The beating of cilia is the primary method of moving mucus in healthy subjects. We need to understand the forces that cilia produce and how they couple to the mucus overlayer. Experiments have primarily focused on the cilia beat frequency, with no reports of measurements of the force of individual cilia in lung cell cultures. Modeling efforts of axonemal structures have focused on flagella, which display symmetric beat patterns distinctly different from the asymmetric pattern of cilia. We need to place cilia within a complete numerical model to understand how mucus rheology places severe limits on cilia-induced flow and how chemical signals that modify cilia motion and force generation affect mucus flow. Finally, we need to understand the interaction of mucus with the cilia and epithelial cell glycocalyx as a possible active mechanism of PCL volume regulation. The thickness of the periciliary layer (PCL) is critical for effective propulsion of mucus by cilia. If the PCL height is too thick then the cilia tips do not engage the lower mucus layer. If the PCL is too thin, then the cilia will bend under the layer and no longer have an effective beat. In considering an active mechanism for PCL volume regulation, there must be sensors that trigger epithelial effectors. We propose that primary candidates for the volume sensor are cilia or glycocalyx linked mechanoreceptors for sensing PCL depletion and inducing secretion of liquid. These two roles of cilia, as actuator and potentially as sensor, are united through Newton’s 3rd law which states that if the cilia apply a force to the mucus, then the cilia has an identical force applied to it from the mucus. Therefore, our multiscale numerical model, and our experimental measurements of cilia forces are intimately related to both roles of cilia, actuator and sensor, that constitute this project.