In Cystic fibrosis (CF), the most common genetic disease in the caucasian polulation, the mutation of the CFTR (cystic fibrosis transmembrane conductance regulator) implicate a defective Cl^- secretion leading to Na⁺ hyperabsorption mediated by ENaC (epithelial sodium channel).

The disturbance of this membrane transport causes the severe symptoms of the CF. For the research on the molecular causes of this disease and the development of potential drugs and therapies two established human epithelial cell lines could serve as model system: The CFBE41o- cells, homozygous for the CF mutation ࢞F508, and 16HBE14o-, acting as model for non-CF epithelia. In functional Ussing chamber analyses both cell lines show Cl^- secretion representative for CF or non-CF cells. But they fail to show any amiloride-sensitive ENaC current and hence do not express the CF phenotype correctly. Thus, we tried to induce the functional ENaC expression by the use of the glucocorticoid Dexamethasone (Dex), which is known to have a positive effect on ENaC expression.

We analyzed the time and dose depended influence of Dex in functional Ussing chamber studies. Moreover, we performed Western Blot analyses to proof which ENaC subunit is responsible for this effect.

Thereby we could show that the application of Dex is able to increase the ENaC expression on the functional and, depended on the analyzed ENaC subunit, also on the protein level.

Therefore, we conclude that by the induction of the ENaC expression by Dex these cell lines could represent a good model for CF in the human airway epithelia.