Excessive intake of dietary fats is strongly associated with an increased risk of various chronic diseases, such as obesity, diabetes, hepatic metabolic disorders, cardiovascular disease, chronic intestinal inflammation, and certain cancers. A significant portion of the adverse effects of high-fat diet on disease risk is mediated through modifications in the gut microbiota. Specifically, high-fat diets are linked to reduced microbial diversity, an overgrowth of gram-negative bacteria, an elevated Firmicutes-to-Bacteroidetes ratio, and alterations at various taxonomic levels. These microbial alterations influence the intestinal metabolism of small molecules, which subsequently increases intestinal permeability, exacerbates inflammatory responses, disrupts metabolic functions, and impairs signal transduction pathways in the host. Consequently, diet-induced changes in the gut microbiota play a crucial role in the initiation and progression of chronic diseases. This review explores the relationship between high-fat diets and gut microbiota, highlighting their roles and underlying mechanisms in the development of chronic metabolic diseases. Additionally, we propose probiotic interventions may serve as a promising adjunctive therapy to counteract the negative effects of high-fat diet-induced alterations in gut microbiota composition.

Dysbiosis of gut microbiota is well established in coronavirus disease 2019 (COVID-19). While studies have attempted to establish a link between the gut commensal Akkermansia muciniphila (A. muciniphila) and COVID-19, the findings have been inconsistent and sometimes controversial. The intestinal microbial abundance information of COVID-19 patients was acquired and analysed from GMrepo database. Subsequently, A. muciniphila's metabolites, target-genes, and metabolite-target relationships was extracted from GutMGene database. Lastly, coronascape module in Metascape database is used for gene annotation and enrichment analysis in various host cells and tissues after SARS-CoV-2 infection. The results indicated that, in comparison to healthy people, A. muciniphila was significantly elevated in COVID-19 patients. This bacterium was found to be associated with heightened expression of IL-10, TLR2, TLR4, CLGN, CLDN4, TJP2, and TJP3, while concurrently experiencing a reduction in the expression of IL-12A and IL-12B in humans. The regulatory genes of A. muciniphila primarily enhance responses to viruses and cytokines, positively regulate cell migration, and control epithelial cell proliferation. Our study revealed a significant increase in the gut commensal A. muciniphila in COVID-19 patients. This bacterium can modulate host immune responses and may also serve as a probiotic with antiviral properties.

Following ingestion via contaminated food, Listeria monocytogenes faces multiple hurdles through the human digestive system, thereby influencing its capacity to cause infection. This review provides a comprehensive overview of the multifaceted mechanisms employed by L. monocytogenes to overcome gastrointestinal hurdles and interact with the host's microbiota, facing chemical and physical barriers such as saliva, stomach acidity, bile salts and mechanical clearance. Proposed evasion strategies will be highlighted, exploring the bacteriocins produced by L. monocytogenes, such as the well-described bacteriocin Listeriolysin S (LLS), a bacteriocin that inhibits inflammogenic species - Lmo2776, and a phage tail-like bacteriocin, monocin. The competitive dynamic interactions within the gut microbiota, as well as the modulation of microbiota composition and immune responses, will also be explored. Finally, the adhesion and invasion of the intestinal epithelium by L. monocytogenes is described, exploring the mechanism of pathogenesis, biofilm and aggregation capacities and other virulence factors. Unlike previous reviews that may focus on individual aspects of L. monocytogenes pathogenicity, this review offers a holistic perspective on the bacterium's ability to persist and cause infection, integrating information about survival strategies, including bacteriocin production, immune modulation, and virulence factors. By connecting recent findings on microbial interactions and infection dynamics, this review incorporates recent developments in the field and connects various lines of research that explore both host and microbial factors influencing infection outcomes.

Inflammatory bowel disease (IBD) is a chronic and relapsing immune-mediated disorder characterized by intestinal inflammation and epithelial injury. The underlying causes of IBD are not fully understood, but genetic factors have been implicated in genome-wide association studies, including CTLA-4, an essential negative regulator of T cell activation. However, establishing a direct link between CTLA-4 and IBD has been challenging due to the early lethality of CTLA-4 knockout mice. In this study, we identified zebrafish Ctla-4 homolog and investigated its role in maintaining intestinal immune homeostasis by generating a Ctla-4-deficient (ctla-4-/-) zebrafish line. These mutant zebrafish exhibited reduced weight, along with impaired epithelial barrier integrity and lymphocytic infiltration in their intestines. Transcriptomics analysis revealed upregulation of inflammation-related genes, disturbing immune system homeostasis. Moreover, single-cell RNA-sequencing analysis indicated increased Th2 cells and interleukin 13 expression, along with decreased innate lymphoid cells and upregulated proinflammatory cytokines. Additionally, Ctla-4-deficient zebrafish exhibited reduced diversity and an altered composition of the intestinal microbiota. All these phenotypes closely resemble those found in mammalian IBD. Lastly, supplementation with Ctla-4-Ig successfully alleviated intestinal inflammation in these mutants. Altogether, our findings demonstrate the pivotal role of Ctla-4 in maintaining intestinal homeostasis. Additionally, they offer substantial evidence linking CTLA-4 to IBD and establish a novel zebrafish model for investigating both the pathogenesis and potential treatments.

Astaxanthin (ASX) gains wide interest in food and nutritional sciences due to its great antioxidant and anti-inflammatory properties. However, ASX faces challenges such as poor water solubility, low bioavailability, and sensitivity to environmental factors. In this study, we employ Akkermansia muciniphila (AKK) with mucoadhesive property as a carrier for ASX to enhance ASX stability and bioaccessibility. The complex multilayered cell envelope of AKK cell provided space for ASX loading. Immersion loading yielded the highest ASX encapsulation efficiency (10.80 ± 2.29 μg/mg in ASX@AKK group and 11.47 ± 3.52 μg/mg in ASX@AKK-Heat group), whereas osmoporation loading and vacuum loading yielded ASX encapsulation efficiencies of 4-6 μg/mg. The encapsulated ASX demonstrated improved thermostability, tolerating pasteurization, and was predominantly amorphous in state, interacting with AKK primarily through hydrophobic interactions and partial hydrogen bonding interactions. The ASX@AKK system facilitated precise ASX release in the intestine and markedly enhanced bioaccessibility, increasing approximately 25.7-fold in simulated intestinal fluid and 77.6-fold in simulated colonic fluid. Importantly, ASX encapsulation did not impair AKK's adhesive affinity to mucus. Therefore, the newly developed integrated dietary supplements have both the functional activity of inactivated AKK as a postbiotic and the antioxidant property of the intestine-targeted released ASX, showing dual-functional activities. These findings highlight a paradigm shift in the functional application of probiotics, showcasing their potential as innovative vehicles for targeted nutrient delivery with improved bioaccessibility and synergistic health effects.

