In this vein, during acute respiratory distress syndrome (ARDS), recruited alveolar neutrophils and Mos/macrophages acquire a classically activated phenotype (Mo1/M1) responsible for the release of several growth factors and proinflammatory cytokines, including CXCL1, CXCL2, CXCL10, CCL2, and TNF-α. This evidence concerns the gene CXCL2 and acute respiratory distress syndrome.