Ontology highlight
ABSTRACT:
PROVIDER: PRJEB87721 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7894910_cleaned.contigs.fa.gz | Other | |||
| SRR7894914_cleaned.contigs.fa.gz | Other | |||
| SRR7894898_cleaned.contigs.fa.gz | Other | |||
| SRR7894918_cleaned.contigs.fa.gz | Other | |||
| SRR7894919_cleaned.contigs.fa.gz | Other |
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Project description:Clostridioides difficile is one of the most common nosocomial pathogens and a global public health threat. Upon colonization of the gastrointestinal tract, C. difficile is exposed to a rapidly changing polymicrobial environment and a dynamic metabolic milieu. Despite the link between the gut microbiota and susceptibility to C. difficile, the impact of synergistic interactions between the microbiota and pathogens on the outcome of infection is largely unknown. Here, we show that microbial cooperation between C. difficile and Enterococcus has a profound impact on the growth, metabolism, and pathogenesis of C. difficile.. Through a process of nutrient restriction and metabolite cross-feeding, E. faecalis shapes the metabolic environment in the gut to enhance C. difficile fitness and increase toxin production. These findings demonstrate that members of the microbiota, such as Enterococcus, have a previously unappreciated impact on C. difficile behavior and virulence.
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Project description:Oral environment is closely linked to blood pressure regulation, yet the underlying mechanisms remain poorly understood. In this study, we demonstrated that saliva, abundantly secreted in the oral cavity, played a critical role in sustaining the abundance of Bacteroides thetaiotaomicron (Bt) in the gut microbiota, contributing to lowering blood pressure. Further investigation revealed that the mechanism driving this process originated from mucins and metal ions in saliva, which work synergistically to promote Bt growth. In turn, the significantly increased gut abundance of Bt contributed to blood pressure downregulation indirectly by synthesizing short-chain fatty acids and regulating sodium ion channels in the gut. Based on these findings, a unique saliva-driven surface-engineered probiotic strain was developed to advance clinical translational potential by boosting in vivo bioavailability, thus improving blood pressure management. This study not only revealed that saliva lowered blood pressure through gut microbiota but also proposes a novel perspective to hypertension management.
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Project description:The larynx is essential for swallowing, breathing, coughing, and voice production, supported by its unique microbial and immunological environment. Our previous research highlighted the role of resident laryngeal microbiota in shaping local immune responses. With growing interest in the gut-lung axis—the bidirectional communication between gut and respiratory immunity—the potential influence of gut microbiota on laryngeal immunity warrants exploration. We hypothesized that a gut-larynx axis may exist, where both resident laryngeal and gut microbiota contribute to immune modulation in the larynx. To investigate this, we treated conventionally raised, wild-type C57BL/6J mice with an oral antibiotic regimen known to disrupt gut microbiota, comparing them to untreated controls. Following treatment, the gut microbiota was significantly disrupted, while the laryngeal microbiota remained largely unchanged. However, antibiotic-treated mice exhibited marked changes in epithelial and immune cell proportions, as well as fibroblasts. Differential gene expression across cell types highlighted pathways related to epithelial barrier integrity, immune signaling, and bacterial response. Additionally, gut dysbiosis affected gene regulatory networks, with the activity of regulons Etv4(+), Irf3(+), Hltf(+), Mga(+), and Nfil3(+) showing significant changes. Notably, cell-cell communication was also altered, especially in immune-epithelial interactions, with integrin-mediated signaling emerging as a key ligand-receptor pathway in these intercellular communications. These findings suggest that gut and laryngeal microbiota may work synergistically to modulate immune responses in the larynx, underscoring the importance of considering gut-larynx interactions in studies of respiratory immunity.
