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. 2005 Feb;73(2):965-71.
doi: 10.1128/IAI.73.2.965-971.2005.

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

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

James R Johnson et al. Infect Immun. 2005 Feb.

Abstract

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 VSports手机版. 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. .

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Figures (V体育2025版)

FIG. 1.
FIG. 1.
Adherence of laboratory E. coli to T-84 uroepithelial cells, with and without cloned Iha. Shown is E. coli ORN172 transformed with pSK+ (A) or pSK+Iha-CRT073 (B). Panel B demonstrates the typical adherence of E. coli ORN172 transformed with pSK+Iha-CFT073 to cells, but the adherence intensity is variable, with some cells quite densely covered (B, inset). Numbers are values associated with cellular adherence for the corresponding recombinant strains. The P value in panel B is relative to the vector control (Mann-Whitney U test). Bars, 20 μm.
FIG. 2.
FIG. 2.
OMPs of E. coli ORN172, with and without recombinant IhaCFT073, and wild-type and derivative E. coli. (A) Immunoblots of OMPs from strain ORN172 transformed with pSK+ (lane 1), pSK+Iha-O157:H7 (lane 2), pSK+Iha-CFT073 (lane 3), E. coli CFT073 (lane 4), UPEC76 (lane 5), and E. coli O157:H7 (lane 6). (B to D) Immunoblots of OMPs from CFT073 (B, lane 1), CFT073Δiha-CFT073 (B, lane 2), UPEC76 (C, lane 1), UPEC76Δiha-CFT073 (B, lane 2), UPEC76 (C, lane 1), UPEC76Δiha-CFT073 (C, lane 2), and CFT073 grown in LB broth (D, lane 2) or DMEM (D, lane 2). The single immunoreactive bands in panels B to D represent the 76-kDa Iha antigen.
FIG. 3.
FIG. 3.
Comparative urovirulences in mice of CFT073 and UPEC76 versus those of their respective ΔihaCFT073 mutants. Mice were challenged via the urethra with 20 μl containing ca. 2 × 109 CFU of a mixture of CFT073 and CFT073Δiha-CFT073 (A) or UPEC76 and UPECΔihaCFT073 (B). CIs were calculated as the parent/deletion mutant ratios, normalized to the corresponding input ratio. X, no growth; horizontal bars, median values.

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