The gut microbiota-derived protein Amuc_1100, a key outer membrane component of Akkermansia muciniphila, has emerged as a groundbreaking therapeutic agent with unique structural and functional properties. Amuc_1100 exerts multifaceted immune-metabolic effects through novel mechanisms, including modulation of TLR2/4 and JAK/STAT pathways. This review highlights its unique multi-component structure that enables synergistic biological activity, and its pharmacological properties, which underlies its ability to enhance intestinal barrier integrity, restore microbiota balance, and suppress systemic inflammation. Crucially, Amuc_1100 demonstrates unprecedented therapeutic versatility across both intestinal disorders (e.g., inflammatory bowel disease, antibiotic-associated diarrhea) and extraintestinal conditions-notably improving neuropsychiatric symptoms via gut-serotonin axis regulation, combating cancer through CD8+ T cell activation, and mitigating cardiotoxicity via gut-heart immune crosstalk. Emerging innovations in targeted delivery systems, including gut-retentive nano-formulations and engineered probiotic vectors, further amplify its clinical potential. We critically evaluate recent advances distinguishing Amuc_1100's mechanisms from live bacterial interventions. By synthesizing evidence from preclinical models, this work positions Amuc_1100 as a prototype for next-generation microbiome-derived therapeutics, bridging microbial ecology with precision medicine.

Polysaccharides are one of the primary active components of Radix Hedysari, although their regulatory effects on gut microbiota remain poorly understood. In this study, Radix Hedysari polysaccharides (RHPS) were isolated and purified, yielding three fractions: RHPS-1, RHPS-2, and RHPS-4. The yields of these fractions were 51.33 %, 3.15 %, and 2.34 %, respectively, with weight-average molecular weights of 18.781, 25.660, and 100.149 kDa. The three polysaccharides were composed of arabinose, galactose, glucose, glucuronic acid. RHPS-1 exhibits good antioxidant, antibacterial, and immune-enhancing activities. Further purification of RHPS-1 yielded RHPS-1-1, and it was found that RHPS-1-1 enhances the growth of beneficial bacteria while suppressing the growth of harmful bacteria in mice. Additionally, mice treated with RHPS-1-1 were primarily involved in bile acid, short-chain fatty acid, and energy metabolism pathways. Our results represent the first demonstration that RHPS-1-1 exhibits good biological activity and possesses the ability to regulate the gut microbiota and its metabolites in mice.

Research has established links between the gut microbiome (GM) and both obesity and type 2 diabetes (T2D), which is much discussed, but underexplored. This study employed body mass index (BMI) as the measurement of obesity to delve deeper into the correlations from a genetic perspective.

We performed the Mendelian randomization (MR) analysis to examine the causal effects of GM on T2D and BMI, and vice versa. Genome-wide association study (GWAS) summary datasets were utilized for the analysis, including T2D (N = 933,970), BMI (N = 806,834), and two GM datasets from the international consortium MiBioGen (211 taxa, N = 18,340) and the Dutch Microbiome Project (DMP) (207 taxa, N = 7,738). These datasets mainly cover European populations, with additional cohorts from Asia and other regions. To further explore the potential mediating role of GM in the connections between BMI and T2D, their interaction patterns were summarized into a network.

MR analysis identified 9 taxa that showed protective properties against T2D. Seven species were within the Firmicutes and Bacteroidales phyla in the DMP, and two were from the MiBioGen (Odds Ratio (OR): 0.94-0.95). Conversely, genetic components contributing to the abundance of 12 taxa were associated with increased risks of T2D (OR: 1.04-1.12). Furthermore, T2D may elevate the abundance of seven taxa (OR: 1.03-1.08) and reduce the abundance of six taxa (OR: 0.93-0.97). In the analysis of the influence of the genetic component of BMI on GM composition, BMI affected 52 bacterial taxa, with 28 decreasing (OR: 0.75-0.92) and 24 increasing (OR: 1.08-1.27). Besides, abundances of 25 taxa were negatively correlated with BMI (OR: 0.95-0.99), while positive correlations were detected for 14 taxa (OR: 1.01-1.05). Notably, we uncovered 11 taxa genetically associated with both BMI and T2D, which formed an interactive network.

Our findings provide evidence for the GM-mediated links between obesity and T2D. The identification of relevant GM taxa offers valuable insights into the potential role of the microbiome in these diseases.

Akkermansia muciniphila (A. muciniphila) is an emerging probiotic with potential impact on human health, and there is a growing interest in this area, but an overall analysis of research trends is lacking. This study conducted a detailed bibliometric analysis and visualization of A. muciniphila research to examine the current research status, hotspots, and trends, aiming to inform future research directions.

This study utilized the Web of Science database to search research on A. muciniphila from 2010 to 2024. Bibliometric analysis was conducted using CiteSpace and VOSviewer software to generate yearly publication trends, contributions by countries, institutions, and distinguished researchers, as well as key themes and influential researches. This analysis aimed to visualize and explore the literature over the past 15 years, guiding future researches and identifying gaps in the field of intestinal flora in A. muciniphila.

We searched a total of 4,423 related publications. Wei Chen, Willem de Vos and Patrice D. Cani are the primary contributors to A. muciniphila 's research. The top contributing countries and institutions are China, the United States, South Korea, Spain, and Italy, with research centers such as the Chinese Academy of Sciences, Zhejiang University, the University of Copenhagen, and the University of Helsinki being the main contributors. Current research hotspots focus on the molecular biology of A. muciniphila, such as its role in intestinal barrier maintenance, immune response, and its potential for regulating and treating digestive and metabolic diseases, such as cancer, fatty liver disease, inflammatory bowel disease, etc., through bile acid metabolism, extracellular vesicles, and insulin resistance.

Our study synthesizes current research on A. muciniphila in various disease areas and suggests enhancing collaboration among countries, institutions, and authors to advance A. muciniphila-related clinical and basic research, explore its efficacy in a variety of diseases and the effects of commonly used clinical medications on A. muciniphila, to fill the research gaps in the current field, and to provide valid evidence for the development of A. muciniphila as a novel probiotic supplement.

Shengjiang Xiexin Decoction (SJXXD) is a recognized formulation in traditional Chinese medicine that is commonly employed in diarrhea treatment. It has the potential to be a viable alternative for treating ulcerative colitis (UC), but its therapeutic effects and mechanisms remain unclear.

This study aims to explore the effects and underlying mechanism of SJXXD in a mouse model of UC induced by dextran sulfate sodium (DSS).

The components of SJXXD were analyzed using HPLC-Q/TOF-MS. UC mice model was established by freely drinking of 3% DSS, and SJXXD was administered as an intervention. After 7 days, body weight change, diarrhea, blood stools, colon length, cytokine levels, and key barrier proteins were evaluated to assess the therapeutic effect of SJXXD on UC. Additionally, transcriptome sequencing, quantitative polymerase chain reaction (qPCR), western blotting, intestinal organoids, 16S rRNA sequencing, and heat correlation analysis were employed to investigate the potential mechanisms of SJXXD on treating UC.

SJXXD significantly inhibited weight loss, reduce diarrhea and bloody stools, lower disease activity index (DAI) score, suppressed inflammatory cell infiltration and cytokines secretion in colonic tissues in UC mice. Additionally, SJXXD also enhances the expression of tight junction and mucins. Transcriptome sequencing results indicate that SJXXD primarily activates the Wnt/β-Catenin pathway, thereby enhancing the expression of genes linked to intestinal stem cells and intestinal regeneration markers. At phylum level, SJXXD significantly increases the relative abundance of Verrucomicrobiota, while inhibiting Campylobacterota and Fusobacteriota. Importantly, the relative abundance of these bacterial phyla is significantly correlated with UC and Wnt/β-Catenin signaling pathway.

