In this regard, some evidence has suggested that the COX-2/PGE2 pathway plays an important role in augmenting the inflammatory immune response during ARDS, as the inhibition of PGE2 synthesis prevents edema formation, neutrophil infiltration, pro-inflammatory cytokine production and the expression of adhesion molecules, thereby restoring lung morphology and increasing survival during poly-microbial sepsis [59]. This evidence concerns the gene PTGS2 and acute respiratory distress syndrome.