Apoptosis plays an important role in acute lung injury (ALI), and alveolar macrophages (AMs) are known to secrete proinflammatory cytokines and promote alveolar inflammation. The authors have previously reported that AMs can be depleted by inhalation of 1 mM 2-chloroadenosine (2-CA). In this study, the authors evaluated the effect of AM depletion by 2-CA inhalation on apoptosis in Candida-induced ALI. The results of in situ terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end-labeling (TUNEL) and immunohistochemical studies and measurement of cytokine levels and caspase 3 activities in lung homogenates indicated that the Fas-FasL system and apoptosis of alveolar epithelial cells are suppressed by depletion of AMs by 2-CA inhalation.