...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Virology >West Nile virus infection modulates human brain microvascular endothelial cells tight junction proteins and cell adhesion molecules: Transmigration across the in vitro blood-brain barrier.
【24h】

West Nile virus infection modulates human brain microvascular endothelial cells tight junction proteins and cell adhesion molecules: Transmigration across the in vitro blood-brain barrier.

机译：西尼罗河病毒感染可调节人脑微血管内皮细胞紧密连接蛋白和细胞粘附分子：跨体外血脑屏障的迁移。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Neurological complications such as inflammation, failure of the blood-brain barrier (BBB), and neuronal death contribute to the mortality and morbidity associated with WNV-induced meningitis. Compromised BBB indicates the ability of the virus to gain entry into the CNS via the BBB, however, the underlying mechanisms, and the specific cell types associated with WNV-CNS trafficking are not well understood. Brain microvascular endothelial cells, the main component of the BBB, represent a barrier to virus dissemination into the CNS and could play key role in WNV spread via hematogenous route. To investigate WNV entry into the CNS, we infected primary human brain microvascular endothelial (HBMVE) cells with the neurovirulent strain of WNV (NY99) and examined WNV replication kinetics together with the changes in the expressions of key tight junction proteins (TJP) and cell adhesion molecules (CAM). WNV infection of HBMVE cells was productive as analyzed by plaque assay and qRT-PCR, and did not induce cytopathic effect. Increased mRNA and protein expressions of TJP (claudin-1) and CAM (vascular cell adhesion molecule and E-selectin) were observed at days 2 and 3 after infection, respectively, which coincided with the peak in WNV replication. Further, using an in vitro BBB model comprised of HBMVE cells, we demonstrate that cell-free WNV can cross the BBB, without compromising the BBB integrity. These data suggest that infection of HBMVE cells can facilitate entry of cell-free virus into the CNS without disturbing the BBB, and increased CAM may assist in the trafficking of WNV-infected immune cells into the CNS, via 'Trojan horse' mechanism, thereby contributing to WNV dissemination in the CNS and associated pathology.
机译：神经系统并发症，例如炎症，血脑屏障（BBB）衰竭和神经元死亡，都导致与WNV诱发的脑膜炎相关的死亡率和发病率。受损的BBB表示病毒具有通过BBB进入CNS的能力，但是，与WNV-CNS贩运相关的潜在机制和特定细胞类型尚不清楚。脑微血管内皮细胞是血脑屏障的主要成分，代表病毒传播到中枢神经系统的障碍，并可能在通过血源途径传播的西尼罗病毒中起关键作用。为了研究WNV进入中枢神经系统的过程，我们用WNV（NY99）的神经毒株感染了原代人脑微血管内皮（HBMVE）细胞，并检查了WNV复制动力学以及关键紧密连接蛋白（TJP）和细胞表达的变化。粘附分子（CAM）。通过噬斑测定和qRT-PCR分析，HBMVE细胞的WNV感染是有生产力的，并且不引起细胞病变作用。感染后第2天和第3天，分别观察到TJP（claudin-1）和CAM（血管细胞粘附分子和E-选择素）的mRNA和蛋白质表达增加，这与WNV复制的峰值一致。此外，使用由HBMVE细胞组成的体外BBB模型，我们证明了无细胞的WNV可以穿越BBB，而不会损害BBB的完整性。这些数据表明，HBMVE细胞的感染可以促进无细胞病毒进入中枢神经系统而不会干扰血脑屏障，而增加的CAM可以通过“特洛伊木马”机制协助感染WNV的免疫细胞向中枢神经系统的运输，从而有助于WNV在CNS和相关病理学中的传播。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号