The ability of an attaching and effacing pathogen to trigger localized actin assembly contributes to virulence by promoting mucosal attachment

Cell Microbiol. 2014 Sep;16(9):1405-24. doi: 10.1111/cmi.12302. Epub 2014 Jun 2.

Abstract

Enterohaemorrhagic Escherichia coli (EHEC) colonizes the intestine and causes bloody diarrhoea and kidney failure by producing Shiga toxin. Upon binding intestinal cells, EHEC triggers a change in host cell shape, generating actin 'pedestals' beneath bound bacteria. To investigate the importance of pedestal formation to disease, we infected genetically engineered mice incapable of supporting pedestal formation by an EHEC-like mouse pathogen, or wild type mice with a mutant of that pathogen incapable of generating pedestals. We found that pedestal formation promotes attachment of bacteria to the intestinal mucosa and vastly increases the severity of Shiga toxin-mediated disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism*
  • Animals
  • Enterohemorrhagic Escherichia coli / pathogenicity*
  • Enterohemorrhagic Escherichia coli / physiology*
  • Escherichia coli Infections / metabolism
  • Escherichia coli Infections / microbiology*
  • HeLa Cells
  • Humans
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / microbiology*
  • Mice
  • Shiga Toxin / metabolism
  • Virulence / physiology*

Substances

  • Actins
  • Shiga Toxin