Ecoli Nissle
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ABSTRACT:
PROVIDER: PRJEB71393 | ENA |
REPOSITORIES: ENA
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Project description:Intervention group:High flavonoid content fruit and vegetable diet guidance;Control group:No
Primary outcome(s): Flavonoid markers;Salivary cortisol;Blood cortisol;Gut microbiota;Mental Health Assessment Questionnaire;Fecal short chain fatty acids;Changes in defecation habits and traits
Study Design: Parallel
| 2717029 | ecrin-mdr-crc
Project description:Intracerebral hemorrhage (ICH) induces alterations in the gut microbiota composition, significantly impacting neuroinflammation post-ICH. However, the impact of gut microbiota absence on neuroinflammation following ICH-induced brain injury remain unexplored. Here, we observed that the gut microbiota absence was associated with reduced neuroinflammation, alleviated neurological dysfunction, and mitigated gut barrier dysfunction post-ICH. In contrast, recolonization of microbiota from ICH-induced SPF mice by transplantation of fecal microbiota (FMT) exacerbated brain injury and gut impairment post-ICH. Additionally, microglia with transcriptional changes mediated the protective effects of gut microbiota absence on brain injury, with Apoe emerging as a hub gene. Subsequently, Apoe deficiency in peri-hematomal microglia was associated with improved brain injury. Finally, we revealed that gut microbiota influence brain injury and gut impairment via gut-derived short-chain fatty acids (SCFA).
2024-05-13 | GSE266602 | GEO
Project description:It has been shown in vitro that only specific dietary-fibers contribute to immunity but studies in vivo are not conclusive. Here we investigated degree of polymerization (DP) dependent effects of β2→1-fructans on immunity via microbiota-dependent and -independent effects. To this end, conventional or germ-free mice received short- or long-chain β2→1-fructan for 5 days. Immune cell populations in the spleen, mesenteric lymph nodes (MLN), and Peyer's patches (PPs) were analyzed with flow cytometry, genome-wide gene expression in the ileum was measured with microarray, and gut microbiota composition was analyzed with 16S rRNA sequencing of fecal samples. We found that β2→1-fructans modulated immunity by both microbiota and microbiota-independent effects. Moreover, effects were dependent on the chain-length of the β2→1-fructans type polymer. Both short- and long-chain β2→1-fructans enhanced T-helper 1 cells in Peyer's patches, whereas only short-chain β2→1-fructans increased regulatory T cells and CD11b-CD103- DCs in the MLN. A common feature after short- and long-chain β2→1-fructan treatment was enhanced Fut2 expression and other IL-22-dependent genes in the ileum of conventional mice. These effects were not associated with shifts in gut microbiota composition, or altered production of short-chain fatty acids. Both short- and long-chain β2→1-fructans also induced immune effects in germ-free animals, demonstrating direct effect independent from the gut microbiota. Also, these effects were dependent on the chain-length of the β2→1-fructans. Short-chain β2→1-fructan induced lower CD80 expression by CD11b-CD103- DCs in PPs, whereas long-chain β2→1-fructan specifically modulated B cell responses in germ-free mice. In conclusion, support of immunity is determined by the chemical structure of β2→1-fructans and is partially microbiota-independent.
2018-03-22 | GSE94516 | GEO
Project description:L. lactis-GLP-1-DA@GN effectively treated T2DM by alleviating hyperglycemia and hyperlipidemia symptoms, restoring damage of major organs, and positively modulating gut microbiota due to the synergy of secreted GLP-1 and generated short-chain fatty acids.
2024-03-30 | PXD051118 |
Project description:Approximately 15% of US adults have circulating levels of uric acid above its solubility limit, which is causally linked to the inflammatory disease gout. In most mammals, uric acid elimination is facilitated by the enzyme uricase. However, human uricase is a pseudogene, having been inactivated early in hominid evolution. Though it has long been known that a substantial amount of uric acid is eliminated in the gut, the role of the gut microbiota in hyperuricemia has not been studied. Here we identify a gene cluster, widely distributed in the gut microbiome, that encodes a pathway for uric acid degradation. Stable isotope tracing demonstrates that gut bacteria metabolize uric acid to xanthine or short chain fatty acids such as acetate, lactate and butyrate. Ablation of the microbiota in uricase-deficient mice causes profound hyperuricemia, and anaerobe-targeted antibiotics increase the risk of gout in humans. These data reveal a role for the gut microbiota in uric acid excretion and highlight the potential for microbiome-targeted therapeutics in hyperuricemia.
2023-06-16 | GSE206419 | GEO
Project description:We analyzed gut microbiota composition in stool, inflammation factor and short chain fatty acid (SCFAs) in plasma, inflammatory and permeability marker in intestinal mucosa in inflammatory depression patients.
2024-03-06 | PXD050388 |
Project description:Commensal microbiota contribute to gut homeostasis and influence mucosal gene expression. We harvested mucosal lining of middle and distal part of the small intestine and colon from germ-free (GF) and gnotobiotic mice monocolonized either with the E.coli strain O6K13 (O) or Nissle 1917 strain (N). The expression profiles of the mucosa samples were compared to the corresponding tissue isolated from conventionally reared mice in order to disclose genes differentially expressed in response to the change in the intestinal microflora composition.
2019-09-13 | E-MTAB-7726 | biostudies-arrayexpress
Project description:Gut microbiota-derived short-chain fatty acids protect against the progression of endometriosis
| PRJNA764669 | ENA
Project description:Acetate, propionate and butyrate are the main short-chain fatty acids (SCFAs) that arise from the fermentation of fibers by the colonic microbiota. While many studies focus on the regulatory role of SCFAs, their quantitative role as a catabolic or anabolic substrate for the host has received relatively little attention. To investigate this aspect, we infused conscious mice with physiological quantities of stable isotopes [1-13C]acetate, [2-13C]propionate or [2,4-13C2]butyrate directly into the cecum, which is the natural production site in mice, and analyzed their interconversion by the microbiota as well as their metabolism by the host. Cecal interconversion - pointing to microbial cross-feeding - was high between acetate and butyrate, low between butyrate and propionate and almost absent between acetate and propionate. As much as 62% of infused propionate was used in whole-body glucose production, in line with its role as gluconeogenic substrate. Conversely, glucose synthesis from propionate accounted for 69% of total glucose production. The synthesis of palmitate and cholesterol in the liver was high from cecal acetate (2.8% and 0.7%, respectively) and butyrate (2.7% and 0.9%, respectively) as substrates, but low or absent from propionate (0.6% and 0.0%, respectively). Label incorporation due to chain elongation of stearate was approximately 8-fold higher than de novo synthesis of stearate. Microarray data suggested that SCFAs exert only a mild regulatory effect on the expression of genes involved in hepatic metabolic pathways during the 6h infusion period. Altogether, gut-derived acetate, propionate and butyrate play important roles as substrates for glucose, cholesterol and lipid metabolism. Mice were infused in cecum with stably-labelled isotopes of the three main short chain fatty acids or control solution. After 6 hrs, livers were removed and pooled RNA samples were subjected to gene expression profiling.
2013-10-21 | E-GEOD-45926 | biostudies-arrayexpress