Naire, Shailesh, and Oliver E. Jensen. Epithelial cell deformation during surfactant-mediated airway reopening: a theoretical model. J Appl Physiol 99: 458 -471, 2005. First published March 31, 2005 doi:10.1152/japplphysiol.00796.2004.-A theoretical model is presented describing the reopening by an advancing air bubble of an initially liquid-filled collapsed airway lined with deformable epithelial cells. The model integrates descriptions of flow-structure interaction (accounting for nonlinear deformation of the airway wall and viscous resistance of the airway liquid flow), surfactant transport around the bubble tip (incorporating physicochemical parameters appropriate for Infasurf), and cell deformation (due to stretching of the airway wall and airway liquid flows). It is shown how the pressure required to drive a bubble into a flooded airway, peeling apart the wet airway walls, can be reduced substantially by surfactant, although the effectiveness of Infasurf is limited by slow adsorption at high concentrations. The model demonstrates how the addition of surfactant can lead to the spontaneous reopening of a collapsed airway, depending on the degree of initial airway collapse. The effective elastic modulus of the epithelial layer is shown to be a key determinant of the relative magnitude of strains generated by flow-induced shear stresses and by airway wall stretch. The model also shows how epithelial-layer compressibility can mediate strains arising from flow-induced normal stresses and stress gradients. recruitment; atelectrauma; volutrauma; fluid-structure interaction; surface tension SUCCESSFUL RECRUITMENT OF liquid-filled airways is a process of fundamental importance in human respiration, from the first breath onward, and is critical in the treatment of conditions such as infant or acute respiratory distress syndrome (ARDS). It is of particular current interest in the context of ARDS, where atelectrauma [damage to airway epithelium through the repeated opening and closing of airways and alveoli (9, 13, 43)], volutrauma [airway overdistension (56, 58)], and biotrauma (inflammatory airway insult secondary to mechanical injury) are candidate mechanisms of ventilator-induced lung injury (49, 53). Mechanisms of atelectrauma, for example, involve processes interacting over widely varying length scales: at the scale of the whole lung (involving forced inflation of a heterogeneous airway network); at the scale of an individual airway (where surface tension, airway compliance, and airway liquid viscosity are significant); at the scale of an airway epithelial cell (deforming in response to its local mechanical environment); and at the scale of individual molecules (for example epithelial-cell mechanosensors such as stretchactivated ion channels). Mathematical and computational models provide powerful tools with which to integrate descriptions of processes operating across such disparate scales. This paper seeks to contribute to the development of a theoretical framework for airway recruitment and specifically aims ...