As described above, ROS derived from PMN NADPH oxidase through interaction between PMNs and AMφ or PMNs and lung ECs mediate an augmented upregulation of TLR2 in the AMφ and ECs following HS, and in turn, sensitize the cells to TLR2 agonists, exaggerate inflammatory response, and promote the development of ALI. The gene discussed is TLR2; the disease is acute respiratory distress syndrome.