TY - JOUR
T1 - Enterohaemorrhagic Escherichia coli serogroup O111 inhibits NF-κB-dependent innate responses in a manner independent of a type III secreted OspG orthologue
AU - Nobe, Rika
AU - Nougayrède, Jean Philippe
AU - Taieb, Frédéric
AU - Oswald, Eric
AU - Bardiau, Marjorie
AU - Cassart, Dominique
AU - Navarro-Garcia, Fernando
AU - Mainil, Jacques
AU - Hayashi, Tetsuya
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
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U2 - 10.1099/mic.0.030759-0
DO - 10.1099/mic.0.030759-0
M3 - Article
C2 - 19628559
AN - SCOPUS:70449643732
VL - 155
SP - 3214
EP - 3225
JO - Microbiology
JF - Microbiology
SN - 1350-0872
IS - 10
ER -