Name: Proteomic analysis of the intestinal epithelial cell response to enteropathogenic Escherichia coli
Keywords: Not available

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Proteomic analysis of the intestinal epithelial cell response to enteropathogenic Escherichia coli

ABSTRACT: Not available

INSTRUMENT(S): instrument model

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Attila Csordas

PROVIDER: PRD000461 | Pride | 2012-07-26

REPOSITORIES: Pride

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			Action	DRS
	PRIDE_Exp_Complete_Ac_17905.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_17905.pride.mztab.gz	Mztab
	PRIDE_Exp_Complete_Ac_17905.xml.gz	Xml

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Publications

Proteomic analysis of the intestinal epithelial cell response to enteropathogenic Escherichia coli.

Hardwidge Philip R PR Rodriguez-Escudero Isabel I Goode David D Donohoe Sam S Eng Jimmy J Goodlett David R DR Aebersold Reudi R Finlay B Brett BB

The Journal of biological chemistry 20040226 19

We present the first large scale proteomic analysis of a human cellular response to a pathogen. Enteropathogenic Escherichia coli (EPEC) is an enteric human pathogen responsible for much childhood morbidity and mortality worldwide. EPEC uses a type III secretion system (TTSS) to inject bacterial proteins into the cytosol of intestinal epithelial cells, resulting in diarrhea. We analyzed the host response to TTSS-delivered EPEC effector proteins by infecting polarized intestinal epithelial monola ...[more]

PMID: 14988394

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Shiga toxin remodels the intestinal epithelial transcriptional response to Enterohemorrhagic Escherichia coli.

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Human intestinal epithelial cell-derived molecule(s) increase enterohemorrhagic Escherichia coli virulence.

Project description:To better understand the role of host cell-derived molecules on enterohemorrhagic Escherichia coli (EHEC) infection, we studied EHEC virulence gene expression when exposed to cell-free spent (conditioned) medium (CM) from HCT-8 intestinal epithelial cells. Exposure to HCT-8 CM for 1 h and 3 h increased the expression of 32 of 41 EHEC locus of enterocyte effacement (LEE) virulence genes compared with fresh medium (FM). Expression of the Shiga toxin 1 (stx1B) gene was up-regulated at 1 h of exposure. Seventeen genes encoded by prophage 933W, including those for Stx2, were also up-regulated at both time-points. The increase in 933W prophage expression was mirrored by a 2.7-fold increase in phage titers. Consistent with the increase in virulence gene expression, we observed a fivefold increase in EHEC attachment to epithelial cells when exposed to CM. The increase in EHEC attachment was abolished when CM was heated to 95 °C or treated with proteinase K to degrade the proteins. The host cell-derived molecule(s) were larger than 3 kDa, which suggests that the molecule(s) that increase EHEC virulence and attachment are protein-based.

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A Proteomic and Transcriptomic Approach Reveals New Insight into b-methylthiolation of Escherichia coli Ribosomal Protein S12

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Shiga toxin remodels the intestinal epithelial transcriptional response to Enterohemorrhagic Escherichia coli

Project description:Enterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes diarrheal disease and the potentially lethal hemolytic uremic syndrome. Here, we used an infant rabbit model of EHEC infection that recapitulates many aspects of human intestinal disease to comprehensively assess the host colonic epithelial and lamina propria cell transcriptional responses to EHEC infection. Furthermore, comparisons of colonic pathology and intestinal transcriptomic profiles in animals infected with EHEC strains containing or lacking Shiga toxins (∆∆stx) were carried out to investigate how these potent toxins shape the host response to the pathogen. We found that Stx is required for severe, multi-focal hemorrhage and extensive apoptosis in the colon. RNA-sequencing revealed that EHEC infection elicits a robust innate immune response in the colonic epithelium that is dramatically shaped by Stx. Over 1400 genes were differentially expressed in animals infected with WT versus ∆∆stx EHEC strains. Several pathways linked to innate immune responses were dependent on Stx. Upregulated genes in the presence of toxin included cytokines IL23a and CXCL8, as well as F3, the gene encoding the coagulation initiator Tissue Factor. RNA FISH revealed that these elevated transcripts were found almost exclusively in epithelial cells, suggesting that Stx remodels the transcriptional profile of the epithelium. Collectively, these findings reveal that Stx potently modulates the innate immune response to EHEC in the intestine, and suggest that Stx drives the response to infection towards type 3 immunity.

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Project description:Not available

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Transcriptional modulation of enterotoxigenic Escherichia coli virulence genes in response to epithelial cell interactions.

Project description:Enterotoxigenic Escherichia coli (ETEC) strains are a leading cause of morbidity and mortality due to diarrheal illness in developing countries. There is currently no effective vaccine against these important pathogens. Because genes modulated by pathogen-host interactions potentially encode putative vaccine targets, we investigated changes in gene expression and surface morphology of ETEC upon interaction with intestinal epithelial cells in vitro. Pan-genome microarrays, quantitative reverse transcriptase PCR (qRT-PCR), and transcriptional reporter fusions of selected promoters were used to study changes in ETEC transcriptomes. Flow cytometry, immunofluorescence microscopy, and scanning electron microscopy were used to investigate alterations in surface antigen expression and morphology following pathogen-host interactions. Following host cell contact, genes for motility, adhesion, toxin production, immunodominant peptides, and key regulatory molecules, including cyclic AMP (cAMP) receptor protein (CRP) and c-di-GMP, were substantially modulated. These changes were accompanied by visible changes in both ETEC architecture and the expression of surface antigens, including a novel highly conserved adhesin molecule, EaeH. The studies reported here suggest that pathogen-host interactions are finely orchestrated by ETEC and are characterized by coordinated responses involving the sequential deployment of multiple virulence molecules. Elucidation of the molecular details of these interactions could highlight novel strategies for development of vaccines for these important pathogens.

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