ICAM1 and acute respiratory distress syndrome: Complement activation is an early step in ALI; the next complement activation products, such as C5a and/or the membrane attack complex (C5b-9), can activate the neutrophils to adhere to the pulmonary capillary endothelium and directly activate endothelial cells to increase P-selectin or work with TNF-α to make up for the upregulation of ICAM-1 and E-selectin [33, 40].