Open AccessEnterohaemorrhagic E scherichia coli O 157: H 7 S higa‐like toxin 1 is required for full pathogenicity and activation of the p38 mitogen‐activated protein kinase pathway in C aenorhabditis elegans
Author(s) -
Chou TC.,
Chiu HC.,
Kuo CJ.,
Wu CM.,
Syu WJ.,
Chiu WT.,
Chen CS.
Publication year - 2013
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12030
Subject(s) - biology , virulence , caenorhabditis elegans , escherichia coli , microbiology and biotechnology , shiga toxin , innate immune system , genetic screen , colicin , host (biology) , pathogen , gene , genetics , immune system , mutant
Summary Enterohaemorrhagic E scherichia coli ( EHEC ) causes life‐threatening infections in humans as a consequence of the production of S higa‐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, C aenorhabditis 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 O 157: H 7, 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 O 157: H 7 were concomitantly demonstrated in vivo . Genetic analysis indicated that the S higa‐like toxin 1 ( S tx1) of E . coli O 157: H 7 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 S tx1‐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.