Abstract： Objective To study the mechanism of sepsis- induced acute respiratory distress syndrome (ARDS) and its correlation with renin-angiotensin system. Methods Male BALB/c mice were randomly divided into 3 groups (n=20)-the normal group, sham group, and cecal ligation and puncture (CLP) group. Sepsis-induced ARDS models were established by CLP. Blood gas, wet/dry lung weight ratio (W/D) , lung tissue histology as lung injury markers were examined 18 h post-CLP. Moreover, levels of several key enzymes from RAS [angiotensin converting enzyme (ACE), ACE2 and angiotensin Ⅱ (Ang Ⅱ)] were detected 6 h post-CLP. Results CLP group mice showed a significant increase in lung water (W/D: 6.08±0.64 vs 4.38±0.93, P<0.01), hypoxia aggravation [PaO2: (40.80±5.03) mm Hg vs (72.80±4.32) mm Hg, P<0.01] and decrease in oxygenation index (PaO2/FiO2: 194.30±23.90 vs 346.70±20.50, P<0.01) 18 h post-CLP compared to sham group. In addition, lung histology revealed inflammatory infiltration, alveolar edema and alveolar-capillary membrane thickening in CLP mice. Six hours after CLP, Ang Ⅱ protein was markedly increased in mice lung and plasma of CLP group than that of sham group, P<0.01. Immunohistochemistry showed an obvious expression of ACE in mice lung vessel wall in sham and CLP group associated with a decrease of lung ACE2 in CLP group than that of the other two groups. Conclusions RAS is activated in sepsis-induced ARDS. The increase of Ang Ⅱ expression can promote lung injury, and the increase of Ang Ⅱ may be correlated with the decrease of ACE2.