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Microbiology 155 (2009), 3214-3225; DOI  10.1099/mic.0.030759-0
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Microbiology 155 (2009), 3214-3225; DOI  10.1099/mic.0.030759-0
© 2009 Society for General Microbiology

Enterohaemorrhagic Escherichia coli serogroup O111 inhibits NF-{kappa}B-dependent innate responses in a manner independent of a type III secreted OspG orthologue

Rika Nobe1,2, Jean-Philippe Nougayrède1,2, Frédéric Taieb1,2, Marjorie Bardiau3, Dominique Cassart4, Fernando Navarro-Garcia5, Jacques Mainil3, Tetsuya Hayashi6 and Eric Oswald1,2

1 INRA, UMR1225, ENVT, F-31076 Toulouse, France
2 Université de Toulouse, ENVT, UMR1225, F-31076 Toulouse, France
3 Department of Infectious Diseases, Bacteriology, Faculty of Veterinary Medicine, University of Liège, Sart Tilman, Liège B4000, Belgium
4 Department of Morphology and Pathology, Faculty of Veterinary Medicine, University of Liège, Sart Tilman, Liège B4000, Belgium
5 Department of Cell Biology, Centro de Investigación y de Estudios Avanzados (CINVESTAV-IPN), Ap. Postal 14-740, 07000 Mexico DF, Mexico
6 Division of Bioenvironmental Science, Frontier Science Research Center, University of Miyazaki, 5200 Kiyotake, Miyazaki 889-1692, Japan

Enterohaemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC) inject a repertoire of effector proteins into host cells via a type III secretion system (T3SS) encoded by the locus of enterocyte effacement (LEE). OspG is an effector protein initially identified in Shigella that was shown to inhibit the host innate immune response. In this study, we found ospG homologues in EHEC (mainly of serogroup O111) and in Yersinia enterocolitica. The T3SS encoded by the LEE was able to inject these different OspG homologues into host cells. Infection of HeLa cells with EHEC O111 inhibited the NF-{kappa}B-dependent innate immune response via a T3SS-dependent mechanism. However, an EHEC O111 ospG mutant was still able to inhibit NF-{kappa}B p65 transfer to the nucleus in infected cells stimulated by tumour necrosis factor {alpha} (TNF-{alpha}). In addition, no difference in the inflammatory response was observed between wild-type EHEC O111 and the isogenic ospG mutant in the rabbit ligated intestinal loop model. These results suggest that OspG is not the sole effector protein involved in the inactivation of the host innate immune system during EHEC O111 infection.

Correspondence
Eric Oswald
e.oswald{at}envt.fr

Abbreviations: EEL, exchangeable effector loci; EHEC, enterohaemorrhagic Escherichia coli; EIEC, enteroinvasive Escherichia coli; EPEC, enteropathogenic Escherichia coli; FCS, fetal calf serum; FRT, Flp recombination target; IL, interleukin; IS, insertion sequence; LEE, locus of enterocyte effacement; TNF-{alpha}, tumour necrosis factor {alpha}; T3SS, type III secretion system

The GenBank/EMBL/DDBJ accession numbers for the sequences (between the lom and yciE genes) reported in this paper are AB438937 (strain 12009), and AB438936 (strain 11128).






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