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1
Contribution of Catalase and Superoxide Dismutase to the Intracellular Survival of Clinical Isolates of Staphylococcus aureus in Murine Macrophages.过氧化氢酶和超氧化物歧化酶对金黄色葡萄球菌临床分离株在小鼠巨噬细胞内生存的贡献。
Indian J Microbiol. 2010 Oct;50(4):375-84. doi: 10.1007/s12088-011-0063-z. Epub 2011 Jan 25.
2
Intracellular survival of Staphylococcus aureus: correlating production of catalase and superoxide dismutase with levels of inflammatory cytokines.金黄色葡萄球菌的细胞内存活:过氧化氢酶和超氧化物歧化酶的产生与炎性细胞因子水平的相关性
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3
Intracellularly survived Staphylococcus aureus after phagocytosis are more virulent in inducing cytotoxicity in fresh murine peritoneal macrophages utilizing TLR-2 as a possible target.吞噬后细胞内存活的金黄色葡萄球菌在利用TLR-2作为可能靶点诱导新鲜小鼠腹腔巨噬细胞产生细胞毒性方面更具毒性。
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Possible role of Toll-like receptor-2 in the intracellular survival of Staphylococcus aureus in murine peritoneal macrophages: involvement of cytokines and anti-oxidant enzymes.Toll 样受体 2 在金黄色葡萄球菌在鼠腹腔巨噬细胞内生存中的可能作用:细胞因子和抗氧化酶的参与。
Scand J Immunol. 2014 Aug;80(2):127-43. doi: 10.1111/sji.12195.
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Simultaneous lack of catalase and beta-toxin in Staphylococcus aureus leads to increased intracellular survival in macrophages and epithelial cells and to attenuated virulence in murine and ovine models.金黄色葡萄球菌中过氧化氢酶和β毒素同时缺失会导致其在巨噬细胞和上皮细胞内的存活率增加,并导致在小鼠和绵羊模型中的毒力减弱。
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Staphylococcal catalase protects intracellularly survived bacteria by destroying H2O2 produced by the murine peritoneal macrophages.葡萄球菌过氧化氢酶通过破坏小鼠腹膜巨噬细胞产生的过氧化氢来保护细胞内存活的细菌。
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Expression of CXCR1 (IL-8 receptor A) in splenic, peritoneal macrophages and resident bone marrow cells after acute live or heat killed Staphylococcus aureus stimulation in mice.小鼠经急性活的或热灭活的金黄色葡萄球菌刺激后,脾、腹膜巨噬细胞及骨髓常驻细胞中CXCR1(白细胞介素8受体A)的表达
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Catalase, superoxide dismutase, and virulence of Staphylococcus aureus. In vitro and in vivo studies with emphasis on staphylococcal--leukocyte interaction.过氧化氢酶、超氧化物歧化酶与金黄色葡萄球菌的毒力。体外和体内研究,重点关注葡萄球菌与白细胞的相互作用。
J Clin Invest. 1975 Mar;55(3):561-6. doi: 10.1172/JCI107963.
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Killing of Staphylococcus aureus by allylpyrocatechol is potentiated by induction of intracellular oxidative stress and inhibition of catalase activity.烯丙基焦儿茶酚通过诱导细胞内氧化应激和抑制过氧化氢酶活性增强金黄色葡萄球菌的杀灭作用。
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COMMD10-Guided Phagolysosomal Maturation Promotes Clearance of Staphylococcus aureus in Macrophages.COMMD10 引导的吞噬溶酶体成熟促进巨噬细胞中金黄色葡萄球菌的清除。
iScience. 2019 Apr 26;14:147-163. doi: 10.1016/j.isci.2019.03.024. Epub 2019 Mar 27.
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Oxidative stress in the oral cavity is driven by individual-specific bacterial communities.口腔中的氧化应激是由个体特异性细菌群落驱动的。
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本文引用的文献

