Expression data from murine colon tissue after exposure to 4% DSS for 6 days DSS followed by 4 days of water or 1% L-arginine
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE34874 | GEO | 2012/06/27
SECONDARY ACCESSION(S): PRJNA150105
REPOSITORIES: GEO
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Project description:L-Arginine (L-Arg) is the substrate for both inducible nitric oxide synthase and arginase, which are upregulated in human IBD and in mouse colitis models. We have found that L-Arg supplementation enhances wound restitution in vitro, and improves the clinical parameters of weight loss, survival, and colon weight/length, in dextran sulfate sodium (DSS) induced murine colitis. Our aim was to further identify the potential mechanisms underlying the clinical benefit of L-Arg supplementation. 12 Total samples were analyzed, 3 samples from each of 4 groups. We generated the following pairwise comparisons: Ctrl vs Ctrl + L-Arg; Ctrl vs DSS; DSS vs DSS + L-Arg; Ctrl + L-Arg vs DSS, Ctrl + L-Arg vs DSS + L-Arg. Genes with a p-value < 0.01 and a fold-change ≥2 were selected. To identify genes that were altered in response to L-Arg, we performed the following multiple sample comparisons using a p-value < 0.01 and a fold-change ≥2: Ctrl vs DSS vs DSS + L-Arg
2012-06-26 | E-GEOD-34874 | biostudies-arrayexpress
Project description:In the DSS-induced colitis model, the epithelial damage and resulting inflammation is restricted to the colon, with a potential influence on the microbial composition in the adjacent cecum. Several studies have reported changes of the gut microbiota in the DSS-induced colitis model and other mouse models of IBD. Furthermore, metaproteomics analysis of the gut microbiome in a mouse model of Crohn’s disease demonstrated that disease severity and location are microbiota-dependent, with clear evidence for the causal role of bacterial dysbiosis in the development of chronic ileal inflammation. We have developed a refined model of chronic DSS-induced colitis that reflects typical symptoms of human IBD without a risky body weight loss usually observed in DSS models [Hoffmann et al., submitted]. In this study, we used metaproteomics to characterize the disease-related changes in bacterial protein abundance and function in the refined model of DSS-induced colitis. To assess the structural and functional changes, we applied 16S rRNA gene sequencing and metaproteomics analysis of the intestinal microbiota in three different entities of the intestinal environment, i.e. colon mucus, colon content and cecum content.
2020-03-17 | PXD007220 | Pride
Project description:STAT3 is a pleiotropic transcription factor with important functions in cytokine signalling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. Here we demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IEC). Studies in genetically engineered mice showed that epithelial STAT3 activation in DSS colitis is dependent on IL-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis and pathways associated with wound healing in IEC. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22-dependent mucosal wound healing. 4 samples of colon epithelium were analyzed from 4 mice (2 per group Stat3flfl VillinCre- and Stat3flfl VillinCre+, respectively) after they had been treated with DSS (2.5%) for 5 days
2009-05-08 | E-GEOD-15955 | biostudies-arrayexpress
Project description:STAT3 is a pleiotropic transcription factor with important functions in cytokine signalling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. Here we demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IEC). Studies in genetically engineered mice showed that epithelial STAT3 activation in DSS colitis is dependent on IL-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis and pathways associated with wound healing in IEC. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22-dependent mucosal wound healing.
2009-05-08 | GSE15955 | GEO
Project description:Background: Preterm infants are at high risk of infection and sepsis, which is associated with arginine (ARG) deficiency. Optimal nutrition for preterm newborns suspected with infection is critical to prevent sepsis development. Citrulline (CIT) supplementation is known to prevent sepsis in adult rodents, by maintaining sufficient blood ARG levels and vascular stabilization. We hypothesized that CIT therapy improve sepsis outcomes in infected preterm newborns via CIT and ARG metabolism.Results: After infection, oral CIT supplementation led to higher mortality, blood bacterial load, and circulating and hepatic inflammation, compared with the infected controls. Intravenous CIT administration also showed increased inflammation and bacterial burdens without increased mortality. Liver transcriptomics and data from in vitro blood stimulation indicated that CIT induces enhanced immunosuppression, which may impair resistance response to bacteria at early stage of infection and later cause excessive inflammation and tissue damage. Conclusion: Early stage of CIT supplementation exacerbates sepsis severity in infected preterm pigs, likely via induced enhanced systemic immunosuppression.
