Introduction. An important factor for delayed healing of chronic wounds is the presence of bacteria. Quorum sensing (QS), a cell density-dependent signalling system, controls the production of many virulence factors and biofilm formation in Pseudomonas aeruginosa.Aim. Inhibition by sodium salicylate (NaSa) of QS-regulated virulence expression was evaluated in QS-characterized clinical wound isolates of P. aeruginosa, cultured in serum-containing medium.Methodology. Fourteen clinical P. aeruginosa strains from chronic wounds were evaluated for the production of QS signals and virulence factors. Inhibition of QS by NaSa in P. aeruginosa clinical strains, wild-type PAO1 and QS reporter strains was evaluated using in vitro assays for the production of biofilm, pyocyanin, siderophores, alkaline protease, elastase and stapholytic protease.Results. Six clinical strains secreted several QS-associated virulence factors and signal molecules and two were negative for all factors. Sub-inhibitory concentrations of NaSa downregulated the expression of the QS-related genes lasB, rhlA and pqsA and reduced the secretion of several virulence factors in PAO1 and clinical strains cultured in serum. Compared to serum-free media, the presence of serum increased the expression of QS genes and production of siderophores and pyocyanin but decreased biofilm formation.Conclusions. Pseudomonas aeruginosa from chronic wound infections showed different virulence properties. While very few strains showed no QS activity, approximately half were highly virulent and produced QS signals, suggesting that the targeting of QS is a viable and relevant strategy for infection control. NaSa showed activity as a QS-inhibitor by lowering the virulence phenotypes and QS signals at both transcriptional and extracellular levels.

中文翻译：

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水杨酸钠干扰模拟伤口液中铜绿假单胞菌的慢性伤口分离株的群体感应调节的毒力。

介绍。慢性伤口延迟愈合的重要因素是细菌的存在。群体感应（QS）是一种依赖细胞密度的信号系统，可控制铜绿假单胞菌（Pseudomonas aeruginosa）中许多毒力因子的产生和生物膜的形成。水杨酸钠（NaSa）对QS表征的铜绿假单胞菌临床伤口分离株（在含血清的培养基中培养）的QS抑制毒力表达的抑制作用进行了评估。评价了来自慢性伤口的十四种临床铜绿假单胞菌菌株的QS信号和毒力因子的产生。NaSa对铜绿假单胞菌临床菌株，野生型PAO1和QS报告基因菌株对QS的抑制作用通过体外测定生物膜，绿脓素，铁载体，碱性蛋白酶，弹性蛋白酶和溶血性蛋白酶的产生进行了评估。6株临床菌株分泌了几种QS相关毒力因子和信号分子，其中2株对所有因子均呈阴性。NaSa的亚抑制浓度下调QS相关基因lasB，rhlA和pqsA的表达，并减少PAO1和血清中培养的临床菌株中几种毒力因子的分泌。与无血清培养基相比，血清的存在增加了QS基因的表达以及铁载体和绿脓素的产生，但减少了生物膜的形成。慢性伤口感染的铜绿假单胞菌显示出不同的毒力特性。尽管极少数菌株没有QS活性，但大约有一半具有高毒力并产生QS信号，这表明以QS为靶标是一种可行且相关的感染控制策略。