Norepinephrine represses the expression of toxA and the siderophore genes in Pseudomonas aeruginosa.

Norepinephrine represses the expression of toxA and the siderophore genes in Pseudomonas aeruginosa.
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去甲肾上腺素抑制铜绿假单胞菌中 toxA 和铁载体基因的表达。

DOI:
10.1111/j.1574-6968.2009.01739.x
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发表时间:
2009-10
影响因子:
2.1
通讯作者:
Hamood, Abdul N.
Hamood, Abdul N.
中科院分区:
生物学4区
文献类型:
--
作者:
Li, Wang;Lyte, Mark;Freestone, Primrose P.;Ajmal, Aziba;Colmer-Hamood, Jane A.;Hamood, Abdul N.

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铜绿假单胞菌产生的不同细胞外毒力因子包括外毒素A(ETA)和绿脓菌荧光素和绿脓菌螯铁蛋白铁载体。ETA和铁载体的产生需要铁饥饿σ因子PvdS、转录激活因子RegA和AraC激活因子PchR的功能。铁通过抑制pvdS、regA和pchR的表达来抑制ETA和铁载体的产生。PvdS调节ETA基因、toxA、regA和绿脓菌荧光素合成基因的表达。儿茶酚胺去甲肾上腺素(NE)通过从宿主结合蛋白转移铁来促进病原菌的生长。在这项研究中,我们阐明了NE和其他儿茶酚胺诱导铜绿假单胞菌生长的机制。我们还研究了NE是否调节toxA和铁载体基因的表达,以及这种调节的机制。NE通过从转铁蛋白中提供铁来促进铜绿假单胞菌的生长。铁抑制toxA、绿脓菌荧光素基因pvdD和pvdE及其调节因子pvdS、regA和pchR的表达,表明NE通过PvdS和PchR实现这种抑制。此外,NE绕过PvdS并支持pvdS缺失突变体的生长,表明NE不依赖于绿脓菌荧光素将铁转移至铜绿假单胞菌。因此,NE通过影响铜绿假单胞菌的生长模式和毒力因子的产生而明显影响其发病机制。
Among the different extracellular virulence factors produced by Pseudomonas aeruginosa are exotoxin A (ETA) and the pyoverdine and pyochelin siderophores. Production of ETA and the siderophores requires the function of the iron-starvation sigma factor PvdS, the transcriptional activator RegA, and the AraC-activator PchR. Iron represses production of ETA and the siderophores by repressing expression of pvdS, regA, and pchR. PvdS regulates the expression of the ETA gene, toxA, regA, and the pyoverdine synthesis genes. The catecholamine norepinephrine (NE) enhances the growth of pathogenic bacteria by transferring iron from host binding proteins. In this study, we elucidated the mechanism by which NE and other catecholamines induce P. aeruginosa growth. We also investigated if NE regulates expression of toxA and the siderophore genes; and the mechanism of this regulation. NE enhanced the growth of P. aeruginosa by supplying iron from transferrin. This provision of iron repressed expression of toxA, the pyoverdine genes pvdD and pvdE, and their regulators, pvdS, regA, and pchR, suggesting that NE accomplishes this repression through PvdS and PchR. Additionally, NE bypassed PvdS and supported the growth of a pvdS deletion mutant indicating that NE transfers iron to P. aeruginosa independently of pyoverdine. Thus, NE apparently influences the pathogenesis of P. aeruginosa by affecting its pattern of growth and the production of virulence factors.
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