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首页> 外文期刊>Infection and immunity >Mannheimia haemolytica Leukotoxin Induces Apoptosis of Bovine Lymphoblastoid Cells (BL-3) via a Caspase-9-Dependent Mitochondrial Pathway
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Mannheimia haemolytica Leukotoxin Induces Apoptosis of Bovine Lymphoblastoid Cells (BL-3) via a Caspase-9-Dependent Mitochondrial Pathway

机译：溶血性曼恩氏菌白细胞毒素通过Caspase-9依赖性线粒体途径诱导牛淋巴母细胞（BL-3）的凋亡。

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Mannheimia haemolytica is a key pathogen in the bovine respiratory disease complex. It produces a leukotoxin (LKT) that is an important virulence factor, causing cell death in bovine leukocytes. The LKT binds to the β2 integrin CD11a/CD18, which usually activates signaling pathways that facilitate cell survival. In this study, we investigated mechanisms by which LKT induces death in bovine lymphoblastoid cells (BL-3). Incubation of BL-3 cells with a low concentration of LKT results in the activation of caspase-3 and caspase-9 but not caspase-8. Similarly, the proapoptotic proteins Bax and BAD were significantly elevated, while the antiapoptotic proteins Bcl-2, BclXL and Akt-1 were downregulated. Following exposure to LKT, we also observed a reduction in mitochondrial cytochrome c and corresponding elevation of cytosolic cytochrome c, suggesting translocation from the mitochondrial compartment to the cytosol. Consistent with this observation, tetramethylrhodamine ethyl ester perchlorate staining revealed that mitochondrial membrane potential was significantly reduced. These data suggest that LKT induces apoptosis of BL-3 cells via a caspase-9-dependent mitochondrial pathway. Furthermore, scanning electron micrographs of mitochondria from LKT-treated BL-3 cells revealed lesions in the outer mitochondrial membrane, which are larger than previous reports of the permeability transition pore through which cytochrome c is usually released.
机译：溶血性曼海姆氏菌是牛呼吸系统疾病的重要病原体。它产生一种重要的毒力因子白细胞毒素（LKT），导致牛白细胞死亡。 LKT与β 2 整合素CD11a / CD18结合，后者通常激活促进细胞存活的信号通路。在这项研究中，我们调查了LKT诱导牛淋巴母细胞（BL-3）死亡的机制。用低浓度的LKT孵育BL-3细胞会导致caspase-3和caspase-9激活，而不激活caspase-8。同样，凋亡蛋白Bax和BAD显着升高，而抗凋亡蛋白Bcl-2，Bcl XL 和Akt-1被下调。暴露于LKT之后，我们还观察到线粒体细胞色素 c 的减少和相应的胞质细胞色素 c 升高，表明从线粒体区室转移到细胞质。与该观察结果一致，四甲基罗丹明乙酯高氯酸盐染色显示线粒体膜电位显着降低。这些数据表明，LKT通过caspase-9依赖性线粒体途径诱导BL-3细胞凋亡。此外，用LKT处理过的BL-3细胞的线粒体的扫描电子显微镜照片揭示了线粒体外膜上的损伤，该损伤大于以前通常通过其释放细胞色素 c 的通透性过渡孔的报道。

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