Ontology highlight
ABSTRACT:
PROVIDER: PRJNA679432 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13101602.fastq.gz | Fastqsanger.gz | |||
| SRR13101603.fastq.gz | Fastqsanger.gz | |||
| SRR13101604.fastq.gz | Fastqsanger.gz | |||
| SRR13101605.fastq.gz | Fastqsanger.gz | |||
| SRR13101606.fastq.gz | Fastqsanger.gz |
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Project description:Ulcerative colitis (UC), belonging to inflammatory bowel disease (IBD), is a chronic and relapsing inflammatory disorders of the gastrointestinal tract, which is not completely cured so far. Valeriana jatamansi is a Chinese medicine used clinically to treat "diarrhea", which is closely related to UC. This study was to elucidate the therapeutic effects of V. jatamansi extract (VJE) on dextran sodium sulfate (DSS)-induced UC in mice and its underlying mechanism. In this work, VJE effectively ameliorate the symptoms, histopathological scores and reduce the production of inflammatory factors of UC mice. The colon untargeted metabolomics analysis and 16S rDNA sequencing showed remarkable differences in colon metabolite profiles and intestinal microbiome composition between the control and DSS groups, and VJE intervention can reduce these differences. Thirty-two biomarkers were found and modulated the primary pathways including pyrimidine metabolism, arginine biosynthesis and glutathione metabolism. Meanwhile, twelve significant taxa of gut microbiota were found. Moreover, there is a close relationship between endogenous metabolites and intestinal flora. These findings suggested that VJE ameliorates UC by inhibiting inflammatory factors, recovering intestinal maladjustment, and regulating the interaction between intestinal microbiota and host metabolites. Therefore, the intervention of V. jatamansi is a potential therapeutic treatment for UC.
2023-07-24 | PXD043047 | Pride
Project description:Effect of Sichuan pepper on DSS induced IBD model mice
| PRJDB16518 | ENA
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: 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. 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-59649 | biostudies-arrayexpress
Project description:To acquire a better understanding of the role of ITGB6 in the development of inflammatory bowel disease (IBD), we performed mRNA-Req to compare gene expression in two kinds of mice (wild-type C57BL/6 mice and ITGB6-overexpressing transgenic mice) in DSS-induced intestinal fibrosis model.
2024-11-01 | GSE188361 | 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. Gene expression profiles were established for normal miR-21-/- mice and wild type c57BL/6 mice (WT). Total of 6 samples with replicates were included in this study.
2014-07-23 | E-GEOD-59648 | biostudies-arrayexpress
Project description:Increased intestinal permeability is associated to the onset of inflammatory bowel disease (IBD) since the exposition to luminal content causes an immunological response that promotes intestinal inflammation. Several studies have been shown that microRNAs (miRNAs) are involved in IBD pathogenesis. Here, we aimed to functionally characterize the role of miRNAs in the regulation of intestinal permeability. miRNA profile of intestinal epithelial cells (IECs) isolated by colon of a UC mice model were identified using microarray. To predict the target genes of modulated miRNAs, we performed a bioinformatic analysis. To validate biologically miRNA targets, we performed transient transfection experiments in HT-29, Caco2 and T84 cell lines. To assess their role in barrier function, trans-epithelial electrical resistance and dextran flux assays were used. To investigate the in vivo effect of miR-195-5p, we employed a DSS-induced colitis model in mice. We identified 18 deregulated miRNAs in IECs from UC mice model and control mice. Among them, down-regulated miR-195-5p targeted CLDN2 and are involved in altered intestinal permeability. CLDN2 expression levels were increased in UC mice models and negatively correlated with the miR-195-5p expression. We demonstrated that the gain-of-function of miR-195-5p in colonic epithelial cell lines decreased the CLDN2 levels. We in vitro confirmed that miR-195-5p was able to control the intestinal barrier integrity. We also in vivo demonstrated that miR-195-5p attenuated the colonic inflammatory response in DSS-induced colitis and reduced the colonic permeability. All together our data support a previously unreported role of miR-195-5p in intestinal permeability and provide a potential pharmacological target for new therapeutic approaches in IBD.
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Project description:IBD is characterized by chronic recurrences of intestinal inflammation and intestinal immune disturbances.Bacteroides vulgatus can alleviate DSS-induced colitis in mice, but the mechanism is unknown. The aim of this study was to examine the changes in gene expression in the intestinal tissue of mice with colitis following treatment with Bacteroides vulgatus by RNA sequencing.
2023-12-06 | GSE246118 | GEO
Project description:Inflammatory bowel disease (IBD) is a multiple-genes-involved chronic disease and current available targeted drugs for IBD only deliver moderate efficacy. Whether there is a single gene that systematically regulates IBD is not yet known. Here we showed that the expression of miR-146a in colon was elevated in Dextran Sulfate Sodium Salt (DSS)-induced IBD mice and patients with IBD. DSS induced dramatic body weight loss and much more rectal bleeding, shorter colon length and colitis in miR-146a knock-out mice than wild type (WT) mice. The miR-146a mimics alleviated DSS-induced symptoms in both DSS-induced miR-146a-/- and WT mice. Further RNA sequencing illustrated that deficiency of miR-146a de-repressed majority of DSS-induced IBD-related genes which cover multiple genetic regulatory networks in IBD, and supplement of miR-146a mimics inhibited expression of many IBD-related genes. DOI 10.3389/fimmu.2024.1366319
2024-04-24 | GSE247433 | GEO