Virulence of EnteropathogenicEscherichia coli, a Global Pathogen

Abstract

Enteropathogenic Escherichia coli (EPEC) remains an important cause of diarrheal disease worldwide. Research into EPEC is intense and provides a good virulence model of other E. coli infections as well as other pathogenic bacteria. Although the virulence mechanisms are now better understood, they are extremely complex and much remains to be learnt. The pathogenesis of EPEC depends on the formation of an ultrastructural lesion in which the bacteria make intimate contact with the host apical enterocyte membrane. The formation of this lesion is a consequence of the ability of EPEC to adhere in a localized manner to the host cell, aided by bundle-forming pili. Tyrosine phosphorylation and signal transduction events occur within the host cell at the lesion site, leading to a disruption of the host cell mechanisms and, consequently, to diarrhea. These result from the action of highly regulated EPEC secreted proteins which are released via a type III secretion system, many genes of which are located within a pathogenicity island known as the locus of enterocyte effacement. Over the last few years, dramatic increases in our knowledge of EPEC virulence have taken place. This review therefore aims to provide a broad overview of and update to the virulence aspects of EPEC

Escherichia coli virulence factors

“…The E. coli best known type 4 fimbriae, or Bundle-Forming Pili (BFP) are produced by typical enteropathogenic E. coli (tEPEC) (Table 1), a sub-class of human EPEC (Wu and Fives-Taylor, 2001;Clarke et al, 2003;Bardiau et al, 2010). Non BFP-producing EPEC from humans and animals are called atypical (a) EPEC (Nataro and Kaper, 1998;Trabulsi et al, 2002;Kaper et al, 2004;Hernandes et al, 2009).…”

“…Those appendices are shafts protruding from the bacterial cell surface and comprise different proteins (Wu and Fives-Taylor, 2001;Bann et al, 2002;Clarke et al, 2003;Mainil, 2003aMainil, , 2005aBarnhart and Chapman, 2006). Structurally the shaft is made of several hundreds copies of a protein, whose generic name is "major subunit" of a molecular weight between 15 and 20 kDa, but that received different other names according to the actual appendix (pilin, fimbrin, or curlin f.i.).…”

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

“…The formation of attaching and effacing (A/E) lesions is required for these microbes to cause diarrheal disease (8,34,42); thus, many studies have characterized the virulence factors used by A/E bacteria to infect their hosts. The formation of A/E lesions depends on a type III secretion system (T3SS) encoded within the locus of enterocyte effacement (LEE), a pathogenicity island that contains all the genes required for A/E lesion formation (9). These pathogens use the LEE-encoded T3SS to inject an array of effector proteins, including the translocated intimin receptor (Tir), into host cells, where they interfere with normal cellular function (9).…”

“…The formation of A/E lesions depends on a type III secretion system (T3SS) encoded within the locus of enterocyte effacement (LEE), a pathogenicity island that contains all the genes required for A/E lesion formation (9). These pathogens use the LEE-encoded T3SS to inject an array of effector proteins, including the translocated intimin receptor (Tir), into host cells, where they interfere with normal cellular function (9).…”

“…Enteropathogenic Escherichia coli (EPEC) is a prominent cause of diarrheal disease, causing the deaths of hundreds of thousands of children each year in developing countries (8,9). Belonging to a family of related gram-negative pathogenic bacteria that includes enterohemorrhagic E. coli (EHEC) and the mouse pathogen Citrobacter rodentium (28), EPEC strains are noninvasive, infecting their hosts by attaching to intestinal epithelial cells (IEC), effacing the epithelial microvilli, and producing pedestal-like structures (2,29).…”