In:
Infection and Immunity, American Society for Microbiology, Vol. 73, No. 2 ( 2005-02), p. 965-971
Kurzfassung:
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 Iha CFT073 is a virulence factor and might be a target for anti-UTI interventions.
Materialart:
Online-Ressource
ISSN:
0019-9567
,
1098-5522
DOI:
10.1128/IAI.73.2.965-971.2005
Sprache:
Englisch
Verlag:
American Society for Microbiology
Publikationsdatum:
2005
ZDB Id:
1483247-1
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