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光动力失活降低了粘质沙雷氏菌群体感应介导的毒力因子产生和生物膜形成。

Photodynamic inactivation diminishes quorum sensing-mediated virulence factor production and biofilm formation of Serratia marcescens.

机构信息

Department of Microbiology, School of Biology, College of Science, University of Tehran, Tehran, 1417614411, Iran.

出版信息

World J Microbiol Biotechnol. 2019 Nov 25;35(12):191. doi: 10.1007/s11274-019-2768-9.

Abstract

Serratia marcescens is an opportunistic human pathogen causing nosocomial infections and displays expanded resistance towards the conventional antibiotics. In S. marcescens, quorum sensing (QS) mechanism coordinates the population-dependent behaviors and regulates the virulence factors production. Photodynamic inactivation (PDI) is a promising alternative for the treatment of infections caused by drug resistant bacteria. Although PDI should be applied at lethal doses, it is possible that during PDI treatment, pathogens encounter sub-lethal doses of PDI (sPDI). sPDI cannot kill microorganisms, but it can considerably influence the microbial virulence. So, in this study, the effect of methylene blue (MB)-mediated PDI on QS-mediated virulence factor production and biofilm formation of S. marcescens at lethal and sub-lethal doses was evaluated. The biofilm formation and virulence factor production of S. marcescens ATCC 13,880 and S. marcescens Sm2 were assessed before and after PDI treatment. Besides, the effect of lethal and sub-lethal PDI on expression of bsmA and bsmB (Biofilm maturation), fimA and fimC (Major fimbrial protein), flhD (Regulator of flagellar mediated swarming and swimming motility) and swrR (AHL-dependent regulator) genes were evaluated by quantitative real time polymerase chain reaction. Lethal and sub-lethal PDI resulted in a significant decrease in biofilm formation, swimming/swarming motility, and pigment and hemolysin production ability of S. marcescens strains. bsmA, bsmB, flhD and swrR genes were down-regulated after PDI treatments. In conclusion, QS-mediated virulence factor production and biofilm formation ability of the two studied S. marcescens strains decreased after both lethal and sub-lethal PDI.

摘要

粘质沙雷氏菌是一种机会致病菌,可引起医院感染,并对传统抗生素表现出广泛的耐药性。在粘质沙雷氏菌中,群体感应(QS)机制协调种群依赖性行为并调节毒力因子的产生。光动力灭活(PDI)是治疗耐药菌引起的感染的一种有前途的替代方法。尽管 PDI 应该在致死剂量下应用,但在 PDI 治疗期间,病原体可能会遇到亚致死剂量的 PDI(sPDI)。sPDI 不能杀死微生物,但它可以极大地影响微生物的毒力。因此,在这项研究中,评估了亚甲蓝(MB)介导的 PDI 在致死和亚致死剂量下对粘质沙雷氏菌的 QS 介导的毒力因子产生和生物膜形成的影响。在 PDI 处理前后评估了粘质沙雷氏菌 ATCC 13,880 和 Sm2 的生物膜形成和毒力因子产生。此外,通过定量实时聚合酶链反应评估了致死和亚致死 PDI 对 bsmA 和 bsmB(生物膜成熟)、fimA 和 fimC(主要菌毛蛋白)、flhD(鞭毛介导的游动和游泳运动调节剂)和 swrR(AHL 依赖性调节剂)基因表达的影响。致死和亚致死 PDI 导致粘质沙雷氏菌菌株的生物膜形成、游动/群集运动、色素和溶血素产生能力显著下降。PDI 处理后,bsmA、bsmB、flhD 和 swrR 基因下调。总之,两种研究的粘质沙雷氏菌菌株的 QS 介导的毒力因子产生和生物膜形成能力在致死和亚致死 PDI 后均降低。

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