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目的探讨结核杆菌感染中巨噬细胞凋亡的信号传导通路及分子机理。方法用透射电镜、荧光染色对凋亡细胞的形态特征进行分析;琼脂糖凝胶电泳检测巨噬细胞DNA片段化水平;流式细胞术测定不同时期小鼠巨噬细胞凋亡率、膜表面Toll样受体2(TLR2)和胞内Bcl2蛋白的水平。结果结核杆菌强毒力株H37Rv感染组的巨噬细胞凋亡率在1～7d内逐渐升高,至7d时最高可达32.2%,感染的9～11d以后,凋亡率逐渐降低;H37Rv感染组Bcl2水平于感染9～11d后逐渐升高,与卡介苗(BCG)组比较差异有统计学意义;H37Rv感染组和BCG组的巨噬细胞膜表面的TLR2水平均高于正常对照组;各组组内不同时期的TLR2水平无明显变化。结论结核杆菌H37Rv株在感染的早期对宿主巨噬细胞有较强的致凋亡作用,而Bcl2表达的增加能显著抑制这种凋亡。结核杆菌在体内感染过程中,TLR2蛋白可能与巨噬细胞凋亡及Bcl2表达无关。
Objective To investigate the signal transduction pathway of macrophage apoptosis in Mycobacterium tuberculosis infection and its molecular mechanism. Methods Morphological characteristics of apoptotic cells were analyzed by transmission electron microscopy and fluorescent staining. DNA fragmentation of macrophages was detected by agarose gel electrophoresis. Apoptosis rate of macrophages at different periods was measured by flow cytometry. Like receptor 2 (TLR2) and intracellular Bcl2 protein levels. Results The apoptotic rates of macrophages in H37Rv infected group increased gradually from 1 to 7 days and reached 32.2% up to 7 days. After 9 to 11 days of infection, the apoptotic rate of H37Rv infection gradually decreased. H37Rv infection The level of Bcl2 increased gradually from 9 to 11 days after infection, which was significantly different from BCG group (P <0.05). The levels of TLR2 on membrane of macrophages in H37Rv infected group and BCG group were higher than those in normal control group There was no significant change in TLR2 levels in different periods. Conclusion Mycobacterium tuberculosis H37Rv strain has a strong apoptosis-inducing effect on host macrophages in the early stage of infection, while the increase of Bcl2 expression can significantly inhibit this apoptosis. Mycobacterium tuberculosis infection in vivo, TLR2 protein may be related to apoptosis and Bcl2 expression of macrophages.