FPR1 and acute respiratory distress syndrome: In mouse models of LPS-induced ALI, neutrophil autophagy is required for the activation of cells and the release of particulate contents from these cells; during ALI, the increased autophagy in neutrophils increases the release of particulate contents, and therefore, inhibiting neutrophil autophagy and Atg5 (an autophagy gene) ameliorate the effect of LPS and fMLP on the release of MPO from neutrophils and inhibit the release of particulate contents, thereby alleviating ALI [34].