In the development of ALI/ARDS, the loss of epithelial cells in the lungs with consecutive impairment of the integrity of the alveolo-capillary barrier is commonly noted (19, 104) . Type I epithelial cells make up approximately 90% of the pulmonary surface, and, while type II epithelial cells account for only 10%, they are critical because they produce surfactant and may differentiate into type I cells (17) . Impairment of the alveolar epithelial barrier is, in many ways, important in the development of ALI. On the one hand, the epithelial barrier is, under physiologic conditions, less permeable when compared with the endothelial barrier, thus, destruction of its integrity prompts a progressive influx of proteinrich fluid into the alveoli (17, 102) . On the other hand, the loss of epithelial integrity represents an impairment of the physiologic trans-epithelial fluid transport and further inhibits the re-absorption of the alveolar edema (105, 106) . Thus, while an isolated injury to the endothelium still leaves intact the capacity of the epithelium to counteract pulmonary edema formation, the fluid balance becomes rapidly disturbed upon injury of the lung epithelium (107, 108) . Therefore, it is not surprising that the extent of epithelial damage and impaired edema re-absorption was linked clinically to outcome in ALI (109) . Additionally, the accompanying reduction of surfactant production led, via an increase in the surface tension, to an augmented respiratory effort affecting gas exchange (110, 111) .