Gene Array Analysis of Methylthioadenosine Supplementation in Dextran Sulfate Sodium Induced Colitis
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE34553 | GEO | 2011/12/20
SECONDARY ACCESSION(S): PRJNA151361
REPOSITORIES: GEO
Similar Datasets
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
2011-12-20 | E-GEOD-34553 | biostudies-arrayexpress
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.
2020-11-03 | E-MTAB-8543 | biostudies-arrayexpress
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).
2008-11-13 | E-GEOD-9281 | biostudies-arrayexpress
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.
2021-08-16 | GSE181959 | GEO
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:The gut and brain are increasingly linked in human disease, with neuropsychiatric conditions classically long attributed to the brain showing an involvement of the intestine and inflammatory bowel diseases displaying an ever-lengthening list of neurological comorbidities. To identify molecular systems that underpin this gut-brain connection and thus discover therapeutic targets, experimental models of gut dysfunction must be evaluated for brain effects. In the present study, we examine disturbances along the gut-brain axis in a widely used murine model of colitis, the dextran sodium sulfate (DSS) model, using high-throughput transcriptomics and an unbiased network analysis strategy coupled with standard outcome measures, yielding a comprehensive approach to identify key disease processes in both colon and brain. We examine the reproducibility of colitis induction with this model and its resulting genetic programs during different phases of disease, finding that DSS-induced colitis is largely reproducible with a few site-specific molecular features. We focus on the circulating immune system, which exhibits an activation of pro-inflammatory innate immunity during colitis, as the vessel between gut and brain. Our unbiased approach provides supporting evidence for immune activation in the brain during colitis, suggests that myelination may be a vulnerable system with intestinal permeability, and identifies a possible role for oxidative stress and brain oxygenation. Overall, we provide a comprehensive evaluation of multiple systems in a prevalent experimental model of intestinal permeability, which will inform future studies using this model and others, assist in the identification of druggable targets, and contribute to our understanding of the concomitance of intestinal and neuropsychiatric dysfunction.
2023-08-01 | GSE239820 | GEO
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.
2015-02-08 | E-GEOD-35651 | biostudies-arrayexpress
Project description:Within the secreted phospholipase A2 (sPLA2) family, group X sPLA2 (sPLA2-X) has the highest capacity to hydrolyze cellular membranes and has long been thought to promote inflammation by releasing arachidonic acid (AA), a precursor of pro-inflammatory eicosanoids. Unexpectedly, we found that transgenic mice globally overexpressing human sPLA2-X (PLA2G10-Tg) displayed striking immunosuppressive and lean phenotypes with lymphopenia and increased M2-like macrophages, accompanied by marked elevation of free omega-3 polyunsaturated fatty acids (PUFAs) and their metabolites. Studies using Pla2g10-deficient mice revealed that endogenous sPLA2-X, which is highly expressed in the colon epithelium and spermatozoa, mobilized omega-3 PUFAs or their metabolites to protect against dextran sulfate sodium (DSS)-induced colitis and to promote fertilization, respectively. In colitis, sPLA2-X deficiency increased colorectal expression of Th17 cytokines, and omega-3 PUFAs attenuated their production by lamina propria cells partly through the fatty acid receptor GPR120. In comparison, cytosolic phospholipase A2 (cPLA2alpha) protects from colitis by mobilizing omega-6 AA metabolites including prostaglandin E2. Thus, our results underscore a previously unrecognized role of sPLA2-X as an omega-3 PUFA mobilizer in vivo, segregated mobilization of omega-3 and omega-6 PUFA metabolites by sPLA2-X and cPLA2alpha, respectively, in protection against colitis, and the novel role of a particular sPLA2-X-driven PUFA in fertilization.
2016-02-01 | GSE77144 | GEO
Project description:Tristetraprolin (TTP, encoded by Zfp36) is an RNA-binding protein that plays a major role in the control of inflammation. Zfp36 -/-mice spontaneously develop a complex multi-organ inflammatory syndrome that shares many features with spondyloarthritis. Herein, we show that Zfp36 -/-mice are paradoxically protected from Dextran Sulfate Sodium (DSS)-induced colitis. This effect was maintained on a Rag2 -/- background but was lost in Rag2 -/-Il2rg -/-Zfp36 -/-mice that lack innate lymphoid cells (ILCs). Furthermore, we observed a local expansion of type 3 ILCs in the lamina propria of Zfp36 -/-mice. These cells produced large amounts of Interleukin (IL)-22 and were expanded in response to systemic inflammation. Finally, we show that IL-22 contributed to protection of Zfp36 -/-mice against DSSinduced colitis but had a minor impact on their spontaneous inflammatory syndrome. Taken together, these data highlight the complex role of TTP in the control of organ-specific inflammation.
2023-08-01 | GSE236230 | GEO
Project description:Luminal (cecal) metabolome of DSS-colitis mice and control mice were compared.
2019-09-12 | ST001250 | MetabolomicsWorkbench