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1
Sputum culture conversion with moxifloxacin-containing regimens in the treatment of patients with newly diagnosed sputum-positive pulmonary tuberculosis in South India.莫西沙星含药方案治疗印度南部新诊断为痰阳性肺结核患者的痰培养转换。
Clin Infect Dis. 2014 Nov 15;59(10):e142-9. doi: 10.1093/cid/ciu550. Epub 2014 Jul 14.
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Medical treatment of pulmonary multidrug-resistant tuberculosis.肺部耐多药结核病的药物治疗
Infect Chemother. 2013 Dec;45(4):367-74. doi: 10.3947/ic.2013.45.4.367. Epub 2013 Dec 27.
3
Salvage therapy for multidrug-resistant tuberculosis.耐多药结核病的挽救治疗。
Clin Microbiol Infect. 2014 May;20(5):441-6. doi: 10.1111/1469-0691.12335. Epub 2013 Aug 30.
4
Contribution of reactive oxygen species to pathways of quinolone-mediated bacterial cell death.活性氧物种在喹诺酮类介导的细菌细胞死亡途径中的作用。
J Antimicrob Chemother. 2010 Mar;65(3):520-4. doi: 10.1093/jac/dkp486. Epub 2010 Jan 12.
5
Contribution of oxidative damage to antimicrobial lethality.氧化损伤对抗菌杀伤力的作用。
Antimicrob Agents Chemother. 2009 Apr;53(4):1395-402. doi: 10.1128/AAC.01087-08. Epub 2009 Feb 17.
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Transposon site hybridization in Mycobacterium tuberculosis.结核分枝杆菌中的转座子位点杂交
Methods Mol Biol. 2008;416:45-59. doi: 10.1007/978-1-59745-321-9_4.
7
A common mechanism of cellular death induced by bactericidal antibiotics.杀菌性抗生素诱导细胞死亡的常见机制。
Cell. 2007 Sep 7;130(5):797-810. doi: 10.1016/j.cell.2007.06.049.
8
Quinolone-mediated bacterial death.喹诺酮介导的细菌死亡。
Antimicrob Agents Chemother. 2008 Feb;52(2):385-92. doi: 10.1128/AAC.01617-06. Epub 2007 Aug 27.
9
RuvABC is required to resolve holliday junctions that accumulate following replication on damaged templates in Escherichia coli.在大肠杆菌中，RuvABC是解决在受损模板上复制后积累的霍利迪连接所必需的。
J Biol Chem. 2006 Sep 29;281(39):28811-21. doi: 10.1074/jbc.M603933200. Epub 2006 Aug 7.
10
Moxifloxacin lethality against Mycobacterium tuberculosis in the presence and absence of chloramphenicol.在有和没有氯霉素的情况下，莫西沙星对结核分枝杆菌的致死性。
Antimicrob Agents Chemother. 2006 Aug;50(8):2842-4. doi: 10.1128/AAC.00250-06.

霍利迪连接体解离酶参与氟喹诺酮介导的耻垢分枝杆菌杀伤作用。

Involvement of Holliday junction resolvase in fluoroquinolone-mediated killing of Mycobacterium smegmatis.

作者信息

Long Quanxin, Du Qinglin, Fu Tiwei, Drlica Karl, Zhao Xilin, Xie Jianping

机构信息

Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, Key Laboratory of Ministry of Education Eco-Environment of the Three Gorges Reservoir Region, School of Life Sciences, Southwest University, Beibei District, Chongqing, China Second Affiliated Hospital and the Key Laboratory of Molecular Biology of Infectious Diseases of the Ministry of Education, Chongqing Medical University, Yuzhong District, Chongqing, China.

Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, Key Laboratory of Ministry of Education Eco-Environment of the Three Gorges Reservoir Region, School of Life Sciences, Southwest University, Beibei District, Chongqing, China.

出版信息

Antimicrob Agents Chemother. 2015 Mar;59(3):1782-5. doi: 10.1128/AAC.04434-14. Epub 2014 Dec 22.

DOI:10.1128/AAC.04434-14
PMID:25534729
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4325773/
Abstract

The absence of the Holliday-junction Ruv resolvase of Mycobacterium smegmatis increased the bacteriostatic and bactericidal activities of the fluoroquinolone moxifloxacin, an important antituberculosis agent. The treatment of ruvAB-deficient cells with thiourea and 2,2'-bipyridyl lowered moxifloxacin lethality to wild-type levels, indicating that the absence of ruvAB stimulates a lethal pathway involving reactive oxygen species. A hexapeptide that traps the Holliday junction substrate of RuvAB potentiated moxifloxacin-mediated lethality, supporting the development of small-molecule enhancers for moxifloxacin activity against mycobacteria.

摘要

耻垢分枝杆菌中霍利迪连接体Ruv解旋酶的缺失增强了重要抗结核药物氟喹诺酮莫西沙星的抑菌和杀菌活性。用硫脲和2,2'-联吡啶处理ruvAB缺陷型细胞可将莫西沙星的致死率降低至野生型水平，这表明ruvAB的缺失激活了一条涉及活性氧的致死途径。一种能捕获RuvAB霍利迪连接体底物的六肽增强了莫西沙星介导的致死作用，这为开发增强莫西沙星对分枝杆菌活性的小分子增强剂提供了支持。