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
Project description:Increased levels of tissue inhibitor of metalloproteinase-1 (TIMP-1) have been detected in fibrotic strictures in Crohnâs disease. In a murine model of chronic inflammation, fibrosis was associated with an increase in TIMP-1 and inhibition of matrix metalloproteinase (MMP)-mediated degradation. We investigated the effect of TIMP-1 deficiency on the colonic gene expression in acute and chronic murine models of colitis, using whole genome gene expression arrays. Colitis was induced via oral administration of dextran sodium sulphate (DSS) to B6.129S4-Timp1tm1Pds/J knock-out (KO) and C57BL/6J wild-type (WT) mice. Total RNA extracted from snap frozen colon was used to analyze mRNA expression via Affymetrix Mouse Gene 1.0 ST Arrays
Project description:We showed different function of monocyte derived cells in the lamina propria of the colon under steady state and inflammatory conditions. We used microarrays to detail the global programme of gene expression and identified distinct clusters of regulated genes during this process. Different subsets of mononuclear phagocytes were sorted from the colonic lamina propria as well as the spleen. Sorting was done in C57BL/6 mice in steady state and under inflammatory conditions (Dextran Sodium Sulphate induced colitis model)
Project description:The lack of suitable animal models reflecting chronically relapsing inflammation and tissue remodeling have hindered fibrosis research in inflammatory bowel diseases (IBD). This study investigated changes in connective tissue in a chronic murine model using different cycles of dextran sodium sulphate (DSS) to mimic the relapsing nature of the disease. We used whole gene expression arrays to study differences in colonic gene expression levels between acute and more chronic DSS colitis, Acute and chronic relapsing colonic inflammation was induced in C57BL6 female mice using several cycles of exposure to DSS in drinking water, followed by recovery phases. Total RNA, extracted from snap frozen colon from five mice per condition was used to analyze mRNA expression via Affymetrix Mouse Gene 1.0 ST arrays.
Project description:The current study was designed to clarify signalling pathways and assess possible beneficial effect of new probiotic mixture in DSS (dextran sulphate sodium) – induced colitis mouse model. Manipulation of intestinal microbiota with probiotics represents a promising alternative or adjunct therapy in gastrointestinal disorders and inflammation. RNA extracted from the middle part of colon tissue from ~11 weeks female C57BL/6JOlaHsd mouse strain was used for examination of the global gene expression using Affymetrix GeneChip Mouse Gene 2.0 ST microarrays.
Project description:Smarcad1 is one of the most conserved chromatin remodelling factors, from yeast to human, with suggested functions in gene silencing, heterochromatin maintenance and genome stability. However, its role in tissue function is poorly understood. As this factor is highly expressed in the stem- and proliferative zone in the intestinal epithelium, we explored the role of this factor in this tissue. Specific deletion of Smarcad1 in the intestinal epithelium led to colitis resistance in the dextran sodium sulphate colitis model. We identified candidate members of the gut microbiome that elicit an epithelial Smarcad1-dependent colitis response.