Thirty years ago Staphylococcus aureus and not Pseudomonas aeruginosawas considered to be the most important lung pathogen in cystic fibrosis.1 Those who believed that P aeruginosa was a pathogen in cystic fibrosis thought that various virulence factors such as exotoxin A, exoenzyme S, elastase, alkaline protease, phospholipase C, lipopolysaccharide and phenazine pigments were responsible for the lung tissue damage by drawing parallels with acute P aeruginosa infections in patients with burns or leukaemia.2 Only acute exacerbations, frequently caused by a virus,3 were therefore treated with antibiotics, although invasive disseminatingP aeruginosa infection including bacteraemia was never found in cystic fibrosis.4 However, a very pronounced antibody response to P aeruginosaantigens, including its virulence factors, was detected in patients with cystic fibrosis and the pathogenesis of the lung tissue damage was subsequently found to be caused by immune complex mediated inflammation dominated by polymorphonuclear leucocytes releasing proteolytic enzymes.5-7 Since the annual mortality of cystic fibrosis patients with chronic P aeruginosa infection in the Danish Cystic Fibrosis Centre increased to nearly 20% in 1974, a comprehensive therapeutic approach was started to try to reduce the inflammation by (1) reducing the antigenic load by …