Abstract

Cystic fibrosis (CF) is one of the most common genetic childhood diseases, affecting 1:2500 newborns in Europe. The disease is caused by loss-of-function mutations in the anion channel Cystic Fibrosis Transmembrane Conductance Regulator (CFTR). Deletion of F508 in CFTR (ΔF508 CFTR) is the most prevalent mutation, occurring in more than 70% of CF patients. Children with CF suffer from unusually thick mucus in the lung, which promotes recurrent bacterial infections, causes obstruction of the airways and eventually leads to inflammation, tissue damage and respiratory failure (1).

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