Enterohaemorrhagic Escherichia coli O157:H7 Shiga-like toxin 1 is required for full pathogenicity and activation of the p38 mitogen-activated protein kinase pathway in Caenorhabditis elegans

Cell Microbiol. 2013 Jan;15(1):82-97. doi: 10.1111/cmi.12030. Epub 2012 Oct 9.


Enterohaemorrhagic Escherichia coli (EHEC) causes life-threatening infections in humans as a consequence of the production of Shiga-like toxins. Lack of a good animal model system currently hinders in vivo study of EHEC virulence by systematic genetic methods. Here we applied the genetically tractable animal, Caenorhabditis elegans, as a surrogate host to study the virulence of EHEC as well as the host immunity to this human pathogen. Our results show that E. coli O157:H7, a serotype of EHEC, infects and kills C. elegans. Bacterial colonization and induction of the characteristic attaching and effacing (A/E) lesions in the intact intestinal epithelium of C. elegans by E. coli O157:H7 were concomitantly demonstrated in vivo. Genetic analysis indicated that the Shiga-like toxin 1 (Stx1) of E. coli O157:H7 is a virulence factor in C. elegans and is required for full toxicity. Moreover, the C. elegans p38 mitogen-activated protein kinase (MAPK) pathway, an evolutionarily conserved innate immune and stress response signalling pathway, is activated in the regulation of host susceptibility to EHEC infection in a Stx1-dependent manner. Our results validate the EHEC-C. elegans interaction as suitable for future comprehensive genetic screens for both novel bacterial and host factors involved in the pathogenesis of EHEC infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caenorhabditis elegans / enzymology*
  • Caenorhabditis elegans / immunology
  • Caenorhabditis elegans / microbiology*
  • Escherichia coli Infections
  • Escherichia coli O157 / pathogenicity*
  • Host-Pathogen Interactions*
  • Intestinal Mucosa / microbiology
  • Intestinal Mucosa / pathology
  • Models, Animal
  • Shiga Toxin 1 / metabolism*
  • Survival Analysis
  • Virulence Factors / metabolism*
  • p38 Mitogen-Activated Protein Kinases / biosynthesis*


  • Shiga Toxin 1
  • Virulence Factors
  • p38 Mitogen-Activated Protein Kinases