Department of Respiratory Medicine, The Affiliated Hospital of Qingdao University, Qingdao, PR China.
Department of Respiratory Medicine, People's Hospital of Rizhao Lanshan, Rizhao, PR China.
Indian J Med Res. 2018 Apr;147(4):400-406. doi: 10.4103/ijmr.IJMR_2010_16.
BACKGROUND & OBJECTIVES: Pseudomonas aeruginosa is an opportunistic pathogen that can cause nosocomial bloodstream infections in humans. This study was aimed to explore the association of furanone C-30 with biofilm formation, quorum sensing (QS) system and antibiotic resistance in P. aeruginosa.
An in vitro model of P. aeruginosa bacterial biofilm was established using the standard P. aeruginosa strain (PAO-1). After treatment with 2.5 and 5 μg/ml of furanone C-30, the change of biofilm morphology of PAO-1 was observed, and the expression levels of QS-regulated virulence genes (lasB, rhlA and phzA2), QS receptor genes (lasR, rhlR and pqsR) as well as QS signal molecule synthase genes (lasI, rhlI, pqsE and pqsH) were determined. Besides, the AmpC expression was quantified in planktonic and mature biofilm induced by antibiotics.
Furanone C-30 treatment significantly inhibited biofilm formation in a dose-dependent manner. With the increase of furanone C-30 concentration, the expression levels of lasB, rhlA, phzA2, pqsR, lasI, rhlI pqsE and pqsH significantly decreased in mature biofilm bacteria while the expression levels of lasR and rhlR markedly increased. The AmpC expression was significantly decreased in both planktonic and biofilm bacteria induced by imipenem and ceftazidime.
INTERPRETATION & CONCLUSIONS: Furanone C-30 may inhibit biofilm formation and antibiotic resistance in P. aeruginosa through regulating QS genes. The inhibitory effect of furanone C-30 on las system appeared to be stronger than that on rhl system. Further studies need to be done with different strains of P. aeruginosa to confirm our findings.
铜绿假单胞菌是一种机会致病菌，可导致人类发生医院获得性血流感染。本研究旨在探讨呋喃酮 C-30 与铜绿假单胞菌生物膜形成、群体感应（QS）系统和抗生素耐药性的关系。
采用标准铜绿假单胞菌株（PAO-1）建立铜绿假单胞菌细菌生物膜体外模型。用 2.5 和 5μg/ml 呋喃酮 C-30 处理后，观察 PAO-1 生物膜形态的变化，测定 QS 调控毒力基因（lasB、rhlA 和 phzA2）、QS 受体基因（lasR、rhlR 和 pqsR）以及 QS 信号分子合成酶基因（lasI、rhlI、pqsE 和 pqsH）的表达水平。此外，还定量检测了抗生素诱导的浮游和成熟生物膜中 AmpC 的表达。
呋喃酮 C-30 处理呈剂量依赖性显著抑制生物膜形成。随着呋喃酮 C-30 浓度的增加，成熟生物膜细菌中 lasB、rhlA、phzA2、pqsR、lasI、rhlI、pqsE 和 pqsH 的表达水平显著降低，而 lasR 和 rhlR 的表达水平显著升高。亚胺培南和头孢他啶诱导的浮游和生物膜细菌中 AmpC 的表达均显著降低。
呋喃酮 C-30 可能通过调节 QS 基因抑制铜绿假单胞菌生物膜形成和抗生素耐药性。呋喃酮 C-30 对 las 系统的抑制作用似乎强于 rhl 系统。需要用不同的铜绿假单胞菌菌株进一步研究以证实我们的发现。
