Latva-Hirvelä J, Kytö V, Saraste A, Eriksson S, Vuorinen T, Pettersson K, Saukko P
University of Turku, Turku, Finland.
Eur J Clin Invest. 2009 Jun;39(6):457-62. doi: 10.1111/j.1365-2362.2009.02113.x. Epub 2009 Apr 8.
Autoantibodies against various endogenous proteins are found in myocarditis. Troponin autoantibodies are detected in patients with chronic dilated cardiomyopathy, but their presence in myocarditis remains unknown. We set out to study the presence of troponin autoantibodies in experimental viral myocarditis.
BALB/c mice infected with coxsackievirus B3 Nancy strain were followed-up at days 1-7 and 2, 4, 8 and 12 weeks after infection. Levels of circulating cardiac troponin I and circulating troponin autoantibodies were measured. Transthoracic echocardiography was performed. Myocarditis was histopathologically graded and cardiomyocyte apoptosis was quantified (TUNEL).
Histopathologically relatively mild acute myocarditis followed by persistent cardiomyocyte damage was observed. Rate of cardiomyocyte apoptosis was the highest on day 5 (0.16 +/- 0.01% vs. 0.03 +/- 0.01% in controls, P < 0.001). Circulating troponin I levels were increased to day 5 (45.2 +/- 6.5 ng mL(-1), P < 0.005 vs. controls). Troponin autoantibodies were detected from 2 weeks after infection (20% of animals had autoantibodies at 2 weeks, 60% at 4 and 8 weeks and 20% at 12 weeks, P < 0.05 vs. controls). Fractional shortening remained decreased after acute myocarditis (0.36 +/- 0.02 at 4 weeks, 0.30 +/- 0.02 at 8 and 12 weeks vs. 0.41 +/- 0.01 before infection, P < 0.01) parallel to development of troponin autoantibodies.
Troponin autoantibodies are formed in experimental virus induced myocarditis following troponin I release and cardiomyocyte apoptosis. The definite role of these autoantibodies remains to be further characterized.
在心肌炎患者中可检测到针对多种内源性蛋白质的自身抗体。在慢性扩张型心肌病患者中可检测到肌钙蛋白自身抗体，但其在心肌炎中的存在情况尚不清楚。我们着手研究实验性病毒性心肌炎中肌钙蛋白自身抗体的存在情况。
对感染柯萨奇病毒B3 Nancy株的BALB/c小鼠在感染后第1 - 7天以及第2、4、8和12周进行随访。检测循环心肌肌钙蛋白I水平和循环肌钙蛋白自身抗体水平。进行经胸超声心动图检查。对心肌炎进行组织病理学分级，并对心肌细胞凋亡进行定量分析（TUNEL法）。
观察到组织病理学上相对较轻的急性心肌炎，随后出现持续性心肌细胞损伤。心肌细胞凋亡率在第5天最高（0.16±0.01%，而对照组为0.03±0.01%，P<0.001）。循环肌钙蛋白I水平在第5天升高（45.2±6.5 ng mL⁻¹，与对照组相比P<0.005）。感染后2周开始检测到肌钙蛋白自身抗体（2周时20%的动物有自身抗体，4周和8周时为60%，12周时为20%，与对照组相比P<0.05）。急性心肌炎后左室短轴缩短率持续降低（4周时为0.36±0.02，8周和12周时为0.30±0.02，而感染前为0.41±0.01，P<0.01），与肌钙蛋白自身抗体的出现平行。
在实验性病毒诱导的心肌炎中，肌钙蛋白I释放和心肌细胞凋亡后会形成肌钙蛋白自身抗体。这些自身抗体的确切作用仍有待进一步明确。
