| First Author | Litvak Y | Year | 2017 |
| Journal | PLoS Pathog | Volume | 13 |
| Issue | 7 | Pages | e1006472 |
| PubMed ID | 28671993 | Mgi Jnum | J:251919 |
| Mgi Id | MGI:5917109 | Doi | 10.1371/journal.ppat.1006472 |
| Citation | Litvak Y, et al. (2017) Epithelial cells detect functional type III secretion system of enteropathogenic Escherichia coli through a novel NF-kappaB signaling pathway. PLoS Pathog 13(7):e1006472 |
| abstractText | Enteropathogenic Escherichia coli (EPEC), a common cause of infant diarrhea, is associated with high risk of mortality in developing countries. The primary niche of infecting EPEC is the apical surface of intestinal epithelial cells. EPEC employs a type three secretion system (TTSS) to inject the host cells with dozens of effector proteins, which facilitate attachment to these cells and successful colonization. Here we show that EPEC elicit strong NF-kappaB activation in infected host cells. Furthermore, the data indicate that active, pore-forming TTSS per se is necessary and sufficient for this NF-kappaB activation, regardless of any specific effector or protein translocation. Importantly, upon infection with wild type EPEC this NF-kappaB activation is antagonized by anti-NF-kappaB effectors, including NleB, NleC and NleE. Accordingly, this NF-kappaB activation is evident only in cells infected with EPEC mutants deleted of nleB, nleC, and nleE. The TTSS-dependent NF-kappaB activation involves a unique pathway, which is independent of TLRs and Nod1/2 and converges with other pathways at the level of TAK1 activation. Taken together, our results imply that epithelial cells have the capacity to sense the EPEC TTSS and activate NF-kappaB in response. Notably, EPEC antagonizes this capacity by delivering anti-NF-kappaB effectors into the infected cells. |
