Project description:Study hypothesized that oral supplementation of methylthioadenosine (MTA) would reduce the inflammatory response in mice exposed to an agent that induces colitis (DSS) and that this reduction in inflammatory response would lead to reduced clinical disease burden. Total RNA was collected from isolated colons of mice in the following treatment groups: untreated controls, DSS only, DSS+MTA
Project description:Study hypothesized that oral supplementation of methylthioadenosine (MTA) would reduce the inflammatory response in mice exposed to an agent that induces colitis (DSS) and that this reduction in inflammatory response would lead to reduced clinical disease burden.
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. Experiment Overall Design: Experimental design: DSS was administered to animals in drinking water as follows:5%DSS from day 1 to 7, 3%DSS from day 8 to 15, 0% DSS from day 16 to 23. Samples were recovered at days 1, 3, 5, 7 (5%DSS), 9, 11, 13, 15 (2%DSS), 17, 19, 21 and 23 (0%DSS). According to inflammatory markers (Myeloperoxidase activity activity, body weight loss, colonic weigth/length ratio), three replicates at each time point were selected for genomic analysis and 6 control healthy rats (42 arrays). Experiment Overall Design: RNA was extracted from homogenized full-thickness colonic tissues in Trizol® reagent (Invitrogen) and purified with RNeasy affinity columns (Qiagen), according to manufacturer´s protocol. The microarray analysis was performed by Progenika Biopharma (Bilbao, Spain) on GeneChip® Rat Genome 230 2.0 Array (Affymetrix). All sample labeling (biotin), hybridization, staining and scanning procedures were carried out using Affimetrix, standard protocols (www.affymetrix.com). Normalization was carried out using Bioconductor sofware (affyPLM package).
Project description:Objective: In this study, we aimed to evaluate the anti-inflammatory properties of nicotine and anatabine in a dextran sulfate sodium (DSS) mouse model of ulcerative colitis (UC). Methods: C57BL/6 male mice (10 groups with 8 animals each) were orally administered nicotine at a concentration of 5 or 20 mg/kg body weight or anatabine at a concentration of 5 or 20 mg/kg body weight for a total of 21 days. Colitis was induced by oral administration of 3.5% DSS in drinking water ad libitum during days 14–21. Colonic samples were collected for transcriptomic analysis and multi-analyte profiling (MAP). Results: Oral administration of anatabine, but not nicotine, reduced the clinical symptoms of DSS-induced colitis. The result of gene expression analysis suggested that anatabine had a restorative effect on global DSS-induced gene expression profiles, while nicotine only had limited effects. Accordingly, MAP findings revealed that anatabine reduced the colonic abundance of DSS-associated cytokines and increased IL‑10 abundance. Conclusions: Our results support the reduction of inflammatory effects by anatabine in the DSS mouse model of UC.
Project description:To understand the role of ATF6a and ATF6b in non-canonical endoplasmic reticulum stress response pathway, we have employed whole genome microarray expression profiling to identify the genes regulated by ATF6s. WIild type or, ER stress mediators,ATF6a or ATF6b-knockout mice were treated with 3% DSS for 3days. Genes responsible for DSS in each mediator-dependent manner were extracted and categorized by Gene Ontology. Among them, expression of three cell structure-related genes (Muc2, Muc3, Muc4) was quantified in the RNA samples from another mice treated with DSS by real-time PCR. Colitis was induced with 3% DSS, 36,000-50,000 M.W. (MP Biomedicals,) in the drinking water for 3 days. Genes responsible for DSS treatment in each mediator-dependent manner were extracted and categorized by Gene Ontology in GeneRanker program of Genomatix platform.
Project description:TMT proteomics for colonic mucosa in DSS-induced colitis mice with or without administrated Cyanidin-3-O-glucoside was used for discovery of differential expressed proteins.
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: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:We compared the transcriptional signatures of the colonic mucosa from control mice (WT) versus mice deficient for the epithelial pantetheinase Vnn1 (Vnn1KO) or overexpressing Vnn1 specifically in intestinal epithelial cells (VIVA transgenic mice), during the development of DSS-induced colitis.
Project description:Liver injury is a common complication of inflammatory bowel disease (IBD). However, the mechanisms of liver injury development are not clear in IBD patients. Gut microbiota is thought to be engaged in IBD pathogenesis. Here, by an integrated analysis of host transcriptome and colonic microbiome, we have attempted to reveal the mechanism of liver injury in colitis mice. In this study, dextran sulfate sodium (DSS) -induced mice colitis model was constructed. Liver and colon transcriptome results showed that immune response and lipid metabolism-related pathways were dramatically altered, while DNA damage repair-related pathways were only significantly down-regulated in the colon. The microbiota of DSS-treated mice underwent strong transitions. Correlation analyses identified genes associated with liver and colon injury, whose expression was associated with the abundance of liver and gut health-related bacteria Collectively, the results indicate that the liver injury in colitis mice may be related to the intestinal dysbiosis and host-microbiota interactions. These findings may provide new insights for identifying potential targets for the treatment of IBD and its induced liver injury.