In the model of ALI, LPS engages the TLR4/NF-kB pathway inducing inflammation and neutrophil recruitment to the lungs, activating them to produce reactive oxygen species, increase the expression of adhesion proteins such as integrin (CD18), as well as the production of cytokines, such as TNF-a, IL-1β, IL-6, and the release neutrophil extracellular traps (NETs—free DNA, myeloperoxidase, histone), promoting diffuse alveolar damage and, consequently, difficulty in gas exchange [5]. This evidence concerns the gene MPO and acute respiratory distress syndrome.