Scientific evidence validating spiritual beliefs for controlling pathogenic microbes in the Ganga river.

Da-Bu-Yin-Wan and Qian-Zheng-San regulate neuroinflammation and intestinal permeability through the microbiota-gut-brain axis in Parkinson's disease mice.

Effects of diet, dietary inflammatory index, modified antiinflammatory dietary intervention via diet management platform on short-term prognosis in patients with ulcerative colitis: A prospective study.

The global prevalence of metabolic dysfunction-associated steatohepatitis (MASH) is rising, driven by a complex interplay of metabolic disturbances, inflammation, and fibrosis, yet effective treatment options remain limited. This study examined the relationships among intestinal microbial dysbiosis, ammonia production, and hepatic CD8+ T cell activity in MASH, then assessed the therapeutic potential of DT-109, a glycine-based tripeptide. We investigated the gut/liver axis across human cohorts and both nonhuman primate and mouse MASH models. Multiomics approaches were used to characterize ileal microbiota, ammonia levels, and hepatic immune and metabolic pathways. Causality was verified through microbiota transplantation, C. perfringens NirA-knockout mutants, and functional validation in vitro and in vivo. The efficacy of DT-109 was evaluated in nonhuman primates and mice. Our results revealed a significant increase in the ammonia-producing gut bacterium C. perfringens, which led to elevated intestinal ammonia and disruption of the intestinal barrier in MASH. Elevated ammonia levels triggered FosB-mediated upregulation of CCL5 in CD8+ T cells, which in turn drove T cell cytotoxicity in the liver. Notably, DT-109 effectively lowered C. perfringens abundance, reduced intestinal ammonia, restored intestinal barrier integrity, and alleviated CD8+ T cell dysregulation in MASH. These results identify a distinct mechanism in which gut-derived ammonia drives CD8+ T cell-mediated MASH and demonstrate that DT-109 effectively targets this axis by inhibiting C. perfringens and reducing ammonia, ultimately ameliorating MASH.

The skin microbiome plays an important role in aging, yet most aging biomarkers predominantly focus on gut bacteria, overlooking the skin microbial communities, especially its fungal component. To comprehensively profile the skin bacterial and fungal microbiome across age, sex, and anatomical sites (sun-exposed forehead vs. non-sun-exposed back) and develop an integrated microbial model for age prediction. A total of 160 skin swabs from 80 healthy individuals stratified into four age groups (centered at 10, 30, 50, 70 years) were conducted by DNA sequencing for microbial analysis. An age-predictive model was built using a random forest classifier trained on bacterial and fungal composition data. We found clear age- and sex-specific differences in the skin microbiome. Fungal diversity was significantly higher in females, while bacterial diversity decreased markedly around age 30 in both sexes. Malassezia dominated fungal communities; its abundance peaked at 30 years, declining with age, especially on female foreheads. Age-dependent shifts occurred in dominant Malassezia species (e.g., M. globosa in children, M. arunalokei in the elderly). Bacterial communities shifted from diverse childhood profiles (e.g., Pseudomonas, Streptococcus) to Cutibacterium dominance in young adulthood, which declined in older individuals. Correlation analysis revealed stronger age-microbe associations in males. Finally, we developed a predictive model using four key microbial markers-Lactarius (fungus), Chryseobacterium, Gordonia, and Psychrobacter-that showed good performance in age-group classification (AUC = 0.97). Collectively, these findings reveal distinct age- and sex-related patterns in the skin microbiome, highlight the importance of including fungi in microbiome studies, and demonstrate the potential of microbial profiles as candidate age-associated signatures.

Neonatal jaundice (NJ) affects 60-80% of neonates, yet the underlying microbial mechanisms remain elucidated, despite known links between gut dysbiosis and bilirubin and bile acid (BA) metabolism. Through two-stage shotgun metagenomic-metabolomic analysis of 150 fecal samples from 120 neonates, we identified key taxa linked to bile acid (BA) metabolism in moderate-to-severe NJ. Furthermore, multi-omics integration revealed significant interkingdom correlations among gut phages, bacteria, and BAs. Dysbiosis featured enriched Streptococcus and Escherichia, depleted Bifidobacterium animalis, and group-specific phage signatures. In the independent clinical validation cohort, jaundice intervention normalized the dysbiotic profile, demonstrating significant suppression of pathogenic taxa concomitant with restoration of B. animalis abundance. In vitro, B. animalis subsp. lactis Y103-OTU5 remodeled BA via deconjugation. In a phenylhydrazine hydrochloride (PHZ)-induced murine model of hemolytic jaundice, oral administration of isolated B. animalis subsp. lactis Y103-OTU5 significantly attenuated hyperbilirubinemia and hepatic inflammation, likely via Cyp7a1/Cyp7b1-dependent modulation of BA synthesis and detoxification pathways. Structural equation modeling revealed a tripartite regulatory network: phages indirectly modulated BA through bacterial remodeling, while B. animalis directly regulated BA pathways, positioning it as a potential therapeutic candidate for hemolysis-associated neonatal jaundice. Collectively, these findings reveal a gut phage-bacteria-BA network in NJ, highlighting B. animalis as a therapeutic candidate with dual modulation of BA metabolism and phage-bacteria interactions.

