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首页> 外文期刊>Cell biology international. >Effects of respiratory syncytial virus infection and major basic protein derived from eosinophils in pulmonary alveolar epithelial cells (A549).
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Effects of respiratory syncytial virus infection and major basic protein derived from eosinophils in pulmonary alveolar epithelial cells (A549).

机译：对肺泡上皮细胞（A549）呼吸道合胞病毒感染和嗜酸性粒细胞衍生的主要碱性蛋白的影响。

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RSV (respiratory syncytial virus)-induced pneumonia and bronchiolitis may be associated with hyperresponsive conditions, including asthma. Eosinophilic proteins such as MBP (major basic protein) may also be associated with the pathophysiology of asthma. To elucidate the roles of RSV infection and MBP in the pathogenesis of pneumonia with hyperresponsiveness, we investigated the effects of RSV infection and MBP on A549 (alveolar epithelial) cells. CPE (cytopathic effects) in A549 cells were observed by microscopy. Apoptosis and cell death was evaluated by flow cytometric analysis and modified MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. We also measured 15 types of cytokines and chemokines in A549 cell supernatants. Although RSV alone did not affect the CPE of A549, high concentrations of MBP resulted in cell death within 24 h. Combinations of RSV and MBP synergistically induced cell death. In A549 cells infected with RSV alone, the release of GM-CSF (granulocyte-macrophage colony-stimulating factor) was significantly enhanced compared with control cells (no infection). In the cells treated with MBP alone, the production of IL (interleukin)-2, 4, 5, 7, 10, 12, 13, 17, IFN (interferon)-gamma, GM-CSF, G-CSF (granulocyte colony-stimulating factor) and MIP (macrophage inflammatory protein)-1beta was significantly increased compared with control cells. Notably, the levels of GM-CSF and IL-17 in RSV/MBP-treated cells were significantly higher than those treated with MBP alone. These results suggest that MBP synergistically enhanced the release of various cytokines/chemokines and the cell death of RSV-infected A549 cells, indicating that MBP may be closely associated with the pathophysiology of allergic reactions in bronchiolitis/pneumonia due to RSV.
机译：RSV（呼吸道合胞病毒）引起的肺炎和细支气管炎可能与包括哮喘在内的高反应性疾病有关。嗜酸性蛋白如MBP（主要碱性蛋白）也可能与哮喘的病理生理有关。为了阐明RSV感染和MBP在高反应性肺炎发病机理中的作用，我们研究了RSV感染和MBP对A549（肺泡上皮）细胞的影响。通过显微镜观察A549细胞中的CPE（细胞病变效应）。通过流式细胞术和改良的MTT [3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑溴化物]分析评估细胞凋亡和细胞死亡。我们还测量了A549细胞上清液中的15种细胞因子和趋化因子。尽管单独使用RSV不会影响A549的CPE，但高浓度的MBP会在24小时内导致细胞死亡。 RSV和MBP的组合协同诱导细胞死亡。在单独感染RSV的A549细胞中，与对照细胞（无感染）相比，GM-CSF（粒细胞-巨噬细胞集落刺激因子）的释放显着增强。在单独用MBP处理的细胞中，IL（白介素）-2、4、5、7、10、12、13、17，IFN（干扰素）-γ，GM-CSF，G-CSF（粒细胞集落-与对照组相比，刺激因子）和MIP（巨噬细胞炎性蛋白）-1β明显增加。值得注意的是，RSV / MBP处理的细胞中GM-CSF和IL-17的水平明显高于单独使用MBP处理的细胞。这些结果表明MBP协同增强了各种细胞因子/趋化因子的释放以及RSV感染的A549细胞的细胞死亡，表明MBP可能与由于RSV引起的细支气管炎/肺炎的过敏反应的病理生理密切相关。

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