The effect of interleukin-18 on airway inflammation in asthmatic murine models and its mechanisms.

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, 1 microg) 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-gamma) 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-gamma in groups A, B and C were 31+/-3, 40+/-5 and 63+/-5 pg/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-gamma.