DSS-induced Colitis Rats
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ABSTRACT:
PROVIDER: PRJNA634709 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of the effect of A. caninum ES proteins on a DSS-induced mouse model of colitis
2016-12-05 | PXD004369 | Pride
Project description:Background & Aims: Dextran sulphate sodium (DSS) induced colitis in rats is one of the most widely used models of inflammatory bowel disease. Animal models can provide new insights into the pathogenesis of intestinal inflammation, which is still unknown. We have performed a genomic analysis of the DSS rat colitis including an acute and a recovery phase. Methods: Expression profile of 6 control rats were compared with colitic rats at day 1 every other day until day 23 after DSS treatment using the GeneChip Rat Genome 230 2.0 Array (Affymetrix). Functional and pathways analysis were made with the differentially expressed genes. Keywords: Time course and differentially expressed genes analysis
2008-11-01 | GSE9281 | GEO
Project description:To identify potential unique miRs that contribute to shaping the intestinal stemness in colitis, we analyzed the miRNome of colonic crypt stem cells from DSS-induced colitis mice.
2019-09-24 | GSE137892 | GEO
Project description:Alistipes putredinis 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 Alistipes putredinis by RNA sequencing.
2024-12-31 | GSE247421 | GEO
Project description:Commensal intestinal bacteria play key roles in regulating cells mediating immune tolerance; however, bacterial strains and related metabolites directly involved in this regulation are largely unknown. Here, using a mouse model of dextran sulfate sodium (DSS)-induced colitis combined with different antibiotic treatment, Enterobacter ludwigii, abundant in microbiota of mice treated with metronidazole, was screened out to have prophylactic and therapeutic effects on DSS-induced colitis with or without the presence of complex intestinal bacteria. E. ludwigii was demonstrated to induce CD103+DC and Treg-mediated immune tolerance for colitis remission using in vitro and in vivo experiments. Moreover, choline, one of E. ludwigii metabolites, was identified to increase DCs’ immune tolerance to promote Treg differentiation. E. ludwigii was found to induce DCs’ immune tolerance ability for Treg differentiation through choline and α7nAChR-mediated RA and TGF-β upregulation, resulting in protecting mice against DSS-induced colitis. This study provides potential therapeutic approaches for IBD.
2024-08-05 | MTBLS5585 | MetaboLights
Project description:Background: MicroRNAs (miRNAs) acting as negative regulators of gene expression are differentially expressed in intestinal tissues of patients with inflammatory bowel disease (IBD). Assessing the functional role of miRNAs in murine models of colitis facilitates elucidating the role of specific miRNAs in human IBD. The aim of this study was to determine the miRNA signature of murine models of colitis and to assess the influence of miR-21 on intestinal inflammation. Methods: miRNAs expression was accessed by microarray for acute and chronic murine model of colitis induced by DSS or TNBS. miR-21-deficient mouse and littermates controls were assessed in the standard DSS, TNBS and CD4+ T cell transfer models of colitis. RNAs of mouse colon and CD4+CD45RBHigh cells were analyzed by miRNA and mRNA microarray, and quantitative RT-PCR. Th1 polarization was accessed by flow-cytometry and ELISA. Results: Alterations of in miRNAs expression were identified for acute and chronic DSS colitis and TNBS colitis, receptively. The Expression of miRs-21, -142-3p and -223 was were distinct between DSS and TNBS models while overlap of numerous miRNAs was seen. Importantly, miRs-19b, -192 and -215, that are decreased in IBD, were significantly decreased in all 4 models of colitis. miR-21, which is increased in IBD, was increased in TNBS colitis but not the DSS colitis models. Further assessment of the miR-21-deficient 1-/- mice revealed that the deletion of miR-21 results in the exacerbation of both the TNBS and T cell-transfer models of colitis. Conclusions: miRNAs are differentially expressed in both human IBD and murine colitis, with overlap of several IBD-associated miRNAs. The demonstration that miR-21 deletion exacerbated CD4+ T cell-mediated models of colitis provides further evidence that miRNAs play significant roles in the pathogenesis of IBD. miRNAs expression was accesed for acute and chronic murine model of colitis induced by DSS or TNBS.Total of 20 samples with duplicates were analyed in this study.
2014-07-23 | E-GEOD-59649 | biostudies-arrayexpress
Project description:We reported the gene expression profiles of hCYP1A mouse colitis epithelial tissues on Day 1, 3 and 7 after the treatment with DSS or DSS/PhIP for 5 days.
2019-09-14 | GSE137387 | GEO
Project description:Paneth cells, intestine-originated innate immune-like cells, are important for maintenance of the intestinal stem cell niche, gut microbiota, and gastrointestinal barrier. Dysfunctional Paneth cells under pathological conditions are a site of origin for intestinal inflammation. However, mechanisms underlying stress-induced Paneth cell dysregulation remains unclear. We have previously reported that deletion of SIRT1 in the intestinal epithelium (SIRT1 iKO) leads to hyperaction of Paneth cells along with an increased sensitivity to Dextran sodium sulfate (DSS)-induced colitis. We recently generated a Paneth-cell specific SIRT1 KO mouse model (SIRT1 PKO). Similar to mice with SIRT1 iKO mice, SIRT1 PKO mice had increased abundance as well as hyperactivation of Paneth cells in vivo and in cultured intestinal organoids. However, in contrast to the hypersensitivity of SIRT1 iKO mice to chemical- or age-induced inflammation, SIRT1 PKO mice were protected from Dextran sodium sulfate (DSS)-colitis.
2025-03-31 | GSE262546 | GEO
Project description:The spider venom-derived peptide GsMTx4 specifically inhibits mechanosensory ion channels. It has been reported that GsMTx4 plays an immunoregulatory role in several inflammatory conditions. Therefore, we administrated GsMTx4 to mice with dextran sodium sulfate (DSS)-induced acute colitis, to explore whether it regulates inflammatory responses in colitis.
2023-10-15 | GSE215772 | GEO
Project description:TFEB in IEC has a protective role in DSS colitis. The goal is to examine what genes/pathways are TFEB target during DSS colitis
2018-02-22 | GSE98266 | GEO