The FcγR imbalance leads to IC-ALI via alveolar macrophage production of proteases, early response cytokines (TNFα and IL-1β), and LTs (predominantly LTB4 (47)), which with C5a increase the expression of adhesion molecules on vascular endothelial cells, and induce CXCR1/2 chemokines. This evidence concerns the gene CXCR1 and acute respiratory distress syndrome.