†These authors contributed equally to this work.
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
Article first published online: 8 OCT 2012
© 2012 Blackwell Publishing Ltd
Volume 15, Issue 1, pages 82–97, January 2013
How to Cite
Chou, T.-C., Chiu, H.-C., Kuo, C.-J., Wu, C.-M., Syu, W.-J., Chiu, W.-T. and Chen, C.-S. (2013), 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. Cellular Microbiology, 15: 82–97. doi: 10.1111/cmi.12030
- Issue published online: 14 DEC 2012
- Article first published online: 8 OCT 2012
- Accepted manuscript online: 17 SEP 2012 06:39AM EST
- Manuscript Accepted: 10 SEP 2012
- Manuscript Revised: 7 SEP 2012
- Manuscript Received: 9 MAY 2012
- NSC. Grant Numbers: 98-2311-B-006-002-MY3, 101-2311-B-006-005
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, anevolutionarily 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.