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在结核分枝杆菌(Mycobacterium tuberculosis,MTB)与宿主巨噬细胞的相互作用中,巨噬细胞的凋亡对抵御及杀灭MTB起着重要的作用。为了探讨MTB的BCG和H37Ra两个弱毒株对巨噬细胞凋亡的影响及其相关机制,本研究比较了体外培养的BCG和H37Ra两种菌株感染小鼠(Mus musculus)巨噬细胞后对细胞凋亡的影响,并检测了肿瘤坏死因子-alpha(tumor necrosis factor-α,TNF-α)、凋亡相关蛋白半胱氨酸蛋白酶-3(Caspase-3)和B淋巴细胞瘤-2(B-cell lymphoma-2,Bcl-2)的表达情况。结果发现,与对照组相比,BCG和H37Ra感染后显著提高了巨噬细胞的凋亡率(P<0.05),TNF-α和Caspase-3的表达及活性也显著增加(P<0.01或P<0.05),同时极显著抑制了Bcl-2的表达(P<0.01)。但BCG感染组细胞凋亡率极显著高于H37Ra组(P<0.01),BCG感染组Caspase-3的表达和活性极显著高于H37Ra组(P<0.01),而Bcl-2和TNF-α的表达在BCG和H37Ra感染组间差异不显著(P>0.05)。结果提示,BCG和H37Ra两个弱毒株感染后对巨噬细胞凋亡的影响不同,可能与Caspase-3的表达相关,而与Bcl-2和TNF-α的表达无关。本研究为深入研究MTB毒力与巨噬细胞凋亡的相互作用机制提供了基础资料。
In the interaction of Mycobacterium tuberculosis (MTB) with host macrophages, apoptosis of macrophages plays an important role in the defense and killing of MTB. In order to investigate the effects of two attenuated BCG and H37Ra strains on macrophage apoptosis and their related mechanisms, we compared the effects of two strains of BCG and H37Ra cultured in vitro on murine (Mus musculus) macrophages, (TNF-α), caspase-3 and B lymphoblastoma-2 (B -cell lymphoma-2, Bcl-2) expression. The results showed that, compared with the control group, BCG and H37Ra significantly increased the apoptosis rate of macrophages (P <0.05) and the expression and activity of TNF-α and Caspase-3 significantly increased (P <0.01 or P <0.05), meanwhile significantly inhibited the expression of Bcl-2 (P <0.01). However, the apoptosis rate of BCG infection group was significantly higher than that of H37Ra group (P <0.01). The expression and activity of Caspase-3 in BCG infection group were significantly higher than those in H37Ra group (P <0.01) There was no significant difference between BCG and H37Ra infection (P> 0.05). The results suggest that BCG and H37Ra attenuated the apoptosis of macrophages after infection, which may be related to the expression of Caspase-3 but not to the expression of Bcl-2 and TNF-α. This study provides the basic information for further study on the mechanism of MTB virulence and macrophage apoptosis.