enhanced biofilm formation. We evaluate the efficacy and limitations of both old and new antibacterials, noting how newer materials that selectively remove C. acnes IA1 can reduce non-inflammatory acne lesions, supporting a key role for this phylotype in the pathogenesis of acne.},
}

*Acne Vulgaris/microbiology/drug therapy/pathology
Humans
*Propionibacterium acnes/pathogenicity/drug effects
Anti-Bacterial Agents/therapeutic use/pharmacology
Sebum/metabolism
Biofilms/drug effects/growth & development

@article {pmid41897395,
year = {2026},
author = {Micke, B and Novotny, J},
title = {Longitudinal Analysis of Rat Gut Microbiome Composition and Fecal Metabolism Markers Following Prolonged Morphine Exposure.},
journal = {Biomolecules},
volume = {16},
number = {3},
pages = {},
doi = {10.3390/biom16030460},
pmid = {41897395},
issn = {2218-273X},
support = {SVV-260790//Charles University/ ; },
mesh = {Animals ; *Morphine/pharmacology/administration & dosage ; *Gastrointestinal Microbiome/drug effects ; *Feces/microbiology/chemistry ; Rats ; Rats, Wistar ; Male ; Metabolome/drug effects ; RNA, Ribosomal, 16S/genetics ; Metabolomics ; Fatty Acids, Volatile/metabolism ; Biomarkers/metabolism ; Bacteria/genetics/classification ; Longitudinal Studies ; },
abstract = {This study investigated temporal group-level changes in gut microbiome composition and fecal metabolic markers in Wistar rats following a 10-day administration of morphine. Fecal samples were collected at predefined post-discontinuation time points and analyzed using 16S rRNA gene sequencing and GC×GC-TOF/MS-based metabolomics, with a focus on short-chain fatty acids (SCFAs). Morphine exposure was associated with transient alterations in gut microbiome structure at early post-treatment time points, including changes in alpha diversity and shifts in the relative abundance of major bacterial taxa. Unsupervised multivariate analysis of fecal metabolomic profiles revealed substantial inter-individual variability without persistent global separation between control and morphine-treated groups. Targeted analysis identified transient reductions in the relative signal intensities of selected SCFAs shortly after morphine withdrawal, while no significant differences were observed at later time points. These findings suggest that morphine-associated perturbations of the gut microbiome and fecal metabolome are predominantly time-dependent and tend to diminish during extended post-discontinuation phases.},
}

Animals
*Morphine/pharmacology/administration & dosage
*Gastrointestinal Microbiome/drug effects
*Feces/microbiology/chemistry
Rats
Rats, Wistar
Male
Metabolome/drug effects
RNA, Ribosomal, 16S/genetics
Metabolomics
Fatty Acids, Volatile/metabolism
Biomarkers/metabolism
Bacteria/genetics/classification
Longitudinal Studies

@article {pmid41897480,
year = {2026},
author = {Jang, NY and Jaiswal, V and Park, M and Lee, HJ},
title = {Immune-Enhancement Effects of 6-Methoxykaempferol on Cyclophosphamide-Induced Immunosuppression via Improving Antioxidant Enzyme Expression, NF-κB and MAPK Signaling, and Modulating Gut Microbiome.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {3},
pages = {},
doi = {10.3390/antiox15030334},
pmid = {41897480},
issn = {2076-3921},
support = {Project No. RS-2022-RD010230//Cooperative Research Program for Agriculture, Science and Technology Development of the Rural Development Administration, Republic of Korea./ ; },
abstract = {The immune system maintains homeostasis through coordinated innate and adaptive responses, and its imbalance increases disease susceptibility. The immunomodulatory effects of 6-methoxykaempferol (6MK), a methoxylated flavonoid found in sweet cherries, were studied in a mouse model of cyclophosphamide (CPA)-induced immunosuppression. The expression of key signaling proteins in the NF-κB and MAPK pathways was studied to explore the underlying molecular mechanisms. The Toll-like receptor-4/myeloid differentiation factor-2 receptor complex (TLR4/MD2), which can stimulate the immune response by activating these pathways, was used to study possible interactions with 6MK using docking analysis. 6MK administration significantly restored immune organ integrity (spleen up to 15.1% and thymus up to 16.8%), enhanced NK cell function (up to 43.8%), promoted T (up to 24.5%) and B cell proliferation (up to 26.4%), increased pro- and anti-inflammatory cytokine (IL-1β, IL-6, TNF-α, IL-4, IL-10, and TGF-β) levels, and elevated NO (up to 25.6%) and immunoglobulin (IgG, IgA, and IgM) concentrations. Additionally, 6MK upregulated antioxidant enzymes (CAT, HO-1, and SOD) and reactivated suppressed NF-κB and MAPK pathways. The docking-supported hypothesis, based on putative interactions and the estimated free energy of binding, suggests that 6MK possesses agonistic potential for the TLR4/MD2. Changes in the gut microbiome due to 6MK treatment, such as an increase in alpha diversity, abundance of Dorea longicatena, and the upregulation of formaldehyde-consuming pathways, may also contribute to immune enhancement. These findings show that 6MK may alleviate immunosuppression, suggesting its potential for future studies targeting immune-related diseases and conditions.},
}

