Programmed cell death/apoptosis of lung epithelial cells represents a potentially important mechanism contributing to the loss of this cell type in the development of ALI (Figure 1 ). Bachhofen et al. reported that patients who died from ARDS exhibited excessive apoptotic alterations in the chromatin of their alveolar type II cells (19) . Subsequent studies then confirmed these DNA fragmentations (112) as well as an increased expression of the pro-apoptotic protein Bax (Bcl-2 associated X protein) (113) . More recent studies also have suggested a role for lung epithelial cell apoptosis in pediatric ARDS (114) . Importantly, epithelial cell and PMN apoptosis is differentially regulated during ARDS. While, as mentioned earlier, PMNs show a decreased rate of apoptosis, it is increased markedly in epithelial cells (107) . Local mediators in the lungs of these patients may regulate these opposing effects (115, 116) . Interestingly, the induction of lung epithelial cell apoptosis appears to lead to the development of ALI, which is further aggravated, when apoptosis is additionally induced in macrophages (117) . Furthermore, inhibition of apoptosis, using a caspase inhibitor, protected mice from the lethal consequences of endotoxin-associated ALI (118) . In addition, Bcl-x(L) treatment reduced albumin leakage and lung tissue damage in LPS-mediated ALI (119).