In patients without motile cilia, as a result of genetic defect or environmental impact, mucus clearance is maintained through sustained coughing. Apparently, this is possible as long as the mucus is not adhered to the epithelial cell surface. Therefore it is very important to understand how the airflow, which can reach 100 miles per hour during cough, couples to the mucus to produce movement. How is this coupling transferred to the mucus/cell surface to release and cause the mucus to slip? In addition, cough is an important for producing a cascade of biochemical responses to modify mucus volume and rheology. There has been speculation that during tidal volume breathing, airflow generates a finite shear stress (approximately 1 dyne/cm2) on the cell surface that releases sufficient nucleotide to account for the basal mass of nucleotides on airway surfaces. Estimates suggest that during cough, shear can approach 1700 dynes.cm 2 on airway surfaces. Depending on the volume of PCL, the concentration of nucleotides/nucleosides is predicted to vary as a function of shear and this concentration may be a signal that regulates the pattern of ion transport. However, little is known about the velocity profile of mucus or PCL along epithelial surfaces and hence the sites of maximal shear, e.g., at the cell surface vs. apex of the glycocalyx.