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have read and approved the manuscript.”
“Background Cystic selleck chemicals llc fibrosis (CF), an inherited disorder caused by mutations in the gene that encodes the cystic fibrosis DAPT transmembrane conductance regulator, affects approximately 30,000 Americans, primarily those of Northern European origin [1, 2]. These mutations cause a deficiency in chloride secretion with ensuing accumulation of thick, stagnant mucus within the lung alveoli of the patients [1–4]. Nutrients in the thick mucus facilitate the colonization of various bacterial pathogens, including Pseudomonas aeruginosa, Staphylococcus aureus, and Haemophilus influenzae[3, 5]. Colonization by these pathogens elicits a strong host inflammatory response which leads to destruction of the lung

tissue and, ultimately, death from respiratory failure [1, 6, 7]. P. aeruginosa is one of the significant pathogens in chronic lung infections of CF patients [1, 8]. Among the different factors that contribute to the virulence of P. aeruginosa is its ability to form a biofilm, a community within which bacteria are attached to a substratum or to each other [9]. Within the biofilm, the bacteria are surrounded by extracellular polymeric substance (EPS), which protects them from the effects of the host immune system and from diverse antibiotics [10–12]. Biofilm development occurs in stages that require specific bacterial factors at each stage. For example, during the initial (attachment) stage of biofilm formation, bacteria depend on both the flagellum-mediated swimming motility and the pili-mediated twitching motility [13]. A number of P.