These results indicate that SJXXD can significantly treat DSS-induced mouse UC model by activating the Wnt/β-Catenin pathway and modulating intestinal flora. SJXXD may serve as a promising therapeutic approach for the management of UC.

Ischemic stroke (IS) is a cerebrovascular disease that predominantly affects middle-aged and elderly populations, exhibiting high mortality and disability rates. At present, the incidence of IS is increasing annually, with a notable trend towards younger affected individuals. Recent discoveries concerning the "gut-brain axis" have established a connection between the gut and the brain. Numerous studies have revealed that intestinal microbes play a crucial role in the onset, progression, and outcomes of IS. They are involved in the entire pathophysiological process of IS through mechanisms such as chronic inflammation, neural regulation, and metabolic processes. Although numerous studies have explored the relationship between IS and intestinal microbiota, comprehensive analyses of specific microbiota is relatively scarce. Therefore, this paper provides an overview of the typical changes in gut microbiota following IS and investigates the role of specific microorganisms in this context. Additionally, it presents a comprehensive analysis of post-stroke microbiological therapy and the relationship between IS and diet. The aim is to identify potential microbial targets for therapeutic intervention, as well as to highlight the benefits of microbiological therapies and the significance of dietary management. Overall, this paper seeks to provide key strategies for the treatment and management of IS, advocating for healthy diets and health programs for individuals. Meanwhile, it may offer a new perspective on the future interdisciplinary development of neurology, microbiology and nutrition.

Propolis, a natural mixture rich in bioactive compounds, has shown the potential to relieve exercise-induced fatigue. However, the underlying mechanism remains unclear. This study aimed to explore the anti-fatigue effects of ethanol extract of propolis (EEP) and its potential mechanisms.

Male C57BL/6 mice aged 6-8 weeks were subjected to swim training with or without EEP supplementation (400 mg/kg.bw) for 3 weeks, followed by a exhaustive swimming test to simulate exercise-induced fatigue. The exhaustion time and fatigue-related biochemical indices were measured to assess the anti-fatigue effects. The anti-fatigue mechanism of EEP was further investigated using untargeted serum metabolomics and 16S rRNA gene sequencing of the gut microbiota.

The results showed that supplementation with EEP significantly increased the exhaustive swimming time of the mice by 27.64%, with no significant effects on body weight, food intake, or viscera and muscle index among the 3 groups. Biochemical analysis indicated that EEP effectively alleviated fatigue-related biochemical indices caused by excessive exercise, including liver glycogen (LG), muscle glycogen (MG), blood lactate (BLA), blood urea nitrogen (BUN), lactate dehydrogenase (LDH), interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), superoxide dismutase (SOD), total antioxidant capacity (T-AOC), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA). Serum metabolomics analysis revealed that EEP reversed the levels of 6 key metabolites (Gamma-Aminobutyric acid, pipecolic acid, L-isoleucine, sucrose, succinic acid, and L-carnitine), which are involved in 7 metabolic pathways related to energy metabolism, amino acid metabolism, and carbohydrate metabolism. 16S rRNA sequencing analysis of the cecal contents showed that EEP altered the composition and structure of the gut microbiota, increasing the abundance of butyrate-producing bacteria and reducing the abundance of harmful bacteria. Correlation analysis revealed that specific bacterial genera were closely related to certain differential metabolites and biochemical indices.

Our study showed that EEP significantly increased exercise endurance in mice and exerted anti-fatigue effects by modulating key metabolites and the gut microbiota.

Pullorum disease (PD) caused by Salmonella Pullorum (SP) results in high mortality in chicks and potential carriers in adult chickens, negatively affecting growth and egg production. This study identified SP infection in 100-day-old White Plymouth Rock hens by serum plate agglutination and fecal and anal swab polymerase chain reaction. SP-infected broilers were classified into positive (P) and negative (N) groups using hematoxylin-and-eosin staining, metabolome sequencing, and 16S rDNA to investigate the effects of SP infection on the metabolites and microorganisms in the cecum of broilers. Groups had different degrees of inflammatory cell infiltration in the cecum, spleen, liver, and lung tissues. The diversity of bacterial flora in the cecum of Groups P and N differed significantly (P < 0.05). o__Lactobacillales and o__Verrucomicrobiota were significantly higher in Group P than in Group N (P < 0.05). At the genus level, g__Akkermansia was significantly higher in Group N (P < 0.05). Metabolome sequencing of cecum contents in Groups P and N screened 77 differential metabolites at the secondary metabolite level. 11 metabolites, including 2,4-dimethylbenzaldehyde, 3a,6b,7b,12a-tetrahydroxy-5b-cholanoic acid, and LysoPG 19:1, were differentially expressed in Group P (P < 0.05). A combined analysis of 16S rDNA sequencing and cecal content metabolomics identified 28 genera significantly associated with 38 metabolites in the cecum (P < 0.05). Specific bacterial genera such as Corynebacterium and Roseobacter have particularly prominent effects on metabolites. These findings highlight the significant alterations in gut microbial composition and metabolic functions due to SP infection. The differential metabolites and bacterial taxa identified in this study may provide insights into the underlying mechanisms of PD pathogenesis and potential biomarkers for disease management.

The gut microbiota plays a pivotal role in influencing the metabolism and immune responses of the body. A balanced microbial composition promotes metabolic health through various mechanisms, including the production of beneficial metabolites, which help regulate inflammation and support immune functions. In contrast, imbalance in the gut microbiota, known as dysbiosis, can disrupt metabolic processes and increase the risk of developing diseases, such as obesity, type 2 diabetes, and inflammatory disorders. The composition of the gut microbiota is dynamic and can be influenced by environmental factors such as diet, medication, and the consumption of live bacteria. Since the early 1900s, bacteria isolated from food and have been used as probiotics. However, the human gut also offers an enormous reservoir of bacterial strains, and recent advances in microbiota research have led to the discovery of strains with probiotic potentials. These strains, derived from a broad spectrum of microbial taxa, differ in their ecological properties and how they interact with their hosts. For most probiotics bacterial structural components and metabolites, such as short-chain fatty acids, contribute to the maintenance of metabolic and immunological homeostasis by regulating inflammation and reinforcing gut barrier integrity. Metabolites produced by probiotic strains can also be used for bacterial cross-feeding to promote a balanced microbiota. Despite the challenges related to safety, stability, and strain-specific properties, several newly identified strains offer great potential for personalized probiotic interventions, allowing for targeted health strategies.

Akkermansia muciniphila is a gut bacterium that colonizes the gut mucosa, has a role in maintaining gut health and shows promise for potential therapeutic applications. The discovery of A. muciniphila as an important member of our gut microbiome, occupying an extraordinary niche in the human gut, has led to new hypotheses on gut health, beneficial microorganisms and host-microbiota interactions. This microorganism has established a unique position in human microbiome research, similar to its role in the gut ecosystem. Its unique traits in using mucin sugars and mechanisms of action that can modify host health have made A. muciniphila a subject of enormous attention from multiple research fields. A. muciniphila is becoming a model organism studied for its ability to modulate human health and gut microbiome structure, leading to commercial products, a genetic model and possible probiotic formulations. This Review provides an overview of A. muciniphila and Akkermansia genus phylogeny, ecophysiology and diversity. Furthermore, the Review discusses perspectives on ecology, strategies for harnessing beneficial effects of A. muciniphila for human mucosal metabolic and gut health, and its potential as a biomarker for diagnostics and prognostics.

