Infectious response to E. coli: molecular and genetic pathways.

Urinary tract infections are most commonly caused by type 1-piliated Escherichia coli (UPEC) and result in urothelial apoptosis, local cytokine release and neutrophil infiltration. A human urothelial cell line was incubated with various E. coli isolates and was then characterized by flow cytometry. UPEC induced rapid urothelial apoptosis that was dependent upon interactions mediated by type 1 pili. Laboratory isolates expressing type 1 pili-induced approximately 50% less apoptosis. UPEC blocked activity of a NF-kappaB-dependent reporter in response to inflammatory stimuli by stabilizing IkappaBalpha and UPEC rapidly altered cellular signalling pathways. Finally, blocking NF-kappaB activity increased the level of the laboratory strain-induced apoptosis to the level of apoptosis induced by UPEC. These results suggest that UPEC blocks NF-kappaB and enhances type 1 pili-induced apoptosis as a component of the uropathogenic programme.