The main function of epithelium is to secret water and solutes. A method to quantify water transport is to measure the flux of marker molecules like fluorescein or ¹⁴C-mannitol. But this allows only assessing the paracellular transport while transcellular water secretion remains unconsidered. In our approach we grow wtCFTR expressing 16HBE14o- and dF508-CFTR expressing CFBE41o- bronchial epithelium cells to confluence on filter membranes. These filter membranes were mounted on a glass cover slip using a clamp ring. Height changes of the whole filter membrane were recorded under physiological conditions by repetitive AFM line scans of the apical surface. Both cell lines as well as empty filters show no height changes under basal conditions. During stimulation of wtCFTR expressing 16HBE14o- with cyclic AMP the complete filter membrane sinks by 2mm within 10 min. The downward movement of the filter could be stopped by application of the CFTR specific inhibitor CFTR_inh-172. Filters with dF508-CFTR expressing CFBE41o- cells contrarily show almost no height change during stimulation. It is known that cAMP induces a CFTR mediated secretion of salt and water from the basolateral to the apical side. The filter mounting procedure causes that a small volume of liquid remains trapped beneath the filter membrane. We assume that cAMP induces transepithelial transport of this trapped liquid which consequently leads to a downward movement of the whole filter. This hypothesis is supported by the finding that the secretion of wtCFTR expressing cells (downward movement of the filter) could be stopped completely by application of CFTR_inh-172 while filters with dF508-CFTR expressing cells shown no movement upon cAMP. We can calculate the secretion rate from the height change, filter area and time. For 16HBE14o- cells we determined a cAMP induced secretion rate of about 2.5 ml/h/cm². From these date we conclude that we developed a reliable method to quantify transepitehlial water transport by AFM.