The Role of Quorum Sensing Genes (Las and Rhl) in Biofilm Forming Pseudomonas Aeruginosa Isolates

Abstract

Background: Quorum sensing (QS) is a bacterial cell-cell communication process that involves the production, detection, and response to extracellular signaling molecules called autoinducers (AIs). Processes controlled by QS include bioluminescence, sporulation, competence, antibiotic production, biofilm formation, and virulence factor secretion. Pseudomonas aeruginosa (P. aeruginosa) produces multiple virulence factors and causes different types of infections. Objectives: to determine if deficiency within the QS system decreases the ability of P. aeruginosa to establish biofilm formation and infections in humans or not. Methodology: This was achieved through determination of the levels of P. aeruginosa autoinducers as well as the presence of QS-controlled genes (lasI, lasR, rhlI and rhlR) within the biofilm-forming clinical samples. Results: We collected 186 P. aeruginosa isolates, 89.3% were significantly biofilm producer strains. About 66% were strong, 28% were moderate and 15% were weak biofilm producer clinical isolates. Autoinducers evaluation revealed that, 8-clinical isolates (CIs) for 3OC 12 -HSL and/or C 4 -HSL concentration were deficient. The amount of 3OC 12 -HSL produced by 8-CIs was significantly lower than that produced by PAO1. While 6-CIs produced no C 4 -HSL and 2-CIs produced detectable levels of C 4 -HSL. Polymerase chain reaction (PCR) analysis of autoinducers deficient CIs revealed that, two isolates contained all four QS genes (lasI, lasR, rhlI and rhlR) and were moderate-biofilm producers while three isolates lacked all QS genes and were non-biofilm producer strains. Analysis of remaining autoinducers deficient CIs revealed that, they were weak-biofilm producer strains and they had intact las system in two strains and lacked lasR in third one while they were completely lacked the rhl system. Patients had autoinducers deficient CIs were isolated from cardiac catheterization, tracheostomy tubes, sputum, and wound infections. Conclusion: Naturally occurring QS-deficient strains of P. aeruginosa were capable of causing different infections despite the loss of optimum gene. QS-deficient genes affected the severity of biofilm formation. So the development of efficient cell-to-cell signaling blockers may reduce P. aeruginosa biofilm formation on medical devices.