Our model presented some of the main features of experimental endotoxin-induced ALI (46), such as: (1) histological evidence of tissue injury characterized by accumulation of neutrophils in the interstitial space, thickening of the alveolar wall, interstitial edema, and atelectasis; (2) an inflammatory response characterized by increased lung myeloperoxidase activity (a surrogate marker of neutrophil activity) and concentrations of proinflammatory cytokines in lung tissue; and (3) evidence of physiological dysfunction characterized by hypoxemia and changes in lung mechanics (25, 46). This evidence concerns the gene MPO and acute respiratory distress syndrome.