Some studies indicated that inflammatory reactants such as interleukin-6 (IL-6), C-reactive protein (CRP) and monocyte chemoattractant protein-1 (MCP-1) were significantly increased in blood or lung tissues from ATAAD patients with ALI, and these reactants could directly or indirectly promote the apoptosis and barrier dysfunction of pulmonary microvascular endothelial cells (PMVECs), which contributed to the elevation of endothelial permeability and the formation of ALI6–8. This evidence concerns the gene CCL2 and acute respiratory distress syndrome.