减毒结核菌苗联用过量维生素A干预小鼠哮喘性肺炎的作用机制

Mechanism of BCG vaccine united hypervitamin A interfered in asthma pneumonia of experiment mice

目的:探讨过量维生素A(Vit A)联用减毒结核菌苗(BCG)对哮喘性肺炎的作用机制。方法:实验第1天45只小鼠腹腔注射卵蛋白(OVA)致敏构建哮喘性肺炎模型,当天BCG组(14只)和Vit A+BCG治疗组(17只)皮内注射BCG,10天后其中一个治疗组口服过量Vit A100 u,余用生理盐水对照。实验2周后全部小鼠雾化OVA激发哮喘,组织化学、ELISA法检查肺、脾病理学。结果:哮喘组过敏性肺炎病程长,IL-13、TNF-α水平显著升高。致敏同时BCG接种出现Th1反应和Th2反应抑制;过量Vit A加重了BCG诱导的肺淋巴细胞炎症,Vit A促进体内单核-巨噬细胞向肺炎症区转移,自释放溶酶体酶加重肺泡炎症;血IL-13、TNF-α因子水平明显下降,IFN-γ水平低,过量Vit A改变了BCG接种诱导的Th1类型,诱发非Th1、非Th2反应。结论:过量Vit A联用BCG促进细胞溶酶体酶释放,加重急性期肺炎,诱导非Th1、非Th2免疫反应,缩短病程。

Objective：To investigate the mechanism of attenuad bacillus calmette-guerin （BCG） unite high dose of vitamin A（ Vit A） interfered in asthma pneumonia. Methods ： All mice were allergized by intraperitoneal injection of ovum albumin （OVA） and two treatment groups were endermic injeced with BCG at 1st day of experiment. The mice of one of treatment groups took orally high dose of vitamin A 100 u after 10 days and other contrasted by NS. All mice atomization OVA were stimulated asthma after experiment, two weeks and were examined with methods pathology, histochemis-try, ELISA . Results： Longer course of severe allergic pneumonia, significant higher IL-13 and TNF-α factors of Th2 reaction in the group of asthma. The mice of group sensitization with OVA and BCG innoculation occurrenced Thl reaction and Th2 reaction suppressed. Another mice of group with overdose VitA and BCG inoculation aggravated lung lymphoid inflammation. Vit A promoted mononuclear-macrophages shifted into the inflammation site of lung, aggratated alveolitis by oneself lysosomal enzyme release. Down blood plasma IL-13 and TNF-α factors level obviously, and hypolevel IFN-γ. Overdose VitA changed Thl type induced by BCG inoculation, provocated non-Th1, non-Th2 reaction. Conclusions： BCG unite high dose of vitamin A possible activation lysosomal hydrolase of cell to aggrav pneumonia at acute stage, can provocated non-Th1, non-Th2 reaction and shorten the course of disease.