ROS Is Involved in Disruption of Tight Junctions of Human Nasal Epithelial Cells Induced by HRV16
ROS Is Involved in Disruption of Tight Junctions of Human Nasal Epithelial Cells Induced by HRV16
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DOI：
10.1002/lary.27510
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发表时间：
2018-12-01
期刊：
影响因子：
2.6
通讯作者：
Kim, Seon Tae
中科院分区：
文献类型：
--
作者：
Kim, Kyeong Ah;Jung, Joo Hyun;Kim, Seon Tae
鼻病毒（RV）是大多数普通感冒的罪魁祸首，可诱导粘液分泌过多、血管通透性增加和继发性细菌感染。这些症状主要是由细胞间连接控制的屏障功能破坏引起的。在这项研究中，我们研究了活性氧（ROS）是否与RV感染诱导的人鼻上皮（HNE）原代细胞紧密连接破坏密切相关。方法和结果RV孵育导致HNE细胞紧密连接蛋白（ZO-1、E-cadherin、claudin-1和occludin）的破坏。用二苯碘（DPI）预处理可减少rv诱导的HNE细胞紧密连接的破坏。DPI可减少rv诱导的ROS生成。然而，与RV孵育后，鱼藤酮在HNE细胞中不受抑制。鼻病毒导致HNE细胞蛋白磷酸酶活性显著降低，蛋白酪氨酸磷酸化水平显著升高。二苯碘抑制rv诱导的磷酸酶失活和蛋白酪氨酸磷酸化。此外，氧化苯larsin抑制蛋白酪氨酸磷酸酶导致HNE细胞蛋白磷酸酶活性显著降低，紧密连接蛋白被破坏。结论ros介导的磷酸酶抑制在RV破坏HNE细胞紧密连接中起着至关重要的作用。这些数据提示RV感染可能会损害鼻上皮屏障功能。
Objective Rhinoviruses (RV), which are responsible for the majority of common colds, induce mucus overproduction, increased vascular permeability, and secondary bacterial infection. These symptoms are primarily caused by barrier function disruption, which is controlled by intercellular junctions. In this study, we investigated whether reactive oxygen species (ROS) are closely involved in tight junction disruption of primary human nasal epithelial (HNE) cells induced by infection of RV . Methods and Results Incubation with RV resulted in disruption of tight junction proteins (ZO-1, E-cadherin, claudin-1, and occludin) in HNE cells. Pretreatment with diphenylene iodonium (DPI) decreased RV-induced disruption of tight junction in HNE cells. RV-induced generation of ROS was diminished by DPI. However, rotenone was not inhibited in HNE cells following incubation with RV. Rhinoviruses resulted in a marked decrease in protein phosphatases activity and an increase in protein tyrosine phosphorylation levels in HNE cells. Diphenylene iodonium inhibited the RV-induced inactivation of phosphatases and phosphorylation of protein tyrosine. In addition, inhibition of protein tyrosine phosphatases with phenylarsine oxide resulted in a marked decrease in protein phosphatase activity and disruption of tight junction proteins in HNE cells. Conclusion Our results suggest that ROS-mediated inhibition of phosphatases plays a crucial role in disruption of tight junctions in HNE cells by RV. The data suggest that RV infection may damage nasal epithelial barrier function.