Infectious response to E. coli: Molecular and genetic pathways

Anthony J. Schaeffer*, David J. Klumpp, Adam C. Weiser, Shomit Sengupta, Sarah G. Forrestal, Robert A. Batler

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

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-κB-dependent reporter in response to inflammatory stimuli by stabilizing IκBα and UPEC rapidly altered cellular signalling pathways. Finally, blocking NF-κB 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-κB and enhances type 1 pili-induced apoptosis as a component of the uropathogenic programme.

Original languageEnglish (US)
Pages (from-to)57-60
Number of pages4
JournalInternational Journal of Antimicrobial Agents
Volume24
Issue numberSUPPL. 1
DOIs
StatePublished - Sep 2004

Keywords

  • Type 1-piliated E. coli
  • Urinary tract infection
  • Urothelial apoptosis

ASJC Scopus subject areas

  • Microbiology (medical)
  • Infectious Diseases
  • Pharmacology (medical)

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