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1
Glucose 6-phosphate dehydrogenase is required for Salmonella typhimurium virulence and resistance to reactive oxygen and nitrogen intermediates.葡萄糖6-磷酸脱氢酶是鼠伤寒沙门氏菌致病以及抵抗活性氧和氮中间产物所必需的。
Infect Immun. 1999 Jan;67(1):436-8. doi: 10.1128/IAI.67.1.436-438.1999.
2
Control of redox balance by the stringent response regulatory protein promotes antioxidant defenses of Salmonella.严格反应调节蛋白对氧化还原平衡的控制促进了沙门氏菌的抗氧化防御。
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3
Periplasmic superoxide dismutase protects Salmonella from products of phagocyte NADPH-oxidase and nitric oxide synthase.周质超氧化物歧化酶保护沙门氏菌免受吞噬细胞NADPH氧化酶和一氧化氮合酶产物的侵害。
Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13997-4001. doi: 10.1073/pnas.94.25.13997.
4
Evaluation of bacterial survival and phagocyte function with a fluorescence-based microplate assay.基于荧光的微孔板分析法评估细菌存活率和吞噬细胞功能。
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Salmonella enterica serovar Typhimurium periplasmic superoxide dismutases SodCI and SodCII are required for protection against the phagocyte oxidative burst.肠炎沙门氏菌鼠伤寒血清型周质超氧化物歧化酶SodCI和SodCII是抵御吞噬细胞氧化爆发所必需的。
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Homocysteine antagonism of nitric oxide-related cytostasis in Salmonella typhimurium.鼠伤寒沙门氏菌中同型半胱氨酸对一氧化氮相关细胞生长抑制的拮抗作用。
Science. 1996 Apr 19;272(5260):414-7. doi: 10.1126/science.272.5260.414.
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Alkyl hydroperoxide reductase subunit C (AhpC) protects bacterial and human cells against reactive nitrogen intermediates.烷基过氧化氢还原酶亚基C（AhpC）可保护细菌和人类细胞免受活性氮中间体的侵害。
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Nitric oxide and antimicrobial activity of reactive oxygen intermediates.一氧化氮与活性氧中间体的抗菌活性
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Role of KatG catalase-peroxidase in mycobacterial pathogenesis: countering the phagocyte oxidative burst.KatG过氧化氢酶-过氧化物酶在分枝杆菌致病机制中的作用：对抗吞噬细胞的氧化爆发。
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Responses to reactive oxygen intermediates and virulence of Salmonella typhimurium.
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本文引用的文献

