Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1193223 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31579231_1.fastq.gz | Fastqsanger.gz | |||
| SRR31579231_2.fastq.gz | Fastqsanger.gz | |||
| SRR31579232_1.fastq.gz | Fastqsanger.gz | |||
| SRR31579232_2.fastq.gz | Fastqsanger.gz | |||
| SRR31579233_1.fastq.gz | Fastqsanger.gz |
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Project description:Aim: The precise role of microRNAs in inflammatory disease has been less clear. The present study investigated the effect of microRNA (miR-146b) on improving intestinal inflammation. Methods: The microRNA profile in IL-10-deficient mice was examined using microRNA arrays and miR-146b was selected for the following experiments. The expression vectors containing either the whole sequence of miR-146b or its siRNA were intraperitoneally administered to the dextran sulfate sodium (DSS)-induced colitis mouse. Results: The overexpression of miR-146b activated the NF-kB pathway, improved the epithelial barrier function, relieved intestinal inflammation in the DSS-induced colitis mice, and improved the survival rate of mice with lethal colitis. Furthermore, this amelioration of the intestinal inflammation by miR-146b was negated by the inhibitor for NF-kB pathway. Conclusion: The modulation of miR-146b expression is a potentially useful therapy for the treatment of intestinal inflammation through the activation of the NF-kB pathway.
2012-09-10 | GSE40708 | GEO
Project description:Inflammatory bowel disease (IBD), comprising CrohnM-BM-4s disease and Ulcerative colitis, is characterized by chronic relapsing inflammation of the gut. It has been shown that increased proteasomal activity is associated with the expression of immunoproteasomes, which enhances NF-kB activation and thus promotes inflammation in IBD-patients. Here, we investigate whether modulation of the proteasomal activity is a suitable therapeutic approach to limit inflammation in colitis. This concept was tested in two different experimental setups. First, development of dextran sulfate sodium (DSS)-induced colitis was tested in lmp7-/--mice, which lack the essential immunoproteasome-subunit LMP7 or in wildtype-mice treated with the proteasome inhibitor bortezomib. Compared to WT mice, lmp7-/- mice revealed significantly attenuated colitis resulting from reduced NF-kB activation in the absence of LMP7. Further, treatment with bortezomib revealed dose-dependent amelioration of DSS-induced inflammation. In both approaches proteasome modulation limited the infiltration of neutrophils, consequently reducing tissue damage. In summary our experiments demonstrate that modulation of the proteasomal activity is effective in attenuating experimental colitis. In particular, our data suggest that the immunoproteasome-subunit LMP7 is a suitable target for the therapy of IBD. Microarray experiments were performed as dual-color hybridizations. To compensate for dye-specific effects, a dye-reversal color-swap was applied. Samples of proximal colon were cut longitudinally, washed in PBS, shortly incubated in 4M Guanidinium-isothiocyanat and transferred to TRIzol (Invitrogen).
2010-07-06 | E-GEOD-18163 | biostudies-arrayexpress
Project description:Inflammatory bowel disease (IBD), comprising Crohn´s disease and Ulcerative colitis, is characterized by chronic relapsing inflammation of the gut. It has been shown that increased proteasomal activity is associated with the expression of immunoproteasomes, which enhances NF-kB activation and thus promotes inflammation in IBD-patients. Here, we investigate whether modulation of the proteasomal activity is a suitable therapeutic approach to limit inflammation in colitis. This concept was tested in two different experimental setups. First, development of dextran sulfate sodium (DSS)-induced colitis was tested in lmp7-/--mice, which lack the essential immunoproteasome-subunit LMP7 or in wildtype-mice treated with the proteasome inhibitor bortezomib. Compared to WT mice, lmp7-/- mice revealed significantly attenuated colitis resulting from reduced NF-kB activation in the absence of LMP7. Further, treatment with bortezomib revealed dose-dependent amelioration of DSS-induced inflammation. In both approaches proteasome modulation limited the infiltration of neutrophils, consequently reducing tissue damage. In summary our experiments demonstrate that modulation of the proteasomal activity is effective in attenuating experimental colitis. In particular, our data suggest that the immunoproteasome-subunit LMP7 is a suitable target for the therapy of IBD.
2010-07-07 | GSE18163 | 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 current study was designed to clarify signalling pathways and assess possible beneficial effect of new probiotic mixture in DSS (dextran sulphate sodium) – induced colitis mouse model. Manipulation of intestinal microbiota with probiotics represents a promising alternative or adjunct therapy in gastrointestinal disorders and inflammation. RNA extracted from the middle part of colon tissue from ~11 weeks female C57BL/6JOlaHsd mouse strain was used for examination of the global gene expression using Affymetrix GeneChip Mouse Gene 2.0 ST microarrays.
