Phagocytic and cytotoxic killing of P. aeruginosa is thwarted by various bacterial adaptations such as biofilm formation, LPS antigen modifications, loss of virulence factors such as flagella, and formation of persister cells, but also by impaired immune function in cells such as macrophages and neutrophils which may be secondary to chronic inflammatory stimuli and, in the case of CF, CFTR-intrinsic defects. Here, CFTR is linked to cystic fibrosis.