1
The transcriptional regulator SoxS is required for resistance of Salmonella typhimurium to paraquat but not for virulence in mice.转录调节因子SoxS是鼠伤寒沙门氏菌对百草枯产生抗性所必需的，但对小鼠的毒力并非必需。
Infect Immun. 1997 Dec;65(12):5371-5. doi: 10.1128/iai.65.12.5371-5375.1997.
2
Periplasmic superoxide dismutase protects Salmonella from products of phagocyte NADPH-oxidase and nitric oxide synthase.周质超氧化物歧化酶保护沙门氏菌免受吞噬细胞NADPH氧化酶和一氧化氮合酶产物的侵害。
Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13997-4001. doi: 10.1073/pnas.94.25.13997.
3
Murine salmonellosis studied by confocal microscopy: Salmonella typhimurium resides intracellularly inside macrophages and exerts a cytotoxic effect on phagocytes in vivo.通过共聚焦显微镜研究的鼠类沙门氏菌病：鼠伤寒沙门氏菌在巨噬细胞内寄生，并在体内对吞噬细胞发挥细胞毒性作用。
J Exp Med. 1997 Aug 18;186(4):569-80. doi: 10.1084/jem.186.4.569.
4
Involvement of the oxidative pentose phosphate pathway in thiamine biosynthesis in Salmonella typhimurium.氧化戊糖磷酸途径参与鼠伤寒沙门氏菌硫胺素的生物合成。
J Bacteriol. 1996 Mar;178(5):1476-9. doi: 10.1128/jb.178.5.1476-1479.1996.
5
Homocysteine antagonism of nitric oxide-related cytostasis in Salmonella typhimurium.鼠伤寒沙门氏菌中同型半胱氨酸对一氧化氮相关细胞生长抑制的拮抗作用。
Science. 1996 Apr 19;272(5260):414-7. doi: 10.1126/science.272.5260.414.
6
Purification and regulatory properties of MarA protein, a transcriptional activator of Escherichia coli multiple antibiotic and superoxide resistance promoters.大肠杆菌多重抗生素和超氧化物抗性启动子的转录激活因子MarA蛋白的纯化及调控特性
J Bacteriol. 1995 Dec;177(24):7100-4. doi: 10.1128/jb.177.24.7100-7104.1995.
7
Recombination-deficient mutants of Salmonella typhimurium are avirulent and sensitive to the oxidative burst of macrophages.鼠伤寒沙门氏菌的重组缺陷型突变体无毒力，且对巨噬细胞的氧化爆发敏感。
Mol Microbiol. 1993 Mar;7(6):933-6. doi: 10.1111/j.1365-2958.1993.tb01184.x.
8
SoxS, an activator of superoxide stress genes in Escherichia coli. Purification and interaction with DNA.SoxS，大肠杆菌中超氧化物应激基因的激活剂。纯化及其与DNA的相互作用。
J Biol Chem. 1994 Jul 15;269(28):18371-7.
9
Genetic definition of the Escherichia coli zwf "soxbox," the DNA binding site for SoxS-mediated induction of glucose 6-phosphate dehydrogenase in response to superoxide.大肠杆菌zwf“soxbox”的遗传学定义，即SoxS介导的超氧化物响应下葡萄糖6-磷酸脱氢酶诱导的DNA结合位点。
J Bacteriol. 1995 Apr;177(7):1742-50. doi: 10.1128/jb.177.7.1742-1750.1995.
10
Mouse model of X-linked chronic granulomatous disease, an inherited defect in phagocyte superoxide production.X连锁慢性肉芽肿病的小鼠模型，一种吞噬细胞超氧化物产生的遗传性缺陷。
Nat Genet. 1995 Feb;9(2):202-9. doi: 10.1038/ng0295-202.

葡萄糖6-磷酸脱氢酶是鼠伤寒沙门氏菌致病以及抵抗活性氧和氮中间产物所必需的。

Glucose 6-phosphate dehydrogenase is required for Salmonella typhimurium virulence and resistance to reactive oxygen and nitrogen intermediates.

作者信息

Lundberg B E, Wolf R E, Dinauer M C, Xu Y, Fang F C

机构信息

Department of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA.

出版信息

Infect Immun. 1999 Jan;67(1):436-8. doi: 10.1128/IAI.67.1.436-438.1999.

DOI:10.1128/IAI.67.1.436-438.1999
PMID:9864251
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC96332/
Abstract

Salmonella typhimurium zwf mutants lacking glucose 6-phosphate dehydrogenase (G6PD) activity have increased susceptibility to reactive oxygen and nitrogen intermediates as well as attenuated virulence in mice. Abrogation of the phagocyte respiratory burst oxidase during experimental infection with zwf mutant Salmonella causes a prompt restoration of virulence, while inhibition of inducible nitric oxide synthase results in delayed lethality. These observations suggest that G6PD-dependent bacterial antioxidant defenses play an important pathogenic role during early salmonellosis and additionally may help to antagonize NO-dependent antimicrobial mechanisms later in the course of infection.

摘要

缺乏葡萄糖-6-磷酸脱氢酶（G6PD）活性的鼠伤寒沙门氏菌zwf突变体对活性氧和氮中间体的敏感性增加，并且在小鼠中的毒力减弱。在用zwf突变体沙门氏菌进行实验性感染期间，吞噬细胞呼吸爆发氧化酶的缺失导致毒力迅速恢复，而诱导型一氧化氮合酶的抑制则导致致死延迟。这些观察结果表明，G6PD依赖性细菌抗氧化防御在早期沙门氏菌病期间发挥重要的致病作用，并且在感染过程后期可能有助于对抗NO依赖性抗菌机制。