1887

Abstract

Uropathogenic (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 Δ mutant was created in the UPEC clinical isolate NU149. The Δ mutant had a growth defect compared with the wild-type strain under osmotic stress conditions; this defect was complemented by the full-length 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 Δ 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 Δ mutant strain was complemented with wild-type , but not when the alanine-substituted 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.

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2009-06-01
2024-04-18
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