敲除pck A基因的结核杆菌引起的免疫反应的研究  

Histological and Immune Responses Induced by pckA Gene Mutated Mycobacterium bovis BCG

作　　者：柏雪莲[1] 刘克义[1] 于进芝 李桂萍[1] 李瑾[1] 魏庆宽[1] 韩广东[1] 崔勇[1] 

机构地区：[1]山东省寄生虫病防治研究所,山东济宁272033 [2]美国康乃尔大学

出　　处：《微生物学杂志》2005年第6期19-22,共4页Journal of Microbiology

基　　金：国家自然科学基金(30340073)

摘　　要：研究结核杆菌pckA基因编码的磷酸烯醇型丙酮酸羧激酶(PEPCK)诱导机体产生的保护性免疫反应。用敲除pckA基因的牛结核杆菌BCG和野生型BCG分别感染小鼠,取肝、肺、脾进行病理分析,并进行脾细胞培养,检测CD4+、CD4+/CD8+、细胞因子IFNI-γI、L-12和TNF等。用敲除pckA基因的BCG感染的小鼠比野生型BCG感染的小鼠体内产生的结核结节少且不典型,炎性程度低。野生型BCG感染的小鼠脾脏内的CD4+T细胞和CD4+/CD8+、细胞因子IFN-γ、IL-12、TNF均明显高于敲除pckA基因BCG感染的小鼠。pckA基因为结核杆菌生长所必需,其编码产物PEPCK能够刺激机体产生免疫反应,是一种很好的疫苗候选分子。Protective immune responses induced by phosphoenolpyruvate carboxykinase （PEPCK） of Mycobacterium boris BCG were studied. Mice were infected with wild type BCG and pckA mutated BCG respectively. The histology of their liver, lung, and spleen were checked. CD4 T cell, CD4^＋/CD8 and the cytokines of IFN-γ, IL-12 and TNF from the infected spleens were also checked. The results showed that granulomas in pckA mutated BCG （BCVGΔpckA） infected mice were less and atypical than those in the mice infected with wild type （BCG-WT）. CD4 T cell, CD4^＋/CD8 and the cytokines of IFN-γ, IL-12 and TNF in the BCG-WT infected mice were significantly higher than those in the BCVGΔpckA infected mice. Therefore, pckA gene is necessary for the growth of Mycobacterium tuberculosis. PEPCK can effectively induce immune responses via the increased activity of cytokines and T cells and can be a candidate for vaccine.

关 键 词：结核杆菌 pckA基因 磷酸烯醇型丙酮酸羧激酶(PEPCK) 细胞因子 免疫反应 

分 类 号：R52[医药卫生—内科学]