E-GEOD-20523
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA125133
PROVIDER: E-GEOD-20523 | ExpressionAtlas | 2014-09-05
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in epithelial cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression. RESULTS: The deficiency of PPAR g in epithelial cells does not significantly affect disease activity or body weight but worsens colon histopathlogy. WT mice have greater CD4+IL10+ T cells and fewer MHC II+ macrophages in mesenteric lymph nodes. Global gene expression analysis reveals greater changes after 7 days of DSS challenge (compared to 2 days). Colonic mucosa from VC- (WT) and VC+ (PPARg knock-out in epithelial cells) mice were sampled at 0 (no DSS), 2, and 7 days of DSS-induced experimental colitis
2010-07-08 | E-GEOD-20621 | biostudies-arrayexpress
Project description:BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in epithelial cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression. RESULTS: The deficiency of PPAR g in epithelial cells does not significantly affect disease activity or body weight but worsens colon histopathlogy. WT mice have greater CD4+IL10+ T cells and fewer MHC II+ macrophages in mesenteric lymph nodes. Global gene expression analysis reveals greater changes after 7 days of DSS challenge (compared to 2 days).
2010-06-21 | GSE20621 | GEO
Project description:Experimental colitis was induced in mice by the administration of 2% (w/v) Dextran sulfate sodium salt (DSS, colitis grade, 36-50kDa, MP Biomedicals) in the drinking water for 7 days followed by normal drinking water w/o DSS. Distal colons were collected two days later.
2023-10-01 | E-MTAB-12655 | biostudies-arrayexpress
Project description:Experimental colitis was induced in mice by the administration of 1.5% (w/v) Dextran sulfate sodium salt (DSS, colitis grade, 36-50kDa, MP Biomedicals) in the drinking water for 7 days followed by normal drinking water w/o DSS. Distal colons were collected two days later.
2023-10-01 | E-MTAB-12737 | biostudies-arrayexpress
Project description:Background and Aims: The impact of cigarette smoke on inflammatory bowel disease has been established by a large number of epidemiological, clinical, and preclinical studies. Exposure to cigarette smoke is associated with a higher risk of developing Crohn’s disease but is inversely correlated with the development, disease risks, progression, and relapse rate of ulcerative colitis. Few mechanistic studies have investigated the effect of cigarette smoke on intestinal inflammation and microbial composition. Methods: Three groups of mice were exposed to three different concentrations of cigarette smoke for a total of 4 weeks, including 5 days of dextran sulfate sodium treatment to induce colitis and a 7-day recovery period. A comprehensive and integrated comparative analysis of the global colon transcriptome and microbiome, as well as classical endpoints, was performed. Results: Cigarette smoke exposure significantly decreased the severity induced colitis. Colon transcriptome analysis revealed that cigarette smoke downregulated specific pathways in a concentration-dependent manner, affecting both the inflammatory state and composition of the gut microbiome. Metagenomics analysis demonstrated that cigarette smoke can modulate dextran sulfate sodium-induced dysbiosis of specific bacterial genera, contributing to resolve the inflammation or accelerate recovery. Conclusions: Cigarette smoke alters gut microbial composition and reduces inflammatory responses in a concentration-dependent manner. The present study lays the foundation for investigating potential molecular mechanisms responsible for the attenuation of colitis by cigarette smoke.
2020-03-03 | E-MTAB-7988 | biostudies-arrayexpress
Project description:BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in T cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression. METHODS: Wild-type (WT) or PPAR g flfl; CD4 Cre+ (CD4cre) mice in a C57BL/6 background were challenged with 2.5% DSS in their drinking water for 0, 2, or 7 days. Mice were scored on disease severity both clinically and histopathologically. Flow cytometry was used to assess lymphocyte and macrophage populations in the blood, spleen, and mesenteric lymph nodes (MLN). Global gene expression in colonic mucosa was profiled using Affymetrix microarrays. RESULTS: Both disease severity and inflammation-related body weight loss were accelerated by the deficiency of PPAR g in T cells. Examination of colon histopathology revealed significantly greater epithelial erosion, leukocyte infiltration, and mucosal thickening in the CD4cre mice on day 7. CD4cre mice had more CD8+ T cells than wt mice and fewer CD4+FoxP3+ regulatory T cells (Treg) and IL10+CD4+ T cells in blood and MLN, respectively. Transcriptomic profiling revealed around 3000 genes being transcriptionally altered as a result of DSS challenge in CD4cre mice. These included up-regulated adhesion molecules on day 7 and proinflammatory cytokines interleukin-6 (IL-6) and IL-1b, and suppressor of cytokine signaling 3 (SOCS-3) mRNA expression. CONCLUSIONS: These findings suggest that T cell PPAR g down-regulates inflammation during DSS colitis by inhibiting colonic expression of inflammatory mediators and increasing MLN Treg. Colonic mucosa from wt and CD4cre mice were sampled at 0 (no DSS), 2, and 7 days of DSS-induced experimental colitis
2010-07-08 | E-GEOD-20523 | biostudies-arrayexpress
Project description:This study uses whole-transcriptome sequencing to characterize the transcriptomes of the AOM/DSS mouse model. In this model, mice are treated with dextran sodium sulfate (DSS) to induce colitis. When this treatment is preceded by injections of the weak carcinogen azoxymethane (AOM) the mice develop intestinal tumors. Our results identify sets of differentially expressed genes which are correlated with methylation changes of the corresponding genes.
2015-06-17 | GSE57533 | GEO
Project description:This study examines how bone marrow (BM)-resident hematopoietic stem and progenitor cells (HSPCs) are activated by bacterial insults for lineage specification to replenish the host hemato-immune system. We use the dextran sulfate sodium (DSS) colitis model to cause acute gut inflammation and observe molecular changes that occur in MPP2s, which expand both in the BM and MLN upon DSS treatment.
2022-07-07 | GSE207403 | GEO
Project description:The goal of this project is to investigate the role of glucocorticoids and their receptor, glucocorticoid receptor (GR), in intestinal stress response and tissue homeostasis. Using a mouse model with specific deletion of GR in intestinal epithelium (GR iKO mice), we recently discovered that intestinal epithelial GR deficiency deteriorates acute colitis while reducing chronic inflammation-associated colon cancer formation in mice. To understand the molecular mechanisms underlying these phenotypes, we examined colonic transcriptomes of Flox control and GR iKO mice treated with or without dextran sulfate sodium (DSS) for 7 days by microarray analysis.
2021-11-15 | GSE146048 | GEO
Project description:The goal of the experiment was to compare the liver transcriptional profile of wild-type and IL-10 knockout mice with colitis. Colitis was induced in 6 week old female wild-type and IL-10-deficient C57BL/6 mice by administration of 3% dextran sulfate sodium (DSS) in the drinking water for 7 days. At necropsy, segments of liver were homogenized in Trizol and total RNA prepared for the transcriptional profiling.
2014-05-01 | GSE52168 | GEO