發(fā)布時間：2018-07-22 12:32

【摘要】：背景 登革病毒感染可以引起從自限性發(fā)熱(Dengue Fever，DF)到登革出血熱(Dengue Haemorrhagic Fever，DHF)或登革休克綜合征(Dengue Shock Syndrome，DSS)等不同程度的臨床癥狀。其中DHF／DSS最明顯的標(biāo)志是血漿滲漏和全身出血，血漿滲漏通常是毛細(xì)血管通透性升高造成的，提示血管的功能病變在DHF／DSS的發(fā)生發(fā)展中起重要的作用。 血管內(nèi)皮細(xì)胞(Vessel endothelial cells，VECs)在調(diào)節(jié)血管滲透性和維持血液生理狀態(tài)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則過度表達(dá)分泌一些粘附分子，參與炎癥因子和炎癥細(xì)胞的聚集、滲出和炎癥反應(yīng)的發(fā)生。DV可以感染人VECs，但DV對VECs表達(dá)粘附分子是否存在影響尚不清楚。血管的炎癥損傷誘發(fā)血管通透性升高，血漿滲漏和出血，這些可能是誘導(dǎo)DHF／DSS發(fā)生發(fā)展的重要原因之一。因此從分子角度推測：活化和損傷的血管內(nèi)皮細(xì)胞，一旦功能失常，引起相應(yīng)的分子表達(dá)和分泌失常，進(jìn)而改變血管內(nèi)環(huán)境的穩(wěn)態(tài)，造成血管通透性升高，對誘發(fā)DHF／DSS血漿滲漏和出血發(fā)揮著重要的作用。 臨床和體外相關(guān)研究資料也為DV感染VECs產(chǎn)生的功能變化提供相應(yīng)的佐證，目前由于尚無理想的動物模型，對DHF／DSS中血管內(nèi)皮細(xì)胞損傷的研究大多停留在體外。目前，關(guān)于DV感染對血管內(nèi)皮細(xì)胞表面粘附分子表達(dá)的影響及在血液滲漏和出血中的作用還不完全清楚。因此，體外研究DV誘導(dǎo)VECs粘附分子表達(dá)變化，對進(jìn)一步完善DHF／DSS的血漿滲漏和出血的發(fā)病機制具有重要的意義。 目的 本研究擬在體外以人臍靜脈內(nèi)皮細(xì)胞為靶細(xì)胞，研究登革病毒Ⅱ型(dengue 2，DV_2)對人臍靜脈內(nèi)皮細(xì)胞表達(dá)粘附分子中的細(xì)胞間粘附分子(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

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