摘要
目的 探讨白细胞介素 18(IL 18)对支气管哮喘 (哮喘 )小鼠气道炎症及核转录因子κB(NF κB)的影响。方法 BALB c小鼠随机分为正常对照组 (A组 ,10只 )、哮喘模型组 (B组 ,10只 )、IL 18注射组 (C组 ,10只 )。B组和C组用经紫外线灭活的呼吸道合胞病毒 (RSV)激发法建立小鼠哮喘模型 ,分别于 1、2、7、8、9、2 1、2 2d腹腔注射生理盐水 (0 .1ml)和IL 18(1μg)。第 2 3天用HE染色切片观察动物气道炎症细胞的改变 ,用免疫组化和蛋白质定量分析法 (Westernblot)测定肺组织中NF κB的活性。结果 B组小鼠哮喘发作症状最明显 ,C组小鼠仅表现为轻度哮喘发作症状 ,A组小鼠无症状。A组支气管粘膜下未见嗜酸性粒细胞 (EOS)和浆细胞 ,B组支气管粘膜下可见EOS[15± 3(平均每视野计数 ,下同 ) ]和浆细胞 (10± 2 ) ,C组支气管粘膜下EOS(6± 2 )和浆细胞 (2± 1)较B组减少 (P<0 .0 5 )。肺组织冰冻切片免疫组化染色发现 :B组NF κB核表达最强 ,C组表达较弱 ,A组无表达。NF κB的抑制蛋白 (IκB)的Westernblot定量分析发现 :A组、C组的IκB含量分别是B组的 3.5和 2 .5倍 ,即说明B组NF κB的含量明显高于其他两组。结论 IL 18对支气管哮喘气道炎症有抑制作用 ,其机制之一可能与IL 18抑制了支气管哮喘小鼠肺组织中NF
Objective To investigate the effects of IL-18 on airway inflammation and nuclear factor kappa-B 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 UV-inactivated respiratory syncytial virus (RSV). Saline (0.1ml) and IL-18(0.1ml, 1μg) were respectively injected in group B and C at day 1, 2, 7, 8, 9, 21, 22. The symptoms and the numbers of eosinophils (EOS) and plasmacytes in the airways were observed and the expression of NF-κB activation in the lung was analyzed by Immohistochemistry (ISH) and Western blot. Results The symtoms of group C were more severe than group 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 increased significantly. Numbers of eosinophils and plasmacytes in group C were significantly decreased comparing 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 group 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 as shown by Western blot. Conclusion IL-18 inhibit asthmatic airway inflammation in mice and its mechamism may be explained by fact that IL-18 inhibit the activation of NF-κB in the murine asthmatic model.
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
2002年第2期139-142,共4页
Chinese Journal of Microbiology and Immunology
