探讨Mce4E蛋白在牛结核分枝杆菌致病机理中的作用。以Mce4E蛋白刺激肺泡巨噬细胞24和48h后,MTT检测分析表明。Mce4E蛋白对巨噬细胞的活性有显著的抑制作用(P〈0.05);用重组表达的Mce4E蛋白、人分枝杆菌纯化蛋白衍生物(Purified Protein Derivative of M.tuberculosis,MtbPPD)、牛结核分枝杆菌纯化蛋白衍生物(Purified Protein Derivative of M.bov/s,MbPPD)、卡介苗(Bacille Calmette Guerin,BCG)和刀豆蛋白A(concanavalin A,ConA)分别刺激肺泡巨噬细胞48h后,real—time PCR方法检测显示,Mce4E蛋白能够促使牛肺泡巨噬细胞TNF-α和IL-6mRNA的表达上调(P〈0.05)、抑制肺泡巨噬细胞iNO的mRNA表达(P〈0.05)而对IL-12表达没有影响(P〉0、05)。Mce4蛋白能够促使肺泡巨噬细胞分泌炎性细胞因子。并对肺泡巨噬细胞有抑制作用,证实Mce4蛋白在分枝杆菌中具有重要的作用。
A large body of research has confirmed that mammalian cell entry proteins (Mce) are related to the virulent Mycobacterium bovis. MTT (3, (4, 5 dimethylthiazol-2yl)-2, 5 diphenylc-tetrazolium bromide) analysis showed that Mce4E protein could inhibit macrophage activity. In real-time RT-PCR assay, Mce4E protein stimulated alveolar macrophage for 48 hours, which significantly (P 〈 0.05) induced the expression of TNF-α and enhanced IL-6 mRNA but the expression of iNO was reduced (P〈 0.05). There was no effect on the IL-12 expression in the macrophage. We conclude that Mce4E proteins can induce an inflammatory response on exposure to M. boris and therefore play an important role in the immune response.