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Elevated Extracellular cGMP Produced after Exposure to Enterotoxigenic Escherichia coli (ETEC) Heat-Stable Toxin (ST) Induces Epithelial IL-33 Release and Alters Intestinal Immunity

ABSTRACT: Elevated Extracellular cGMP Produced after Exposure to Enterotoxigenic Escherichia coli (ETEC) Heat-Stable Toxin (ST) Induces Epithelial IL-33 Release and Alters Intestinal Immunity

PROVIDER: PRJNA681781 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13172430_1.fastq.gz	Fastqsanger.gz
	SRR13172430_2.fastq.gz	Fastqsanger.gz
	SRR13172431_1.fastq.gz	Fastqsanger.gz
	SRR13172431_2.fastq.gz	Fastqsanger.gz
	SRR13172432_1.fastq.gz	Fastqsanger.gz

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Elevated Extracellular cGMP Produced after Exposure to Enterotoxigenic Escherichia coli (ETEC) Heat-Stable Toxin (ST) Induces Epithelial IL-33 Release and Alters Intestinal Immunity

Project description:The purpose of our study was to examine the effect of enterotoxigenic E. coli (ETEC) heat-stable toxin (ST) on global T84 gene expression at selected time points following intoxication, with the goal of understanding the functional effects of ST on host epithelium. RNASeq analysis relvealed that ST alters inflammatory gene expression, including the IL-1 family member IL33, which is induced downstream of cGMP.

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Expression data of enterotoxigenic (ETEC) isolate E24377A

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Expression data of enterotoxigenic (ETEC) isolate E24377A

Project description:ETEC is an important human pathogen. Although the mechanism of diarrhea is known in ETEC, the regulatory networks are less understood. This study was conducted to understand the global expression of ETEC isolate E24377A under different growth and environemental conditions. ETEC isolate E24377A was grown in the presence of several chemical signals, including bile salts, glucose, and pre-conditioned media (PCM) from other enteric pathogens. E24377A was also grown to different densities, to see if a quorum sensing mechanism was in place The isolate was grown in different types of media, with different ammendments, and at different growth densities. The overall goal was to determine how expression gene expression changes in the presence of chemical signals; a special emphasis was placed on the expression of known and suspected virulence and colonization factors

2012-03-01 | E-GEOD-31804 | biostudies-arrayexpress

Elevated Extracellular cGMP Produced after Exposure to Enterotoxigenic Escherichia coli Heat-Stable Toxin Induces Epithelial IL-33 Release and Alters Intestinal Immunity.

Project description:Enterotoxigenic Escherichia coli (ETEC) is a major diarrheal pathogen in children in low- to middle-income countries. Previous studies identified heat-stable enterotoxin (ST)-producing ETEC as a prevalent diarrheal pathogen in children younger than 5 years. While many studies have evaluated the interaction of ETEC heat-labile enterotoxin (LT) with host epithelium and immunity, few investigations have attempted similar studies with ST. To further understand ST pathogenesis, we examined the impact of ST on cGMP localization, epithelial cell cytokine production, and antibody development following immunization. In addition to robust intracellular cGMP in T84 cells in the presence of phosphodiesterase inhibitors (PDEis) that prevent the breakdown of cyclic nucleotides, we found that prolonged ST intoxication induced extracellular cGMP accumulation in the presence or absence of PDEis. Further, ST intoxication induced luminal cGMP in vivo in mice, suggesting that secreted cGMP may have other cellular functions. Using transcriptome sequencing (RNA-seq) and quantitative PCR (qPCR), we demonstrated that ST intoxication, or treatment with the clinically used ST mimic linaclotide, altered inflammatory cytokine gene expression, including the interleukin 1 (IL-1) family member IL-33, which could also be induced by cell-permeative 8-Br-cGMP. Finally, when present during immunization, ST suppressed induction of antibodies to specific antigens. In conclusion, our studies indicate that ST modulates epithelial cell physiology and the interplay between the epithelial and immune compartments.

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