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Infection and Immunity, July 2008, p. 3019-3026, Vol. 76, No. 7
0019-9567/08/$08.00+0 doi:10.1128/IAI.00022-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
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Division of Cell Biology and Immunology, Pathology Department, University of Utah, Salt Lake City, Utah 84112-0565
Received 7 January 2008/ Returned for modification 7 March 2008/ Accepted 28 April 2008
Hfq is a bacterial RNA chaperone involved in the posttranscriptional regulation of many stress-inducible genes via small noncoding RNAs. Here, we show that Hfq is critical for the uropathogenic Escherichia coli (UPEC) isolate UTI89 to effectively colonize the bladder and kidneys in a murine urinary tract infection model system. The disruption of hfq did not affect bacterial adherence to or invasion of host cells but did limit the development of intracellular microcolonies by UTI89 within the terminally differentiated epithelial cells that line the lumen of the bladder. In vitro, the hfq mutant was significantly impaired in its abilities to handle the antibacterial cationic peptide polymyxin B and reactive nitrogen and oxygen radicals and to grow in acidic medium (pH 5.0). Relative to the wild-type strain, the hfq mutant also had a substantially reduced migration rate on motility agar and was less prone to form biofilms. Hfq activities are known to impact the regulation of both the stationary-phase sigma factor RpoS (
S) and the envelope stress response sigma factor RpoE (
E). Although we saw similarities among hfq, rpoS, and rpoE deletion mutants in our assays, the rpoE and hfq mutants were phenotypically the most alike. Cumulatively, our data indicate that Hfq likely affects UPEC virulence-related phenotypes primarily by modulating membrane homeostasis and envelope stress response pathways.
Published ahead of print on 5 May 2008.
Supplemental material for this article may be found at http://iai.asm.org/.
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