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Genome-wide transcriptional profiles of intestinal macrophages from WT and Csf1r-EP4-/- mice during dextran sodium sulfate induced colitis.

ABSTRACT: Genome-wide transcriptional profiles of intestinal macrophages from WT and Csf1r-EP4-/- mice during dextran sodium sulfate induced colitis.

PROVIDER: PRJNA592057 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10545000.fastq.gz	Fastqsanger.gz
	SRR10545001.fastq.gz	Fastqsanger.gz
	SRR10545002.fastq.gz	Fastqsanger.gz
	SRR10545003.fastq.gz	Fastqsanger.gz
	SRR10545004.fastq.gz	Fastqsanger.gz

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Genome-wide transcriptional profiles of intestinal macrophages from WT and Csf1r-EP4-/- mice during dextran sodium sulfate induced colitis.

Project description:To define the mechanisms that underlie regeneration driven by EP4+ macrophages, we transcriptionally compared the WT and Csf1r-EP4-/- mature macrophages isolated from colon by 39 days post DSS treatment.

2019-11-28 | GSE141093 | GEO

Whole ileal tissue from day 6 Dextran Sodium Sulfate (DSS) administered Il17rafl/fl;Atoh1-cre+/- mice

Project description:Total RNA sequencing (RNA-seq) of the terminal ileum of day 6 Dextran Sodium Sulfate (DSS) administered Il17rafl/fl;Atoh1-cre+ mice and littermate cre- mice was performed.

2022-01-25 | GSE189219 | GEO

Dextran sodium sulfate treatment of Pirc rats alters colonic and tumor gene expression

2014-01-14 | GSE54035 | GEO

Myeloperoxidase gene deletion in dextran sodium sulfate-induced colitis

Project description:Myeloperoxidase gene deletion in dextran sodium sulfate-induced colitis

| PRJEB66447 | ENA

Dextran sodium sulfate treatment of wild type and Pirc rats alters colonic normal tissue gene expression

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RNA-Seq of wild type and somatostatin 3 CrispR/Cas9 zebrafish mutants treated with dextran sodium sulfate (DSS)

Project description:Wild type and somatostatin 3 (Sst3) gene CrispR/Cas9 mutants of the AB zebrafish strain were treated with dextran sodium sulfate (DSS) to determine the role of sst3 in the innate immune response.

2020-07-31 | E-MTAB-9018 | biostudies-arrayexpress

Dextran sodium sulfate treatment of wild type and Pirc rats alters colonic normal tissue gene expression

Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine which genes are altered in the normal colonic epithelium, and which changes depend on the Pirc mutation. 97 day old (ACIxF344)F1 wild type and Pirc male rats either untreated or given 4% DSS in the drinking water from 40-47 and 54-61 days of age, housed in 12 hour light:12 dark, ad lib feeding. Normal colonic tissue was collected from the distal colon at 97 days of age.

2014-01-14 | E-GEOD-54005 | biostudies-arrayexpress

Dextran sodium sulfate treatment of Pirc rats alters colonic and tumor gene expression

Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine whether genes altered in the normal colonic epithelium or tumor differed between sporadic and inflammation-associated tumor development. 97 day old (ACIxF344)F1-Pirc male rats either untreated or given 4% DSS in the drinking water from 40-47 and 54-61 days of age, housed in 12 hour light:12 dark, ad lib feeding and drinking conditions. Normal colonic tissue and tumors were harvested from the distal colon at 97 days of age. A two color, reference design experiment hybridized according to Agilent protocols against a reference pool of RNA made up from colon tissue taken from pooled wild type rats which was labeled with Cy5.

2014-01-14 | E-GEOD-54035 | biostudies-arrayexpress

Determination of the influence of caNrf2 expression and/or Dextran Sulfate Sodium treatment on genome wide mRNA expression in whole colon wall or colon epithelial cells

Project description:The transcription factor NF-E2-related factor 2 (Nrf2) is a major modulator of the cellular antioxidant response. To study the role of Nrf2 on mucosal inflammation we used transgenic mice expressing a constitutively active Nrf2 in epithelial cells and induced mucosal inflammation by administration of dextran sulfate sodium. Genome wide expression was studied by mRNA sequencing.

2016-09-22 | GSE68156 | GEO

The reduction of dextran sulfate sodium-induced colitis severity in mice exposed to cigarette smoke is accompanied by specific gene pathway and microbial shifts.

Project description:Background and Aims: The impact of cigarette smoke on inflammatory bowel disease has been established by a large number of epidemiological, clinical, and preclinical studies. Exposure to cigarette smoke is associated with a higher risk of developing Crohn’s disease but is inversely correlated with the development, disease risks, progression, and relapse rate of ulcerative colitis. Few mechanistic studies have investigated the effect of cigarette smoke on intestinal inflammation and microbial composition. Methods: Three groups of mice were exposed to three different concentrations of cigarette smoke for a total of 4 weeks, including 5 days of dextran sulfate sodium treatment to induce colitis and a 7-day recovery period. A comprehensive and integrated comparative analysis of the global colon transcriptome and microbiome, as well as classical endpoints, was performed. Results: Cigarette smoke exposure significantly decreased the severity induced colitis. Colon transcriptome analysis revealed that cigarette smoke downregulated specific pathways in a concentration-dependent manner, affecting both the inflammatory state and composition of the gut microbiome. Metagenomics analysis demonstrated that cigarette smoke can modulate dextran sulfate sodium-induced dysbiosis of specific bacterial genera, contributing to resolve the inflammation or accelerate recovery. Conclusions: Cigarette smoke alters gut microbial composition and reduces inflammatory responses in a concentration-dependent manner. The present study lays the foundation for investigating potential molecular mechanisms responsible for the attenuation of colitis by cigarette smoke.

2020-03-03 | E-MTAB-7988 | biostudies-arrayexpress

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