@article {pmid41897542,
year = {2026},
author = {Ferreira, IM and Martins, SA and Gonçalves, L and Jesus, M and Brandão, E and Soares, S},
title = {Beyond Sensory Properties: Molecular Interactions of Antioxidant Flavour-Active Polyphenols Across the Food-Oral-Gut Axis.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {15},
number = {3},
pages = {},
doi = {10.3390/antiox15030397},
pmid = {41897542},
issn = {2076-3921},
support = {GA 101040462/ERC_/European Research Council/International ; CA22161//European Cooperation in Science and Technology/ ; project UID/50006/2025//Laboratório Associado para a Química Verde/ ; CEECIND/01598/2018//Fundação para a Ciência e Tecnologia/ ; 2023.00959.BD//Fundação para a Ciência e Tecnologia/ ; COMPETE2030-FEDER-00914400 (project 15462)//Fundação para a Ciência e Tecnologia/ ; },
abstract = {Dietary antioxidants are widely valued for their potential health benefits, but incorporating them into functional foods is not straightforward. Polyphenols are among the most abundant and important antioxidants in foods, and this review focuses on them because the same structural features linked to their health-promoting effects can also cause pronounced bitterness and astringency, ultimately limiting consumer acceptance. This review examines how these challenges are interconnected across three levels: food matrix interactions, bioavailability, and consumer psychobiology. We describe how non-covalent interactions between polyphenols, proteins, and polysaccharides can have both positive and negative effects. While these interactions may alter oral lubrication and flavour release, they also protect highly reactive bioactive compounds from gastric degradation. Furthermore, we broaden the concept of bioavailability by exploring the microbiota-mediated "colonic rescue" of polyphenols that are not released during earlier digestion. We also highlight the role of extraoral bitter taste receptors (TAS2Rs) along the gastrointestinal (GI) tract. Activation of these receptors during digestion can trigger relevant metabolic and endocrine responses, indicating that systemic absorption is not the only pathway to bioactivity. Finally, we connect these mechanisms to individual differences in food acceptance, showing that genetic factors (e.g., TAS2R38 and the salivary proteome) and psychological traits (such as neophobia and reward sensitivity) can shape rejection or flavour-nutrient learning. Overall, the successful development of functional foods will require a "sensory-by-design" approach. This strategy utilises matrix interactions strategically to improve both consumer acceptance and physiological efficacy.},
}

@article {pmid41897732,
year = {2026},
author = {Lee, H and Na, W and Sohn, C},
title = {Comparative Microbiome Profiles of Korean Fermented Foods Based on Production Type and Additive Use.},
journal = {Foods (Basel, Switzerland)},
volume = {15},
number = {6},
pages = {},
doi = {10.3390/foods15061010},
pmid = {41897732},
issn = {2304-8158},
support = {NRF-RS-2024-00463020//National Research Foundation of Korea/ ; },
abstract = {Fermented foods are produced through controlled microbial activity and are valued for their extended shelf life, sensory attributes, and potential health benefits. This study examined the effects of production methods on microbial ecology by comparing microbial community structure, Shannon diversity, and pH changes in traditional and commercially produced Korean fermented foods. Cabbage and radish kimchi were fermented for four weeks to assess microbial succession and physicochemical changes, and additional fermented foods, including soy sauce, soybean paste, pepper paste, fruit vinegar, yogurt, and aged kimchi, were compared according to production method. Microbial communities were analyzed using amplicon sequencing targeting the V3-V4 regions of the bacterial 16S rRNA gene and the fungal internal transcribed spacer (ITS) region. Traditionally produced cabbage kimchi exhibited high microbial diversity at the early fermentation stage, initially dominated by Weissella and Leuconostoc, followed by a gradual shift toward lactic acid bacteria dominance at later stages. In contrast, commercially produced cabbage kimchi maintained a simplified microbial community dominated by a limited number of lactic acid bacteria throughout fermentation. Radish kimchi showed production-method-dependent patterns, with the rapid dominance of lactic acid bacteria during traditional fermentation and partial recovery of microbial diversity during commercial fermentation. Shannon diversity was consistently higher in traditionally produced kimchi during fermentation. In contrast, commercially produced kimchi exhibited more rapid acidification. Across other fermented foods, traditionally produced soy-based products exhibited complex microbial communities dominated by Bacillus spp., whereas commercially produced products were characterized by yeast-dominant profiles. Fruit vinegar and yogurt showed low microbial diversity regardless of the production method. These findings demonstrate the importance of production strategies in shaping microbial ecology, fermentation dynamics, and resulting product characteristics across various Korean fermented foods.},
}

