Background: Acute lung injury (ALI) and acute respiratory distress syndrome have still high mortality. However, there are few therapeutic options. We have to devise the method to decrease cell death of lung epithelium and endothelium in ALI. Autophagy is involved in both cell survival and cell death, which is not known well in the field of ALI. In this work, we wished to determine the role of autophagy in ALI and the physiological significance of the autophagic response. Materials and Methods: In vitro experiment, lipopolysaccharide(LPS) was exposed to RAW 264.7 cell and autophagy was monitored by measurement of expression level of LC3-I and LC3-II using western blotting(WB). In vivo experiment, LPS was instilled into C57BL/6 mice intratracheally and fixed lung tissue and mouse lung lysates were analyzed by WB, LM and EM. N-acetylcysteine was treated to in vivo and in vitro ALI models and protein extracts from lung and cells were prepared for western blot analysis. Results: Preliminary studies indicated that LPS induced autophagy in RAW 264.7 cells in dose and time dependent manner, as assessed by increased expression of LC3II. Parallel studies in mice also showed an increase in LC3II in lung by LPS, which also induced ALI. We next investigated the effect of NAC upon the LPS induced autophagy. We observed that LPS induced autophagy was attenuated by NAC both in vitro and vivo experiment. Conclusion: We found that LPS induced autophagy in the model of ALI. Oxidative signaling might be involved in the induction mechanism of autophagy by LPS.