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J Infect Dis. 2012 Nov 15;206(10):1589-96. doi: 10.1093/infdis/jis554. Epub 2012 Sep 21.

Escherichia coli-mediated impairment of ureteric contractility is uropathogenic E. coli specific.

Author information

1
Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, United Kingdom. floyd78@liv.ac.uk

Abstract

BACKGROUND:

Ureters are fundamental for keeping kidneys free from uropathogenic Escherichia coli (UPEC), but we have shown that 2 strains (J96 and 536) can subvert this role and reduce ureteric contractility. To determine whether this is (1) a widespread feature of UPEC, (2) exhibited only by UPEC, and (3) dependent upon type 1 fimbriae, we analyzed strains representing epidemiologically important multilocus sequence types ST131, ST73, and ST95 and non-UPEC E. coli.

METHODS:

Contractility and calcium transients in intact rat ureters were compared between strains. Mannose and fim mutants were used to investigate the role of type 1 fimbriae.

RESULTS:

Non-UPEC had no significant effect on contractility, with a mean decrease after 8 hours of 8.8%, compared with 8.8% in controls. UPEC effects on contractility were strain specific, with decreases from 9.47% to 96.7%. Mannose inhibited the effects of the most potent strains (CFT073 and UTI89) but had variable effects among other UPEC strains. Mutation and complementation studies showed that the effects of the UTI89 cystitis isolate were fimH dependent.

CONCLUSIONS:

We find that (1) non-UPEC do not affect ureteric contractility, (2) impairment of contractility is a common feature of UPEC, and (3) the mechanism varies between strains, but for the most potent UPEC type 1 fimbriae are involved.

PMID:
23002447
PMCID:
PMC3475635
DOI:
10.1093/infdis/jis554
[Indexed for MEDLINE]
Free PMC Article
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