The Effect of Interleukin-18 on Airway Inflammation in Asthmatic Murine Models and Its Mechanisms  

作　　者：张惠兰 张珍祥 徐永健 邢丽华 刘剑波 

机构地区：[1]Department of Respiratory Diseases, Tongji Hospital, Tongji Medical School, Huazhong University of Science and Technology

出　　处：《Journal of Huazhong University of Science and Technology(Medical Sciences)》2007年第5期501-504,共4页华中科技大学学报（医学英德文版）

基　　金：The project was supported by a grant from the National Natural Sciences Foundation of China (No 30500224)

摘　　要：In order to investigate the effect of interleukin-18 （IL-18） on airway inflammation in asthmatic murine models and its mechanisms, BALB/C mice were randomly divided into three groups （n=10 in each group）： group A （control group）; group B （asthmatic model group）; group C （IL-18-treated group）. The asthmatic model was established in groups B and C by respiratory syncytial virus （RSV） killed by ultraviolet. Saline solution （0.1 mL） and IL-18 （0.1 mL, 1μg） were intraperitoneally injected respectively in groups B and C at 7 time points （day 1, 2, 7, 8, 9, 21, 22）. The number of eosinophils （EOS） and plasmacytes in the airway was observed. The levels of interferon gamma （IFN-γ） in bronchoalveolar lavage fluid （BALF） were measured by ELISA. The results showed that symptoms of asthma in group C were more severe than in groups A and B. In group A, there were no EOS and plasmacytes in the airway submucosa. The number of EOS [ 15±3 （average cell counts per microscopic visual field, the same below）] and plasmacytes （10±2） in group B were increased significantly. However, the number of EOS and plasmacytes in group C （6±2 and 2±1, respectively） was decreased significantly as compared with group B （both P〈0.05）. The levels of IFN-γ in groups A, B and C were 31±3, 40±5 and 63±5 μg/mL respectively, and those in group C were significantly higher than in groups A and B （both p〈0.05）. It was suggested that the mechanism by which IL-18 inhibited the airway inflammation in asthmatic mice might be contributed to the fact that IL-18 could induce the induction of IFN-γ.In order to investigate the effect of interleukin-18 （IL-18） on airway inflammation in asthmatic murine models and its mechanisms, BALB/C mice were randomly divided into three groups （n=10 in each group）： group A （control group）; group B （asthmatic model group）; group C （IL-18-treated group）. The asthmatic model was established in groups B and C by respiratory syncytial virus （RSV） killed by ultraviolet. Saline solution （0.1 mL） and IL-18 （0.1 mL, 1μg） were intraperitoneally injected respectively in groups B and C at 7 time points （day 1, 2, 7, 8, 9, 21, 22）. The number of eosinophils （EOS） and plasmacytes in the airway was observed. The levels of interferon gamma （IFN-γ） in bronchoalveolar lavage fluid （BALF） were measured by ELISA. The results showed that symptoms of asthma in group C were more severe than in groups A and B. In group A, there were no EOS and plasmacytes in the airway submucosa. The number of EOS [ 15±3 （average cell counts per microscopic visual field, the same below）] and plasmacytes （10±2） in group B were increased significantly. However, the number of EOS and plasmacytes in group C （6±2 and 2±1, respectively） was decreased significantly as compared with group B （both P〈0.05）. The levels of IFN-γ in groups A, B and C were 31±3, 40±5 and 63±5 μg/mL respectively, and those in group C were significantly higher than in groups A and B （both p〈0.05）. It was suggested that the mechanism by which IL-18 inhibited the airway inflammation in asthmatic mice might be contributed to the fact that IL-18 could induce the induction of IFN-γ.

关 键 词：interleukin- 18 ASTHMA EOSINOPHIL plasmacyte interferon gamma 

分 类 号：R562.25[医药卫生—呼吸系统]