Bacterial extracellular vesicles (EVs) play a pivotal role in host-microbe communication. Akkermansia muciniphila, a symbiotic bacterium essential for intestinal health, is hypothesized to exert its effects via EVs. Here, we successfully isolated and characterized EVs derived from A. muciniphila (Am-EVs) using ultracentrifugation. Am-EVs exhibited a double-membrane structure, with an average diameter of 92.48 ± 0.28 nm and a proteomic profile comprising 850 proteins. In an in vitro model of lipopolysaccharide (LPS)-induced inflammation in human colorectal adenocarcinoma cells (Caco-2), treatment with both 25 and 50 μg/mL Am-EVs significantly reduced oxidative stress markers, including reactive oxygen species (ROS), nitric oxide (NO), and malondialdehyde (MDA), while restoring catalase activity (CAT). Am-EVs also suppressed the expression of pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). Subsequent transcriptomic sequencing and Western blot experiments revealed that Am-EVs attenuate the MAPK signaling pathway by downregulating TRIF, MyD88, p38 MAPK, and FOS while upregulating TGFBR2. These findings suggest that Am-EVs mediate anti-inflammatory effects through modulation of MAPK signaling, highlighting their potential as therapeutic agents in intestinal inflammation.

Pediatric-onset ulcerative colitis (pUC) represents a more aggressive disease phenotype compared with adult-onset UC. We hypothesized that this difference can, in part, be explained by the composition of the microbiota.

In a prospective, longitudinal study, we included pediatric (N = 30) and adult (N = 30) patients with newly or previously (>1 year) diagnosed UC. We analyzed the microbiota composition in the mucosa-adherent microbiota at baseline, using 16S rRNA gene sequencing, and the fecal microbiota at baseline and at 3-month intervals, using shotgun metagenomics.

For fecal samples, the bacterial composition differed between pUC and aUC in newly diagnosed patients (β-diversity, Bray Curtis: R2 = 0.08, P = .02). In colon biopsies, microbial diversity was higher in aUC compared with pUC (α-diversity, Shannon: estimated difference 0.54, P = .006). In the mucosa-adherent microbiota, Alistipes finegoldii was negatively associated with disease activity in pUC while being positively associated in aUC (estimate: -0.255 and 0.098, P = .003 and P = .02 in pUC and aUC, respectively). Finally, we showed reduced stability of the fecal microbiota in pediatric patients, evidenced by a different composition of the fecal microbiota in newly and previously diagnosed pUC, a pattern not found in adults.

Our results indicate that pediatric UC patients have a more unstable fecal microbiota and a lower α diversity than adult patients and that the microbiota composition differs between aUC and pUC patients. These findings offer some explanation for the observed differences between pUC and aUC and indicate that individualized approaches are needed if microbiota modifications are to be used in the future treatment of UC.

As the largest mucosal surface, the gut has built a physical, chemical, microbial, and immune barrier to protect the body against pathogen invasion. The disturbance of gut microbiota aggravates pathogenic bacteria invasion and gut barrier injury. Fecal microbiota transplantation (FMT) is a promising treatment for microbiome-related disorders, where beneficial strain engraftment is a significant factor influencing FMT outcomes. The aim of this research was to explore the effect of FMT on antibiotic-induced microbiome-disordered (AIMD) models infected with enterotoxigenic Escherichia coli (ETEC). We used piglet, mouse, and intestinal organoid models to explore the protective effects and mechanisms of FMT on ETEC infection. The results showed that FMT regulated gut microbiota and enhanced the protection of AIMD piglets against ETEC K88 challenge, as demonstrated by reduced intestinal pathogen colonization and alleviated gut barrier injury. Akkermansia muciniphila (A. muciniphila) and Bacteroides fragilis (B. fragilis) were identified as two strains that may play key roles in FMT. We further investigated the alleviatory effects of these two strains on ETEC infection in the AIMD mice model, which revealed that A. muciniphila and B. fragilis relieved ETEC-induced intestinal inflammation by maintaining the proportion of Treg/Th17 cells and epithelial damage by moderately activating the Wnt/β-catenin signaling pathway, while the effect of A. muciniphila was better than B. fragilis. We, therefore, identified whether A. muciniphila protected against ETEC infection using basal-out and apical-out intestinal organoid models. A. muciniphila did protect the intestinal stem cells and stimulate the proliferation and differentiation of intestinal epithelium, and the protective effects of A. muciniphila were reversed by Wnt inhibitor. FMT alleviated ETEC-induced gut barrier injury and intestinal inflammation in the AIMD model. A. muciniphila was identified as a key strain in FMT to promote the proliferation and differentiation of intestinal stem cells by mediating the Wnt/β-catenin signaling pathway.

The mosquito microbiota represents an intricate assemblage of microorganisms, comprising bacteria, fungi, viruses, and protozoa. Factors modulating microbiome abundance and composition include host genetic background, environmental parameters, and pathogen exposure. Conversely, the microbiome profoundly influences pathogen infection of the mosquito host and thus harbours considerable potential to impact the transmission of vector-borne diseases. As such, there is a growing interest in using the microbiome in novel vector-control strategies, including exploiting the natural ability of some microbes to interfere with infection of the vectors by pathogens. However, before novel microbiome-based vector control approaches can move towards translation, a more complete understanding of the interactions between mosquitoes, their microbiome, and the pathogens they transmit, is required to better appreciate how variation in the microbiome of field mosquitoes affects these interactions. To examine the impact of the host background and the associated diversity of microbiomes within distinct hosts, but without artificially manipulating the microbiome, we exposed several laboratory-reared and field-collected Aedes aegypti mosquito lines to Zika virus (ZIKV) and correlated their microbial load and composition to pathogen exposure and viral infection success. We observed significant differences in ZIKV exposure outcomes between the different mosquito lines and their associated microbiomes, and found that ZIKV alteration of the microbiomes was distinct in different lines. We also identified microbial taxa correlating with either ZIKV infection or a lack of infection. In summary, our study provides novel insights into the variability of pathogen interactions within the mosquito holobiont. A more complete understanding of which factors influence the tripartite interactions between Aedes mosquitoes, their microbiome, and arboviral pathogens, will be critical for the development of microbial-based interventions aimed at reducing vector-borne disease burden.

Akkermansia muciniphila is a human microbial symbiont residing in the mucosal layer of the large intestine. Its main carbon source is the highly heterogeneous mucin glycoprotein, and it uses an array of carbohydrate-active enzymes and sulfatases to access this complex energy source. Here we describe the biochemical characterization of 54 glycoside hydrolases, 11 sulfatases and 1 polysaccharide lyase from A. muciniphila to provide a holistic understanding of their carbohydrate-degrading activities. This was achieved using a variety of liquid chromatography techniques, mass spectrometry, enzyme kinetics and thin-layer chromatography. These results are supported with A. muciniphila growth and whole-cell assays. We find that these enzymes can act synergistically to degrade the O-glycans on the mucin polypeptide to completion, down to the core N-acetylgalactosaime. In addition, these enzymes can break down human breast milk oligosaccharide, ganglioside and globoside glycan structures, showing their capacity to target a variety of host glycans. These data provide a resource to understand the full degradative capability of the gut microbiome member A. muciniphila.

