In the induction of lung apoptosis during ALI, Fas-(an apoptotic death receptor pathway) mediated cell death also appears to play a major role (Figure 2 ). In this regard, during endotoxin-induced ALI, an increase of Fas expression on epithelial cells, as well as an immigration of Fas-ligand (FasL) expressing cells in(to) the lung, was observed (120). Human lung epithelial cells also expressed Fas and were, particularly in the distal airways, sensitive to Fas-mediated apoptosis (121) . Caspase-cleaved cytokeratin-18, a marker for epithelial cell apoptosis, also was increased in BALF during ARDS (122) . During ALI and ARDS, an increased concentration of Fas and FasL in patients' BALF and lung tissue was detected (122, 123) and BALF from ARDS patients was shown to induce apoptosis in healthy lung epithelial cells (116) . Furthermore, ARDS non-survivors exhibited markedly higher FasL concentrations when compared with survivors (116) . Particularly during septic ALI, an infection-severity dependent activation of the Fas-FasL system in the lung was observed (124) . FasL concentrations have been reported to be much higher locally than systemically, suggesting its origin is pulmonary (122, 123) . In this respect, there appear to be several potential sources of FasL: infiltrating monocytes have been implicated (but not alveolar macrophages) (125), PMNs have been implicated (126) , and FasL may be cleaved from cell membranes by the activation of matrix metalloproteinases 3 and 7 (127, 128) . However, anti-apoptotic proteins such as soluble Fas (129) also appear to be increased during ARDS (122, 123) and have been described to correlate with clinical features such as the PaO 2 /FiO 2 ratio (122) . This may point toward a simultaneous activation of protective anti-apoptotic mechanisms during ALI.