Objective To investigate the role of moderate hypothermia in the lung inflammation of rat acute lung injury induced by lipopolysaccharide(LPS). Methods A rat model of acute lung injury (ALI) was established by intra-tracheal instillation of lipopolysaccharide (1.5 mg/kg, 0.5 ml) at 16 h after LPS (1.0 mg/kg) intraperitoneal administration. Thirty-four male Sprague Dawley rats were randomly divided into four groups: control group, receiving saline only; LPS group, receiving LPS; hypothermia group, treated with hypothermia without LPS; LPS+hypothermia group, treated with LPS and cooled to 32.5℃～33.0℃ as PaO 2/FiO 2 was below 300 mmHg. Hemodynamics and blood gases were recorded every hour throughout the study. Rats were killed 4 h after ALI, and lung lavage was performed to measure the tumor necrosis factor α (TNF-α), interleukin-6 (IL-6) and interleukin-10 (IL-10) concentrations in bronchoalveolar lavage fluid (BALF) by using enzyme-linked immunosorbent assay (ELISA). Results PaO 2/FiO 2 was significantly decreased and PaCO 2 was increased in the LPS group as compared to their baseline values(P<0.01). Treatment with hypothermia inhibited the increase in PaCO 2 (P<0.05) but had no effect on PaO 2/FiO 2 in the presence of LPS. The administration of LPS significantly increased the concentrations of TNF-α, IL-6 and IL-10 in BALF as compared to the control experiment(P<0.05,P<0.01). Moderate hypothermia reduced the expressions of TNF-α and IL-6(P<0.01) but had no effect on the production of IL-10(P>05). Conclusion Moderate hypothermia significantly inhibits proinflammatory cytokine expressions in lipopolysaccharide-induced acute lung injury. Objective To investigate the role of moderate hypothermia in the lung inflammation of rat acute lung injury induced by lipopolysaccharide (LPS). Methods A rat model of acute lung injury (ALI) was established by intra-tracheal instillation of lipopolysaccharide (1.5 mg / kg, 0.5 ml) at 16 h after LPS (1.0 mg / kg) intraperitoneal administration. Thirty-four male Sprague Dawley rats were differentiated into four groups: control group, receiving saline only; LPS group, receiving LPS; hypothermia group, treated with hypothermia LPS + hypothermia group, treated with LPS and cooled to 32.5 ° C ~ 33.0 ° C as PaO 2 / FiO 2 was below 300 mmHg. Rats were killed 4 h after ALI, and lung lavage was performed to measure the tumor necrosis factor α (TNF-α), interleukin-6 (IL-6) and interleukin-10 concentrations in bronchoalveolar lavage fluid (BALF) by using enzyme-linked immunosorbent assay (ELISA) Treatment with hypothermia inhibited the increase in PaCO 2 (P <0.05) but had no effect on PaO (P <0.05), but PaO 2 / FiO 2 was significantly decreased in the LPS group as compared to their baseline values The administration of LPS significantly increased the concentrations of TNF-α, IL-6 and IL-10 in BALF as compared to the control experiment (P <0.05, P <0.01). Moderate hypothermia Reduced expressions of TNF-α and IL-6 (P <0.01) but had no effect on the production of IL-10 (P> 05). Conclusion Moderate hypothermia significantly inhibits proinflammatory cytokine expressions in lipopolysaccharide-induced acute lung injury.