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目的研究结核分枝杆菌(MTB)感染的小鼠腹腔巨噬细胞L-型钙通道(L-type calcium channel,LTCC)的mRNA表达水平,并探讨其免疫学意义。方法结核分枝杆菌强毒株H37Rv、弱毒株H37Ra、卡介菌(简称BCG)分别感染小鼠24h后,腹腔灌洗收获巨噬细胞,用逆转录-聚合酶链反应(RT-PCR)半定量技术检测巨噬细胞LTCC mRNA的表达情况,并选择正常小鼠和金黄色葡萄球菌(金葡菌)感染小鼠作对照。结果巨噬细胞LTCC mRNA表达水平(相对含量)MTB H37Rv组为0.42±0.14),H37Ra组为0.35±0.09,BCG组为0.32±0.10,与正常未感染组0.20±0.08比较差异有统计学意义(P<0.01或P<0.05);H37Rv、H37Ra感染组与金葡菌感染组0.24±0.07比较差异有统计学意义(P<0.01或P<0.05);BCG感染组与金葡菌感染组之间差异无统计学意义(P>0.05);金葡菌感染组与正常未感染组之间差异也无统计学意义(P>0.05);BCG感染组、H37Ra感染组和H37Rv感染组间差异无统计学意义(P>0.05);不同抗菌谱的金葡菌感染组间差异也无统计学意义(P>0.05)。结论 MTB感染小鼠后巨噬细胞LTCC mRNA表达量显著增加,提示LTCC在MTB的致病机制和机体的免疫保护机制中均发挥了一定的作用。
Objective To study the mRNA expression level of L-type calcium channel (LTCC) in mouse peritoneal macrophages infected with Mycobacterium tuberculosis (MTB) and to explore its immunological significance. Methods Mycobacterium tuberculosis virulent strain H37Rv, attenuated strain H37Ra and bacillus Calmette-Guerin (BCG) were infected respectively for 24 hours. After peritoneal lavage, macrophages were harvested and transfected by reverse transcriptase-polymerase chain reaction (RT-PCR) Quantitative technique was used to detect the expression of LTCC mRNA in macrophages. Normal mice and S. aureus were selected as control. Results The level of LTCC mRNA in macrophages was 0.42 ± 0.14 in MTB H37Rv group, 0.35 ± 0.09 in H37Ra group, 0.32 ± 0.10 in BCG group, and 0.20 ± 0.08 in normal non-infected group (P <0.05) P <0.01 or P <0.05). There was significant difference between H37Rv and H37Ra infection groups and 0.24 ± 0.07 of S.aureus infection group (P <0.01 or P <0.05); between BCG infection group and S.aureus infection group (P> 0.05). There was also no significant difference between S.aureus infection group and normal non-infection group (P> 0.05). There was no statistical difference between BCG infection group, H37Ra infection group and H37Rv infection group (P> 0.05). There was also no significant difference between different antibacterial spectrum of S. aureus infection (P> 0.05). Conclusion The expression of LTCC mRNA in macrophages increased significantly after MTB infection, suggesting that LTCC may play a role in the pathogenesis of MTB and the mechanism of immune protection.