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Reactive oxygen species involved in apoptosis induction of human respiratory epithelial (A549) cells by Streptococcus agalactiae

机译:无乳链球菌参与人类呼吸道上皮(A549)细胞凋亡诱导的活性氧

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Streptococcus agalactiae (Group B Streptococcus; GBS) is an important pathogen and is associated with pneumonia, sepsis and meningitis in neonates and adults. GBS infections induce cytotoxicity of respiratory epithelial cells (A549) with generation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential (ψm). The apoptosis of A549 cells by GBS was dependent on the activation of caspase-3 and caspase-9 with increased pro-apoptotic Bim and Bax molecules and decreased Bcl-2 pro-survival protein. Treatment of infected A549 cells with ROS inhibitors (diphenyleniodonium chloride or apocynin) prevented intracellular ROS production and apoptosis. Consequently, oxidative stress is included among the cellular events leading to apoptosis during GBS human invasive infections.
机译:无乳链球菌(B组链球菌; GBS)是重要的病原体,与新生儿和成人的肺炎,败血症和脑膜炎有关。 GBS感染通过产生活性氧(ROS)和线粒体膜电位(ψm)丧失,诱导呼吸道上皮细胞(A549)发生细胞毒性。 GBS对A549细胞的凋亡依赖于caspase-3和caspase-9的激活,促凋亡的Bim和Bax分子增加,而Bcl-2的促生存蛋白降低。用ROS抑制剂(氯化二苯基亚硝基鎓或载脂蛋白)处理感染的A549细胞可防止细胞内ROS的产生和凋亡。因此,氧化应激包括在导致GBS人为感染期间凋亡的细胞事件中。

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