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Effect of Bacteroides vulgatus on colitis and depressive-like behavior in a murine model of inflammatory bowel disease: involvement of the gut-brain axis

ABSTRACT: IBD is characterized by chronic recurrences of intestinal inflammation and intestinal immune disturbances.Bacteroides vulgatus can alleviate DSS-induced colitis in mice, but the mechanism is unknown. The aim of this study was to examine the changes in gene expression in the intestinal tissue of mice with colitis following treatment with Bacteroides vulgatus by RNA sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE246118 | GEO | 2023/12/06

REPOSITORIES: GEO

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Bacteroides thetaiotaomicron ameliorates colon inflammation in preclinical models of Crohn’s Disease [Bacteroides]

Project description:Analysis of the Bacteroides thetaiotaomicron(BT) transcriptome during co-culture with Caco-2 intestinal epithelial cells To identify potential bacterial protein(s) involved in the anti-inflammatory effect of BT in colitis, BT was incubated with Caco-2 human intestinal epithelial cells for 2 hours, and bacterial gene expression was assessed on a Bacteroides thetaiotaomicron VPI-5482 specific microarray. Forty-three BT genes were up-regulated by five-fold or more and of these, twenty genes encoded hypothetical proteins.

2019-03-06 | GSE118525 | GEO

Transcriptome of IL-13 treated small intestinal tissue in Nod2-/- mice

Project description:We previously found that mice deficient in the CD susceptibility gene Nod2 develop small intestinal abnormalities including impaired mucus production by goblet cells and susceptibility to injury, which were associated with interferon-gamma producing intraepithelial lymphocytes. These abnormalities were caused by a striking expansion of a common member of the microbiota, Bacteroides vulgatus. Remarkably, infection of Nod2-deficient mice with the helminth Trichuris muris led to a TH2 response that eliminated B. vulgatus colonization and intestinal abnormalities. In addition, treatment with recombinant IL13 (rIL13) or recombinant IL4 reduced B. vulgatus levels and eliminated goblet cell defects, suggesting that type 2 cytokines alone can reverse intestinal abnormalities in the absence of helminth infection. To determine the mechanism by which type 2 cytokines protected Nod2-/- mice from intestinal abnormalities, we performed RNA-seq on small intestinal tissue from WT, Nod2-/- and rIL13 treated Nod2-/- mice. We found that rIL13 treatment induced a wound healing response characterized by M2 macrophage activation genes. Hence, type 2 cytokines can reverse inflammatory imbalances in the composition of the gut microbiota that occurs in a genetically susceptible host.

2016-04-28 | GSE76504 | GEO

Bacteroides vulgatus CAG:6

Project description:Bacteroides vulgatus CAG:6 overview

| PRJNA207247 | ENA

single bacterial species LC-MS/MS

Project description:Analysis of six types of single bacterial species, including Bacteroides vulgatus ATCC 8482,Bacteroides ovatus ATCC 8483, Bacteroides uniformis ATCC 8492, Blautia hydrogenotrophica DSM 10507, Bacteroides thetaiotaomicron ATCC 29148, Escherichia coli DSM 101114

2023-03-11 | PXD037839 | Pride

The Enterotoxigenic Bacteroides fragilis (ETBF) in intestinal inflammation and colorectal carcinogenesis [exosomes]

Project description:To elucidate whether Enterotoxigenic Bacteroides fragilis (ETBF) plays a role in intestinal inflammation and colorectal carcinogenesis, a RNA-seq analysis was performed to compare the microRNA profiles of exosomes derived from ETBF-treated HCT116 colorectal cancer cell lines.

2023-11-08 | GSE161048 | GEO

The Enterotoxigenic Bacteroides fragilis (ETBF) in intestinal inflammation and colorectal carcinogenesis [whole cell RNA]

2023-11-08 | GSE161047 | GEO

Specific Gut Microbial Enzymes Drive Colitis Promotion by Triclosan

Project description:Triclosan (TCS), an antimicrobial agent in thousands of consumer products, is a risk factor for colitis and colitis-associated colorectal cancer. While the intestinal toxicities of TCS require the presence of gut microbiota, the molecular mechanisms involved have not been defined. Here we show that intestinal commensal microbes mediate metabolic activation of TCS in the colon and drive its gut toxicology. Using a range of in vitro, ex vivo, and in vivo approaches, we identify specific microbial β-glucuronidase (GUS) enzymes involved and pinpoint molecular motifs required to metabolically activate TCS in the gut. Finally, we show that targeted inhibition of bacterial GUS enzymes abolishes the colitis-promoting effects of TCS, supporting the essential roles of specific microbial proteins in TCS toxicity. Our results define a mechanism by which intestinal microbes cause the gut toxicity of environmental chemicals and suggest a therapeutic approach to alleviate colitis and associated diseases.