@article {pmid41897851,
year = {2026},
author = {Fragomeni, B and Hird, SM and Zezeski, AL and Geary, TW and McCoski, SR and Hay, EH},
title = {Vaginal Microbiome Is Associated with Breed and Pregnancy Status in Beef Cattle.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/ani16060874},
pmid = {41897851},
issn = {2076-2615},
support = {3030-31000-019-000D//USDA-ARS CRIS/ ; },
abstract = {Reproductive performance is a key determinant of overall livestock productivity. In both beef and dairy systems, reproductive failure represents a leading cause of cow culling. Reproductive traits are complex in nature and present a low heritability in general. Additionally, the collection of such phenotypes usually relies on indirect measures of fertility, such as conception success. Therefore, further investigation into genetic and non-genetic factors of reproductive traits in cattle is necessary. The hosts' microbiome plays a crucial role in vertebrate biology, including reproduction. We, therefore, hypothesize that microbiome indicators may serve as a biomarker of fertility. This study explored the relationship between vaginal microbiome profiles and pregnancy among three beef cattle genetic groups using field data. Vaginal swabs were collected from 74 cows at Fort Keogh, MT, including 23 Angus, 23 Hereford Line 1, and 28 crossbreds, and DNA was extracted and analyzed via 16S rRNA gene amplification. Significant differences in alpha diversity (p < 0.05) were found among Line 1 cows compared to Angus and crossbreds in many indicators of alpha diversity. Pregnancy status did not influence alpha diversity of samples significantly, but trends toward significance were observed. PERMANOVA analysis indicated that genetic groups and pregnancy status affected microbial composition (p < 0.05), but their interaction was not significant. Each genetic group showed unique compositions of operational taxonomic units (OTUs), with higher proportions of Ureaplasma and Mycoplasma families in Line 1. Additionally, variations in microbial communities were observed between pregnant and non-pregnant cows, with certain uncultured bacteria more prevalent in non-pregnant cows. While field data are useful for such studies and represent a real production system, better-designed experiments are necessary to validate findings and test hypotheses. These results suggest variation in vaginal microbiomes across breeds and pregnancy status, emphasizing the need for further research to identify factors affecting these changes.},
}

@article {pmid41897857,
year = {2026},
author = {Yang, Y and Wang, J and Wang, Z and Li, C and Hu, X and Liao, S and Wang, L},
title = {Airborne Microbiome of Tropical Ostrich Farms: Diversity, Antibiotic Resistance, and Biogeochemical Cycling Potential.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/ani16060880},
pmid = {41897857},
issn = {2076-2615},
support = {42367014//The National Natural Science Foundation of China/ ; },
abstract = {The expansion of tropical specialty livestock farming raises urgent concerns about airborne pathogen and antibiotic resistance dissemination. Ostrich farming, characterized by high-density stocking and feed exposure, yet their microbial ecology remain poorly characterized. This study analyzed 48 bioaerosols samples from an ostrich farm in Hainan, China, across dry and rainy seasons using 16S rRNA sequencing and metagenomics. The bacterial community were dominated by Firmicutes, Proteobacteria, and Actinobacteria, followed by Staphylococcus, Bacillus, and Acinetobacter as predominant genera, with particle size significantly shaping their structure. Large particles (>7.0 μm) carried higher species richness, while medium particles (2.1-3.3 μm) exhibited the highest diversity and evenness. Notably, small particles (0.65-1.1 μm), which can penetrate deep into the lungs, were enriched with Brevibacillus and Corynebacterium. Metagenomic analysis identified 638 antibiotic resistance genes (ARGs), dominated by efflux pump-associated determinants. The detection of clinically relevant ARGs (e.g., mcr-1 and blaTEM) reflects the genetic potential of the airborne resistome, rather than confirmed resistance phenotypes or active horizontal gene transfer. Functional analysis revealed a strong potential for organic matter degradation, driven by abundant carbohydrate-active enzymes (CAZymes) and their corresponding CAZyme genes, as well as a nitrogen cycle dominated by assimilation and reduction pathways, while genes for nitrogen fixation and nitrification were absent. Our findings demonstrate that ostrich farming enhanced airborne microbial diversity and functional potential, facilitating the ARG dissemination and nitrogen transformation. This study provides critical insights into the ecological and health risks of bioaerosols in tropical livestock farms, informing environmental monitoring and risk management strategies.},
}

