TNF-α were often synergistically functioned with IL-1β [33], which could stimulate the production and release of a variety of inflammatory cells, trigger the release of oxygen free radicals and lipid metabolites, and then cause damage of the alveolar surface active material and endothelial cells, as well as blood capillary leakage, eventually leading to ALI [34]. Here, TNF is linked to acute respiratory distress syndrome.