1
Pharmacodynamic evaluation of the intracellular activities of antibiotics against Staphylococcus aureus in a model of THP-1 macrophages.在THP-1巨噬细胞模型中对抗生素针对金黄色葡萄球菌的细胞内活性进行药效学评估。
Antimicrob Agents Chemother. 2006 Mar;50(3):841-51. doi: 10.1128/AAC.50.3.841-851.2006.
2
4-hydroxycinnamate lowers plasma and hepatic lipids without changing antioxidant enzyme activities.4-羟基肉桂酸可降低血浆和肝脏脂质水平,而不改变抗氧化酶活性。
Ann Nutr Metab. 2003;47(3-4):144-51. doi: 10.1159/000070037.
3
Euglycemic hyperinsulinemia augments the cytokine and endocrine responses to endotoxin in humans.正常血糖高胰岛素血症增强人体对内毒素的细胞因子和内分泌反应。
Am J Physiol Endocrinol Metab. 2002 Jun;282(6):E1276-85. doi: 10.1152/ajpendo.00535.2001.
4
Discrepancy between uptake and intracellular activity of moxifloxacin in a Staphylococcus aureus-human THP-1 monocytic cell model.莫西沙星在金黄色葡萄球菌-人THP-1单核细胞模型中的摄取与细胞内活性之间的差异。
Antimicrob Agents Chemother. 2002 Feb;46(2):288-93. doi: 10.1128/AAC.46.2.288-293.2002.
5
TNF-alpha controls intracellular mycobacterial growth by both inducible nitric oxide synthase-dependent and inducible nitric oxide synthase-independent pathways.肿瘤坏死因子-α通过诱导型一氧化氮合酶依赖性和诱导型一氧化氮合酶非依赖性途径控制细胞内分枝杆菌的生长。
J Immunol. 2001 Jun 1;166(11):6728-34. doi: 10.4049/jimmunol.166.11.6728.
6
Role of macrophages in Staphylococcus aureus-induced arthritis and sepsis.巨噬细胞在金黄色葡萄球菌诱导的关节炎和败血症中的作用。
Arthritis Rheum. 2000 Oct;43(10):2276-82. doi: 10.1002/1529-0131(200010)43:10<2276::AID-ANR15>3.0.CO;2-C.
7
Role of catalase in Campylobacter jejuni intracellular survival.过氧化氢酶在空肠弯曲菌细胞内存活中的作用。
Infect Immun. 2000 Nov;68(11):6337-45. doi: 10.1128/IAI.68.11.6337-6345.2000.
8
Staphylococcus aureus RN6390 replicates and induces apoptosis in a pulmonary epithelial cell line.金黄色葡萄球菌RN6390在一种肺上皮细胞系中复制并诱导细胞凋亡。
Infect Immun. 2000 Sep;68(9):5385-92. doi: 10.1128/IAI.68.9.5385-5392.2000.
9
Survival of Staphylococcus aureus inside neutrophils contributes to infection.金黄色葡萄球菌在中性粒细胞内的存活会导致感染。
J Immunol. 2000 Apr 1;164(7):3713-22. doi: 10.4049/jimmunol.164.7.3713.
10
Characterization of the major superoxide dismutase of Staphylococcus aureus and its role in starvation survival, stress resistance, and pathogenicity.金黄色葡萄球菌主要超氧化物歧化酶的特性及其在饥饿存活、应激抗性和致病性中的作用。
J Bacteriol. 1999 Jul;181(13):3898-903. doi: 10.1128/JB.181.13.3898-3903.1999.

过氧化氢酶和超氧化物歧化酶对金黄色葡萄球菌临床分离株在小鼠巨噬细胞内生存的贡献。

Contribution of Catalase and Superoxide Dismutase to the Intracellular Survival of Clinical Isolates of Staphylococcus aureus in Murine Macrophages.

机构信息

Department of Physiology, Immunology Laboratory, University of Calcutta, 92, APC Road, Kolkata, 700009 West Bengal India.

出版信息

Indian J Microbiol. 2010 Oct;50(4):375-84. doi: 10.1007/s12088-011-0063-z. Epub 2011 Jan 25.

DOI:10.1007/s12088-011-0063-z
PMID:22282603
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3209836/
Abstract

The present study was performed in order to carefully investigate the interaction of Staphylococcus aureus with murine macrophages and the contribution of catalase and superoxide dismutase in intracellular persistence of Staphylococcus aureus within murine macrophages during in vitro infection. We have reported that Staphylococcus aureus internalized by murine macrophages did not appear to be rapidly killed. Data indicating the contribution of a single catalase and superoxide dismutase in intracellular survival of Staphylococcus aureus were provided using established biochemical assays. The results of the present experiment suggest that the survival of Staphylococcus aureus within phagocytic cells is facilitated by its ability to resist oxidative products. Organisms in the log phase of growth clearly demonstrate a resistance to oxidative products.

摘要

本研究旨在仔细研究金黄色葡萄球菌与小鼠巨噬细胞的相互作用,以及过氧化氢酶和超氧化物歧化酶在金黄色葡萄球菌在体外感染小鼠巨噬细胞内的细胞内持续存在中的作用。我们已经报道了被小鼠巨噬细胞内化的金黄色葡萄球菌似乎不会被迅速杀死。使用已建立的生化测定法提供了表明单个过氧化氢酶和超氧化物歧化酶在金黄色葡萄球菌细胞内存活中的作用的数据。本实验的结果表明,金黄色葡萄球菌在吞噬细胞内的存活是通过其抵抗氧化产物的能力来促进的。处于对数生长期的生物体显然对氧化产物具有抗性。