Abstract

Enterotoxigenic Escherichia coli (ETEC) strains are among the most common causes of diarrheal illness worldwide. These pathogens disproportionately afflict children in developing countries, where they cause substantial morbidity and are responsible for hundreds of thousands of deaths each year. Although these organisms are important targets for enteric vaccines, most development efforts to date have centered on a subset of plasmid-encoded fimbrial adhesins known as colonization factors and heat-labile toxin (LT). Emerging data suggest that ETEC undergoes considerable changes in its surface architecture, sequentially deploying a number of putative adhesins during its interactions with the host. We demonstrate here that one putative highly conserved, chromosomally encoded adhesin, EaeH, engages the surfaces of intestinal epithelial cells and contributes to bacterial adhesion, LT delivery, and colonization of the small intestine.

Highlights

  • Enterotoxigenic Escherichia coli (ETEC) strains are among the most common causes of diarrheal illness worldwide

  • The eaeH gene is predicted to encode an outer membrane protein with a putative signal sequence at its amino-terminal end [34, 35], followed by the mature peptide which shares a region of homology with intimin (EaeA) that corresponds to a transmembrane ␤-barrel (Fig. 1a) [43]

  • Another feature shared with intimin [44], invasin [45], and a diverse superfamily of bacterial virulence proteins [46] is a series of tandem bacterial immunoglobulin-like (BIg) domains similar to those involved in eukaryotic cell surface adhesion proteins such as ICAMs [47]

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Summary

Introduction

Enterotoxigenic Escherichia coli (ETEC) strains are among the most common causes of diarrheal illness worldwide These pathogens disproportionately afflict children in developing countries, where they cause substantial morbidity and are responsible for hundreds of thousands of deaths each year. These organisms are important targets for enteric vaccines, most development efforts to date have centered on a subset of plasmid-encoded fimbrial adhesins known as colonization factors and heatlabile toxin (LT). The emerging data suggest that these sophisticated interactions of ETEC strains with their host might be exploited in outlining novel strategies for vaccine development [23]

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