2018-03-23 | GSE89851 | GEO
Project description:IL17B protected mice from dextran sodium sulfate (DSS)-induced colitis since IL17B deficiency resulted in severe DSS-induced colitis with exaggerated weight loss, shorter colon length, and elevated proinflammatory cytokine production in colon. For mechanism study, we use single cell transcriptional analyses of CD45+ immune cells in colonic lamina propria to detect the effect of IL-17B on colon LP immune cells in colitis. We found increased inflammatory macrophages infiltration in colon lamina propria after colitis induction expressing inflammatory cytokines such as S100a9, S100a8, Tnf, which was confirmed by real-time PCR and flow cytometry. Reconstitute of Il17b-/- mice with recombinant IL17B alleviated the severity of DSS-induced colitis. IL17B treatment also inhibited LPS-induced inflammation in bone marrow derived macrophage and in mice. These data indicate that IL17B exerting its inhibitory role in inflammation by regulating inflammatory macrophage response. In view of the protective effect of IL17B on DSS-induced colitis and LPS-induced inflammation, IL17B might represent a novel potential therapeutic approach to treat the inflammation.
2023-01-17 | GSE162062 | GEO
Project description:IL17B protected mice from dextran sodium sulfate (DSS)-induced colitis since IL17B deficiency resulted in severe DSS-induced colitis with exaggerated weight loss, shorter colon length, and elevated proinflammatory cytokine production in colon. For mechanism study, we use single cell transcriptional analyses of CD45+ immune cells in colonic lamina propria to detect the effect of IL-17B on colon LP immune cells in colitis. We found increased inflammatory macrophages infiltration in colon lamina propria after colitis induction expressing inflammatory cytokines such as S100a9, S100a8, Tnf, which was confirmed by real-time PCR and flow cytometry. Reconstitute of Il17b-/- mice with recombinant IL17B alleviated the severity of DSS-induced colitis. IL17B treatment also inhibited LPS-induced inflammation in bone marrow derived macrophage and in mice. These data indicate that IL17B exerting its inhibitory role in inflammation by regulating inflammatory macrophage response. In view of the protective effect of IL17B on DSS-induced colitis and LPS-induced inflammation, IL17B might represent a novel potential therapeutic approach to treat the inflammation.
2023-01-17 | GSE161987 | GEO
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:BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in epithelial cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression. RESULTS: The deficiency of PPAR g in epithelial cells does not significantly affect disease activity or body weight but worsens colon histopathlogy. WT mice have greater CD4+IL10+ T cells and fewer MHC II+ macrophages in mesenteric lymph nodes. Global gene expression analysis reveals greater changes after 7 days of DSS challenge (compared to 2 days). Colonic mucosa from VC- (WT) and VC+ (PPARg knock-out in epithelial cells) mice were sampled at 0 (no DSS), 2, and 7 days of DSS-induced experimental colitis
2010-07-08 | E-GEOD-20621 | biostudies-arrayexpress
Project description:Aim: The precise role of microRNAs in inflammatory disease has been less clear. The present study investigated the effect of microRNA (miR-146b) on improving intestinal inflammation. Methods: The microRNA profile in IL-10-deficient mice was examined using microRNA arrays and miR-146b was selected for the following experiments. The expression vectors containing either the whole sequence of miR-146b or its siRNA were intraperitoneally administered to the dextran sulfate sodium (DSS)-induced colitis mouse. Results: The overexpression of miR-146b activated the NF-kB pathway, improved the epithelial barrier function, relieved intestinal inflammation in the DSS-induced colitis mice, and improved the survival rate of mice with lethal colitis. Furthermore, this amelioration of the intestinal inflammation by miR-146b was negated by the inhibitor for NF-kB pathway. Conclusion: The modulation of miR-146b expression is a potentially useful therapy for the treatment of intestinal inflammation through the activation of the NF-kB pathway. Mice: The present studies were approved by the Institutional Animal Care and Use Committee of the Asahikawa Medical College. C57BL/6 and IL-10-/- mice were purchased from Sankyo Labo Service Co., Inc. (Tokyo, Japan) and Jackson Laboratories (Bar Harbor, ME), respectively. Large intestines with or without treatments were removed, rinsed with saline, and the epithelium was gently sheared off with glass slides for protein determination. microRNA arrays: RNA was extracted from the large intestines of mice with Trizol and then was immediately frozen in liquid nitrogen. Next, the microRNA expression profiles of large intestine in wild-type and IL-10-deficient mouse were investigated using the mirVanaTM miRNA bioarray (Filgene, Inc., Japan). Any more than 2-fold differences were considered to indicate a significant change.
2012-09-10 | E-GEOD-40708 | biostudies-arrayexpress