Objective To investigate the effects of Interleukin-18 (IL-18) on asthmatic airway inflammation and nuclear factor kappa-B (NF-κB) in a murine asthmatic model. Methods BALB/C mice were randomly divided into three groups: group A(control group,n=10); group B (asthmatic model group, n=10); group C (IL-18 injection group, n=10). The asthmatic model was established in group B and C by respiratory syncytial virus (RSV) killed by ultraviolet light. Saline solution (0.1 ml) and IL-18 (0.1 ml, 1 μg) was injected in groups B and C at seven time points (1, 2, 7, 8, 9, 21, 22 d). The symptoms and the numbers of eosinophils and plasmacytes in the airways were observed and the expression of NF-κB activation in the lung was analyzed by Immohistochemistry (IHC) and Western blot. Results The symtoms of group C were more severe than in groups A and B. Group A did not have EOS and plasmacytes in the airway submucosal while the numbers of eosinophils [15±3 (average cell counts per microscopic visual field, the same below)] and plasmacytes (10±2) in group B were found to have increased significantly. But the numbers of eosinophils and plasmacytes in group C were decreased significantly when compared with group B (6±2 and 2±1, respectively, both P <0.05). ISH showed that the expression of NF-κB activation in group B was stronger than that in groups A and C. The amount of NF-κB inhibitor (IκB) in group A and group C were 3.5 times and 2.5 times more than that of group B respectively via Western blot. Conclusion IL-18 can inhibit asthmatic airway inflammation in mice and its mechamism may be due to the fact that IL-18 can inhibit the activation of NF-κB in the murine asthmatic model. Objective To investigate the effects of Interleukin-18 (IL-18) on asthmatic airway inflammation and nuclear factor kappa-B (NF-κB) in a murine asthmatic model. Methods BALB / C mice were randomly divided into three groups: group A group B (asthmatic model group, n = 10); group C (IL-18 injection group, n = 10). The asthmatic model was established in group B and C by respiratory syncytial virus Saline solution (0.1 ml) and IL-18 (0.1 ml, 1 μg) were injected in groups B and C at seven time points (1, 2, 7, 8, 9, 21, 22 d) . The symptoms and the numbers of eosinophils and plasmacytes in the airways were observed and the expression of NF-κB activation in the lung was analyzed by Immohistochemistry (IHC) and Western blot. Results The symtoms of group C were more severe than in groups A and B. Group A did not have EOS and plasmacytes in the airway submucosal while the numbers of eosinophils [15 ± 3 (average cell counts per microscopic vis ual field, the same below]] and plasmacytes (10 ± 2) in group B were found to have increased significantly. But the numbers of eosinophils and plasmacytes in group C were decreased significantly compared to group B (6 ± 2 and 2 ± 1, respectively, both P <0.05). ISH showed that the expression of NF-κB activation in group B was stronger than that in groups A and C. The amount of NF-κB inhibitor (IκB) in group A and group C were 3.5 times and 2.5 times more than that of group B respectively via Western blot. Conclusion IL-18 can inhibit asthmatic airway inflammation in mice and its mechamism may be due to the fact that IL-18 can inhibit the activation of NF-κB in the murine asthmatic model.