Huilan Zhang1, Zhenxiang Zhang, Yongjian Xu. 1. Department of Respiratory Diseases, Tongji Hospital, Tongji Medical School, Huazhong University of Science and Technology, Wuhan 430030, China. huilanz_76@163.com
Abstract
OBJECTIVE: To investigate the effects of Interleukin-18 (IL-18) on asthmatic airway inflammation and nuclear factor kappa-B (NF-kappaB) 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 micro g) 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-kappaB activation in the lung was analyzed by immunohistochemistry (IHC) and Western blot. RESULTS: The symptoms 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-kappaB activation in group B was stronger than that in groups A and C. The amount of NF-kappaB inhibitor (IkappaB) 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 mechanism may be due to the fact that IL-18 can inhibit the activation of NF-kappaB 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-kappaB) 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 micro g) 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-kappaB activation in the lung was analyzed by immunohistochemistry (IHC) and Western blot. RESULTS: The symptoms 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-kappaB activation in group B was stronger than that in groups A and C. The amount of NF-kappaB inhibitor (IkappaB) 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 mechanism may be due to the fact that IL-18 can inhibit the activation of NF-kappaB in the murine asthmatic model.