2025-03-04 | GSE290718 | GEO
Project description:Adequate sleep is essential for relieving stress and rejuvenating the mind; however, undesirable physiological and pathological responses resulting from sleep insufficiency or sleep deprivation (SD) are becoming increasingly common. However, the influence of sleep deficiency on gut microbiota and microbiota-associated human diseases, especially on cardiac diseases remain controversial. Here, we constructed the experimental SD model in mice and found it significantly resulted in weakness, depression-like behaviors, and multiple organs dysfunction. Intriguingly, SD mice developed pathogenic cardiac hypertrophy and fibrosis with poor ejection fraction as well as fractional shortening. 16s rRNA sequencing demonstrated that SD-induced the pathogenic effects of gut microbiota, which was also observed in mice received by fecal microbe from SD mice in fecal microbiota transplantation (FMT) assays. Next, we investigated the therapeutic effects and underlying mechanisms of oxygen therapy in gut microbiota-associated cardiac fibrosis and dysfunction. The environment of 30% oxygen concentration effectively ameliorated the pathological effects on cardiac function. Transcriptome data also found oxygen therapy targeted several hypoxia-dependent pathways and suppressed cardiac collagen production. In conclusion, these results indicated the importance of sufficient sleep in gut microbiota and may represent a potential therapeutic strategy of oxygen environment exerts protective effects in sleepless sufferings through gut microbiota.
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Project description:Maternal secretor status is one of the determinants of human milk oligosaccharides (HMOs) composition, which in turn changes the gut microbiota composition of infants. To understand if this change in gut microbiota impacts immune cell composition, intestinal morphology and gene expression, day 21-old germ-free mice were transplanted with fecal microbiota from infants whose mothers were either secretors (SMM) or non-secretors (NSM) or from infants consuming dairy-based formula (MFM). For each group, one set of mice was supplemented with HMOs. HMO supplementation did not significantly impact the microbiota diversity however, SMM mice had higher abundance of genus Bacteroides, Bifidobacterium, and Blautia, whereas, in the NSM group, there were higher abundance of Akkermansia, Enterocloster, and Klebsiella. In MFM, gut microbiota was represented mainly by Parabacteroides, Ruminococcaceae_unclassified, and Clostrodium_sensu_stricto. In mesenteric lymph node, Foxp3+ T cells and innate lymphoid cells type 2 (ILC2) were increased in MFM mice supplemented with HMOs while in the spleen, they were increased in SMM+HMOs mice. Similarly, serum immunoglobulin A (IgA) was also elevated in MFM+HMOs group. Distinct global gene expression of the gut was observed in each microbiota group, which was enhanced with HMOs supplementation. Overall, our data shows that distinct infant gut microbiota due to maternal secretor status or consumption of dairy-based formula and HMO supplementation impacts immune cell composition, antibody response and intestinal gene expression in a mouse model.
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Project description:Background Alterations of the gut microbiome have been linked to multiple chronic diseases. However, the drivers of such changes remain largely unknown. The oral cavity acts as a major route of exposure to exogenous factors including pathogens, and processes therein may affect the communities in the subsequent compartments of the gastrointestinal tract. Here, we perform strain-resolved, integrated multi-omic analyses of saliva and stool samples collected from eight families with multiple cases of type 1 diabetes mellitus (T1DM). Results We identified distinct oral microbiota mostly reflecting competition between streptococcal species. More specifically, we found a decreased abundance of the commensal Streptococcus salivarius in the oral cavity of T1DM individuals, which is linked to its apparent competition with the pathobiont Streptococcus mutans. The decrease in S. salivarius in the oral cavity was also associated with its decrease in the gut as well as higher abundances in facultative anaerobes including Enterobacteria. In addition, we found evidence of gut inflammation in T1DM as reflected in the expression profiles of the Enterobacteria as well as in the human gut proteome. Finally, we were able to follow transmitted strain-variants from the oral cavity to the gut at the metagenomic, metatranscriptomic and metaproteomic levels, highlighting not only the transfer, but also the activity of the transmitted taxa along the gastrointestinal tract. Conclusions Alterations of the oral microbiome in the context of T1DM impact the microbial communities in the lower gut, in particular through the reduction of “oral-to-gut” transfer of Streptococcus salivarius. Our results indicate that the observed oral-cavity-driven gut microbiome changes may contribute towards the inflammatory processes involved in T1DM. Through the integration of multi-omic analyses, we resolve strain-variant “mouth-to-gut” transfer in a disease context.
2022-10-05 | PXD031579 | Pride