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

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences 2007-10, Vol.27 (5), p.501-504
• Main Author: 张惠兰 张珍祥 徐永健 邢丽华 刘剑波
• Format: Article
• Language: English
• Subjects: Animals; Asthma - drug therapy; Asthma - metabolism; Asthma - virology; Bronchoalveolar Lavage Fluid - chemistry; Female; Inflammation - complications; Inflammation - metabolism; Inflammation - virology; Interferon-gamma - metabolism; Interleukin-18 - therapeutic use; Mice; Mice, Inbred BALB C; Random Allocation; Respiratory syncytial virus; Respiratory Syncytial Viruses; 内白细胞素-18; 发病机理; 嗜曙红细胞; 干扰素-γ; 支气管哮喘
• ISSN: 1672-0733; 1993-1352
• DOI: 10.1007/s11596-007-0506-2

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.