Journal
INFECTION AND IMMUNITY
Volume 73, Issue 7, Pages 3999-4006Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.73.7.3999-4006.2005
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Funding
- NICHD NIH HHS [K12-HD00850, K12 HD000850] Funding Source: Medline
- NIDDK NIH HHS [K08 DK067894, P50 DK064540, F32 DK010168, P50-DK64540, R01-DK51406, K08-DK067894, R01 DK051406] Funding Source: Medline
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Urinary tract infections are most commonly caused by uropathogenic strains of Escherichia coli (UPEC), which invade superficial bladder epithelial cells via a type I pilus-dependent mechanism. Inside these epithelial cells, UPEC organisms multiply to high numbers to form intracellular bacterial communities, allowing them to avoid immune detection. Bladder epithelia] cells produce interleukin-6 (IL-6) and IL-8 in response to laboratory strains of E. coli in vitro. We investigated the ability of UPEC to alter epithelial cytokine signaling by examining the in vitro responses of bladder epithelial cell lines to the cystitis strains UTI89 and NU14. The cystitis strains induced significantly less IL-6 than did the laboratory E. coli strain MG1655 from 5637 and T24 bladder epithelial cells. The cystitis strains also suppressed epithelial cytokine responses to exogenous lipopolysaccharide (LPS) and to laboratory E. coli. We found that insertional mutations in the rfa and rfb operons and in the surA gene all abolished the ability of UT189 to suppress cytokine induction. The rfa and rjb operons encode LPS biosynthetic genes, while surA encodes a periplasmic cis-trans prolyl isomerase important in the biogenesis of outer membrane proteins. We conclude that, in this in vitro model system, cystitis strains of UPEC have genes encoding factors that suppress proinflammatory cytokine production by bladder epithelial cells.
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