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As one of the major pathogens in wound infections,  Pseudomonas aeruginosa  produces several virulence factors and forms biofilms; these processes are under the regulation of various quorum sensing (QS) systems. Therefore, QS has been regarded as a promising target to treat  P. aeruginosa  infections. In the present study, we evaluated the effect of the plant-derived QS inhibitor coumarin on  P. aeruginosa  biofilms and virulence. Coumarin inhibited QS in the  P. aeruginosa  QSIS2 biosensor strain, reduced protease and pyocyanin production, and inhibited biofilm formation in microtiter plates in different  P. aeruginosa  strains. The effects of coumarin in inhibiting biofilm formation in an  in vitro  wound model and reducing  P. aeruginosa  virulence in the  Lucilia sericata  infection model were strain-dependent. Transcriptome analysis revealed that several key genes involved in the  las, rhl, Pseudomonas  quinolone signal (PQS), and integrated QS (IQS) systems were downregulated in coumarin-treated biofilms of  P. aeruginosa  PAO1. Coumarin also changed the expression of genes related to type III secretion and cyclic diguanylate (c-di-GMP) metabolism. The cellular c-di-GMP level of  P. aeruginosa  PAO1 and recent clinical  P. aeruginosa  strains was significantly reduced by coumarin. These results provide new evidence for the possible application of coumarin as an anti-biofilm and anti-virulence agent against  P. aeruginosa  in wound infections.

Coumarin Reduces Virulence and Biofilm Formation in Pseudomonas aeruginosa by Affecting Quorum Sensing, Type III Secretion and C-di-GMP Levels