Yersinia pestis and Y. pseudotuberculosis are able to colonize visceral organs and submucosal intestinal epithelial tissue, respectively, without eliciting infiltrating leukocytes to the site of infection. For both pathogens this ability is dependent on the presence of the virulence plasmid and has been proposed to be due to the ability of Yersinia spp. to inhibit infected cells from releasing pro-inflammatory cytokines. We show that YopJ of Y. pseudotuberculosis. which we show is delivered into the cytoplasm of infected cells by a bacterial typeIII secretion system, blocks the degradation of IkB and the subsequent translocation of NF-kB site-binding transcription factors to the nucleus. This activity is dependent on a region of YopJ that resembles a eukaryotic SH2 domain suggesting that YopJ interacts directly with signalling molecules involved in the early host immune response.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology