Most of the health problems experienced by cystic fibrosis (CF) patients arise from a thick mucus. Mucins are mucus glycoproteins that are kept compact inside the cells. However, when mucus is secreted towards the airways, mucins have to expand to function correctly. In CF, this does not happen and recent data suggest that mucus is so thick in CF not only because of reduced fluid secretion: the lack of bicarbonate secretion across mutated CFTR does not allow mucins to expand. This project aim at studying the structure and viscoelastic properties of mucus released by CF and non-CF airway epithelia in vitro. The plan is to evaluate whether compounds that recover the activity of mutated CFTR protein are able to restore the normal properties of mucus; to study the effects produced by the addition of bicarbonate on the characteristics of airway mucus and on its capacity to kill bacteria. Bicarbonate may be a mutation-independent low cost solution.