The central mechanism of ALI is the formation of aortic coarctation, endothelial cell leakage, tissue factor release, and blood contact with the aortic intima, resulting in the release of histogenic factors, activation of cells associated with the inflammatory response, and the entry of a large number of inflammation-related factors into the blood, such as interleukin-6 (IL-6), interleukin-8 (IL-8), and other proinflammatory factors, resulting in a “waterfall.” This results in a “waterfall-like” inflammatory cascade, leading to extensive alveolar exudation and interstitial edema. Here, CXCL8 is linked to acute respiratory distress syndrome.