LPSEC can contribute to the pathogenesis of ALI and ARDS [37,188,189,190], characterized by infiltration of neutrophils and macrophages, the release of pro-inflammatory mediators such as IL-1β, IL-6, IL-8/CXCL8, IL-18, IL-23, TNF, and MIP-2, the decreased release of anti-inflammatory cytokines such as IL-4 and IL-10, and the disruption of pulmonary alveolar epithelial-capillary barrier integrity [204,206,207,208,209,210,211]. This evidence concerns the gene CXCL2 and acute respiratory distress syndrome.