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目的观察ＣｏｘＢ３感染大鼠单个核细胞，诱导细胞表面ＬＦＡ－１表达的变化，以及ＬＦＡ－１／ＩＣＡＭ－１在ＣｏｘＢ３从单个核细胞向心肌细胞播散感染中的作用。方法制备和培养大鼠心肌细胞和大鼠外周血单个核细胞，并进行病毒感染；制备和纯化分泌抗大鼠ＬＦＡ－１（ＣＤ１１ａ）和抗大鼠ＩＣＡＭ－１（ＣＤ５４）的单克隆抗体；在Ｗｉｓｈ细胞上进行病毒感染性滴定，并观察细胞病变；流式细胞仪分析各组单个核细胞ＬＦＡ－１的表达情况；观察抗－ＬＦＡ－１和抗－ＩＣＡＭ－１单克隆抗体在ＣｏｘＢ３复制和播散感染中的作用。结果ＣｏｘＢ３感染大鼠外周血单个核细胞１８～２４小时可以诱导细胞膜ＬＦＡ－１表达增多，同时释放感染性病毒颗粒感染正常大鼠心肌细胞；加入抗－ＬＦＡ－１或抗－ＩＣＡＭ－１的单克隆抗体均可不同程度地抑制病毒向心肌细胞播散感染，并显著降低培养上清液中病毒滴度。结论ＣｏｘＢ３感染增加白细胞表面ＬＦＡ－１表达可能是病毒病理作用的重要步骤
Objective To observe the changes of LFA-1 expression induced by CoxB3 in rat mononuclear cells and the role of LFA-1 / ICAM-1 in the mononuclear cells to cardiomyocyte dissemination of CoxB3. Methods Rat cardiomyocytes and rat peripheral blood mononuclear cells were prepared and cultured and infected with virus. Monoclonal antibodies against rat LFA-1 (CD11a) and anti-rat ICAM-1 (CD54) were prepared and purified. Viral titration was performed on Wish cells and the cytopathological changes were observed. The expression of LFA-1 in each group of mononuclear cells was analyzed by flow cytometry. The expression of anti-LFA-1 and anti-ICAM-1 monoclonal antibodies in CoxB3 And disseminated the role of infection. Results CoxB3 infected rat peripheral blood mononuclear cells 18 ~ 24 hours can induce an increase of LFA-1 expression in the cell membrane, while the release of infectious virus particles infected normal rat cardiomyocytes; add anti-LFA-1 or anti-ICAM-1 single Clonal antibodies can inhibit the virus to varying degrees, disseminated to the cardiomyocyte infection, and significantly reduce the culture supernatant virus titer. Conclusion CoxB3 infection may increase the expression of LFA-1 on the surface of leukocytes and may be an important step in the pathological process of the virus