酮洛芬抑制铜绿假单胞菌的 Las/Rhl 群体感应系统：分子和对接研究。
Ketoprofen attenuates Las/Rhl quorum-sensing (QS) systems of Pseudomonas aeruginosa: molecular and docking studies.
机构信息
Department of Microbiology, Lahijan Branch, Islamic Azad University, Lahijan, Iran.
出版信息
Mol Biol Rep. 2024 Jan 18;51(1):133. doi: 10.1007/s11033-023-09071-3.
BACKGROUND
Quorum sensing (QS) is the leading cause of persistent infections and recalcitrance to antibiotic treatment of Pseudomonas aeruginosa. Hence, QS inhibitors are promising agents for the potential treatment of P. aeruginosa infections.
METHODS AND RESULTS
Herein, the reducing effect of ketoprofen on virulence factors production including protease, hemolysin, pyocyanin, hydrogen cyanide, biofilm, and motility of P. aeruginosa strains was investigated. Furthermore, the quorum quenching activity of ketoprofen at the molecular level was examined by real-time PCR assessment. Our results showed that ketoprofen significantly attenuates virulence factors and biofilm formation in P. aeruginosa strains. Moreover, ketoprofen down-regulated the expression of lasI, lasR, rhlI, and rhlR genes, by 35-47, 22-48, 34-67, and 43-56%, respectively. As well, molecular docking simulation showed a high binding affinity of ketoprofen with QS regulatory proteins.
CONCLUSIONS
Consequently, this study confirmed the quorum quenching activity of ketoprofen, which could be employed as a useful agent for the treatment of P. aeruginosa infections.
背景
群体感应（QS）是导致铜绿假单胞菌持续感染和抗生素治疗耐药的主要原因。因此，QS 抑制剂是治疗铜绿假单胞菌感染的有前途的药物。
方法和结果
本文研究了酮洛芬对包括蛋白酶、溶血素、绿脓菌素、氰化氢、生物膜和运动性在内的铜绿假单胞菌菌株毒力因子产生的抑制作用。此外，通过实时 PCR 评估研究了酮洛芬在分子水平上的群体感应淬灭活性。结果表明，酮洛芬可显著减弱铜绿假单胞菌菌株的毒力因子和生物膜形成。此外，酮洛芬分别下调了 lasI、lasR、rhlI 和 rhlR 基因的表达 35-47%、22-48%、34-67%和 43-56%。分子对接模拟表明酮洛芬与 QS 调节蛋白具有很高的结合亲和力。
结论
因此，本研究证实了酮洛芬的群体感应淬灭活性，可将其用作治疗铜绿假单胞菌感染的有效药物。
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