Pharmacologic inhibition of autophagy with 3-methyladenine (3-MA) or genetic silencing of ATG5 effectively reduced macrophage apoptosis and alleviated lung injury (134), suggesting that C5a-mediated autophagy activation may exacerbate ALI by promoting macrophage apoptosis.Temporal analyses in lipopolysaccharide (LPS)-induced ALI indicate distinct kinetics of cell death, with autophagy peaking at 2 hours and apoptosis occurring later at around 6 hours (135). This evidence concerns the gene ATG5 and acute respiratory distress syndrome.