Human Leukocyte Antigen (HLA) class-II genes, particularly HLA-DR2 and HLA-DR3, and the gut microbiota are intricately linked to the pathobiology of multiple sclerosis (MS) through their ability to regulate host immunity, a critical factor in disease pathogenesis. An imbalance between anti-inflammatory CD4+ Tregs and pro-inflammatory IL-17A-secreting CD4+ Th17 cells is thought to drive disease. However, a key unresolved question is whether HLA-class II-restricted CD4+IL-17A cells can influence Treg populations and the extent to which gut microbiota regulate this IL-17A-Treg axis. Therefore, we utilized humanized transgenic mice expressing the HLA class-II gene and deficient in mouse class-II molecules, where all CD4+ T cells are selected on the human HLA class-II molecule, closely mimicking human immune responses. Utilizing IL-17A-deficient (DR3.IL-17A-/-) mice expressing HLA-DR3 (HLA-DRβ1*0301), we show that IL-17A deficiency enriches beneficial gut bacteria, including Prevotella species, enhances peroxisome proliferator-activated receptor (PPAR) signaling, and increases FoxP3+ regulatory T (Treg) cells and IL-10 production. The importance of gut microbiota in promoting Tregs and anti-inflammatory responses was confirmed by administering Prevotella copri, a common commensal in human gut, which mirrored the effects observed in IL-17A-deficient mice by inducing PPAR signaling and Treg population. Moreover, DR3.IL-17A-/- mice exhibited a marked reduction in EAE severity compared to IL-17A-sufficient (DR3) mice, underscoring the enhanced functional capacity of the Treg population in mitigating disease progression. Cohousing experiments validated the role of gut microbiota in immune regulation including Treg induction, as demonstrated by the transfer of Prevotella species from IL-17A-deficient mice to IL-17A-sufficient mice, increased Treg populations and attenuated EAE severity in recipient DR3 mice. This study redefines IL-17A's role in immune regulation, emphasizing its ability to directly influence gut microbiota composition and the abundance of Treg-promoting bacteria. Thus, gut microbiota-targeted therapies, particularly those promoting Treg-inducing bacteria like Prevotella species, hold promise for treating autoimmune diseases by modulating host immune responses. Video Abstract.

Gut bacteria in insects play critical roles in host physiology, contributing to both beneficial and harmful functions. However, the functional role of gut bacteria in Tecia solanivora, a major pest of potato crops in Central and South America, remains poorly understood. This study provides the first genomic and functional characterization of bacteria isolated from the gut of T. solanivora, focusing on their contributions to host fitness and their potential applications in pest control. Seven bacterial strains were identified: Duffyella gerundensis Ts1, Enterobacter ludwigii Ts2, Serratia quinivorans Ts3, Duffyella sp. Ts4, Rahnella variigena ATs1, Rahnella variigena ATs2, and Stenotrophomonas sp. ATs4. Genomic analyses revealed genes implicated in digestion and nutrient acquisition (e.g., ribABCDE operon for riboflavin synthesis and the ISA gene for isoamylase synthesis), insecticide detoxification (e.g., nfsAB encoding nitroreductase), and protection against natural enemies (e.g., impABCEFGHJLM operon for type VI secretion system). Experimental validation confirmed the activity of key functions. Notably, E. ludwigii Ts2 and S. quinivorans Ts3 exhibited entomopathogenic activity against their host insect, causing larval mortality rates of 63.3% and 40.8%, respectively. Notably, R. variigena ATs1 and Rahnella variigena ATs2 demonstrated phytopathogenic activity against potato tubers (97% damage), identifying them as opportunistic pathogens. These findings advance understanding of insect-microbe interactions, identify promising candidates for biological pest control, and highlight the importance of comprehensive safety assessments in agricultural applications.

Bacterial swarming on a semi-solid agar surface is a prevalent form of collective motility. Our study focuses on probing the swarm front of a novel species of gut bacteria, Enterobacter sp. SM3, which manifests strong swarming behavior. By depositing a fluid drop on the edge of the swarm, a monolayer of swarming bacteria is observed in minutes. We image these swarming bacteria and segment/identify them with the aid of CellPose, a machine-learning-based software algorithm. To address the challenge of dense, highly motile populations where automated segmentation alone is insufficient, we implement a post-processing approach that leverages particle image velocimetry (PIV) in conjunction with intersection-over-union (IoU) mapping to propagate segmentation masks across consecutive frames. This approach corrects spurious split and merge events introduced by automated segmentation, integrates a scientist-in-the-loop framework for targeted refinement of cell identities, and improves downstream trajectory reconstruction using TrackMate within Fiji. Together, the integration of machine-learning-based segmentation with PIV-IoU post-processing enables robust tracking of individual bacteria in crowded environments, allowing comprehensive analysis of their individual trajectories and collective dynamics.

