Survival of uropathogenic Escherichia coli in the murine urinary tract is dependent on OmpR.
Survival of uropathogenic Escherichia coli in the murine urinary tract is dependent on OmpR.
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DOI：
10.1099/mic.0.026187-0
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发表时间：
2009-06
期刊：
影响因子：
1.5
通讯作者：
W. Schwan
中科院分区：
文献类型：
--
作者：
W. Schwan
致尿性大肠埃希氏菌(UPEC)可在渗透压显著升高的环境中生长，如鼠和人的尿路。OmpR是双组分OmpR-EnvZ调控系统的反应调节器，对渗透胁迫做出反应。为了确定OmpR在UPEC存活中的作用，在UPEC临床分离株NU149中创建了一个DeltaompR突变体。与野生型菌株相比，DeltaompR突变体在渗透胁迫条件下存在生长缺陷；这一缺陷被质粒上的全长ompR基因所弥补，但不能被突变的OmpR所弥补，该突变株在55位的磷酸化位点上用丙氨酸取代天冬氨酸。此外，DeltaompR突变体在感染5天后，与野生型细菌相比，小鼠膀胱和肾脏中的细菌细胞数量显示出高达2log的减少。当DeltaompR突变株与野生型ompR互补时，细菌的生存能力恢复到野生型水平，但当使用丙氨酸取代的ompR基因时，则不能。这项研究通过显示OmpR在小鼠尿路内UPEC存活中发挥的关键作用，实现了分子Koch的假设。
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 DeltaompR mutant was created in the UPEC clinical isolate NU149. The DeltaompR 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 DeltaompR 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 DeltaompR 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.