@article {pmid41897872,
year = {2026},
author = {Yang, X and Liu, K and Yang, W and Jin, T and Li, J and Wang, Z and Li, F},
title = {Reciprocal Hybridization Between Herbivorous and Carnivorous Sub-Cold-Water Fish Reveals Divergent Intestinal Characteristics and Microbiome Assembly.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/ani16060895},
pmid = {41897872},
issn = {2076-2615},
support = {CSTB2023TIAD-KPX0023//Zhijian Wang/ ; },
abstract = {Hybridization is pivotal for germplasm innovation, yet how reciprocal crossing regulates digestive characteristics in sub-cold-water fish remains unclear. This study systematically compared differences in intestinal morphology, physiological function, and microbial community assembly among herbivorous Schizothorax prenanti, carnivorous S. davidi, and their reciprocal hybrids using histological analysis, digestive enzyme assays, and 16S rRNA sequencing. Results indicated that parental intestinal characteristics were highly consistent with their feeding habits. Orthogonal hybrids exhibited a mosaic phenotype, combining the maternal muscular gut structure with high paternal-like lipase activity, and were characterized by an enrichment of the potential probiotic Lactococcus. In contrast, reciprocal hybrids presented a mismatch between morphology and function: despite developed hindgut folds, key digestive enzyme activities were low, and the gut microbiota was dominated by environmental bacteria such as Methylobacterium. Our findings indicate a spatially dependent assembly dynamic: the host genetic background strongly drives microbiome divergence in the anterior segments (foregut and midgut), whereas the long-term administration of a standardized diet ultimately promotes structural convergence in the hindgut. The orthogonal cross yielded a phenotype characterized by an apparent co-occurrence of specific host enzymes and distinct microbiota, suggesting an inferred physiological potential for lipid digestion that requires further multi-omics validation. These findings provide preliminary insights into the associations between genetic background and intestinal traits, providing a theoretical basis for the targeted breeding of Schizothorax species.},
}

@article {pmid41897913,
year = {2026},
author = {An, Q and Chen, S and Ma, S and Bai, R and Lu, Z and Liu, Y and Wang, F and Wang, Q and Song, Y and Zhang, G and Lyu, Y and Wang, L and Wang, Y and Xia, Z},
title = {Shotgun Metagenomics Reveals Gut Microbiome Remodeling with Altered Taxonomic Composition and Functional Potential in Diabetic Dogs.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/ani16060936},
pmid = {41897913},
issn = {2076-2615},
support = {1051-2225006//General Program of the 2025 Talent Fund, Veterinary Teaching Hospital, China Agricultural University/ ; },
abstract = {Gut microbiota dysbiosis is implicated in metabolic disorders, yet taxonomic and functional alterations in canine diabetes remain incompletely defined. Here, we performed shotgun metagenomic sequencing of fecal samples from 38 diabetic dogs and 37 healthy controls under controlled conditions (no recent antibiotic/probiotic exposure and stable commercial diets). Alpha-diversity indices did not differ between groups, whereas beta-diversity revealed significant separation of community structure at both genus and species levels (p < 0.05). Linear discriminant analysis effect size (LEfSe) identified enrichment of opportunistic-associated taxa in diabetic dogs, including Enterobacterales/Enterobacteriaceae (e.g., Escherichia coli, Klebsiella pneumoniae, Salmonella enterica) and Enterococcus faecalis. In contrast, healthy dogs were enriched for putatively beneficial taxa linked to bile acid and short-chain fatty acid (SCFA) metabolism, including Turicibacter spp. and Romboutsia spp. Functional profiling showed higher abundances of pathways related to carbohydrate/energy metabolism, membrane transport, and virulence/colonization in diabetic dogs; 17 KEGG level-3 pathways and 320 KOs differed at FDR < 0.05, with enriched modules including bacterial secretion systems, lipopolysaccharide biosynthesis, chemotaxis/flagellar assembly, and biofilm formation. Collectively, canine diabetes is associated with a remodeled gut microbiome characterized by expansion of opportunistic pathogens and elevated virulence and metabolic potential, supporting exploration of microbiota-targeted strategies as a complement to conventional management.},
}

