结核病疫情形势严峻，迫切需要寻找新的更有效的结核病防治策略与措施。研究表明自噬在巨噬细胞清除结核杆菌中发挥着重要作用。AMPK激活可通过抑制mTOR途径来促进巨噬细胞自噬，增强其清除结核杆菌的能力。我们前期的研究发现饮茶是结核病发生的保护因素；茶叶中最主要的多酚类物质EGCG可上调巨噬细胞自噬相关蛋白的表达。因此我们认为：EGCG激活AMPK进而抑制mTOR途径活化，促进巨噬细胞自噬，增强巨噬细胞清除结核杆菌能力，可能是饮茶抗结核的机制。本研究拟首先通过细胞实验以及动物实验探讨EGCG是否可以通过AMPK通路调控巨噬细胞的自噬，从而影响巨噬细胞对结核分支杆菌的清除能力；然后通过人群病例对照研究探讨AMPKα1亚基编码基因PRKAA1的多态性及其与绿茶的交互作用对结核易感性的影响。研究结果将阐明EGCG抗结核的机制，为探索结核病防治新策略与措施提供理论支持。

The epidemics of tuberculosis (TB) faces severe situation, and it is our top priority to explore innovative and more effective strategies and measures for TB prevention and treatment. Many studies have shown that macrophage autophagy plays an important role in eliminating mycobacterium tuberculosis. In addition, AMPK activation could promote macrophage autophagy via inhibiting mTOR pathway and enhance the anti-tuberculosis capability of macrophage. Our previous results have shown that the intake of tea could decrease the risk of TB, and EGCG, a main polyphenol of tea, could up-regulate the expression of macrophage autophagy-related proteins. We proposed a hypothesis for the mechanism of the anti-tuberculosis effects of EGCG, that is, EGCG activated AMPK to inhibit mTOR pathway, and then enhance autophagy and the anti-tuberculosis capability of macrophage. In this study, we explore the mechanism on whether EGCG could regulate the autophagy of macrophage via AMPK pathway, which then affects the clearance of mycobacterium tuberculosis of macrophage in cell and animal experiments. Then we investigate the impact of polymorphism of PRKAA1 gene, encoding AMPK α1 subunit, and the interaction between PRKAA1 gene and green tea on the susceptibility to tuberculosis by case-control study. The results of this research will clarify the anti-TB mechanism of EGCG and provide theoretical support for exploring new strategies and measures on the TB prevention and treatment.