Introduction
The gene defect in cystic fibrosis (CF) leads to a malfunction
of organs expressing the cystic fibrosis conductance regulator
(CFTR) gene, with the most striking changes seen by the increased
mucus production in the airways (Lyczak et al., 2002). In addition
to increased mucus production, a CFTR mutation leads to dysregulation
of various components of the innate immune system
(Döring and Gulbins, 2009). As a result, the CF lungs are infected
with a complex microbial flora (Harrison, 2007). In most cases,
Pseudomonas aeruginosa becomes the dominant pathogen, which
cannot be eradicated by antibiotic treatment, once a chronic infection
is established (Høiby et al., 2005). However, the reason what
makes P. aeruginosa the dominant pathogen in CF is still not completely
understood.