2023-11-20 | GSE247865 | GEO
Project description:In the present study, we demonstrated that mice deficient in chemerin or IEC-specific CMKLR1 expression were highly susceptible to DSS-induced colitis and subsequent tumorigenesis, which was reversed by suppressing colonic neutrophilic inflammation using CXCR2 inhibitor. Surprisingly, we found that lack of the Chemerin-CMKLR1 signaling specifically reduced colonic epithelial expression of lactoperoxidase (LPO), an epithelial peroxidase which could utilize H2O2 to oxidase thiocyanates to antibiotic compound (Bafort et al., 2014). Importantly, we demonstrated that impaired epithelial LPO expression accounted for outgrowth of potentially pathogenic Gram-negative bacteria following epithelial injury, which led to overproduction of CXCL1/2 and pathological neutrophilic inflammation in mice with epithelial Chemerin-CMKLR1 signaling deficiency. Finally, lack of epithelial Chemerin-CMKLR1 signaling impaired early host defense against enteric bacteria, which was reversed by LPO supplementation. Taken together, our study uncovers a critical role of epithelial Chemerin-CMKLR1 signaling in restricting pathological colonic neutrophilia via potentiating LPO-mediated epithelial innate defense, thereby rendering protection against microbiota-driven colitis and tumorigenesis.
2022-06-30 | GSE178308 | GEO
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.
2011-12-20 | GSE34553 | GEO
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:The relative contribution of polarized macrophages to the maintenance of tolerance is unknown. We examined their roles by in vivo adoptive transfer immunotherapy of M0, M1 and M2a macrophages as pre-treatment of colitis. In other experiments, M2a macrophages were used as pre-treatment or treatment of established colitis followed by immunotherapy with nTreg cells. Survival, weight gain, tissue infiltration, iTreg and Th17 cell development, T cell activation, and the frequency of proinflammatory cytokines were used as outcome measurements. Pre-treatment with M2a but not M1 macrophages increased the development of iTreg and Th17 cells. M2a macrophages used as pre-treatment or in treatment of established colitis allowed for successful therapy with nTreg cells. M1 and M2a macrophages have distinct gene expression profiles.
2016-03-02 | GSE72518 | GEO
Project description:We identified a small molecule, orally active ER-464195-01, inhibits the calreticulin binding to alpha integrins, and clearly suppresses the adherence ability of leukocytes. Our transcriptome analysis with the colon of dextran sodium sulfate (DSS)-treated mice reveals that the increased expression of pro-inflammatory genes was down-regulated by ER-464195-01. Purpose: To gain insight into the molecular mechanisms underlying the prevention of DSS-induced colitis conferred by treatment of ER-464195-01, we performed a comprehensive analysis of ER-464195-01-mediated gene expression changes in DSS-induced colitis using RNA sequencing (RNA-Seq). Methods: Male Balb/c mice (7 weeks) were allowed free access to distilled water (Otsuka Pharmaceutical) containing 2% DSS (molecular weight: 36,000–50,000; ICN Biomedicals) for 6 days to induce colitis. ER-464195-01 (10 mg/kg) or vehicle was orally administered once per day for 6 days. Results: To investigate differentially expressed genes (false discovery rate (FDR) p<0.05, fold change >2) among three groups, we performed pairwise comparisons of RNA-Seq data using the CLC Genomics Workbench software. In comparison with the control, 5,570 (3,483 up- and 2,087 down-regulated) unique genes were significantly changed in the DSS-induced colitis group. Meanwhile, the data set of DSS-induced colitis with ER-464195-01 groups revealed significant changes in 1,808 (837 up- and 971 down-regulated) genes as compared with DSS alone. Notably, of 3,483 genes up-regulated by the DSS treatment, 894 transcripts of which were overlapped with 971 genes down-regulated genes by ER-464195-01.
2018-04-11 | GSE98407 | GEO