Treating a neurological disorder through the gut may seem counterintuitive, yet multiple lines of evidence highlight the gut's important role in Parkinson's disease (PD). Prodromal gastrointestinal symptoms, the presence of aggregated α-synuclein in enteric neurons, increased intestinal inflammation, and impaired epithelial barrier integrity all point to gut-level involvement in PD pathophysiology. The gut microbiome, markedly altered in individuals with PD, may be a key driver of these changes. Fecal microbiota transplantation (FMT) is currently the most effective strategy for achieving broad and durable modifications of gut microbiota composition. However, FMT is a complex, multi-step procedure requiring stringent methodological control. Modulating gut bacteria has demonstrated therapeutic potential in preclinical models of PD, and recent clinical trials have begun evaluating FMT in patients, although outcomes have been variable. In this review, we examine potential explanations for these divergent results, with a particular focus on methodological differences across trials. We also outline future directions for optimizing FMT study design in PD and discuss how these insights may guide the development of next-generation microbiota-targeted therapies.

Over the past few decades, the importance of the human gut microbiota has been cast into the limelight. A growing number of studies are attempting to detangle the complex functions of the gut microbiota for human health; however, one existing shortcoming is an incomplete understanding of the microbiota community composition. Up to 70% of bacteria colonizing the human gastrointestinal tract are estimated to lack complete genomic or functional characterization due to their low abundance within the gastrointestinal tract or challenge to culture. As traditional culture methods often favour fast-growing or easily cultured species, alternative strategies are needed to access the broader gut microbial diversity. Here, we propose a novel approach to improve the growth of difficult-to-culture gut bacteria through single-cell microencapsulation, which will allow for in vitro manipulation. This work provides evidence of high biocompatibility of four-arm poly(ethylene glycol) maleimide (PEG4MAL) for gastrointestinal microbial culture and significant anaerobic gut bacteria proliferation in PEG4MAL microbeads generated via microfluidics. Specifically, we varied the concentration of PEG4MAL and the presence of Arg-Gly-Asp peptide motifs to tune the mechanical properties and porosity of the microbeads, and examined their impact on bacterial viability, confluency, and colony formation.

Cobamides, including vitamin B12, are essential cofactors exchanged between organisms across diverse ecosystems including oceans, soils, and the mammalian gut. Although most organisms depend on cobamides only a minority of prokaryotes perform their metabolically costly biosynthesis. This has led to vitamin B12 uptake from the environment as a common acquisition strategy, but does not explain why B12 producers would allow B12 to become extracellularly available. Our work reconciles this inconsistency, showing that bacteriophages (phages) can facilitate the release of intracellular B12 at physiologically relevant concentrations. Phages are viruses that infect and often lyse their targeted bacteria, which may externalizes intracellular material along with progeny phages. In this work, we aimed to determine whether phage-mediated lysis promotes the externalization of vitamin B12, thereby supporting the growth of B12 dependent bacteria. To test this, we first used genetically well-defined B12-Producer and B12-User bacteria, and found that phage-mediated lysis of the producers releases sufficient B12 to support the growth of the users in co-culture. Next, we show that phage-mediated lysis of the B12-producer can similarly support the growth of various commensal gut bacteria that are also B12-dependent, in co-culture. B12 released by phage-mediated cell lysis induced significant compositional changes among the non-targeted bacteria including an increased diversity that was muted by supplementing B12 in the medium. Collectively, these findings suggest that phage-mediated bacterial lysis is a significant contributor to nutrient externalization in microbial communities, leading to broad compositional changes beyond their host range.

Gut bacteria that produce fatty acid ethanolamides alleviate diarrhea-predominant IBS with insulin resistance.

Retinoic acid-driven expansion of CD16hiCD177+ neutrophils mediates steroid-resistant GI-GVHD.

Acute effects of cadmium and zinc on crayfish (Procambarus clarkii): Insights from deep learning-based behavioral analysis and physiological assessments.

