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Gene expression by RNA-seq in purified paneth cells of WT and panetch cell specific P55 KO mice 3 hours after TNF

ABSTRACT: Gene expression by RNA-seq in purified paneth cells of WT and panetch cell specific P55 KO mice 3 hours after TNF

PROVIDER: PRJNA996563 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25345236.fastq.gz	Fastqsanger.gz
	SRR25345237.fastq.gz	Fastqsanger.gz
	SRR25345238.fastq.gz	Fastqsanger.gz
	SRR25345239.fastq.gz	Fastqsanger.gz
	SRR25345240.fastq.gz	Fastqsanger.gz

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Gene expression by RNA-seq in purified paneth cells of WT and panetch cell specific P55 KO mice 3 hours after TNF

Project description:The study of how gene expression in paneth cells changes 3 hours after TNF admistration in mice were the TNFR1 (P55) genes was deleted in paneth cells using Defa6-cre.

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Project description:After a challenge with TNF, gene expression changes in the liver may result from direct effect of TNF, through liver TNF receptors, and indirect effect. Baterial infiltration of the liver due to leaky gut after TNF is a primary contributor of this effect. In order to evaluate only the direct effects of TNF on lier transcriptome, we performed TNF challenge in normal WT mice and P55 panetch cell KO mice, which do not show the leaky gut syndrome.

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PanethcellTNF-signalinginducesbacterialsepsis: PC transcriptome 15h ater TNF

Project description:Paneth Cells (PCs) are secretory cells located in the crypts of Lieberkühn of the small intestine. They produce antimicrobial peptides (AMPs) and are thought to keep the microbiome under control. The cytokine TNF, which functions mainly via its TNF receptor 1 (TNFR1 or P55), is a driving force in many inflammatory bowel disease (IBD) patients, but its impact on PCs is poorly known. We have generated PC-specific P55 knockout mice (P55Paneth KO) and found that these mice are protected against lethal TNF-induced systemic inflammatory response syndrome (SIRS). The impact of TNF on PCs is characterized by morphological changes and by intestinal bacterial translocation into organs, such as liver, in which these bacteria induce expression of numerous genes, associated with typical sepsis signatures. The presence of these bacteria cause lethality of the mice. Based on bulk RNA-SEQ on pure PCs, P55 signaling stimulated mainly a type-I IFN response in the PCs, which drives the bacterial translocation and lethality via IFNAR1. Interestingly, based on ER stress reporter mice, PCs constitutively have high amounts of spliced XBP1 (XBP1s) protein, presumably to support their secretion of AMPs, and TNF eradicates this XBP1s production, leading to failure of the unfolded protein response (UPR). This causes reduced antimicrobial activity in PCs, in a P55 and IFNAR1-dependent way. Our data suggest a novel axis induced by TNF in PCs, leading to interferon-induced UPR failure causing lethal bacterial translocation to the liver (and other organs)

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PanethcellTNF-signalinginducesbacterialsepsis: PC transcriptome 15h ater TNF in IFNARKO mice

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Gene expression by RNA-seq in purified paneth cells in antibiotics microbiome depleded mice

Project description:The study of how gene expression in paneth cells changes after TNF admistration in mice were the microbiome has been depleted with broad spectrum antibiotics. The depletion of the microbiome excludes the occurence of indirect effects mediated through it by TNF on PC gene expression, only direct TNF effecs on crypt cells are measured

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Project description:Gene expression by RNA-seq in Liver of WT and panetch cell specific P55 KO mice 18 hours after TNF

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Mouse duodenal and ileal Paneth cell single cell RNA sequencing

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