Under experimental conditions, the instillation of Fas-activating antibody into murine lungs induced apoptosis of lung epithelial cells, PMN recruitment and impairment of the alveolo-capillary barrier (130) . This development of Fas-dependent lung injury was linked to Fas-expression on non-myeloid but not myeloid cells (131) . Furthermore, blocking of the Fas-FasL system reduced the development of endotoxin-mediated ALI (120) . Our experiments further demonstrated the relevance of Fas-mediated apoptosis in the lung during HEMinduced septic ALI (132) . Fas and FasL mutant animals exhibited less pulmonary epithelial cell apoptosis in response to the insult when compared with background animals. In addition, the extent of ALI as assessed histologically and by protein influx was diminished significantly. This was associated with a survival benefit for Fas mutant mice when compared with background animals (132) . It also has been reported that Fas-FasL deficiency is associated with a reduction in the degree of injury seen during direct ALI in E. coli, S. aureus, or S. pneumoniae sepsis models (133) . Similar results were described for sepsis induced by Legionella pneumonia (134) . In contrast, data from pulmonary sepsis fol-lowing lung infection with P. aeruginosa suggest a reduction in lung apoptosis in the absence of Fas signaling as well, but a decreased survival rate was observed, associated with an increased dissemination of the bacteria (135) . It should be noted that Fas-mediated apoptosis in the lung appears to be modulated by several factors such as surfactant protein A, Angiotensin II, transforming growth factor (TGF)-beta, decoy receptor 3, etc. (reviewed in 108) , and that other apoptotic pathways, for example, mediated by TNF-α (136) or mitochondria (137) , appear to play a role under certain circumstances, too.