Polyamine-mediated resistance of uropathogenic Escherichia coli to nitrosative stress
Polyamine-mediated resistance of uropathogenic Escherichia coli to nitrosative stress
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DOI：
10.1128/jb.188.3.928-933.2006
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发表时间：
2006-02-01
影响因子：
3.2
通讯作者：
Mulvey, MA
中科院分区：
文献类型：
--
作者：
Bower, JM;Mulvey, MA
在尿路感染的过程中，会产生大量的一氧化氮和活性氮中间体。我们已经发现，许多致尿路感染的大肠杆菌菌株对亚硝化应激的抗性远高于K-12参考菌株MG 1655。通过对泌尿系致病性E. coli转座子突变体不能在酸化亚硝酸盐存在下生长，cadC基因产物被鉴定为亚硝化胁迫抗性的关键促进剂。cadC或其转录靶点cadA和cadB的突变导致多胺尸胺的显著生产损失和对酸化亚硝酸盐的敏感性增加。外源添加尸胺或其他多胺拯救亚硝化胁迫下cad突变体的生长。在野生型细胞中，暴露于酸化的亚硝酸盐会显著增加每个细胞产生的尸胺浓度。多胺介导的亚硝化应激的拯救机制尚不清楚，但它不能仅仅归因于活性氮的化学淬灭或突变频率的降低。
During the course of a urinary tract infection, substantial levels of nitric oxide and reactive nitrogen intermediates are generated. We have found that many uropathogenic strains of Escherichia coli display far greater resistance to nitrosative stress than the K-12 reference strain MG1655. By selecting and screening for uropathogenic E. coli transposon mutants that are unable to grow in the presence of acidified nitrite, the cadC gene product was identified as a key facilitator of nitrosative stress resistance. Mutation of cadC, or its transcriptional targets cadA and cadB, results in loss of significant production of the polyamine cadaverine and increased sensitivity to acidified nitrite. Exogenous addition of cadaverine or other polyamines rescues growth of cad mutants under nitrosative stress. In wild-type cells, the concentration of cadaverine produced per cell is substantially increased by exposure to acidified nitrite. The mechanism behind polyamine-mediated rescue from nitrosative stress is unclear, but it is not attributable solely to chemical quenching of reactive nitrogen species or reduction in mutation frequency.