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本文引用的文献

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Ligand-binding PAS domains in a genomic, cellular, and structural context.配体结合 PAS 结构域的基因组学、细胞生物学和结构背景。
Annu Rev Microbiol. 2011;65:261-86. doi: 10.1146/annurev-micro-121809-151631.
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ArcA-regulated glycosyltransferase lic2B promotes complement evasion and pathogenesis of nontypeable Haemophilus influenzae.ArcA 调控的糖基转移酶 lic2B 促进了不可分型流感嗜血杆菌的补体逃避和发病机制。
Infect Immun. 2011 May;79(5):1971-83. doi: 10.1128/IAI.01269-10. Epub 2011 Feb 28.
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Comparative study of the roles of AhpC and KatE as respiratory antioxidants in Brucella abortus 2308.比较研究 AhpC 和 KatE 在布鲁氏菌 2308 中的呼吸抗氧化作用。
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Glutathione import in Haemophilus influenzae Rd is primed by the periplasmic heme-binding protein HbpA.流感嗜血杆菌 Rd 中的谷胱甘肽摄取由周质血红素结合蛋白 HbpA 引发。
Proc Natl Acad Sci U S A. 2010 Jul 27;107(30):13270-5. doi: 10.1073/pnas.1005198107. Epub 2010 Jul 13.
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The multifaceted capacity of Dps proteins to combat bacterial stress conditions: Detoxification of iron and hydrogen peroxide and DNA binding.Dps蛋白应对细菌应激条件的多方面能力:铁和过氧化氢的解毒作用以及DNA结合。
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The catalase-peroxidase KatG is required for virulence of Xanthomonas campestris pv. campestris in a host plant by providing protection against low levels of H2O2.过氧化氢酶-过氧化物酶KatG对于野油菜黄单胞菌野油菜致病变种在寄主植物中的致病性是必需的,它通过提供对低水平过氧化氢的保护作用来实现。
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Detection of cryptic genospecies misidentified as Haemophilus influenzae in routine clinical samples by assessment of marker genes fucK, hap, and sodC.通过评估标记基因fucK、hap和sodC在常规临床样本中检测被误鉴定为流感嗜血杆菌的隐匿基因种。
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Manganese import is a key element of the OxyR response to hydrogen peroxide in Escherichia coli.锰的导入是大肠杆菌中氧还调节蛋白(OxyR)对过氧化氢反应的关键要素。
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DSB proteins and bacterial pathogenicity.双链断裂(DSB)蛋白与细菌致病性
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流感嗜血杆菌与氧化应激。

Haemophilus influenzae and oxidative stress.

机构信息

The Center for Microbial Pathogenesis, The Research Institute at Nationwide Children's Hospital, Columbus OH, USA. alistair.harrison@ nationwidechildrens.org

出版信息

Front Cell Infect Microbiol. 2012 Mar 28;2:40. doi: 10.3389/fcimb.2012.00040. eCollection 2012.

DOI:10.3389/fcimb.2012.00040
PMID:22919631
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3417577/
Abstract

Haemophilus influenzae is a commensal of the human upper respiratory tract. H. influenzae can, however, move out of its commensal niche and cause multiple respiratory tract diseases. Such diseases include otitis media in young children, as well as exacerbations of chronic obstructive pulmonary disease (COPD), sinusitis, conjunctivitis, and bronchitis. During the course of colonization and infection, H. influenzae must withstand oxidative stress generated by multiple reactive oxygen species produced endogenously, by other co-pathogens and by host cells. H. influenzae has, therefore, evolved multiple mechanisms that protect the cell against oxygen-generated stresses. In this review, we will describe these systems relative to the well-described systems in Escherichia coli. Moreover, we will compare how H. influenzae combats the effect of oxidative stress as a necessary phenotype for its roles as both a successful commensal and pathogen.

摘要

流感嗜血杆菌是人体上呼吸道的共生菌。然而,流感嗜血杆菌可以脱离共生环境并引起多种呼吸道疾病。这些疾病包括幼儿中耳炎,以及慢性阻塞性肺疾病(COPD)、鼻窦炎、结膜炎和支气管炎的恶化。在定植和感染过程中,流感嗜血杆菌必须承受由内源性、其他共病原体和宿主细胞产生的多种活性氧物质产生的氧化应激。因此,流感嗜血杆菌已经进化出多种保护细胞免受氧应激的机制。在这篇综述中,我们将描述这些系统相对于大肠杆菌中描述良好的系统。此外,我们将比较流感嗜血杆菌如何对抗氧化应激的影响,因为这是其作为成功共生菌和病原体的必要表型。