rpoS-mutation variants are selected in Pseudomonas aeruginosa biofilms under imipenem pressure

Cell & Bioscience

Ke Wang¹  Xiangke Duan²  Lianhui Zhang²  Yumei Liu³  Zhao Cai³  Yingdan Zhang³  Moxiao Liu³  Liang Yang³  Yanrong Pan³  Yang Liu⁴ 

[1] Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University;Guangdong Province Key Laboratory of Microbial Signals and Disease Control, Integrative Microbiology Research Center, South China Agricultural University;School of Medicine, Southern University of Science and Technology;Southern University of Science and Technology Hospital;

关键词: Experimental biofilm evolution;    Pseudomonas aeruginosa;    Sigma factor RpoS;    Biofilms;    Cyclic-di-GMP;    Virulence;   

DOI  :  10.1186/s13578-021-00655-9

来源: DOAJ

【 摘 要 】

Abstract Background Pseudomonas aeruginosa is a notorious opportunistic pathogen causing various types of biofilm-related infections. Biofilm formation is a unique microbial strategy that allows P. aeruginosa to survive adverse conditions such as antibiotic treatment and human immune clearance. Results In this study, we experimentally evolved P. aeruginosa PAO1 biofilms for cyclic treatment in the presence of high dose of imipenem, and enriched hyperbiofilm mutants within six cycles in two independent lineages. The competition assay showed that the evolved hyperbiofilm mutants can outcompete the ancestral strain within biofilms but not in planktonic cultures. Whole-genome sequencing analysis revealed the hyperbiofilm phenotype is caused by point mutations in rpoS gene in all independently evolved mutants and the same mutation was found in P. aeruginosa clinical isolates. We further showed that mutation in rpoS gene increased the intracellular c-di-GMP level by turning on the expression of the diguanylate cyclases. Mutation in rpoS increased pyocyanin production and virulence in hyperbiofilm variants. Conclusion Here, our study revealed that antibiotic treatment of biofilm-related P. aeruginosa infections might induce a hyperbiofilm phenotype via rpoS mutation, which might partially explain antimicrobial treatment failure of many P. aeruginosa biofilm-related infections.

【 授权许可】

Unknown