During ALI, excessive ROS generation contributes to the endothelial and epithelial barrier disruption, resulting in leakage of fluids into the pulmonary parenchyma and massive leukocyte (e.g., neutrophils and macrophage) infiltration, as well as robust pro-inflammatory mediator production such as IL-6, TNF-α and IL-8 [1, 33, 34]. This evidence concerns the gene CXCL8 and acute respiratory distress syndrome.