@article {pmid41897927,
year = {2026},
author = {Fukuda, EP and Lu, Y and Fowler, E and Jessup, RW and Drewery, ML},
title = {Metagenomic Insights into the Effects of Dietary Thymol on the Structure and Function of the Rumen Microbial Community in Beef Steers Consuming Forage.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/ani16060950},
pmid = {41897927},
issn = {2076-2615},
support = {2021-77040-34881//National Institute of Food and Agriculture/ ; 2020-38422-32250//National Institute of Food and Agriculture/ ; N/a//Translational Health Research Center/ ; },
abstract = {While essential oils are gaining momentum as a strategy to modulate rumen function and potentially reduce enteric methane in cattle, little is known about how their bioactive components, terpenes, affect rumen microbes. Our objective was to evaluate how in vivo doses of thymol affect the structure and function of the rumen microbial community via whole genome shotgun sequencing (WGS). Four beef steers were used in a 4 × 4 Latin square with four 28 d periods. Steers consumed ad libitum forage and received one of four thymol doses (0 [CON], 120 [120-T], 240 [240-T], and 480 [480-T] mg/kg forage intake). Rumen contents were separated into liquid and solid fractions, DNA was extracted, analyzed via WGS, and assessed with orthogonal contrasts. After FDR correction, no taxa were affected by thymol; however, raw p-values demonstrated responses to thymol supplementation for solid-associated uncultured Lachnospiraceae bacterium (p = 0.04), uncultured Methanobrevibacter (p = 0.05), and uncultured Coriobacteriaceae bacterium (p = 0.02). Liquid-associated uncultured Prevotellaceae bacterium (p = 0.03), Prevotella sp. (p = 0.04), and Bacteroides sp. (p = 0.02) also responded to thymol, with the highest abundances observed at various thymol doses. Genes involved in energy production and amino acid metabolism transport were observed at the highest abundances at 240-T, while genes associated with cell cycle control, cell division, and chromosome partitioning were present in the highest abundances at 120-T. The findings suggest that thymol exerts dose-dependent effects on rumen microbial abundances and functional pathways, with 240 mg/kg forage intake appearing to be the most effective dose to downregulate methanogenic enzymes while also enhancing the enzymes associated with metabolism without negatively impacting microbial diversity.},
}

@article {pmid41897949,
year = {2026},
author = {Wang, Z and Lin, Z and Lin, B and Peng, S and Xu, Y and Wang, X and Wu, H and Xie, B and Chen, B and Zhao, M and Lin, F and Sun, T and Li, Z},
title = {Composite Probiotic Fermented Feed Enhances Growth Performance and Intestinal Health in Weaned Piglets by Modulating the Gut Microbiome and Metabolome.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/ani16060972},
pmid = {41897949},
issn = {2076-2615},
support = {2023N0044//Fujian Provincial Agricultural Guidance (key) Project/ ; 2024S0033 and 2022S0027//Fujian Provincial Department of Science and Technology Spark Program/ ; },
abstract = {This study investigated the effects of compound microbial fermented feed on the growth performance, intestinal architecture, microbiota composition, and metabolic profiles of weaned piglets. Fifty-four weaned piglets were randomly allocated to three dietary treatment groups: a control group (basal diet), a 50% fermented feed group (T1), and a 100% fermented feed group (T2), for a 33-day feeding period. The results indicated that both T1 and T2 diets significantly improved final body weight and average daily gain (ADG), while decreasing the feed-to-gain ratio (F/G) compared with the control (p < 0.05). Morphological assessment revealed that the T1 group significantly elevated the villus height-to-crypt depth ratio in the jejunum and increased the density of goblet cells in the cecum and colon (p < 0.05). Multi-omics analysis indicated that fermented feed significantly reshaped the gut microbiota structure (p < 0.05), characterized by the enrichment of beneficial taxa, including Oscillospiraceae and Lachnospiraceae (p < 0.05), and the modulation of nucleotide and bile acid metabolism. Furthermore, correlation analysis identified significant linkages between the abundance of jejunal Oscillospiraceae and colonic/cecal Lactobacillus with growth performance, intestinal morphology, and key metabolites. This finding systematically elucidates the mechanisms by which compound microbial fermented feed promotes growth and intestinal health in weaned piglets via microbiota-mediated pathways, offering a robust scientific framework for the development of antibiotic-free nutritional strategies.},
}

