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

Rika Nobe, Jean Philippe Nougayrède, Frédéric Taieb, Eric Oswald, Marjorie Bardiau, Dominique Cassart, Fernando Navarro-Garcia, Jacques Mainil, Tetsuya Hayashi

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

Abstract

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-κB-dependent innate immune response via a T3SS-dependent mechanism. However, an EHEC O111 ospG mutant was still able to inhibit NF-κB p65 transfer to the nucleus in infected cells stimulated by tumour necrosis factor α (TNF-α). 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.

Original languageEnglish
Pages (from-to)3214-3225
Number of pages12
JournalMicrobiology
Volume155
Issue number10
DOIs
Publication statusPublished - 2009
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Microbiology

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