Intestinal mucus, a viscoelastic medium with mucin2 (MUC2) as its main component, covers the surface of intestinal epithelial cells and protects the intestine from invasion, forming the first barrier of the intestinal tract. Unlike the small intestine, where the mucus layer is a single layer, the colonic mucus layer can be divided into a sterile inner layer and an outer layer with bacterial colonization. Many of the substances in the mucus layer have beneficial effects on the intestinal epithelium, but the mucus layer is often affected by a variety of factors, mainly microbiological, dietary, and immunological. Inflammatory bowel disease (IBD) is a disease of increasing morbidity worldwide, with a complex etiology and a high relapse rate. In recent years, the mucus barrier in IBD has received increasing attention and is considered a key factor in the pathogenesis of IBD. Loss of goblet cells (GCs) and changes in the composition and properties of the mucus layer material are commonly found in the colon of IBD patients. Damage to the mucus layer may make it easier for microorganisms to access the intestinal epithelium and cause inflammation. There are currently a number of herbs and other therapies that can be used to treat IBD and repair the damaged mucus barrier. This review highlights the important role of the mucus layer in IBD and the therapies that target the mucus layer in IBD.

The Simulator of Human Intestinal Microbial Ecosystem (SHIME) has hindered widespread adoption due to its high cost. This study founded biomimetic multilink fermentation equipment (BMLFE), priced at half or even lower than SHIME. It was improved based on multilink fermentation equipment (MLFE) by modifying materials, peristaltic pumps, fermentation time, and dietary habits while calculating transfer time and volumes and conducted anaerobic fermentation for 15 days followed by monitoring changes in intestinal microbial composition and short-chain fatty acids (SCFAs). We observed that the intestinal microbiota achieved a stable state after the ninth day and retained the predominant bacterial species in the fecal inoculum. The Bacillota/Bacteroidota values of the descending colon (DC) were similar to those in the fecal samples. However, the stability of SCFAs was relatively delayed and reached stability only after the 11th day. Meanwhile, the concentration ratio of acetic acid, propionate, and butyric acid metabolized by transverse colon (TC) and DC on the 11-15th days was close to that in fecal inoculations. Therefore, BMLFE can be used to simulate the human gastrointestinal environment in vitro studies. It is expected to be employed in clinical FMT and may even contribute to establishing stable enterotypes through dietary intervention.

The bacteria living in the human gut are essential for host health. Though the composition and metabolism of these bacteria are well described in both healthy hosts and those with intestinal disease, less is known about the metabolic activity of the gut bacteria prior to, and during, disease development-especially regarding gut bacterial replication. Here, we use a recently developed single-cell technique alongside existing metagenomics-based tools to identify, track, and quantify replicating gut bacteria both ex vivo and in situ in the dextran sodium sulfate (DSS) mouse model of colitis. We show that the proportion of replicating gut bacteria decreases when mice have the highest levels of inflammation and returns to baseline levels as mice begin recovering. In addition, we report significant alterations in the composition of the replicating gut bacterial community ex vivo during colitis development. On the taxa level, we observe significant changes in the abundance of taxa such as the mucus-degrading Akkermansia and the poorly described Erysipelatoclostridium genus. We further demonstrate that many taxa exhibit variable replication rates in situ during colitis, including Akkermansia muciniphila. Lastly, we show that colitis development is positively correlated with increases in the presence and abundance of bacteria in situ which are predicted to be fast replicators. This could suggest that taxa with the potential to replicate quickly may have an advantage during intestinal inflammation. These data support the need for additional research using activity-based approaches to further characterize the gut bacterial response to intestinal inflammation and its consequences for both the host and the gut microbial community.IMPORTANCEIt is well known that the bacteria living inside the gut are important for human health. Indeed, the type of bacteria that are present and their metabolism are different in healthy people versus those with intestinal disease. However, less is known about how these gut bacteria are replicating, especially as someone begins to develop intestinal disease. This is particularly important as it is thought that metabolically active gut bacteria may be more relevant to health. Here, we begin to address this gap using several complementary approaches to characterize the replicating gut bacteria in a mouse model of intestinal inflammation. We reveal which gut bacteria are replicating, and how quickly, as mice develop and recover from inflammation. This work can serve as a model for future research to identify how actively growing gut bacteria may be impacting health, or why these particular bacteria tend to thrive during intestinal inflammation.

Attention-deficit/hyperactivity disorder (ADHD), a common neurodevelopmental disorder in children, is associated with alterations in gut microbiota and short-chain fatty acids (SCFAs), which are metabolites influencing the gut-brain axis. Evidence suggests that psychostimulant medications, widely used to manage ADHD symptoms, may also impact gut microbiota composition and SCFA levels. This study explores these potential effects by examining gut microbiota profiles and SCFA concentrations in unmedicated and medicated children with ADHD, compared to healthy controls. Fecal samples from 30 children aged 6-12 years (10 unmedicated ADHD, 10 medicated ADHD, and 10 healthy controls) were analyzed using 16 S rRNA sequencing and targeted metabolomics. Unmedicated ADHD children show distinct gut microbiota profiles, with lower level of Tyzzerella, Prevotellaceae, and Coriobacteriaceae, compared to controls. Notably, propionic acid levels were negatively associated with ADHD symptom severity, suggesting a potential biomarker role. Medicated ADHD children showed lower gut microbial diversity, unique taxa, and lower SCFA levels, compared to unmedicated children with ADHD. These findings suggest that gut microbiota and SCFAs may be linked to ADHD symptomatology, underscoring the importance of gut-brain interactions in ADHD. This study highlights the potential of gut health monitoring as part of future ADHD management strategies.

The gut microbiome was involved in a variety of physiological processes and played a key role in host environmental adaptation. However, the mechanisms of their response to altitudinal environmental changes remain unclear. In this study, we used 16S rRNA sequencing and LC-MS metabolomics to investigate the changes in the gut microbiome and metabolism of the Yarkand toad-headed agama (Phrynocephalus axillaris) at different altitudes (-80 m to 2000 m). The results demonstrated that Firmicutes, Bacteroidetes, and Proteobacteria were the dominant phylum, Lachnospiraceae and Oscillospiraceae were the most abundant family, and the low-altitude populations had higher richness than high-altitude populations; Akkermansiaceae appeared to be enriched in high-altitude populations and the relative abundance tended to increase with altitude. The gut microbiome of three populations of P. axillaris at different altitudes was clustered into two different enterotypes, low-altitude populations and high-altitude populations shared an enterotype dominated by Akkermansia, Kineothrix, Phocaeicola; intermediate-altitude populations had an enterotype dominated by Mesorhizobium, Bradyrhizobium. Metabolites involved in amino acid and lipid metabolism differed significantly at different altitudes. The above results suggest that gut microbiome plasticity drives the extensive adaptation of P. axillaris to multi-stress caused by different altitudes. With global warming, recognizing the adaptive capacity of wide-ranging species to altitude can help plan future conservation strategies.

