Li Hongdong, Li Xingyuan, Song Chao, Zhang Yunhui, Wang Zhengli, Liu Zhenqiu, Wei Hong, Yu Jialin
Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China.
Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China.
Front Microbiol. 2017 Oct 17;8:1944. doi: 10.3389/fmicb.2017.01944. eCollection 2017.
Bacterial communication systems, such as quorum sensing (QS), have provided new insights of alternative approaches in antimicrobial treatment. We recently reported that one QS signal, named as autoinducer-2 (AI-2), can affect the behaviors of PAO1 in a dose-dependent manner. In this study, we aimed to investigate the effects of AI-2 on PAO1 biofilm formation and virulence factors production , and using a pulmonary infection mouse model. Exogenous AI-2 resulted in increased biofilms architecture, the number of viable cells, and the yield of pyocyanin and elastase virulence factors in wild type PAO1. However, no such effect was observed in mutant strain. , the use of AI-2 significantly increased the mortality, lung bacterial count and histological lung damage of mice with acute PAO1 infection. Our data suggest that AI-2 promotes the formation of PAO1 biofilms and the production of virulence factors by interfering with QS systems, resulting in decreased host survival. AI-2 may be a therapeutic target for the clinical treatment of a co-infection of and AI-2 producing bacteria.
细菌通讯系统,如群体感应(QS),为抗菌治疗的替代方法提供了新的见解。我们最近报道,一种名为自诱导物-2(AI-2)的QS信号可以剂量依赖性方式影响铜绿假单胞菌PAO1的行为。在本研究中,我们旨在研究AI-2对PAO1生物膜形成和毒力因子产生的影响,并使用肺部感染小鼠模型。外源性AI-2导致野生型PAO1中生物膜结构增加、活细胞数量增加以及绿脓菌素和弹性蛋白酶毒力因子产量增加。然而,在突变菌株中未观察到这种效应。此外,使用AI-2显著增加了急性PAO1感染小鼠的死亡率、肺部细菌计数和肺部组织学损伤。我们的数据表明,AI-2通过干扰QS系统促进PAO1生物膜的形成和毒力因子的产生,导致宿主存活率降低。AI-2可能是临床治疗与产生AI-2细菌共感染的治疗靶点。