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本文引用的文献

1
Colistin resistance in Pseudomonas aeruginosa that is not linked to arnB.铜绿假单胞菌中与arnB无关的黏菌素耐药性。
J Med Microbiol. 2017 Jun;66(6):833-841. doi: 10.1099/jmm.0.000456.
2
Emergence of colistin resistance in Pseudomonas aeruginosa ST235 clone in South Korea.韩国铜绿假单胞菌 ST235 克隆中出现多粘菌素耐药性。
Int J Antimicrob Agents. 2017 Jun;49(6):767-769. doi: 10.1016/j.ijantimicag.2017.01.023. Epub 2017 Apr 6.
3
Structural Modification of Lipopolysaccharide Conferred by in Gram-Negative ESKAPE Pathogens.革兰氏阴性ESKAPE病原体中脂多糖的结构修饰
Antimicrob Agents Chemother. 2017 May 24;61(6). doi: 10.1128/AAC.00580-17. Print 2017 Jun.
4
Resistance to polymyxins in Gram-negative organisms.革兰氏阴性菌对多黏菌素的耐药性。
Int J Antimicrob Agents. 2017 May;49(5):526-535. doi: 10.1016/j.ijantimicag.2016.11.029. Epub 2017 Feb 3.
5
The role of whole genome sequencing in antimicrobial susceptibility testing of bacteria: report from the EUCAST Subcommittee.全基因组测序在细菌抗菌药物敏感性试验中的作用:来自 EUCAST 分委会的报告。
Clin Microbiol Infect. 2017 Jan;23(1):2-22. doi: 10.1016/j.cmi.2016.11.012. Epub 2016 Nov 23.
6
The evolution of antimicrobial peptide resistance in Pseudomonas aeruginosa is shaped by strong epistatic interactions.铜绿假单胞菌中抗菌肽耐药性的进化受到强烈上位性相互作用的影响。
Nat Commun. 2016 Oct 3;7:13002. doi: 10.1038/ncomms13002.
7
Molecular mechanisms of polymyxin resistance: knowns and unknowns.多粘菌素耐药的分子机制:已知和未知。
Int J Antimicrob Agents. 2016 Dec;48(6):583-591. doi: 10.1016/j.ijantimicag.2016.06.023. Epub 2016 Aug 4.
8
Extracellular zinc induces phosphoethanolamine addition to Pseudomonas aeruginosa lipid A via the ColRS two-component system.细胞外锌通过ColRS双组分系统诱导磷酸乙醇胺添加到铜绿假单胞菌脂质A中。
Mol Microbiol. 2015 Jul;97(1):166-78. doi: 10.1111/mmi.13018. Epub 2015 May 9.
9
Mechanisms of polymyxin resistance: acquired and intrinsic resistance in bacteria.多粘菌素耐药机制:细菌中的获得性耐药和固有耐药
Front Microbiol. 2014 Nov 26;5:643. doi: 10.3389/fmicb.2014.00643. eCollection 2014.
10
Development of colistin resistance in pmrA-, phoP-, parR- and cprR-inactivated mutants of Pseudomonas aeruginosa.铜绿假单胞菌pmrA、phoP、parR和cprR失活突变体中黏菌素耐药性的发展。
J Antimicrob Chemother. 2014 Nov;69(11):2966-71. doi: 10.1093/jac/dku238. Epub 2014 Jul 2.

脂阿拉伯甘露糖胺化对于铜绿假单胞菌对多黏菌素耐药性的发展至关重要。

Aminoarabinosylation of Lipid A Is Critical for the Development of Colistin Resistance in Pseudomonas aeruginosa.

机构信息

Department of Biology and Biotechnology Charles Darwin, Sapienza University of Rome, Laboratory affiliated with Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Rome, Italy.

Department of Biology and Biotechnology Charles Darwin, Sapienza University of Rome, Laboratory affiliated with Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Rome, Italy

出版信息

Antimicrob Agents Chemother. 2018 Feb 23;62(3). doi: 10.1128/AAC.01820-17. Print 2018 Mar.

DOI:10.1128/AAC.01820-17
PMID:29263076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5826156/
Abstract

Lipid A aminoarabinosylation is invariably associated with colistin resistance in ; however, the existence of alternative aminoarabinosylation-independent colistin resistance mechanisms in this bacterium has remained elusive. By combining reverse genetics with experimental evolution assays, we demonstrate that a functional lipid A aminoarabinosylation pathway is critical for the acquisition of colistin resistance in reference and clinical isolates. This highlights lipid A aminoarabinosylation as a promising target for the design of colistin adjuvants against .

摘要

脂质 A 氨基阿拉伯糖基化与 ; 中的多粘菌素耐药性密切相关;然而,这种细菌中是否存在其他氨基阿拉伯糖基化非依赖性的多粘菌素耐药机制仍不清楚。通过将反向遗传学与实验进化测定相结合,我们证明了功能性脂质 A 氨基阿拉伯糖基化途径对于参考株和临床分离株获得多粘菌素耐药性至关重要。这凸显了脂质 A 氨基阿拉伯糖基化作为设计多粘菌素佐剂的有前途的靶标。