Molecular mechanisms that mediate colonization of Shiga toxin-producing Escherichia coli strains

Abstract

Shiga toxin-producing Escherichia coli (STEC) is a group of pathogens which cause gastrointestinal disease in humans and have been associated with numerous food-borne outbreaks worldwide. The intimin adhesin has been considered for many years to be the only colonization factor in these strains. However, the rapid progress in whole-genome sequencing of different STEC serotypes has accelerated the discovery of other adhesins (fimbrial and afimbrial), which have emerged as important contributors to the intestinal colonization occurring during STEC infection. This review summarizes recent progress to identify and characterize, at the molecular level, novel adhesion and colonization factors in STEC strains, with an emphasis on their contribution to virulence traits, their host-pathogen interactions, the regulatory mechanisms controlling their expression, and their role as targets eliciting immune responses in the host.

Fig 1

Working colonization model for STEC infecting humans and persisting in ruminants. (A) The diagram shows a human intestinal epithelial cell displaying the first stages of colonization by STEC in the lumen. STEC O157 or non-O157 strains interact with the intestine via the Lpf fimbriae; this is followed by the formation of A/E lesions. Stx production occurs in the intestinal tract, and translocation across the intestinal lumen to the bloodstream results in its distribution to target organs, such as the kidneys. (B) STEC O157 and non-O157 strains are also capable of adhering and colonizing other surfaces, such as the bovine intestinal epithelium and the surfaces of different vegetables. Several adhesins, such as HCP, ECP, and flagella, have been associated with persistence in the bovine intestine and the formation of biofilms.