ObjectiveTo investigate the effects of plant-derived phenolic compounds (i.e. caffeic acid, cinnamic acid, ferulic acid and vanillic acid) on the production of quorum sensing regulated virulence factors such as pyocyanin, biofilm formation and swarming motility of Pseudomonas aeruginosa (P. aeruginosa) isolates.MethodsFourteen clinical P. aeruginosa isolates obtained from urine samples and P. aeruginosa PA01 strain were included in the study. The antibacterial effects of phenolic compounds were screened by well diffusion assay. Pyocyanin and biofilm activity were measured from culture supernatants and the absorbance values were measured using a spectrophotometer. Swarming plates supplemented with phenolic acids were point inoculated with P. aeruginosa strains and the ability to swarm was determined by measuring the distance of swarming from the central inoculation site.ResultsTested phenolic compounds reduced the production of pyocyanin and biofilm formation without affecting growth compared to untreated cultures. Moreover, these compounds blocked about 50% of biofilm production and swarming motility in P. aeruginosa isolates.ConclusionsWe may suggest that if swarming and consecutive biofilm formation could be inhibited by the natural products as shown in our study, the bacteria could not attach to the surfaces and produce chronic infections. Antimicrobials and natural products could be combined and the dosage of antimicrobials could be reduced to overcome antimicrobial resistance and drug side effects

Introduction: In the opportunistic pathogen Pseudomonas aeruginosa, the production of several virulence factors depends on quorum sensing (QS) involving N-acylhomoserine lactone signal molecules. In vitro studies have suggested that the QS system is crucial in the pathogenesis of P. aeruginosa. However, it is unclear whether QS systems of P. aeruginosa play the same role during infections. Methodology: In this study, to explore the contribution of QS systems to the pathogenesis of P. aeruginosa during urinary tract infections, we collected 82 clinical isolates. Detection of N-acyl-homoserine lactones (C12-HSL and C4-HSL) was performed on agar plates employing biosensor strains C. violaceum. Elastase and biofilm production were determined spectrophotometrically. QS genes were detected by PCR and subsequently underwent sequencing. Results and conclusion: Six isolates were found to be negative in the production of both C12-HSL and C4-HSL and all virulence factors tested. PCR analysis of these isolates revealed that four isolates contained all four QS genes while one isolate was negative for lasR gene, and one isolate negative for lasI, lasR and rhlR genes. Sequence analyses of these isolates showed that the lasR, lasI, rhlR and rhlI genes had point mutations. The combination of these mutations probably explains their C12-HSL, C4-HSL and virulence factor deficiencies. Results of this study suggest that QS deficient clinical isolates occur and are still capable of causing clinical infections in humans.