The IrgA homologue adhesin Iha is an Escherichia coli virulence factor in murine urinary tract infection

James R. Johnson, Srdjan Jelacic, Laura M. Schoening, Connie Clabots, Nurmohammad Shaikh, Harry L.T. Mobley, Phillip I. Tarr

Research output: Contribution to journalArticlepeer-review

95 Scopus citations


The role of the Escherichia coli iron-regulated gene homologue adhesin (Iha) in the pathogenesis of urinary tract infections (UTIs) is unknown. We performed a series of complementary analyses to confirm or refute the hypothesis that Iha is a virulence factor in uropathogenic E. coli. Fecal E. coli isolates exhibited significantly lower prevalences of iha (range, 14 to 22%) than did clinical isolates from cases of pediatric cystitis or pyelonephritis, adult pyelonephritis or urosepsis, or bacteremia (range, 38 to 74%). Recombinant Iha from E. coli pyelonephritis isolate CFT073 conferred upon nonadherent E. coli ORN172 the ability to adhere to cultured T-24 human uroepithelial cells. In a well-established mouse model of ascending UTI, CFT073 and its derivative UPEC76 (a pap [P fimbriae] mutant version of strain CFT073) each significantly outcompeted their respective iha deletion mutants in CBA/J mice 48 h after bladder challenge (P < 0.03 for urine, both kidneys, and bladders of both constructs, except for bladders of mice challenged with UPEC76 and its deletion mutant, where P = 0.11). These data suggest that IhaCFT073 is a virulence factor and might be a target for anti-UTI interventions.

Original languageEnglish (US)
Pages (from-to)965-971
Number of pages7
JournalInfection and immunity
Issue number2
StatePublished - Feb 2005


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