Microbiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Microbiology 155 (2009), 1832-1839; DOI  10.1099/mic.0.026187-0
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
mic.0.026187-0v1
155/6/1832    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Google Scholar
Right arrow Articles by Schwan, W. R.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schwan, W. R.
Agricola
Right arrow Articles by Schwan, W. R.
Microbiology 155 (2009), 1832-1839; DOI  10.1099/mic.0.026187-0
© 2009 Society for General Microbiology

Survival of uropathogenic Escherichia coli in the murine urinary tract is dependent on OmpR

William R. Schwan

Department of Microbiology, University of Wisconsin-La Crosse, 1725 State St., La Crosse, WI 54601, USA

Uropathogenic Escherichia coli (UPEC) can grow in environments with significantly elevated osmolarities, such as murine and human urinary tracts. OmpR is the response regulator part of a two-component OmpR–EnvZ regulatory system that responds to osmotic stresses. To determine the role of OmpR in UPEC survival, a {Delta}ompR mutant was created in the UPEC clinical isolate NU149. The {Delta}ompR mutant had a growth defect compared with the wild-type strain under osmotic stress conditions; this defect was complemented by the full-length ompR gene on a plasmid, but not with a mutant OmpR with an alanine substitution for aspartic acid at the phosphorylation site at position 55. Furthermore, the {Delta}ompR mutant displayed up to 2-log reduction in bacterial cell numbers in murine bladders and kidneys compared with wild-type bacteria after 5 days of infection. The ability of the bacteria to survive was restored to wild-type levels when the {Delta}ompR mutant strain was complemented with wild-type ompR, but not when the alanine-substituted ompR gene was used. This study has fulfilled molecular Koch's postulates by showing the pivotal role OmpR plays in UPEC survival within the murine urinary tract.

Correspondence
William R. Schwan
schwan.will{at}uwlax.edu







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 2009 Society for General Microbiology.