The consequence of the mutations in the CFTR gene is malfunction of the chloride channel in cystic fibrosis (CF) patients, which leads to decreased volume of the paraciliary fluid in the lower respiratory tract, and that in turn leads to impaired mucociliary clearance of inhaled microbes (Boucher 2004). This impairment of the non-inflammatory defense mechanism of the respiratory tract leads to early recruitment of the inflammatory defense mechanisms, e.g., polymorphonuclear leukocytes (PMN) and antibodies (Armstrong et al. 1995, 2005, Hoiby et al. 2001). CF patients, therefore, from early childhood suffer from recurrent and chronic respiratory tract infections characterized by PMN inflammation.