The inflammatory reaction is a contributory factor to lung damage in cystic fibrosis (CF), the most common lethal autosomal recessive hereditary disease in Caucasian populations. Bacterial colonization of the lower airways and repeated lung infections lead to pulmonary deterioration and shorten the life span of CF patients. Recent studies have shown that inflammation in the lower airways occurs even in asymptomatic children with CF (1, 2). Proinflammatory cytokines like tumour necrosis factor alpha (TNF-a) and interleukin-8 (IL-8) in sputum have proved to be significant markers of the activity of CF lung disease in different patient populations (3, 4). TNF-a is produced in response to bacterial and viral challenges. Bacterial lipopolysaccharides and other cell wall components induce TNF-a and interleukin-1 beta (IL-1b), which in turn induce various other cytokines, nitric oxide, prostaglandin, platelet activating factor and oxygen radicals. TNF-a is produced by macrophages in the lung. It mediates neutrophil chemotaxis and neutrophil activation. IL-8 is probably the most stable cytokine produced in epithelial cells and fibroblasts in response to TNF-a or IL-1a and IL-1b. It has a long duration of action, activates lymphocytes and neutrophils and promotes chemotaxis of neutrophils. Even neutrophils can produce IL-8 and recruit other neutrophils.