登革病毒对血管内皮细胞粘附分子表达的影响
发布时间：2018-07-22 12:32
【摘要】：背景 登革病毒感染可以引起从自限性发热(Dengue Fever，DF)到登革出血热(Dengue Haemorrhagic Fever，DHF)或登革休克综合征(Dengue Shock Syndrome，DSS)等不同程度的临床症状。其中DHF／DSS最明显的标志是血浆渗漏和全身出血，血浆渗漏通常是毛细血管通透性升高造成的，提示血管的功能病变在DHF／DSS的发生发展中起重要的作用。 血管内皮细胞(Vessel endothelial cells，VECs)在调节血管渗透性和维持血液生理状态等方面起重要作用。某些病原微生物感染可以激活VECs，，激活的VECs则过度表达分泌一些粘附分子，参与炎症因子和炎症细胞的聚集、渗出和炎症反应的发生。DV可以感染人VECs，但DV对VECs表达粘附分子是否存在影响尚不清楚。血管的炎症损伤诱发血管通透性升高，血浆渗漏和出血，这些可能是诱导DHF／DSS发生发展的重要原因之一。因此从分子角度推测：活化和损伤的血管内皮细胞，一旦功能失常，引起相应的分子表达和分泌失常，进而改变血管内环境的稳态，造成血管通透性升高，对诱发DHF／DSS血浆渗漏和出血发挥着重要的作用。 临床和体外相关研究资料也为DV感染VECs产生的功能变化提供相应的佐证，目前由于尚无理想的动物模型，对DHF／DSS中血管内皮细胞损伤的研究大多停留在体外。目前，关于DV感染对血管内皮细胞表面粘附分子表达的影响及在血液渗漏和出血中的作用还不完全清楚。因此，体外研究DV诱导VECs粘附分子表达变化，对进一步完善DHF／DSS的血浆渗漏和出血的发病机制具有重要的意义。 目的 本研究拟在体外以人脐静脉内皮细胞为靶细胞，研究登革病毒Ⅱ型(dengue 2，DV_2)对人脐静脉内皮细胞表达粘附分子中的细胞间粘附分子(intercellular
[Abstract]:Background Dengue virus infection can cause various clinical symptoms ranging from dengue fever (DF) to dengue haemorrhagic Feverfever (DHF) or dengue shock syndrome (DSS). The most obvious signs of DHF / DSS are plasma leakage and systemic hemorrhage. Plasma leakage is usually caused by increased capillary permeability, which suggests that vascular functional lesions play an important role in the occurrence and development of DHF / DSS. Vascular endothelial cells (Vessel endothelial cells) play an important role in regulating vascular permeability and maintaining blood physiological state. Some pathogenic microbes can activate VECs, and activated VECs overexpression and secrete some adhesion molecules to participate in the aggregation of inflammatory factors and inflammatory cells. Exudation and inflammatory reaction. DV can infect human VECs, but it is not clear whether DV can affect VECs expression. The inflammatory injury of blood vessel induces the increase of vascular permeability, plasma leakage and hemorrhage, which may be one of the important reasons to induce the development of DHF / DSS. Therefore, from the molecular point of view, the activation and injury of vascular endothelial cells, once the function is abnormal, cause the corresponding molecular expression and secretion to be abnormal, and then change the homeostasis of the vascular environment, resulting in the increase of vascular permeability. It plays an important role in inducing DHF / DSS plasma leakage and hemorrhage. The data of clinical and in vitro studies also provide evidence for the functional changes of VECs caused by DV infection. As there is no ideal animal model, most of the studies on vascular endothelial cell injury in DHF / DSS remain in vitro. At present, the effect of DV infection on the expression of adhesion molecules on vascular endothelial cells and its role in blood leakage and bleeding is still unclear. Therefore, it is of great significance to study the changes of VECs adhesion molecule expression induced by DV in vitro in order to improve the mechanism of plasma leakage and hemorrhage of DHF / DSS. Objective to study human umbilical vein endothelial cells (HUVECs) as target cells in vitro. To study the expression of intercellular adhesion molecule (intercellular) in human umbilical vein endothelial cells (HUVECs) induced by dengue virus type 鈪
本文编号：2137473
[Abstract]:Background Dengue virus infection can cause various clinical symptoms ranging from dengue fever (DF) to dengue haemorrhagic Feverfever (DHF) or dengue shock syndrome (DSS). The most obvious signs of DHF / DSS are plasma leakage and systemic hemorrhage. Plasma leakage is usually caused by increased capillary permeability, which suggests that vascular functional lesions play an important role in the occurrence and development of DHF / DSS. Vascular endothelial cells (Vessel endothelial cells) play an important role in regulating vascular permeability and maintaining blood physiological state. Some pathogenic microbes can activate VECs, and activated VECs overexpression and secrete some adhesion molecules to participate in the aggregation of inflammatory factors and inflammatory cells. Exudation and inflammatory reaction. DV can infect human VECs, but it is not clear whether DV can affect VECs expression. The inflammatory injury of blood vessel induces the increase of vascular permeability, plasma leakage and hemorrhage, which may be one of the important reasons to induce the development of DHF / DSS. Therefore, from the molecular point of view, the activation and injury of vascular endothelial cells, once the function is abnormal, cause the corresponding molecular expression and secretion to be abnormal, and then change the homeostasis of the vascular environment, resulting in the increase of vascular permeability. It plays an important role in inducing DHF / DSS plasma leakage and hemorrhage. The data of clinical and in vitro studies also provide evidence for the functional changes of VECs caused by DV infection. As there is no ideal animal model, most of the studies on vascular endothelial cell injury in DHF / DSS remain in vitro. At present, the effect of DV infection on the expression of adhesion molecules on vascular endothelial cells and its role in blood leakage and bleeding is still unclear. Therefore, it is of great significance to study the changes of VECs adhesion molecule expression induced by DV in vitro in order to improve the mechanism of plasma leakage and hemorrhage of DHF / DSS. Objective to study human umbilical vein endothelial cells (HUVECs) as target cells in vitro. To study the expression of intercellular adhesion molecule (intercellular) in human umbilical vein endothelial cells (HUVECs) induced by dengue virus type 鈪
本文编号：2137473
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