Manganese import protects Salmonella enterica serovar Typhimurium against nitrosative stress,Metallomics

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Manganese import protects Salmonella enterica serovar Typhimurium against nitrosative stress
Metallomics ( IF 2.9 ) Pub Date : 2020-10-20 , DOI: 10.1039/d0mt00178c
Shehla Yousuf ₁ , Joyce E Karlinsey , Stephanie L Neville , Christopher A McDevitt , Stephen J Libby , Ferric C Fang , Elaine R Frawley

Affiliation

Nitric oxide (NO˙) is a radical molecule produced by mammalian phagocytic cells as part of the innate immune response to bacterial pathogens. It exerts its antimicrobial activity in part by impairing the function of metalloproteins, particularly those containing iron and zinc cofactors. The pathogenic Gram-negative bacterium Salmonella enterica serovar typhimurium undergoes dynamic changes in its cellular content of the four most common metal cofactors following exposure to NO˙ stress. Zinc, iron and magnesium all decrease in response to NO˙ while cellular manganese increases significantly. Manganese acquisition is driven primarily by increased expression of the mntH and sitABCD transporters following derepression of MntR and Fur. ZupT also contributes to manganese acquisition in response to nitrosative stress. S. Typhimurium mutants lacking manganese importers are more sensitive to NO˙, indicating that manganese is important for resistance to nitrosative stress.

中文翻译：

锰进口保护沙门氏菌鼠伤寒沙门氏菌免受亚硝化应激

一氧化氮 (NO·) 是哺乳动物吞噬细胞产生的一种自由基分子，是对细菌病原体的先天免疫反应的一部分。它部分地通过削弱金属蛋白的功能发挥其抗菌活性，尤其是那些含有铁和锌辅助因子的蛋白。致病性革兰氏阴性菌沙门氏菌鼠伤寒血清型在暴露于 NO 胁迫后，其四种最常见金属辅助因子的细胞含量发生动态变化。锌、铁和镁均会因 NO˙ 而减少，而细胞中的锰则显着增加。锰的获取主要是由mntH和satABCD 的表达增加驱动的MntR 和 Fur 去抑制后的转运蛋白。ZupT 还有助于锰的获取以响应亚硝化应激。S.缺乏锰进口鼠伤寒沙门氏菌突变体对没有更敏感，这表明锰是用于向亚硝化应激抗性很重要的。

更新日期：2020-11-03

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