@article {pmid41897953,
year = {2026},
author = {Fan, J and Xue, X and Zhang, H and Wang, F and Chao, Z and Wei, L and Liu, H and Ren, Y and Sun, R},
title = {Intestinal Development in Wuzhishan Pigs at Different Growth Phases: Insights from Microbiome and Metabolomics.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/ani16060976},
pmid = {41897953},
issn = {2076-2615},
support = {2021YFF0702804//The National Key R&D Program of China/ ; U22A20508//National Natural Science Foundation of China/ ; 202002011//The 2020 Research Program of Sanya Yazhou Bay Science and Technology City/ ; HNARS-02-Z01//Hainan Local Pig Agricultural Research System/ ; },
abstract = {Wuzhishan pigs are a typical Chinese indigenous miniature pig breed, with thin skin and high amino acid content in muscle; slow weight gain and long feeding phases limit their value. As the primary digestive and absorptive organ, the intestine is crucial for growth, yet current studies on its development are limited. This study aimed to investigate intestinal physiological differences in Wuzhishan pigs across four phases (pre-weaning: 7, 14 days; weaning: 35, 38, 45 days; fattening: 70, 100 days; maturity: 180, 240 days) by evaluating intestinal morphology, digestive enzyme activity, gut microbiota diversity via 16S rRNA gene sequencing, and metabolite characteristics via metabolomic analysis. Results showed poor intestinal morphology and enzyme activity during weaning, significant ileal and colonic microbial diversity differences across phases, increased beneficial bacteria with age, and enriched opportunistic pathogens (Streptococcus, Romboutsia, Terrisporobacter) during weaning; weaning also had lower lipid metabolites, correlated with decreased Fusobacterium, Lactobacillus, and Muribaculaceae. Fattening enhanced amino acid metabolism, with increased Lactobacillus correlated with higher amino acids and muscle-related metabolites, while maturity increased immune-related metabolites (e.g., pyridoxine) in the vitamin B6 pathway. These results explain delayed rapid weight gain in Wuzhishan pigs and provide a theoretical basis for maintaining intestinal stability and production performance.},
}

@article {pmid41897963,
year = {2026},
author = {Del Treste, A and Sacchettino, L and Costanza, D and Trapanese, L and Salzano, A and Napolitano, F and Cortese, L and d'Angelo, D and Campanile, G and Greco, A},
title = {Intestinal Dysbiosis Relating to Gut-Brain Axis and Behavior in Dogs: A Systematic Review with Text Mining Approach.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/ani16060986},
pmid = {41897963},
issn = {2076-2615},
abstract = {The intestinal microbiome plays a fundamental role in canine health and well-being, regulating functions, including digestion, immunity, metabolism, and behavior. Dysbiosis refers to the disruption of the balanced composition of resident commensal communities, and gut bacteria can influence behavior via neurological, metabolic, endocrine, and immune-mediated pathways. Growing evidence supports the existence of a bidirectional communication between the gut and the central nervous system, known as the gut-brain axis, through which intestinal microorganisms may influence behavior via neurological, metabolic, endocrine, and immune-mediated pathways. Despite the expanding interest in this field, the contribution of intestinal dysbiosis to the development and severity of behavioral and neurological disorders in companion dogs remains poorly understood. This review aims to critically analyze the literature from 2011 to 18 September 2025 concerning the association between dysbiosis, the gut-brain axis, and both gastrointestinal and non-gastrointestinal illnesses in dogs. To our knowledge, this review represents the first application of Text Mining (TM) in this domain: TM facilitates the identification and analysis of valuable information from extensive datasets, converting unstructured content into structured data, thereby enabling quantitative analysis. We used the following search terms on three bibliographic databases (PubMed, Scopus, and Web of Science): "dysbiosis" AND "canine" OR "dog" AND "gut-brain axis" AND "behavior". Of the 1176 records retrieved, 35 studies were checked following the PRISMA guidelines, and they met the predefined inclusion criteria in the final analysis.},
}

