Ontology highlight
ABSTRACT:
PROVIDER: PRJNA827781 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18791400_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR18791500_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR18791401_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR18791501_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR18791402_subreads.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:Microbiota dysbiosis has been reported to contribute to the pathogenesis of colitis, to demonstrate whether IL-17D protects against DSS-induced colitis through regulation of microflora, we performed 16S rRNA sequencing in feces from WT and Il17d-deficient mice. Our data indicate that Il17d deficiency results in microbiota dysibiosis in both steady state and DSS-induced colitis.
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Project description:Colonic gene expression profiles of mice with DSS-induced colitis treated with apple peel polyphenolic extract Four-condition experiment: control, DSS-induced colitis, and mice treated with DAPP (two different doses (200 and 400 mg/kg/day) before or during induction and development of DSS-induced colitis.
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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.
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Project description:To investigate the immune regulatory role of microbiota derived interlukin-35 producing B cells in DSS-induced mice colitis. We then performed gene expression profiling analysis using data obtained from RNA-seq of isolated B cells from patches of colitis mice at four different time points.
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Project description:Inflammatory bowel diseases encompass gastrointestinal illnesseses typified by chronic inflammation, loss of epithelial integrity and gastrointestinal microbiota dysbiosis. In an effort to counteract these characteristic perturbations, we used stem cells and/or a probiotic preparation in a murine model of Dextran Sodium Sulfate induced colitis to examine both their efficacy in ameliorating disease and impact on niche-specific microbial communities of the lower GI tract. Colitis was induced in C57BL/6 mice by administering 3% DSS in drinking water for 10 days prior to administering one of three treatment plans: daily probiotic (VSL#3) supplementation for 3 days, a single tail vein injection of 1x106 murine mesenchymal stem cells, or both. Controls included DSS-untreated mice and DSS-treated mice that received no therapy. Ileal, cecal and colonic sections were collected for microbiota and histological analyses. Microbiota profiling revealed distinct bacterial community compositions in the ileum, cecum and colon of control untreated animals, all of which were predicted in silico to be enriched for a number of discrete KEGG pathways, indicating compositional and functional niche specificity in healthy animals. DSS- treatment perturbed community composition in all three niches with ileal communities exhibiting the greatest change relative to control animals. Stem cell, VSL#3 and the combination treated animals exhibited treatment-specific microbiota composition in the lower GI tract, though disease scores were only improved in VSL#3 treated animals. This VSL#3-associated shift in the ileal microbiota was characterized by significant Enterobacteriaceae enrichment compared to colitic animals (p<0.05), Mice (n=40) were randomly divided into five experimental groups, four of which received Dextran Sodium Sulfate (DSS; 3% solution in drinking water) for 10 days to induce colitis. Three of the DSS-treated groups received the following treatment modalities: VSL#3 (VSL#3, n=5), mesenchymal stem cells (MSC, n=5), or VSL#3 + mesenchymal stem cells (DUAL, n=5). The fourth DSS-treated group received no intervention (DSS; n=10). The additional fifth group of animals received neither DSS nor any therapeutic intervention and acted as untreated controls (CNTL, n=15). Following colitis induction (Day 10), DSS administration was halted and mice in the VSL#3, MSC and DUAL groups received the following interventions respectively: daily oral supplementation with 5x106 CFUs per supplement of VSL#3 in 100ul PBS (VSL#3); a single tail vein injection of 1x106 murine mesenchymal stem cells in 100_l PBS on Day 10 (MSC) or a combination of both treatments To provide control data for comparison, CNTL mice (n=5 per time point) were euthanized and sampled on days 1, 10, and 14, while DSS mice (n=5 per time point) were euthanized on days 10 and 14. All MSC, VSL#3, and DUAL mice were euthanized on Day 14. Samples collected from each animal included terminal ileum (1cm proximal to the cecum), cecum (divided transversely and stored as two separate samples), and proximal colon. All samples were added to RNAlater, prior to storage at -80C for analysis. Additional colonic samples were obtained, proximal to the initial sample site for microbiome analyses, and were preserved in paraformaldehyde for histological analyses.
2014-09-01 | E-GEOD-56137 | biostudies-arrayexpress
Project description:Ulcerative colitis (UC), a subtype of inflammatory bowel disease (IBD), is characterized by chronic and relapsing mucosal inflammation initiating in the rectum and extending upward through part or the entire colon in a continuous fashion. Currently, 5-aminosalicylic acid agents, corticosteroids, immunomodulators, and surgery are the main treatments for UC, which are limited in clinical practice due to common nonadherence, serious adverse effects and heavy financial burden. Atractylodes macrocephala Koidz. (Baizhu) has been used for improving gastrointestinal function and treating digestive disorders for thousands of years, and is currently one of the most frequently used traditional Chinese medicines for the treatment of UC. The purpose of this study was to evaluate the effect and underlying mechanism of polysaccharide from Atractylodes macrocephala Koidz. (PAMK) on UC based on a mouse model of dextran sodium sulfate (DSS)-induced colitis. To investigate the mechanism of therapeutic effect of PAMK on colitis, we performed the microarray analysis of colonic tissues in Control, DSS and DSS+PAMK groups. The results indicated that the beneficial effect of PAMK on DSS-induced colitis may rely on the regulation of the immune response.
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Project description:Liver injury is a common complication of inflammatory bowel disease (IBD). However, the mechanisms of liver injury development are not clear in IBD patients. Gut microbiota is thought to be engaged in IBD pathogenesis. Here, by an integrated analysis of host transcriptome and colonic microbiome, we have attempted to reveal the mechanism of liver injury in colitis mice. In this study, dextran sulfate sodium (DSS) -induced mice colitis model was constructed. Liver and colon transcriptome results showed that immune response and lipid metabolism-related pathways were dramatically altered, while DNA damage repair-related pathways were only significantly down-regulated in the colon. The microbiota of DSS-treated mice underwent strong transitions. Correlation analyses identified genes associated with liver and colon injury, whose expression was associated with the abundance of liver and gut health-related bacteria Collectively, the results indicate that the liver injury in colitis mice may be related to the intestinal dysbiosis and host-microbiota interactions. These findings may provide new insights for identifying potential targets for the treatment of IBD and its induced liver injury.
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Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. For the induction of colitis, mice were given drinking water supplemented with 2% (w/v) Dextran sulphate sodium (DSS) for 7 days, then allowed to recover by drinking water alone for 5 additional days. 3 mice of each groups (WT and Card9-/-) were sacrified before DSS administration. 5 WT mice and 4 Card9-/- mice were sacrified 7 days after DSS administration and 5 mice of each group were sacrified at day 12.
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