Ontology highlight
ABSTRACT:
PROVIDER: PRJNA577388 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10273158_1.fastq.gz | Fastqsanger.gz | |||
| SRR10273158_2.fastq.gz | Fastqsanger.gz | |||
| SRR10273159_1.fastq.gz | Fastqsanger.gz | |||
| SRR10273159_2.fastq.gz | Fastqsanger.gz | |||
| SRR10273160_1.fastq.gz | Fastqsanger.gz |
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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:Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice are all more sensitive than wild type (WT) mice to dextran sulfate sodium (DSS)-induced colitis. The purpose of this study was to determine which genes are differentially induced by DSS treatment in the colon of Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice compared to WT mice. The results demonstrate higher induction of proinflammatory gene expression in Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice than in WT mice after DSS treatment. The majority of genes whose expression is increased in Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice but not in WT mice are interferon-inducible genes. Thus, Peptidoglycan Recognition Proteins Pglyrp1, Pglyrp2, Pglyrp3, and Pglyrp4 protect mice from excessive inflammatory response and damage to the colon by limiting expression of interferon-inducible genes in the colon.
2010-08-23 | GSE18859 | GEO
Project description:intestinal mesenchymal stromal cell subset specific accessible elements were analyzed using ATAC-seq Bulk RNA-seq Purpose: The goals of this study are to compare WT and Map3k2 deficient mice colon tissue transcriptome upon Naive and DSS treatment for 1 day Bulk RNA-seq Methods: Colon Tissue mRNA profiles of Naive or 2% DSS treated 16-week-old wild-type (WT) and MEKK2 knockout (Map3k2-/-) mice were generated by deep sequencing, in triplicate, using Illumina NextSeq 500. The sequence reads that passed quality filters were analyzed at the gene level with : Bowtie2 followed by HTSeq-Count and Normalized by DESeq2 Bulk RNA-seq Results: Using an optimized data analysis workflow, we mapped about 20 million sequence reads per sample to the mouse genome (build mm10) and identified 13,284 transcripts in the colon tissues of WT and Map3k2-/- mice. Single-cell RNA-seq Purpose: The goals of this study are to characterize murine colon mesenchymal stromal cell heterogeneity upon DSS treatment for 3 days Single-cell RNA-seq Methods: Mesenchymal Stromal Cell Single Cell Suspension Dissociated from 2% DSS treated 12-week-old wild-type (WT) mice has undergone 10x genomics single cell RNA sequencing using Illumina NextSeq 500. Single-cell RNA-seq Results: Using CellRanger and Seurat we identified 11,284 cells after quality control and filtering
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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:Gut microbiota comparation of Young mice (n=10), Old mice, Young_yFMT (Young mice 14 days after transplant feces from young mice, n=10) and Young_oFMT (Young mice 14 days after transplant feces from old mice, n=10), Antibiotic group (Cefazolin, n=8).
2023-08-28 | E-MTAB-13206 | biostudies-arrayexpress
Project description:Ulcerative colitis (UC) is a form of inflammatory bowel disease (IBD) that predisposes to colorectal cancer (CRC) and is modeled in mice by administration of dextran sodium sulfate (DSS) in drinking water. There are two isoforms of STAT3, STAT3α is pro-inflammatory and anti-apoptotic, while STAT3β has opposing effects on STAT3α. We examined the severity of DSS-induced colitis in transgenic-mice expressing only STAT3α ( / ) and in wild-type (WT) mice administered C188-9, a small molecule direct-inhibitor of STAT3. While manifestations of DSS-induced UC, such as mortality, weight-loss, rectal-bleeding, diarrhea, and colon-shortening, were exacerbated in / transgenic versus cage-control WT mice, all were prevented by C188-9 treatment of WT mice. C188-9 treatment also increased apoptosis of pathogenic CD4+T-cells, reduced colon-levels of IL17-positive cells, down-modulated mRNA-levels of STAT3-genes involved in inflammation, apoptosis-prevention, and colorectal-cancer-metastases. These are the only studies showing efficacy of Thus small-molecule targeting of STAT3 may be a useful novel approach in treating UC and preventing UC-associated colorectal-cancer. We performed genome-wide microarray expression profiling to gain greater understanding of the mechanisms involved in the protective effect of C188-9 in DSS-induced colitis, we examined mRNA levels in the colon of mice receiving DSS or plain water, without or with C188-9 treatment.
2019-07-24 | GSE117355 | GEO