Epithelial cells detect functional type III secretion system of enteropathogenic Escherichia coli through a novel NF-κB signaling pathway

摘要: Enteropathogenic Escherichia coli (EPEC), a common cause of infant diarrhea, is associated with high risk mortality in developing countries. The primary niche infecting EPEC the apical surface intestinal epithelial cells. employs type three secretion system (TTSS) to inject host cells dozens effector proteins, which facilitate attachment these and successful colonization. Here we show that elicit strong NF-κB activation infected Furthermore, data indicate active, pore-forming TTSS per se necessary sufficient for this activation, regardless any specific or protein translocation. Importantly, upon infection wild antagonized by anti-NF-κB effectors, including NleB, NleC NleE. Accordingly, evident only mutants deleted nleB, nleC, nleE. TTSS-dependent involves unique pathway, independent TLRs Nod1/2 converges other pathways at level TAK1 activation. Taken together, our results imply have capacity sense activate response. Notably, antagonizes delivering effectors into