2021-11-04 | PXD025887 | Pride

Genome-wide RNA-seq of Bacteroides thetaiotaomicron VPI-5482 with Bacteroides phage challenge

Project description:Purpose: Examining the transcriptome of Bacteroides thetaiotaomicron VPI-5482 challenged with Bacteroides phage to assess surface molecule expression changes Methods: Bacteroides thetaiotaomicron was grown in BPRM in vitro or Germ-Free mice were monocolonized with Bacteroides thetaiotaomicron and gavaged with ARB25 phage. Fold change was calculated as live phage versus heat-killed phage treated samples with n=3 biological replicates. Once cells reached an optical density corresponding to mid-log phase growth (absorbance between 0.4-0.5), RNA was isolated and rRNA depleted. Samples were multiplexed for sequencing on the Illumina HiSeq platform at the University of Michigan Sequencing Core. Data was analyzed using Arraystar software (DNASTAR, Inc.) using DEseq2 normalization with default parameters. Genes with significant up- or down-regulation were determined by the following criteria: genes with an average fold-change >5-fold and with at least 2/3 biological replicates with a normalized expression level >1% of the overall average, and a p-value < 0.05 (t test with Benjamini-Hochberg correction) Results: Specific capsule expression was increased in wild-type B. thetaiotaomicron during phage infection in vitro and in vivo. Many corresponding in vivo genes were upregulated as well as other surface layer proteins.

2020-05-01 | GSE147071 | GEO

Role of the E3 Ubiquitin-ligase Hakai in intestinal inflammation and cancer bowel disease

Project description:E3 ubiquitin-ligases are important for the cellular protein homeostasis and their deregulation is implicated in cancer. The E3 ubiquitin-ligase Hakai is involved in tumour progression and metastasis, through the regulation of the tumour suppressor E-cadherin. Hakai is overexpressed in colon cancer, however, the implication in colitis-associated cancer is unknown. Here, we investigated the potential role of Hakai in intestinal inflammation and cancer bowel disease.Several mouse models of colitis and associated cancer were used including AOM-DSS, acute colitis, and genetically modified mice deficient for the IL-10 gene, to analyse Hakai expression by immunohistochemistry. Interactome analysis of Hakai was performed and effect on selected protein was determined by plasmid and siRNA transfection, western-blotting, immunoprecipitation, immunofluorescence and ubiquitination assays. Lipid accumulation was assayed by oil red staining. Immunohistochemistry was also performed in inflamed colon biopsies from ulcerative colitis, Crohn's disease and colorectal cancer patients. Our results show that Hakai was downregulated in inflammatory tissues in different mouse models. Fatty Acid Synthase (FASN) protein was identified as a novel Hakai-interacting protein. Hakai induces FASN ubiquitination and degradation via lysosome, thus regulating FASN-mediated lipid accumulation. An inverse expression of FASN with Hakai expression was detected in inflammatory AOM/DSS mouse model. In conclusion, Hakai regulates FASN ubiquitination and degradation, resulting in the regulation of FASN-mediated lipid accumulation, which is associated to the development of inflammatory bowel disease. The interaction between Hakai and FASN may be an important mechanism for the homeostasis of intestinal barrier function and in the pathogenesis of this disease.

2022-10-25 | PXD029136 | Pride

In vitro transcriptional profiling of Bacteroides fragilis in glucose and human milk oligosaccharides

Project description:The factors that govern the retention and abundance of specific microbial lineages within a developing intestinal microbiota remain poorly defined. Human milk oligosaccharides consumed by nursing infnats pass undigested to the distal gut where they may be consumed by microbes. We investigated the transcriptional response of Bacterides fragilis, a prominent gut resident, to the presence of HMOs. In vitro transcriptional profiles of Bacteroides fragilis obtained from biological duplicate cultures taken at middle log phase in minimal media glucose (MM-Glu) and in minimal media with human milk oligosaccharides (MM-HMO).

2012-09-30 | E-GEOD-32207 | biostudies-arrayexpress

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