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Infect. Immun. doi:10.1128/IAI.00922-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Modulation of Host Innate Immune Response in the Bladder by Uropathogenic Escherichia coli

Departments of Urology and Microbiology-Immunology, Northwestern University Feinberg School of Medicine, 16-703 Tarry, 303 East Chicago Avenue, Chicago, IL 60611; Mucosal and Vaccine Research Center, Infectious Diseases, Room 3B-101, VA Medical Center, ONE VETERANS DRIVE, MINNEAPOLIS, MN 55417

^* To whom correspondence should be addressed. Email: d-klumpp{at}northwestern.edu.

	Abstract

Uropathogenic Escherichia coli (UPEC), the most frequent cause of urinary tract infection (UTI), are associated with an inflammatory response which includes the induction of cytokine/chemokine secretion by urothelial cells and neutrophil recruitment to the bladder. Recent studies indicate, however, that UPEC can evade the early activation of urothelial innate immune response in vitro. In this study, we report that the prototypic UPEC strain NU14 suppresses tumor necrosis factor alpha-mediated (TNFa) interleukin-8 (CXCL-8) and interleukin-6 (CXCL-6) secretion from urothelial cell cultures when compared to infection with a type 1 piliated E. coli K-12 strain. Furthermore, examination of a panel of clinical E. coli isolates revealed that 15 of 17 strains also possessed the ability to suppress cytokine secretion. In a murine model of UTI, NU14 infection resulted in diminished levels of mRNAs encoding keratinocyte-derived chemokine (KC), macrophage inflammatory peptide-2 (MIP-2), and CXCL-6 in the bladder relative to infection with an E. coli K-12 strain. Furthermore, reduced stimulation of inflammatory chemokine production during NU14 infection correlated with decreased levels of bladder and urine myeloperoxidase and increased bacterial colonization. These data indicate that a broad phylogenetic range of clinical E. coli isolates, including UPEC, may evade the activation of innate immune response in the urinary tract, thereby providing a pathogenic advantage.

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