@article {pmid41898245,
year = {2026},
author = {Bernstein, C and Bernstein, H},
title = {The Causal Role of Bile Acids in Cancers of the Digestive System.},
journal = {Biomedicines},
volume = {14},
number = {3},
pages = {},
doi = {10.3390/biomedicines14030598},
pmid = {41898245},
issn = {2227-9059},
abstract = {Bile acids are widely distributed in the human gastrointestinal tract. A literature review indicates that bile acids may have a role in initiating cancers in every organ of the digestive system. The estimated number of new digestive system cancers world-wide in 2022 was about 5 million. In the particular case of colon cancer, secondary bile acids produced in response to a high fat diet disrupt colonic epithelial cell mitochondrial membranes. This disruption leads to the release of oxidative free radicals that damage DNA, potentially leading to carcinogenic mutations. High levels of colonic bile acids may also alter the gut microbiome, with some bacteria causing inflammation and increased reactive oxygen species leading to DNA damage. Also, bile acids taken up by receptors on the surface of gastrointestinal tract cells can activate NF-kB. In turn, NF-kB may activate a super-enhancer at an oncogene. Bile acid reflux also plays a significant role in esophageal adenocarcinoma, stomach cancer and small intestine carcinogenesis. In addition, cancers of the pancreas, liver, and biliary tract can be caused by the constriction of the common bile duct leading to reflux of bile acids back into these organs. Gastroesophageal reflux involving bile acids may also contribute to hypopharyngeal squamous cell carcinogenesis. Thus, bile acids are a likely major contributory cause of cancer throughout the digestive tract.},
}

@article {pmid41898284,
year = {2026},
author = {Rosas-Sánchez, GU and Germán-Ponciano, LJ and Pérez-Vega, MI and Gutiérrez-Coronado, O and Muñoz-Carrillo, JL and Soriano-Hernández, AD and Barrientos-Bonilla, AA and Rosales-Muñoz, CG and Soria-Fregozo, C},
title = {Probiotics as Modulators of Adult Neurogenesis and Synaptic Plasticity: New Perspectives in the Pathophysiology and Treatment of Affective Disorders.},
journal = {Biomedicines},
volume = {14},
number = {3},
pages = {},
doi = {10.3390/biomedicines14030637},
pmid = {41898284},
issn = {2227-9059},
abstract = {Affective disorders, such as major depressive disorder and anxiety disorders, represent a major global health burden, with current treatments proving inadequate for a substantial proportion of patients. Emerging research highlights the microbiota-gut-brain (MGB) axis as a crucial bidirectional communication system influencing brain function and neuroplasticity through neural, endocrine, immune, and metabolic pathways. This narrative review examines probiotics-live beneficial microorganisms-as modulators of adult neurogenesis and synaptic plasticity, two processes fundamentally implicated in the pathophysiology of affective disorders. Preclinical evidence demonstrates that specific strains, particularly from the Lactobacillus and Bifidobacterium genera, promote hippocampal neurogenesis and synaptic function through epigenetic regulation via short-chain fatty acids (SCFAs), notably butyrate-mediated histone deacetylase inhibition, modulation of neuroinflammatory pathways, regulation of neurotransmitter receptor expression across glutamatergic, GABAergic, and monoaminergic systems, and production of neuroactive peptides. Clinical evidence from randomized controlled trials and recent meta-analyses indicates that probiotic supplementation produces significant reductions in depressive and anxiety symptoms, with effects correlating to changes in gut microbiota composition and peripheral neuroplasticity biomarkers, particularly brain-derived neurotrophic factor (BDNF). However, significant methodological limitations persist, including small sample sizes, lack of standardization in probiotic strains and dosages, inconsistent outcome measures, and considerable interindividual variability. While the mechanistic and clinical evidence is biologically plausible and directionally promising, it is not yet sufficient to support definitive therapeutic recommendations. Future research must prioritize adequately powered clinical trials with standardized consortia, comprehensive multi-omics biomarker panels, and precision psychobiotic strategies guided by microbiome-defined patient stratification.},
}

