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Myeloperoxidase gene deletion in dextran sodium sulfate-induced colitis

ABSTRACT: Myeloperoxidase gene deletion in dextran sodium sulfate-induced colitis

PROVIDER: PRJEB66447 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR12081505_1.fastq.gz	Fastqsanger.gz
	ERR12081505_2.fastq.gz	Fastqsanger.gz
	ERR12081506_1.fastq.gz	Fastqsanger.gz
	ERR12081506_2.fastq.gz	Fastqsanger.gz
	ERR12081507_1.fastq.gz	Fastqsanger.gz

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

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

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Effect of group X phospholipase A2 deletion in dextran sulfate sodium-induced colitis modeled colon

Project description:Within the secreted phospholipase A2 (sPLA2) family, group X sPLA2 (sPLA2-X) has the highest capacity to hydrolyze cellular membranes and has long been thought to promote inflammation by releasing arachidonic acid (AA), a precursor of pro-inflammatory eicosanoids. Unexpectedly, we found that transgenic mice globally overexpressing human sPLA2-X (PLA2G10-Tg) displayed striking immunosuppressive and lean phenotypes with lymphopenia and increased M2-like macrophages, accompanied by marked elevation of free omega-3 polyunsaturated fatty acids (PUFAs) and their metabolites. Studies using Pla2g10-deficient mice revealed that endogenous sPLA2-X, which is highly expressed in the colon epithelium and spermatozoa, mobilized omega-3 PUFAs or their metabolites to protect against dextran sulfate sodium (DSS)-induced colitis and to promote fertilization, respectively. In colitis, sPLA2-X deficiency increased colorectal expression of Th17 cytokines, and omega-3 PUFAs attenuated their production by lamina propria cells partly through the fatty acid receptor GPR120. In comparison, cytosolic phospholipase A2 (cPLA2alpha) protects from colitis by mobilizing omega-6 AA metabolites including prostaglandin E2. Thus, our results underscore a previously unrecognized role of sPLA2-X as an omega-3 PUFA mobilizer in vivo, segregated mobilization of omega-3 and omega-6 PUFA metabolites by sPLA2-X and cPLA2alpha, respectively, in protection against colitis, and the novel role of a particular sPLA2-X-driven PUFA in fertilization.

2016-02-01 | GSE77144 | 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

Multi-Omics Insights into the Mechanism of Liver Injury in Dextran Sulfate Sodium-Induced Colitis

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.

2021-08-16 | GSE181959 | GEO

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

Expansion of Interleukin-22-producing Innate Lymphoid Cells in Tristetraprolindeficient mice protects against Dextran Sulfate Sodium-induced Colitis

Project description:Tristetraprolin (TTP, encoded by Zfp36) is an RNA-binding protein that plays a major role in the control of inflammation. Zfp36 -/-mice spontaneously develop a complex multi-organ inflammatory syndrome that shares many features with spondyloarthritis. Herein, we show that Zfp36 -/-mice are paradoxically protected from Dextran Sulfate Sodium (DSS)-induced colitis. This effect was maintained on a Rag2 -/- background but was lost in Rag2 -/-Il2rg -/-Zfp36 -/-mice that lack innate lymphoid cells (ILCs). Furthermore, we observed a local expansion of type 3 ILCs in the lamina propria of Zfp36 -/-mice. These cells produced large amounts of Interleukin (IL)-22 and were expanded in response to systemic inflammation. Finally, we show that IL-22 contributed to protection of Zfp36 -/-mice against DSSinduced colitis but had a minor impact on their spontaneous inflammatory syndrome. Taken together, these data highlight the complex role of TTP in the control of organ-specific inflammation.

2023-08-01 | GSE236230 | GEO

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

Single nuclei sequencing to understand mechanism of action of the melanocortin 1 receptor agonist Pl8177 in Dextran sodium sulfate (DSS)-induced colitis in rats

Project description:PL8177 is a potent and selective agonist of the melanocortin 1 receptor (MC1R). PL8177 has shown efficacy in reversing intestinal inflammation in a cannulated rat ulcerative colitis model. To facilitate oral delivery, a novel, polymer-encapsulated formulation of PL8177 was developed and tested in dextran sulfate sodium induced rat ulcerative colitis model. Rats treated with 50 µg oral PL8177 demonstrated significantly lower macroscopic colon damage scores and improvement in colon weight, stool consistency, and fecal occult blood vs the vehicle without active drug. We used single nuclei RNA sequencing of colon tissues to characterize the mechanism of action and identify relative cell population and key gene expression changes between treated, healthy and vehicle.

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Anatabine ameliorates intestinal inflammation and reduces the production of pro-inflammatory factors in a dextran sulfate sodium mouse model of colitis.

Project description:Objective: In this study, we aimed to evaluate the anti-inflammatory properties of nicotine and anatabine in a dextran sulfate sodium (DSS) mouse model of ulcerative colitis (UC). Methods: C57BL/6 male mice (10 groups with 8 animals each) were orally administered nicotine at a concentration of 5 or 20 mg/kg body weight or anatabine at a concentration of 5 or 20 mg/kg body weight for a total of 21 days. Colitis was induced by oral administration of 3.5% DSS in drinking water ad libitum during days 14–21. Colonic samples were collected for transcriptomic analysis and multi-analyte profiling (MAP). Results: Oral administration of anatabine, but not nicotine, reduced the clinical symptoms of DSS-induced colitis. The result of gene expression analysis suggested that anatabine had a restorative effect on global DSS-induced gene expression profiles, while nicotine only had limited effects. Accordingly, MAP findings revealed that anatabine reduced the colonic abundance of DSS-associated cytokines and increased IL‑10 abundance. Conclusions: Our results support the reduction of inflammatory effects by anatabine in the DSS mouse model of UC.

2020-11-03 | E-MTAB-8543 | biostudies-arrayexpress

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