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E-GEOD-36806

ABSTRACT: Chronic TNBS Colitis in the FN14 KO Mouse

OTHER RELATED OMICS DATASETS IN: PRJNA156833

PROVIDER: E-GEOD-36806 | ExpressionAtlas | 2015-07-08

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-36806-analysis-methods.tsv	Tabular
	E-GEOD-36806-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-36806-configuration.xml	Xml
	E-GEOD-36806-configuration.xml.beforeQC	Xml
	E-GEOD-36806-percentile-ranks.tsv	Tabular

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Project description:Chronic TNBS Colitis in the FN14 KO Mouse

| PRJNA156833 | ENA

Chronic TNBS Colitis in the FN14 KO Mouse

Project description:To test TWEAK/Fn14 pathway and relative agents in chronic TNBS colitis Chronic colitis was induced by rectal injection of TNBS with ethanol for 6 weeks in WT or FN14 KO BALB/c mice. Colons were harvested for gene profiling.

2013-06-20 | E-GEOD-36806 | biostudies-arrayexpress

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Study of the role of IL-12p40-related cytokines in colitis of NEMOIEC-KO mice

Project description:Disruption of the epithelial barrier is considered a potential cause of inflammatory bowel disease (IBD). In this study, we employed the NEMOIEC-KO mouse model to study the immune mechanisms triggering chronic colitis downstream of an epithelial barrier defect. Colitis in NEMOIEC-KO mice is driven by commensal bacteria sensing through MyD88 signaling. The IL-12p40-related cytokines are induced upon microbial sensing and are known to act critically in promoting intestinal inflammation. Yet, the relative contribution of IL-12 versus IL-23 in eliciting intestinal pathology has been controversial. Using IL-12p40, IL-12p35 and IL-23p19 knockout mice we assessed the functional contribution of IL-12 and IL-23 to intestinal inflammation in the NEMOIEC-KO model.

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Toll-like receptor 2 deficiency exacerbates dextran sulfate sodium (DSS)-induced intestinal injury by Marinifilaceae dependent attenuating cell cycle signaling

Project description:Ulcerative colitis (UC) is an intestinal pathology characterized by chronic recurrent inflammation, which requires in-depth exploration of its mechanisms. To investigate the biological effects of TLR2 on DSS-induced intestinal inflammation in mice, we constructed the WT and TLR2-KO colitis mice model. We found TLR2-KO mice were severely susceptible to DSS-induced colitis. To determine how TLR2 exerted a protective effect in DSS-induced colitis, we compared the global gene expression profiles in the gut between WT and TLR2-KO mice by RNA-Seq. Results suggested that cell cycle pathway-related genes were significantly downregulated in gut of TLR2-KO colitis mice. 16S rRNA gene sequencing demonstrated remarkable variation in the composition of gut microbiota between WT and TLR2-KO colitis mice. Compared with WT colitis mice, the relative abundance of Marinifilaceae, Rikenellaceae, Desulfovibrionaceae, Tannerellaceae, Ruminococcaceae, Clostridia, Mycoplasmataceae were significantly higher in the gut of TLR2-KO colitis mice at family level. Moreover, we found that the relative abundance of Marinifilaceae was negatively correlated with the expression of cell cycle signaling related genes by microbiome diversity-transcriptome collaboration analysis. We came to this conclusion: TLR 2-KO exacerbated DSS-induced intestinal injury by Marinifilaceae dependent attenuating cell cycle signaling.

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Gene expression in the colon from IL10 KO mice

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Autophosphorylation at serine 166 regulates RIPK1-mediated cell death and inflammation

Project description:NEMO-IEC KO mice spontaneously develop chronic colitis characterized by inflammatory gene expression. We characterized the role of RIPK1 auto-phosphorylation in the upregulation of inlflammatory genes in these mice. We used microarray to study the effect of a RIPK1S166A mutation on the gene expression profile in NEMO IEC-KO mice and detect effects on specific inflammatory genes.

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