@article {pmid41898327,
year = {2026},
author = {Belosic Halle, Z and Tomasic, V and Biscanin, A and Cacic, P and Saric, I and Mustapic, S and Stojic, J and Luetic, K and Bekic, D and Paic, M and Micetic, D and Krznaric Zrnic, I and Olic, I and Razov Radas, M and Skocilic, I and Golčic, M and Rados, L and Radic, J and Prejac, J and Mikolasevic, I},
title = {Immune-Mediated Colitis Induced by Immune Checkpoint Inhibitors: Pathophysiology, Clinical Management, and the Emerging Role of Fecal Microbiota Transplantation.},
journal = {Biomedicines},
volume = {14},
number = {3},
pages = {},
doi = {10.3390/biomedicines14030683},
pmid = {41898327},
issn = {2227-9059},
abstract = {BACKGROUND/OBJECTIVES: Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of various malignancies, but their use is frequently accompanied by immune-related adverse events, among which immune-mediated colitis (IMC) represents one of the most common and clinically significant gastrointestinal toxicities. IMC may lead to treatment interruption, increased morbidity, and compromised quality of life. This review aims to provide a comprehensive overview of the pathophysiology, risk factors, diagnosis, management, and emerging therapeutic strategies with particular emphasis on the role of the gut microbiota and fecal microbiota transplantation (FMT).

METHODS: This review integrates current international guidelines, meta-analyses, clinical trials, and recent translational studies addressing IMC. The available evidence on immunological mechanisms, predictive biomarkers, clinical presentation, diagnostic algorithms, and treatment options was critically synthesized to outline a structured and multidisciplinary management approach.

RESULTS: IMC is driven by dysregulated immune activation, cytokine release, and alterations in gut microbiota. Incidence and severity vary according to ICI class, combination regimens, tumor type, and patient-related factors. Diagnosis requires exclusion of infectious causes, laboratory assessment, and endoscopic and histologic evaluation with CTCAE-based severity grading. Corticosteroids remain the cornerstone of first-line therapy, while infliximab and vedolizumab are effective in steroid-refractory cases. Emerging therapies, including JAK inhibitors and FMT, have shown promising results in refractory disease.

CONCLUSIONS: IMC is a complex and potentially severe complication of ICI therapy that necessitates early recognition, accurate grading, and individualized, multidisciplinary management. Severity-guided treatment, timely escalation to biologics, and careful balancing of immunosuppression with antitumor efficacy are essential for optimal outcomes. Future research should focus on biomarker validation, microbiome-targeted therapies, and prospective trials to refine therapeutic algorithms and define the optimal role and timing of FMT in clinical practice.},
}

@article {pmid41898341,
year = {2026},
author = {Prince, Y and Davison, GM and Matsha, T and Raghubeer, S},
title = {The Role of Fusobacterium in Periodontal Disease and Its Implications for Cardiovascular Health.},
journal = {Biomedicines},
volume = {14},
number = {3},
pages = {},
doi = {10.3390/biomedicines14030697},
pmid = {41898341},
issn = {2227-9059},
support = {MRC-RFA-UFSP-01-2013/ VMH Study//South African Medical Research Council/ ; Grant number: 115450//National Research Foundation/ ; },
abstract = {Fusobacterium species, particularly Fusobacterium nucleatum, is known as a key adhesive bridging microorganism in the development of periodontal disease, inducing microbial imbalances and chronic inflammation within the oral cavity. Their role is to provide a bridge between both early colonisers (such as Streptococcus and Actinomyces) and late colonisers (such as Porphyromonas gingivalis and Treponema denticola), which results in multispecies biofilm formation. This triggers an immune reaction which may provide both a protective and destructive effect on the periodontal ligament and alveolar bone. Recent studies have discovered their significance beyond oral pathology. Therefore, Fusobacterium have been implicated in several systemic diseases, including cardiovascular disease (CVD). Virulent mechanisms, such as adhesion, invasion, modulation of host immunity, and pro-inflammatory signalling, contributes to periodontal tissue bone loss and entry into the circulation. Circulating bacteria interact with vascular endothelium and promote atherosclerotic plaque formation. The role of Fusobacterium nucleatum as a microbial link between periodontal disease and cardiovascular disease is highlighted and discussed. Overall, current evidence is mostly observational and preclinical, supporting an associative link between F. nucleatum-mediated periodontal disease and CVD. The literature highlights key mechanistic pathways while underscoring the important need for longitudinal studies to clarify causality and identify target therapeutic interventions.},
}