Faculty of Biotechnology and Food Engineering, Technion, Haifa 32000, Israel.
J Antimicrob Chemother. 2010 May;65(5):888-96. doi: 10.1093/jac/dkq077. Epub 2010 Mar 17.
Salicylate, a potent inducer of the MarA activator in Salmonella enterica, is the principal metabolite of aspirin, which is often consumed for medicinal and cosmetic uses. Our research was aimed at testing if salicylate activates the mar regulon in macrophage-associated Salmonella (intracellular bacteria), and investigating its effects on bacterial susceptibility to ciprofloxacin extracellularly and intracellularly.
J774 macrophages were infected with S. enterica serovar Typhimurium (wild-type and marA null mutant), treated with ciprofloxacin with and without pre-exposure to salicylate, and the surviving bacteria were counted. Similar experiments were conducted with bacteria in broth (extracellular bacteria). Phe-Arg-beta-naphthylamide (PAbetaN) was added to investigate the role of efflux pumps in resistance. The transcriptional regulation of marRAB, acrAB and micF in extracellular and intracellular Salmonella Typhimurium with and without salicylate and ciprofloxacin was investigated using green fluorescent protein as a marker protein and quantitative real time PCR.
Pre-exposure of Salmonella to salicylate increased the resistance of extracellular but not intracellular bacteria to ciprofloxacin, although salicylate stimulated the expression of mar genes in intracellular and extracellular bacteria. Using marA mutants and the inhibitor PAbetaN, we showed that the improved resistance in extracellular bacteria is derived from the induction of acrAB by salicylate, which is mediated by MarA.
In intracellular bacteria, the expression of acrAB is already higher when compared with extracellular cells; therefore, salicylate does not result in significant acrAB induction intracellularly and subsequent resistance enhancement. Results show that conclusions raised from extracellular studies cannot be applied to intracellular bacteria, although the systems have similar functions.
柳酸盐是沙门氏菌中 MarA 激活物的一种有效诱导物,它是阿司匹林的主要代谢物,阿司匹林常用于医疗和美容用途。我们的研究旨在测试柳酸盐是否能激活与巨噬细胞相关的沙门氏菌(细胞内细菌)的 mar 调控子,并研究其对细菌体外和细胞内对环丙沙星敏感性的影响。
用沙门氏菌 Typhimurium(野生型和 marA 缺失突变体)感染 J774 巨噬细胞,用环丙沙星处理并用柳酸盐预处理,然后计数存活的细菌。在肉汤(细胞外细菌)中进行了类似的实验。加入苯丙氨酸-精氨酸-β-萘酰胺(PAbetaN)以研究外排泵在耐药性中的作用。使用绿色荧光蛋白作为标记蛋白和实时定量 PCR 研究了柳酸盐和环丙沙星存在与否时细胞外和细胞内沙门氏菌 Typhimurium 中 marRAB、acrAB 和 micF 的转录调控。
柳酸盐预处理增加了细胞外细菌对环丙沙星的耐药性,但不增加细胞内细菌的耐药性,尽管柳酸盐刺激了细胞内和细胞外细菌 mar 基因的表达。使用 marA 突变体和抑制剂 PAbetaN,我们表明,细胞外细菌的耐药性增强来自于柳酸盐诱导的 acrAB,这是由 MarA 介导的。
在细胞内细菌中,与细胞外细胞相比,acrAB 的表达已经更高;因此,柳酸盐不会导致细胞内 acrAB 的显著诱导和随后的耐药性增强。结果表明,尽管这些系统具有相似的功能,但从细胞外研究中得出的结论不能应用于细胞内细菌。