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PanethcellTNF-signalinginducesbacterialsepsis: transcriptome of intestinal epithelial cells 8h after TNF

ABSTRACT: PanethcellTNF-signalinginducesbacterialsepsis: transcriptome of intestinal epithelial cells 8h after TNF

PROVIDER: PRJNA1119480 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29270284.fastq.gz	Fastqsanger.gz
	SRR29270285.fastq.gz	Fastqsanger.gz
	SRR29270286.fastq.gz	Fastqsanger.gz
	SRR29270287.fastq.gz	Fastqsanger.gz
	SRR29270288.fastq.gz	Fastqsanger.gz

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PanethcellTNF-signalinginducesbacterialsepsis: transcriptome of intestinal epithelial cells 8h after 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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Project description:Death of intestinal epithelial cells (IECs) is important in the pathological process of intestinal inflammatory diseases. TNF acts as one pathogenic driver for inducing IEC death and substantial intestinal inflammation. However, the physiological protective mechanisms for suppressing TNF-induced IEC death remain poorly understood. Here, we report that EF-hand domain-containing protein D2 (EFHD2), highly expressed in normal intestine tissues but decreased in intestinal biopsy samples of ulcerative colitis patients, protects the intestinal epithelium from TNF-induced IEC apoptosis. EFHD2 inhibits TNF-induced apoptosis in primary IECs and intestinal organoids (enteroids). Mice deficient of Efhd2 in IECs exhibit excessive IEC death and exacerbated experimental colitis. Mechanistically, EFHD2 interacts with Cofilin to suppress the phosphorylation of Cofilin, leading to the inhibition of TNF receptor Ⅰ (TNFR1) internalization and TNF-induced apoptosis. Our findings define EFHD2 as an endogenous suppressor of IEC death to protect intestine inflammation, providing new insight to the regulation of death receptor signaling and control of intestinal inflammatory diseases.

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