Early weaning is frequently accompanied by a significant increase in diarrhea and mortality rates, which reduces rabbits' performance. Although antibiotics can reduce pathogenic bacteria, they also harm beneficial microorganisms and disrupt the normal intestinal microbiota balance. In order to find non-residue and non-toxic alternatives to antibiotics to ensure the safety of animal products, we conducted a study on the effect of compound microecological preparations supplementation on lactating female rabbits and their offspring. A total of 60 female rabbits were randomly assigned to four groups: CON, supplemented with probiotics at 3, 6, and 9 g/female rabbit/day from day 24 of gestation until weaning. We observed that probiotics supplementation significantly enhanced production performance (P < 0.05), immune and antioxidant function (P < 0.05), as well as intestinal flora composition in lactating rabbits and their offspring. Notably, compared with the control group, the experimental group exhibited a 19.23%, 44.22%, and 24.57% increase in milk yield (P = 0.002). Regarding rabbit growth performance, the average body weight of young rabbits in the experimental group showed a significant increase of 3.59%, 10.22%, and 6.74% at day 35 (P = 0.022), whereas the average daily gain (ADG) of rabbits aged between 21 and 35 days was significantly elevated by 4.94%, 17.06%, and 6.28% in the experimental group (P < 0.001). In conclusion, probiotics supplementation can significantly enhance lactation performance, promote growth and disease resistance in rabbits, as well as improve intestinal health when administered at a dosage of 6 g/day. Moreover, the limited sample size in this study may hinder the detection of subtle effects, and augmenting the sample size will bolster the reliability of the study findings.

The intestinal environment of rabbits is fragile and susceptible to environmental influences, leading to inflammatory intestinal diseases. Adding antibiotics to rabbit feed can achieve the effect of preventing and treating inflammation, which can also lead to the imbalance of the gut microbiota and residual antibiotics in agricultural products. Composite probiotics are live microbial feed additives composed of various ratios of probiotics and have become the most promising alternative to antibiotics due to their residue-free and non-toxic properties. The aim of this study was to investigate the impact of compound probiotics on lactating female rabbits and their offspring. Our findings highlight the potential of compound microecological preparations as an effective strategy for enhancing lactation performance, immune function, and antioxidant capacity in rabbits. The supplementation of probiotics through rabbit milk offers a promising approach to optimize the growth and health outcomes of newborn rabbits.

It is critical to sustain the diversity of the microbiota to maintain host homeostasis and health. Growing evidence indicates that changes in gut microbial biodiversity may be associated with the development of several pathologies, including type 2 diabetes mellitus (T2DM). Metformin is still the first-line drug for treatment of T2DM unless there are contra-indications. The drug primarily inhibits hepatic gluconeogenesis and increases the sensitivity of target cells (hepatocytes, adipocytes and myocytes) to insulin; however, increasing evidence suggests that it may also influence the gut. As T2DM patients exhibit gut dysbiosis, the intestinal microbiome has gained interest as a key target for metabolic diseases. Interestingly, changes in the gut microbiome were also observed in T2DM patients treated with metformin compared to those who were not. Therefore, the aim of this review is to present the current state of knowledge regarding the association of the gut microbiome with the antihyperglycemic effect of metformin. Numerous studies indicate that the reduction in glucose concentration observed in T2DM patients treated with metformin is due in part to changes in the biodiversity of the gut microbiota. These changes contribute to improved intestinal barrier integrity, increased production of short-chain fatty acids (SCFAs), regulation of bile acid metabolism, and enhanced glucose absorption. Therefore, in addition to the well-recognized reduction of gluconeogenesis, metformin also appears to exert its glucose-lowering effect by influencing gut microbiome biodiversity. However, we are only beginning to understand how metformin acts on specific microorganisms in the intestine, and further research is needed to understand its role in regulating glucose metabolism, including the impact of this remarkable drug on specific microorganisms in the gut.

Background/Objectives: Managing type 2 diabetes mellitus (T2DM) and obesity requires a multidimensional, patient-centered approach including nutritional interventions (NIs) and physical activity. Changes in the gut microbiota (GM) have been linked to obesity and the metabolic alterations typical of T2DM and obesity, and they are strongly influenced by diet. However, few studies have evaluated the effects on the GM of a very-low-calorie ketogenic diet (VLCKD) in patients with T2DM, especially in the mid-term and long-term. This longitudinal study is aimed at evaluating the mid-term and long-term impact of the VLCKD and Mediterranean diet (MD) on the GM and on the anthropometric, metabolic, and lifestyle parameters of 11 patients with T2DM and obesity (diabesity). This study extends previously published results evaluating the short-term (three months) impact of these NIs on the same patients. Methods: At baseline, patients were randomly assigned to either a VLCKD (KETO group) or a Mediterranean diet (MEDI group). After two months, the KETO group gradually shifted to a Mediterranean diet (VLCKD-MD), according to current VLCKD guidelines. From the fourth month until the end of the study both groups followed a similar MD. Previous published results showed that VLCKD had a more beneficial impact than MD on several variables for 3 months of NI. In this study, the analyses were extended until six (T6) and twelve months (T12) of NI by comparing data prospectively and against baseline (T0). The GM analysis was performed through next-generation sequencing. Results: Improvements in anthropometric and metabolic parameters were more pronounced in the KETO group at T6, particularly for body mass index (-5.8 vs. -1.7 kg/m2; p = 0.006) and waist circumference (-15.9 vs. -5.2 cm; p = 0.011). At T6, a significant improvement in HbA1c (6.7% vs. 5.5% p = 0.02) and triglyceride (158 vs. 95 mg/dL p = 0.04) values compared to T0 was observed only in the KETO group, which maintained the results achieved at T3. The VLCKD-MD had a more beneficial impact than the MD on the GM phenotype. A substantial positive modulatory effect was observed especially up to the sixth month of the NI in KETO due to the progressive increase in bacterial markers of human health. After the sixth month, most markers of human health decreased, though they were still increased compared with baseline. Among them, the Verrucomicrobiota phylum was identified as the main biomarker in the KETO group, together with its members Verrucomicrobiae, Akkermansiaceae, Verrucomicrobiales, and Akkermansia at T6 compared with baseline. Conclusions: Both dietary approaches ameliorated health status, but VLCKD, in support of the MD, has shown greater improvements on anthropometric and metabolic parameters, as well as on GM profile, especially up to T6 of NI.

The advent of checkpoint immunotherapy has dramatically changed the outcomes for patients with cancer. However, a considerable number of patients have little or no response to therapy. We review recent findings on the connection between the gut microbiota and the immune system, exploring whether this link could enhance the effectiveness of immunotherapy.

Clinical studies have reported specific types of bacteria in larger quantities at baseline in responders than in non-responders, especially Akkermansia mucinifila, Ruminococcaceae, Faecalibacterium, and Lachnospiraceae. Following the consumption of a high-fiber diet, bacteria in the gut ferment dietary fiber to short-chain fatty acids (SCFAs), like acetate, propionate, and butyrate. Some of the SCFAs nurture intestinal epithelial cells, and some enter the bloodstream. Here SCFAs can activate DC8 + cytotoxic T-cells to induce cancer cell death. High fiber intake in the diet was associated with a reduced risk of progression or death during checkpoint immunotherapy. Recent findings demonstrate that high-fiber plant-based diets such as the Mediterranean Diet positively influence the gut microbiota whereas antibiotics and proton pump inhibitors can negatively influence outcomes of cancer immunotherapy by changing the gut microbiota. This narrative review provides evidence of an association between types of bacteria and their metabolites and favorable responses to checkpoint immunotherapy. Prospective clinical trials are needed to determine if diet interventions can improve treatment outcomes.

