Acute lung injury (ALI) and the more severe form termed acute respiratory distress syndrome (ARDS) are associated with an estimated mortality of 40–50%1. Causes of ALI may be direct (pneumonia, aspiration, inhalational injury, etc.) or indirect (sepsis, pancreatitis, blood transfusion, etc.). ALI is characterized by increased vascular permeability caused by dysfunction of the alveolar-capillary membrane, lung edema, neutrophil-derived inflammation, and surfactant dysfunction2. During the course of ALI/ARDS, resident lung cells such as alveolar macrophages (AMΦ) are stimulated to release chemoattractants, which recruit inflammatory cells to migrate from the intravascular space across the endothelium and epithelium into the airspaces3.