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目的：研究柯萨基Ｂ３病毒（ＣｏｘＢ３）感染对内皮细胞表面ＩＣＡＭ１表达的诱导作用，及对内皮细胞与单个核细胞粘附的影响，探讨病毒性心肌炎心肌细胞免疫损伤的机理。方法：采用流式细胞仪分析内皮细胞ＩＣＡＭ１表达；粘附试验和单克隆抗体抑制试验观察单个核细胞与内皮细胞的粘附。结果：１００和４００ＴＣＩＤ５０／ｍｌＣｏｘＢ３感染内皮细胞２４和４８ｈ，均可显著增加单个核细胞与内皮细胞的粘附（Ｐ＜００１），分别为对照组的１８和２５倍。经流式细胞仪分析证实，ＣｏｘＢ３感染可以诱导内皮细胞ＩＣＡＭ１表达增加，阳性细胞数增多。用抗ＩＣＡＭ１和抗ＬＦＡ１单克隆抗体均可部分阻断单个核细胞与ＣｏｘＢ３感染内皮细胞的粘附，抗ＩＣＡＭ１单抗的抑制作用较抗ＬＦＡ１单抗更为明显。结论：ＣｏｘＢ３可以通过感染内皮细胞上调膜ＩＣＡＭ１的表达，促进单个核细胞与内皮细胞的粘附。
Objective: To investigate the effect of CoxB3 infection on the expression of ICAM-1 on the surface of endothelial cells and its effect on the adhesion of endothelial cells and mononuclear cells, and to explore the mechanism of cardiomyocyte immune damage in viral myocarditis. Methods: The expression of ICAM-1 in endothelial cells was analyzed by flow cytometry. Adhesion test and monoclonal antibody inhibition test were used to observe the adhesion of mononuclear cells to endothelial cells. Results: The adhesion of mononuclear cells to endothelial cells was significantly increased by both 100 and 400 TCID50 / ml CoxB3 infection for 24 h and 48 h (P <001), which were respectively 1. 8 and 25 times that of the control group. Confirmed by flow cytometry analysis, CoxB3 infection can induce endothelial ICAM 1 expression increased positive cells increased. Anti-ICAM 1 and anti-LFA 1 monoclonal antibodies can be partially blocked mononuclear cells and CoxB3 endothelial cell adhesion, anti-ICAM 1 monoclonal antibody anti-LFA 1 monoclonal antibody was more obvious. Conclusion: CoxB3 can promote the adhesion of mononuclear cells and endothelial cells by up-regulating the expression of ICAM-1 in endothelial cells.