Little is known about the population health status of the world's rarest primate, the Hainan gibbon. Here, the largest gut microbiome dataset yet constructed was generated from all five extant breeding groups of the Hainan gibbons, with 42 samples from individuals spanning all ages and sexes, in addition to dry and wet seasons. Groups A and B exhibited higher diversity of gut microbiota and food resources, in contrast to the subsequently established Groups C, D, and E. Significantly, Group C demonstrated the lowest gut microbial diversity and higher abundance of vector-related Pestivirus, which may be attributed to their proximity to the primary forest edge and the village. We also inferred the origin and possible dispersal paths of the newly established Group E. These findings indicate that Hainan gibbons are still facing viral zoonosis and the threat of extinction, as illuminated by an understanding of the gut microbiome and habitat landscape ecology.

Microorganisms that colonize the intestine communicate with the host in various ways and affect gut function and health. Extracellular vesicles (EVs), especially their encapsulated microRNAs (miRNAs), participate in the complex and precise regulation of microbiota-host interactions in the gut. These roles make miRNAs critically important for the prevention, diagnosis, and treatment of intestinal diseases. Here, we review the current knowledge on how different sources of EVs and miRNAs, including those from diets, gut microbes, and hosts, maintain gut microbial homeostasis and improve the intestinal barrier and immune function. We further highlight the roles of EVs and miRNAs in intestinal diseases, including diarrhea, inflammatory bowel disease, and colorectal cancer, thus providing a perspective for the application of EVs and miRNAs in these diseases.

A Gram-stain-negative bacterium, designated as strain TK19100T, was isolated from the mid-ridge of the Southwest Indian Ocean. Cells of strain TK19100T were strictly aerobic, non-motile and short-rod shaped with fimbriae-like structures around the cell surface. Growth occurred at 15-40 °C, at pH 6.0-9.0 and with 1-10% (w/v) NaCl. Strain TK19100T shared the highest 16S rRNA gene sequence similarity with Cerasicoccus frondis NBRC 105381T of 97.74%, followed by Cerasicoccus arenae KCTC 12870T of 97.69% and Cerasicoccus maritimus NBRC 105382T of 97.40%. The phylogenetic tree based on both 16S rRNA genes and 92 core genes placed strain TK19100T in a new linage within the genus Cerasicoccus. The genome size of strain TK19100T was 5.07 Mb with the DNA G + C content 56.1%. The average nucleotide identity value and the digital DNA-DNA hybridization value of strain TK19100T compared with the closest related species, Cerasicoccus frondis, were 78.39% and 23.70%, respectively. Strain TK19100T encoded a previously unreported combination of GH16 and Carbohydrate Binding Module 96. The major fatty acids of strain TK19100T were C14:0 and C18:1 ω9c. Menaquinone-7 was the sole respiratory quinone. The phenotypic and genotypic characterization analysis indicate that strain TK19100T represents a novel species affiliated to the genus Cerasicoccus, for which the name Cerasicoccus fimbriatus sp. nov. is proposed. The type strain is TK19100T (= CGMCC 1.18957T = NBRC 116189T).

Microbes like bacteria and fungi are crucial for host plant growth and development. However, environmental factors and host genotypes can influence microbiome composition and diversity in plants such as industrial hemp (Cannabis sativa L.). Herein, we evaluated the endophytic and rhizosphere microbial communities of two cannabidiol (CBD; Sweet Sensi and Cherry Wine) and two fibers (American Victory and Unknown). The four hemp varieties showed significant variations in microbiome diversity. The roots had significantly abundant fungal and bacterial endophyte diversity indices, whereas the stem had higher fungal than bacterial diversity. Interestingly, the soil system showed no significant diversity variation across CBD vs. fiber genotypes. In fungal phyla, Ascomycota and Basidiomycota were significantly more abundant in roots and stems than leaves in CBD-rich genotypes compared to fiber-rich genotypes. The highly abundant bacterial phyla were Proteobacteria, Acidobacteria, and Actinobacteria. We found 16 and 11 core-microbiome bacterial and fungal species across genotypes. Sphingomonas, Pseudomonas, and Bacillus were the core bacteria of fiber genotypes with high abundance compared to CBD genotypes. Contrarily, Microbacterium, and Rhizobium were significantly higher in CBD than fiber. The Alternaria and Gibberella formed a core-fungal microbiome of fiber-genotype than CBD. Contrarily, Penicillium, and Nigrospora were significantly more abundant in CBD than fiber genotypes. In conclusion, specific hemp genotypes recruit specialized microbial communities in the rhizosphere and phyllosphere. Utilizing the core-microbiome species can help to maintain and improve the growth of hemp plants and to target specialized traits of the genotype.

Non-Alcoholic Fatty Liver Disease (NAFLD) affects approximately 32.4% of the global population and poses a significant health concern. Emerging evidence underscores the pivotal role of the gut microbiota-including bacteria, viruses, fungi, and parasites-in the development and progression of NAFLD. Dysbiosis among gut bacteria alters key biological pathways that contribute to liver fat accumulation and inflammation. The gut virome, comprising bacteriophages and eukaryotic viruses, significantly shapes microbial community dynamics and impacts host metabolism through complex interactions. Similarly, gut fungi maintain a symbiotic relationship with bacteria; the relationship between gut fungi and bacteria is crucial for overall host health, with certain fungal species such as Candida in NAFLD patients showing detrimental associations with metabolic markers and liver function. Additionally, the "hygiene hypothesis" suggests that reduced exposure to gut parasites may affect immune regulation and metabolic processes, potentially influencing conditions like obesity and insulin resistance. This review synthesizes current knowledge on the intricate interactions within the gut microbiota and their associations with NAFLD. We highlight the therapeutic potential of targeting these microbial communities through interventions such as probiotics, prebiotics, and fecal microbiota transplantation. Addressing the complexities of NAFLD requires comprehensive strategies that consider the multifaceted roles of gut microorganisms in disease pathology.

Angular limb deformities (ALDs) are a common skeletal development disorder in newborn foals. This condition affects the growth and development of foals and severely impacts their future athletic performance and economic value, causing significant financial losses to the horse industry. Placentitis, metritis, and severe metabolic diseases during mare pregnancy are significant causes of ALDs in newborn foals. It has been established that intestinal flora disorders can easily lead to inflammatory and metabolic diseases in the host. However, the incidence of ALDs in foals in Zhaosu County, Xinjiang, a key production area of China's horse industry, remains unclear. Additionally, the relationship between functional changes in foals with ALDs and their mares and changes in their intestinal flora is not well-understood.

This study investigated the status of ALD in newborn foals through clinical observation and imaging examinations. In addition, molecular biological methods were applied to examine the effects of ALDs foals and their mares on physiological and biochemical markers and gut microbiota.

The results showed that the incidence of ALD in Zhaosu area of China was 4.13%. In addition, by comparing and correlating the physiological and biochemical indicators and intestinal flora of foals and mares with ALD with those of healthy horses, it was found that foals and mares with ALD may promote the occurrence and development of the disease through the "blood marker changes-intestinal flora-ALDs" axis. In addition, by comparing the physiological and biochemical indicators and intestinal flora of foals and mares with ALD with the intestinal flora of healthy horses, it was found that the physiological and biochemical indicators and intestinal flora structure and metabolic pathways of foals and mares with ALD had significant changes.