Hyperuricemia (HUA) is a growing global health concern with a younger onset trend. Using a high-purine diet-induced HUA mouse model, this study evaluated kidney, colon, and gut microbiota damage and investigated the effects of Psidium guajava basal postbiotics (PGP). PGP reduced xanthine oxidase activity, modulated purine metabolism, and increased beneficial gut bacteria (Akkermansia muciniphila) and short-chain fatty acids (acetate, butyrate, propionate). This led to decreased blood urea nitrogen, creatinine, and renal malondialdehyde, along with reduced inflammatory factors (IL-8, LPS). Consequently, PGP alleviated HUA and mitigated HUA-induced kidney and colonic damage. This study highlights the therapeutic potential of tropical postbiotics against HUA, offering a theoretical basis for dietary supplements in chronic disease prevention.

The oral microbiota, comprising bacteria, fungi, and viruses, plays a critical role in initiating food digestion, serving as the first defense against pathogenic invasion and maintaining oral homeostasis. In contrast, the gut microbiota, consisting of trillions of microorganisms, functions as a barrier protection, modulating the immune system and facilitating the absorption of nutrients. Although they have distinct anatomical locations, these ecosystems are highly interconnected and play a pivotal role in human health and disease. The most common routes of interaction between the oral and gut microbiota are the enteral, the hematogenous, and the immune cell migration routes. Many oral pathogens interact with intestinal microbes, activating the host's mechanisms that establish dysbiosis and pave the way for the development of various diseases, ranging from inflammatory bowel disease and colorectal cancer to metabolic and neurodegenerative disorders. In this review, we delineate the mechanisms underlying these ecosystems to offer novel insights into disease pathogenesis while also unveiling new avenues for preventive and therapeutic interventions. Although current therapeutic approaches include the administration of antibiotics, prebiotics, and probiotics, novel personalized therapeutic approaches have also emerged. Fecal microbiota transplantation (FMT), gut bacteria engineering, nanomedicine-based techniques, and the use of miRNA to foster microbiota balance in both compartments hold great promise and may prove critical for the prevention and management of systemic diseases.

Interaction of gut microbiota (GM) with dietary sugars (glucose, sorbitol) and choline has been transversely implicated in the pathogenesis of multiple chronic diseases. Our aim was to develop functional PET imaging of GM, using a multi-tracer approach to capture bacteria classes involved in sugar fermentation and choline catabolism at their gastrointestinal (GI) location. Adult and young sex-balanced groups of mice underwent oral administration of [18F]FDG, [18F]FDS or [11C]choline ([11C]cho) and repeated PET imaging over 4-5 h. Antibiotics, probiotic or faecal microbiota transplantation (FMT) served to quantify the specific role and site of bacteria action. GM was sequenced ex-vivo; gut histology and metabolic profiles were assessed in subsets. [18F]FDG and [18F]FDS reflected caecum abundance of Clostridia and Bacteroidia fermenters, with [18F]FDG exhibiting strongest and broadest relations. Clearance of [11C]cho from small gut reflected Bacilli and Lactobacilli abundance. In vitro cultures supported these relationships. Urinary 11C-excretion was nearly abolished by antibiotics. PET imaging was able to differentiate and predict gut bacteria classes in mice receiving FMT from two age-extreme human donors. Urinary [18F]FDS excretion reflected small-gut goblet cell activation; high caecum [18F]FDG retention and small gut [11C]cho clearance predicted body glucose use and low systemic inflammation. Imaging of ingested probes is simple and effective to map GM characteristics in situ and the functional crosstalk with host processes in mice in real-time. Our data confirm that the GI ecosystem is highly diversified, pointing to small intestine and caecum GM as dominant players in gut-body handling of our target nutrients.

The macronutrients in our diets including non-starch polysaccharides such as β-mannans, found in plant cell walls, can impact on human gut health. There is however a paucity of data regarding the ability of gut bacteria, in particular those belonging to the Bacillota (previously Firmicutes) phylum, to depolymerise and ferment β-mannans. In this study, we tested a total of 12 strains, including nine Bacillota, for their ability to metabolise and cross-feed on β-mannans. Three of the six butyrate-producing Bacillota strains, namely Roseburia intestinalis L1-82, Roseburia faecis M72/1, and Coprococcus eutactus ART55/1, were able to metabolise carob galactomannan, konjac glucomannan, and softwood spruce acetylated galactoglucomannan, which corresponded with their carbohydrate active enzyme profiles, whilst Faecalibacterium prausnitzii S3L/3 only grew well on β-mannan endo-mannanase digests. To investigate competition and microbial cross-feeding on β-mannans, growth assays were conducted with co-cultures of up to six strains belonging to both the Bacillota phylum and a Bacteroidetes β-mannan utilising strain, Bacteroides ovatus V975. All strains in the mixes were able to co-exist, including the non-mannan degrading butyrate producers, with butyrate being formed as one of the major fermentation products. These studies suggest that β-mannans may offer a notable prebiotic approach to promoting butyrate-producing bacteria and gut health.

Toll-like receptor 5 protects against nonsteroidal anti-inflammatory drug-induced enteropathy in mice.