Normal lung mechanics maximize gas exchange across the alveolar-capillary membrane. However, pulmonary diseases such as Acute Respiratory Distress Syndrome (ARDS) disrupt this function by allowing edematous fluid from the vasculature to enter and occlude airways and alveoli. ARDS causes about 59,000 deaths per year in the United States with a mortality rate between 36.2 â"u20ac"u201c 44.3%. To improve gas exchange, patients are often treated with mechanical ventilation, which can cause atelectrauma during the recruitment and derecruitment of occluded airways and alveoli. Previous in vitro experiments have modeled the interfacial flow of airway recruitment by introducing a single finger of air into epithelial-lined parallel plate chambers and tubes. The objective of the current study is to longitudinally track the cellular injury and detachment associated with interfacial stresses that arise from 20 cycles of recruitment and derecruitment. We found that cellular injury trends asymptotically from 4.1% after one cycle to 11.2% after 20 cycles. In addition, we found that cellular detachment trends linearly from 0.0 to 6.4% over 20 cycles. The asymptotic behavior of cell damage agrees with conclusions of prior investigations and implies the existence of a â"u20ac˜critical numberâ"u20ac™ of bubble passes, above which no additional damage occurs. This cyclic recruitment and derecruitment model provides a platform for investigating the cellular biomechanics leading to epithelial injury during mechanical ventilation of patients with ARDS. / Thomas A Itin