Acute lung injury (ALI) and its most severe form, the acute respiratory distress syndrome (ARDS) are frequent complications in critically ill patients and are responsible for significant morbidity and mortality (1, 2). Treatment of the underlying disease and excellent supportive care using “lung-protective” strategies of mechanical ventilation (3) contribute to successful clinical outcomes. However, aside from the use of activated protein C in the subset of ALI/ ARDS patients with sepsis (4), specific therapies are lacking, and the cascade of events leading to ALI and ARDS, once initiated, is much less amenable to specific treatment modalities. Regardless of the underlying illness, the clinical and pathologic manifestations of ALI/ARDS are very similar, indicating the existence of final common pathways that represent potential therapeutic targets (1, 5). In essence, these syndromes reflect severe injury leading to dysfunction and compromise of the barrier properties of the pulmonary endothelium and epithelium as a consequence of an unregulated acute inflammatory response (6). In this hypothetical construct, an initiating event (sepsis, shock, trauma, multiple transfusions, pancreatitis, etc.) leads to activation of the acute inflammatory response on a systemic level. One of the earliest manifestations is activation of pulmonary endothelium and macrophages (alveolar and interstitial), upregulation of adhesion molecules, and production of cytokines and chemokines that induce a massive sequestration of neutrophils within the pulmonary microvasculature. These cells transmigrate across the endothelium and epithelium into the alveolar space and release a variety of cytotoxic and proinflammatory compounds, including proteolytic enzymes, reactive oxygen species (ROS) and nitrogen species, cationic proteins, lipid mediators, and additional inflammatory