Defensive remodeling: How bacterial surface properties and biofilm formation promote resistance to antimicrobial peptides

被引:69
作者
Nuri, Reut [1 ]
Shprung, Tal [1 ]
Shai, Yechiel [1 ]
机构
[1] Weizmann Inst Sci, Dept Biol Chem, IL-76100 Rehovot, Israel
来源
BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES | 2015年 / 1848卷 / 11期
关键词
Antimicrobial peptides; Resistance; Surface; Biophysical properties; Biochemical properties; Biofilm; Cross resistance; ENTERICA SEROVAR TYPHIMURIUM; 2-COMPONENT REGULATORY SYSTEM; STAPHYLOCOCCUS-AUREUS; PSEUDOMONAS-AERUGINOSA; SALMONELLA-TYPHIMURIUM; ESCHERICHIA-COLI; OUTER-MEMBRANE; PHOP-PHOQ; LIPID-A; IN-VITRO;
D O I
10.1016/j.bbamem.2015.05.022
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Multidrug resistance bacteria are a major concern worldwide. These pathogens cannot be treated with conventional antibiotics and thus alternative therapeutic agents are needed. Antimicrobial peptides (AMPs) are considered to be good candidates for this purpose. Most AMPs are short and positively charged amphipathic peptides, which are found in all known forms of life. AMPs are known to kill bacteria by binding to the negatively charged bacterial surface, and in most cases cause membrane disruption. Resistance toward AMPs can be developed, by modification of bacterial surface molecules, secretion of protective material and up-regulation or elimination of specific proteins. Because of the general mechanisms of attachment and action of AMPs, bacterial resistance to AMPs often involves biophysical and biochemical changes such as surface rigidity, cell wall thickness, surface charge, as well as membrane and cell wall modification. Here we focus on the biophysical, surface and surrounding changes that bacteria undergo in acquiring resistance to AMPs. In addition we discuss the question of whether bacterial resistance to administered AMPs might compromise our innate immunity to endogenous AMPs. This article is part of a Special Issue entitled: Bacterial Resistance to Antimicrobial Peptides. (C) 2015 Published by Elsevier B.V.
引用
收藏
页码:3089 / 3100
页数:12
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