【作者】 肖瑞；

【导师】 江振友；

【作者基本信息】 暨南大学 ， 病原生物学， 2006， 硕士

【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，DV₂）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更多还原

【Abstract】 BACKGROUNDThe dengue virus can produce a mild, self-limited febril illness or a severe sickness, known as hemorrhagic dengue and Dengue Shock Syndrome, which may endanger the life of patients. The most characteristic features of DHF/DSS and the best indicator of disease are vascular leakage and hemorrhaging which has suggested that dysfunction of blood vessel play an important role in the development of DHF/DSS.Vascular endothelial cells play important roles in regulating vascular permeability and maintaining the normal blood dynamics. DV can infect VECs, but little was known about the CAMs expression induced by DV. Some pathogenic infection can activate VECs and the activated VECs may express and secrete some CAM excessively. The increased production and over-expression of these molecules may take part in the inflammatory cell effusion and enhanced locally inflammatory reactions. So we speculate in the molecular level that the activated and damaged vascular endothelial cells which are in dysfunction can induce the molecules in disorder, change internal environmental homeostasis and increase vascular permeability. These will play important roles in the process of blood leakage and hemorrhage.Clinical and in vitro related studies support the changes of VECs, but because of no ideal animal models, up to now, the studies remain in vitro, and we know little about the changes of CAM induced by DV though the process of plasma leakage and hemorrhage. So the study of the expression of AM on VECs infected by DV may play important roles in completely elucidating the pathogenesis of DHF/DSS.更多还原