The formation of Pseudomonas biofilms is very common in the lungs of cystic fibrosis patients with chronic infections. The colonization of the respiratory tract by this pathogen usually starts with the tissue adhesion of non-mucoid and motile strains. Subsequently they evolve a mucoid phenotype forming sessile communities, with a protective layer around the cells that confers more resistance to antibiotic therapy. Conventional antibiotics are frequently ineffective mainly because of their undesiderable side effects, emergence of resistant strains or because their lacking activity against pathogenic forms. Due to these reasons, novel anti-infective agents are of great interest to the medical community. Here we report on the potent activity and membrane-perturbing effects of the amphibian antimicrobial peptide esculentin(1-21), on both the free-living and sessile forms of P. aeruginosa, as a possible mechanism for biofilm disruption. Moreover Esc(1-21) does not induce resistant strains in vitro after multiple exposure to the peptide. Overall, this peptide is a promising template for the generation of new antibiotic formulations to advance care of infections caused by P. aeruginosa
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