Gene expression profiles in TNBS-induced murine colitis
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE5864 | GEO | 2007/12/10
SECONDARY ACCESSION(S): PRJNA97275
REPOSITORIES: GEO
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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:To test TWEAK/Fn14 pathway and relative agents in chronic TNBS colitis
2013-06-20 | GSE36806 | 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. 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: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:Colitis is the common pathological lesion of inflammatory bowel diseases, the major chronic inflammatory diseases of intestinal tracts in humans. In this study, we investigated the therapeutic effects of ginger extract and its component zingerone in mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Mice were administered with TNBS and/or various amounts of ginger and zingerone by an intrarectal route. The severity of colitis was evaluated by colonic weight/length ratio, macroscopic lesion, and histological examination. The mechanisms of ginger and zingerone were further elucidated by DNA microarray, ex vivo imaging, and immunohistochemical staining. Our data showed that treatment with ginger extract and zingerone ameliorated TNBS-induced colonic inflammation and injury in a dose-dependent manner. Pathway analysis of ginger- and zingerone-regulated gene expression profiles showed that ginger and zingerone significantly regulated cytokine-related pathways. Network analysis showed that nuclear factor-κB (NF-κB) and interleukin-1β (IL-1β) were key molecules involved in the expression of ginger- and zingerone-affected genes. Ex vivo imaging and immunohistochemical staining further verified that ginger and zingerone suppressed TNBS-induced NF-κB activation and decreased the NF-κB and IL-1β protein levels in the colon. In conclusion, our data showed that ginger improved the TNBS-induced colitis in mice via modulation of NF-κB activity and IL-1β signaling pathway. Moreover, zingerone might be the active component of ginger responsible for the amelioration of colitis induced by TNBS. A total of 24 mice was randomly divided into four groups of six mice: mock, mice were given with 0.1 ml of 50% ethanol; TNBS, mice were given with 250 mg/kg TNBS in 0.1 ml of 50% ethanol; TNBS/ginger, mice were administered with mixtures containing 250 mg/kg TNBS and various amounts of ginger extract in 0.1 ml of 50% ethanol; TNBS/zingerone, mice were given with mixtures containing 250 mg/kg TNBS and various amounts of zingerone in 0.1 ml of 50% ethanol. Mice were sacrificed seven days later for histochemical staining, RNA extraction, and ex vivo imaging.
2015-04-28 | E-GEOD-37677 | 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:To obtain insight into the complex traits underlying the local pathophysiological response to the repeated colitis inductions with TNBS, whole genome gene expression was performed on RNA isolated from the distal colon tissue of 5 mice/timepoint Total RNA obtained from isolated from the distal colon of TNBS colitis mice (isolated on day 9, 14, 16, 21, 23, and 28) was compared to those healthy control mice
2013-07-08 | E-GEOD-35609 | biostudies-arrayexpress
Project description:By combining directed evolution and synthetic biology, we engineered novel synthetic yeasts probiotics for the dynamic modulation of intestinal inflammation. In this experiment we treated TNBS-colitis induced mice with these probiotics and test the amelioration of immune response in the transcriptional level in the colon.
2021-04-22 | GSE152869 | GEO
Project description:This study looks at the effect of glycomacropeptide (GMP) treatment on rats with trinitrobenzene sulfuric acid (TNBS) induced colitis.<br><br> Female Wistar rats (175-225 g) were randomly assigned to three different groups. A control group C (n=3) that did not receive the TNBS challenge but 0.25 ml of phosphate buffered saline (PBS) intrarectally, and two groups (group T (n=3) and group GMP (n=5) that received the TNBS challenge as described below. Group GMP received 500 mg kg-1 day-1 of GMP in 1% methylcellulose p.o, starting two days before the TNBS challenge. Treatment was administered to rats for five days after the TNBS challenge using an oesophageal catheter. The T group received the vehicle. Colitis was induced by the method of Morris et al. with minor modifications (13). Briefly, animals were fasted overnight and anaesthetized with halothane. Under these conditions, animals were given 10 mg of TNBS dissolved in 0.25 ml of 50% ethanol (v v-1) by means of a Teflon cannula inserted 8 cm through the anus. Animals were kept in a head-down position for an additional 30 s and returned to their cage. Distal colon samples were obtained. For TNBS treated animals samples were obtained avoiding necrotic tissue.
2009-05-25 | E-MEXP-1631 | biostudies-arrayexpress