The diversity, species composition, and function of the intestinal flora of ALDs and their mares were significantly altered. These findings provide a scientific basis for understanding the etiology of ALDs in foals and offer new perspectives for diagnosing and treatment ALDs in newborn foals.

Luteolibacter sp. strain Populi is a bacterium from the phylum Verrucomicrobiota, isolated from the rhizosphere of a black cottonwood tree, Populus trichocarpa, from the Cascade mountains in Washington. Its 6.6-Mb chromosome was completely sequenced using Oxford Nanopore long-read sequencing and is predicted to encode 5,301 proteins and 60 RNAs.

Glioma poses a serious threat to human health and has a high mortality rate. Therefore, developing natural anti-tumour drugs for cancer treatment is an urgent priority. Schizophyllum commune is an edible and medicinal fungus, with polysaccharides as its main active components, which may have anti-tumour properties. Herein, we characterised S. commune fruiting body polysaccharides (SCFP) structure and evaluated its anti-glioma activity in vitro and in vivo. UV and FTIR spectra, high-performance gel chromatography, and monosaccharide composition analyses demonstrated that SCFP was a heteropolysaccharide with a molecular weight of 290.92 kDa. Among the monosaccharide compositions, mannose, galactose, and glucose were the most abundant. SCFP significantly inhibited the survival of the glioma cell lines U251 and U-87MG. U251 xenograft tumours treated with SCFP via gavage showed a 47.39 % inhibition, with no significant toxic side effects observed. SCFP upregulated aplasia Ras homologue member I (ARHI) expression, thereby regulating PI3K/AKT signalling, inhibiting tumour migration, and inducing apoptosis, to inhibit tumour growth. Furthermore, SCFP treatment increased the relative abundance of beneficial bacteria, including Akkermansia muciniphila, Ligilactobacillus murinus, and Parabacteroides goldsteinii, in tumour-bearing mice and restored the gut microbiota structure to that of the normal group (NG group) mice without tumours. Thus, SCFP has the potential for application as a natural anticancer drug.

Fucoidans, known for their diverse biological properties such as anti-inflammatory, antiviral, antitumor, and immune stimulatory effects, have recently gained attention for their potential benefits in exercise endurance, muscle mass, and anti-fatigue. However, the mechanisms by which fucoidans enhance exercise performance are still unclear. To investigate these effects, we administered 400 mg/kg/day of fucoidan extract derived from Undaria pinnatifida to 64 C57BL/6J mice over 10 weeks. We evaluated changes in running activity, mitochondrial-related gene expression in skeletal muscle, and alterations in the intestinal microbiome. Our results showed that fucoidan supplementation significantly increased daily running distance and muscle mass by 25.5% and 10.4%, respectively, in mice on a standard chow diet, and with more modest effects observed in those on a high-fat diet (HFD). Additionally, fucoidan supplementation led to a significant increase in beneficial gut bacteria, including Bacteroides/Prevotella, Akkermansia muciniphila, and Lactobacillus, along with a notable reduction in the Firmicutes/Bacteroidetes ratio, indicating improved gut microbiome health. Mechanistically, fucoidan supplementation upregulated the mRNA expression of key genes related to mitochondrial biogenesis and oxidative capacity, such as COX4, MYH1, PGC-1α, PPAR-γ, and IGF1, in both standard chow and HFD-fed mice. Our findings suggest that fucoidan supplementation enhances exercise performance, improves muscle function, and positively modulates the gut microbiome in mice, regardless of diet. These effects may be attributed to fucoidans' potential prebiotic role, promoting the abundance of beneficial gut bacteria and contributing to enhanced exercise performance, increased muscle strength, and improved recovery.

Introducing complementary foods is critical for promoting infant health and development. During the weaning period, the dietary patterns provide essential nutrients and facilitate the development of a diverse gut microbiome, which plays significant roles in the regulation of immune, metabolic, and neurological functions. This study enrolled 200 families to assess the impact of complementary feeding on infant growth and health outcomes. Data included detailed records of feeding practices, infant growth measurements, health assessments, and fecal samples and breast milk collected between weeks 12 and 32 postpartum. The gut microbiome was analyzed using 16S rRNA sequencing, while metabolites such as human milk oligosaccharides (HMOs), monosaccharides, and short-chain fatty acids (SCFAs) were measured using chromatography-mass spectrometry. Results revealed a high prevalence of breastfeeding, with complementary food introduced at around 16 weeks. Significant alterations in the infant gut microbiome were observed, particularly in the genera Lactobacillus, Akkermansia, and Staphylococcus. Additionally, the levels of HMOs, monosaccharides, and SCFAs were found to be influenced by the introduction of complementary foods. Significant correlations emerged between complementary feeding practices, gut microbiome diversity, specific bacterial genera (e.g., Streptococcus, Lactobacillus, Bifidobacterium, and Clostridioides), and key metabolites (such as lacto-N-tetraose, lacto-N-neotetraose, mannose, and butyric acid). This study offers valuable insights into the complex interactions between complementary feeding, gut microbiome development, and metabolite profiles during early infant growth. Future research with larger cohorts and targeted dietary interventions is recommended to further elucidate the underlying mechanisms.

Background: Didymin is a dietary flavonoid derived from citrus fruits and has been shown to have extensive biological functions, especially anti-inflammatory effects, but its mechanism is unclear. The purpose of this study was to investigate the potential mechanism of didymin that alleviates ulcerative colitis. Methods and Results: Our results indicated that didymin could alleviate the symptoms of ulcerative colitis, as it inhibited the expressions of interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Didymin also promoted the expressions of claudin-1 and zona occludens-1(ZO-1), which are closely related with restoring colon barrier function. Didymin also increased the abundance of Firmicutes and Verrucomicobiota, while decreasing the abundance of Bacteroidota and Proteobacteria. Meanwhile, didymin significantly altered the levels of metabolites related to arginine synthesis and metabolism, and lysine degradation in the colitis mice. Utilizing network pharmacology and molecular docking, our results showed that the metabolites L-ornithine and saccharin could interact with signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa-B (NF-κB). In this in vitro study, L-ornithine could reduce the expressions of transcription factors STAT3 and NF-κB, and it also inhibited the expressions of IL-6 and IL-1β in the lipopolysaccharides (LPS) induced in RAW264.7 cells, while saccharin had the opposite effect. Conclusions: Taken together, didymin can regulate gut microbiota and alter metabolite products, which can modulate STAT3 and NF-κB pathways and inhibit the expressions of inflammatory factors and inflammatory response in the DSS-induced colitis mice.

Our gut microbiota directly influences human physiology in health and disease. The myriad of surface glycoconjugates in both the bacterial cell envelope and our gut cells dominate the microbiota-host interface and play a critical role in host response and microbiota homeostasis. Among these, peptidoglycan is the basic glycan polymer offering the cell rigidity and a basis on which many other glycoconjugates are anchored. To directly study peptidoglycan in gut commensals and obtain the molecular insight required to understand their functional activities we need effective techniques like chemical probes to label peptidoglycan in live bacteria. Here we report a chemically guided approach to study peptidoglycan in a key mucin-degrading gut microbiota member of the Verrucomicrobia phylum, Akkermansia muciniphila. Two novel non-toxic tetrazine click-compatible peptidoglycan probes with either a cyclopropene or isonitrile handle allowed for the detection and imaging of peptidoglycan synthesis in this intestinal species.