牙本质基质蛋白1和肿瘤坏死因子-α对汉滩病毒感染的脐静脉内皮细胞的作用

Function of DMP1 and TNF-α in hemorrhagic fever of renal syndrome

摘要:

目的  探讨肿瘤坏死因子-α和牙本质基质蛋白1对汉滩病毒感染的脐静脉内皮细胞通透性的影响，为阐明肾综合征出血热发病过程中通透性增高的机制提供实验基础。方法  首先用免疫细胞化学方法检测牙本质基质蛋白1在脐静脉内皮细胞的表达情况，然后通过Transwell单层细胞模型系统检测外源性肿瘤坏死因子-α和牙本质基质蛋白1对汉滩病毒感染的血管内皮细胞通透性的影响。结果  牙本质基质蛋白1可以在血管内皮细胞表达，汉滩病毒感染对牙本质基质蛋白1表达量无显著性影响，汉滩病毒感染后加入肿瘤坏死因子-α使牙本质基质蛋白1表达量显著性增加（P <0.05）。单纯汉滩病毒感染后，通透性无显著性变化（P >
0.05），而感染细胞加入外源性肿瘤坏死因子-α或牙本质基质蛋白1后，内皮细胞通透性显著增加（P <0.05），两者联合作用能促进通透性进一步增加（P <0.05）。结论  牙本质基质蛋白1广泛表达在血管内皮细胞，肿瘤坏死因子-α和牙本质基质蛋白1均可使汉滩病毒感染的脐静脉内皮细胞通透性显著增高，且两者存在联合作用。

Abstract:

Objective To explore the mechanism of hyper-permeability in hemorrhagic fever of renal syndrome (HFRS). Methods Immunocytochemistry was used to detect the production of dentin matrix protein 1 (DMP1). The penetrability changes of human umbilical vein endothelial cells were detected by transwell monolayer system. Uninfected vein endothelial cells were used as the negative control in each experiment. Immunofluorescence was used to guarantee that cells were infected by HTNV before each experiment. Results HTNV infection alone did not change the penetrability of vein endothelial cells. but the penetrability elevated remarkably after TNF-α or DMP1 were added, and increased even more when both two were added. Conclusions TNF-α and DMP1 can increase the penetrability of HTNV infected endothelial cells, and there were combined effects. They may play a role in the immunopathogenesis of HFRS.