New antimicrobials in the management of cystic fibrosis

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Abstract
The chronic Pseudomonas aeruginosa lung infection in cystic fibrosis (CF) is a biofilm1 characterized by (i) the mucoid phenotype producing an abundance of alginate in vitro and in the patients, (ii) microcolonies surrounded by alginate in sputum and in post-mortem investigations and bacteria staying on the surface of the airways as an endobronchiolitis without spreading to the blood or to other organs, (iii) high levels of antibodies against alginate and other P. aeruginosa antigens, and (iv) resistance to the patients' defence mechanisms and to antibiotic treatment.1 Oxygen radicals produced by the inflammatory response (polmorphonuclear leucocytes; PMNs) induce mutations leading to the alginate production that is so characteristic of P. aeruginosa biofilm infection in CF.2 Quorum sensing is also involved in mature biofilm formation in vitro and in vivo.3 The biofilm mode of growth is the survival strategy of environmental bacteria such as P. aeruginosa, and alginate biofilms are also protected against antibiotics and against the immune response in the lungs of the patient.1 The tissue damage is due to immune complex-mediated chronic inflammation dominated by PMNs leading to release of leucocyte proteases.1

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