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本文引用的文献

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Bacterial strategies of resistance to antimicrobial peptides.细菌对抗菌肽的耐药策略。
Philos Trans R Soc Lond B Biol Sci. 2016 May 26;371(1695). doi: 10.1098/rstb.2015.0292.
2
Investigating the lytic activity and structural properties of Staphylococcus aureus phenol soluble modulin (PSM) peptide toxins.研究金黄色葡萄球菌酚溶性调节蛋白(PSM)肽毒素的裂解活性和结构特性。
Biochim Biophys Acta. 2014 Dec;1838(12):3153-61. doi: 10.1016/j.bbamem.2014.08.026. Epub 2014 Sep 3.
3
Phenol-soluble modulins and staphylococcal infection.酚可溶性调节蛋白与葡萄球菌感染。
Nat Rev Microbiol. 2013 Oct;11(10):667-73. doi: 10.1038/nrmicro3110. Epub 2013 Sep 10.
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Isolation, purification and labeling of mouse bone marrow neutrophils for functional studies and adoptive transfer experiments.用于功能研究和过继转移实验的小鼠骨髓中性粒细胞的分离、纯化及标记
J Vis Exp. 2013 Jul 10(77):e50586. doi: 10.3791/50586.
5
Essential Staphylococcus aureus toxin export system.必需的金黄色葡萄球菌毒素外排系统。
Nat Med. 2013 Mar;19(3):364-7. doi: 10.1038/nm.3047. Epub 2013 Feb 10.
6
Neutrophils in innate host defense against Staphylococcus aureus infections.中性粒细胞在先天宿主防御金黄色葡萄球菌感染中的作用。
Semin Immunopathol. 2012 Mar;34(2):237-59. doi: 10.1007/s00281-011-0295-3. Epub 2011 Nov 12.
7
Antimicrobial activity of community-associated methicillin-resistant Staphylococcus aureus is caused by phenol-soluble modulin derivatives.社区相关性耐甲氧西林金黄色葡萄球菌的抗菌活性是由酚可溶性调节素衍生物引起的。
J Biol Chem. 2011 Mar 18;286(11):8933-40. doi: 10.1074/jbc.M111.221382. Epub 2011 Jan 28.
8
Structures of human host defense cathelicidin LL-37 and its smallest antimicrobial peptide KR-12 in lipid micelles.人宿主防御阳离子抗菌肽LL-37及其最小抗菌肽KR-12在脂质微团中的结构。
J Biol Chem. 2008 Nov 21;283(47):32637-43. doi: 10.1074/jbc.M805533200. Epub 2008 Sep 25.
9
The human anionic antimicrobial peptide dermcidin induces proteolytic defence mechanisms in staphylococci.人类阴离子抗菌肽皮肤杀菌素可诱导葡萄球菌的蛋白水解防御机制。
Mol Microbiol. 2007 Jan;63(2):497-506. doi: 10.1111/j.1365-2958.2006.05540.x. Epub 2006 Dec 14.
10
Antimicrobial and host-defense peptides as new anti-infective therapeutic strategies.抗菌肽和宿主防御肽作为新型抗感染治疗策略。
Nat Biotechnol. 2006 Dec;24(12):1551-7. doi: 10.1038/nbt1267.

抗菌肽耐药机制导致金黄色葡萄球菌感染。

Antimicrobial Peptide Resistance Mechanism Contributes to Staphylococcus aureus Infection.

机构信息

Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryl.

Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryl.

出版信息

J Infect Dis. 2018 Mar 13;217(7):1153-1159. doi: 10.1093/infdis/jiy024.

DOI:10.1093/infdis/jiy024
PMID:29351622
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5939666/
Abstract

Antimicrobial peptides (AMPs) constitute an important part of innate host defense. Possibly limiting the therapeutic potential of AMPs is the fact that bacteria have developed AMP resistance mechanisms during their co-evolution with humans. However, there is no direct evidence that AMP resistance per se is important during an infection. Here we show that the Staphylococcus aureus Pmt ABC transporter defends the bacteria from killing by important human AMPs and elimination by human neutrophils. By showing that Pmt contributes to virulence during skin infection in an AMP-dependent manner, we provide evidence that AMP resistance plays a key role in bacterial infection.

摘要

抗菌肽 (AMPs) 是先天宿主防御的重要组成部分。可能限制 AMP 治疗潜力的事实是,细菌在与人类共同进化的过程中已经发展出 AMP 耐药机制。然而,目前没有直接证据表明 AMP 耐药本身在感染过程中很重要。在这里,我们表明金黄色葡萄球菌 Pmt ABC 转运蛋白可防止细菌被重要的人类 AMP 杀死并被人类中性粒细胞清除。通过表明 Pmt 以 AMP 依赖的方式有助于皮肤感染中的毒力,我们提供了 AMP 耐药在细菌感染中起关键作用的证据。