Genomic profile of trinitrobencenesulfonic acid (TNBS)-induced colitis model
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE9293 | GEO | 2008/11/01
SECONDARY ACCESSION(S): PRJNA102933
REPOSITORIES: GEO
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Project description:Trinitrobenzenesulfonic acid (TNBS) rat colitis is one of the most widely used models of inflammatory bowel disease, a condition whose etiology and pathophysiology are incompletely understood. We have characterized the model at the genomic level following a longitudinal approach. Experiment Overall Design: A single enema of 10mg of TNBS in 50% ethanol was administered to rats at day 0. Samples were recovered at days 2, 5, 7 and 14. According to inflammatory markers (myeloperoxidase activity, body weigh loss, colonic weigh/length ratio) we selected three replicates at each time point for the genimoc analysis, and 6 healthy control rats that received a saline enema. 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-9293 | biostudies-arrayexpress
Project description:Experimental colitis is often used as a model for the inflammatory bowel diseases, ulcerative colitis and Crohn’s disease. Results identify the inflammatory processes during acute colitis in affected tissues from TNBS-treated susceptible 5-7 week old SJL mice. Keywords: Disease state analysis
2008-09-08 | GSE12139 | GEO
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.
2014-07-23 | GSE59650 | GEO
Project description:Experimental colitis is often used as a model for the inflammatory bowel diseases, ulcerative colitis and Crohn’s disease. Results identify the inflammatory processes during acute colitis in affected tissues from TNBS-treated susceptible 5-7 week old SJL mice. Keywords: Disease state analysis Two-condition experiment, Treated vs Non-treated. Biological replicates: 4 treated, 4 non-treated. One replicate per array.
2008-09-08 | E-GEOD-12139 | biostudies-arrayexpress
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-59650 | biostudies-arrayexpress
Project description:To test TWEAK/Fn14 pathway and relative agents in chronic TNBS colitis
2013-06-20 | GSE36806 | GEO
Project description:We investigated the relationship between chronic inflammation and fibrosis in a mouse model of chronic colitis. Six weekly Trinitrobenzenesulphonic acid (TNBS) enemas were given to establish colitis and temporal changes in gene expression was elucidated over the next six weeks. Experiment Overall Design: After the six TNBS enemas, mice were sacrificed at 3 days (termed as TNBS-w6, n=6), 2 weeks (TNBS-w8, n=4), 4 weeks (TNBS-w10, n=5), or 6 weeks (TNBS-w12, n=4). The saline control groups were also sacrificed at week 6 (Saline-w6, n=5), week 8 (n=2) and week 10 (n=2). The last two sets were pooled as Saline-w10 (n=4). Two replicates of saline-w6 were analyzed. We compared Saline-w6 with TNBS-w6, and Saline-w10 with TNBS-w8, TNBS-w10, TNBS-w12, respectively.
2008-06-14 | E-GEOD-5864 | biostudies-arrayexpress
Project description:To test TWEAK/Fn14 pathway and relative agents in chronic TNBS colitis Chronic colitis was induced by rectal injection of TNBS with ethanol for 6 weeks in WT or FN14 KO BALB/c mice. Colons were harvested for gene profiling.
2013-06-20 | E-GEOD-36806 | biostudies-arrayexpress
Project description:We investigated the relationship between chronic inflammation and fibrosis in a mouse model of chronic colitis. Six weekly Trinitrobenzenesulphonic acid (TNBS) enemas were given to establish colitis and temporal changes in gene expression was elucidated over the next six weeks. Keywords: disease state analysis
2007-12-10 | GSE5864 | GEO
Project description:Inflammatory bowel disease is a chronic colonic inflammation that displays symptoms like diarrhea and weight loss. Acupuncture has been widely accepted by Western countries for the treatment of pain. In this study, we analyzed the efficacy and mechanism of electroacupuncture (EA) on trinitrobenzene sulphonic acid (TNBS)-induced colitis in mice. Mice were intrarectally administered 250 mg/kg TNBS and electroacupunctured at Quze (PC3) and Neiguan (PC6) acupoints, which have been applied for gastrointestinal disorders. Gene expression profiles in colons and spleens were analyzed by microarray for the elucidation of mechanism of EA. Our data showed that EA at PC3 and PC6 improved macroscopic and microscopic features of colitis, and the improvement displayed a frequency-dependent manner. Administration of TNBS upregulated the expression of most cytokine genes in colons, while EA downregulated the expression of TNBS-induced cytokine genes. Pathway analysis showed that EA significantly affected inflammatory pathways in colons and immunity-associated pathway in spleens. Immunohistochemical staining further showed that EA decreased the expression of interleukin-1? and nuclear factor-?B. In conclusion, this is the first study reporting the global gene expression profiles of EA on TNBS-induced colitis. Our findings suggested that inflammatory and immunity pathways were involved in the anti-inflammatory mechanism of EA on colitis induced by TNBS. In this study, we analyzed the efficacy and mechanism of electroacupuncture (EA) on trinitrobenzene sulphonic acid (TNBS)-induced colitis in mice. Mice were intrarectally administered 250 mg/kg TNBS and electroacupunctured at Quze (PC3) and Neiguan (PC6) acupoints, which have been applied for gastrointestinal disorders. Gene expression profiles in colons and spleens were analyzed by microarray for the elucidation of mechanism of EA.
2014-09-02 | E-GEOD-57771 | biostudies-arrayexpress