A NOVEL EXPERIMENTAL-MODEL OF GIANT-CELL MYOCARDITIS INDUCED IN RATS BY IMMUNIZATION WITH CARDIAC MYOSIN FRACTION
A NOVEL EXPERIMENTAL-MODEL OF GIANT-CELL MYOCARDITIS INDUCED IN RATS BY IMMUNIZATION WITH CARDIAC MYOSIN FRACTION
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DOI：
10.1016/0090-1229(90)90039-s
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发表时间：
1990-11-01
期刊：
影响因子：
--
通讯作者：
SHIBATA, A
中科院分区：
文献类型：
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作者：
KODAMA, M;MATSUMOTO, Y;SHIBATA, A
部分巨细胞心肌炎的发病机制可能与自身免疫性疾病有关。然而，自身免疫的证据很少在临床研究中得到证实。在这项研究中，我们已经证明了一种新的动物模型的自身免疫性心肌炎的特点是外观的多核巨细胞。刘易斯大鼠用完全弗氏佐剂中的人心肌肌球蛋白组分免疫两次。从人心脏的心室肌中制备心肌肌球蛋白组分。第一次免疫后3周，所有大鼠均出现急性和严重的心肌炎。该心肌炎的特征为大量心包积液、心脏增大和心肌灰色变色。显微镜下，有明显的细胞浸润，包括单核细胞、中性粒细胞、成纤维细胞和大量多核巨细胞。还存在广泛的心肌坏死。心脏重量从第3周至第4周逐渐增加，然后逐渐下降。抗肌球蛋白抗体的滴度从第二周开始升高，并保持高水平，直到第六周。在第六周，炎症变得阴燃，多核巨细胞消失。这些结果表明，心肌肌球蛋白组分含有心肌抗原，巨细胞心肌炎可以引起自身免疫性参与。据我们所知，这是第一次报告的实验性巨细胞心肌炎，这是密切相似的人类巨细胞心肌炎的组织学和临床过程。
It is suspected that autoimmune disease processes are involved in the pathogenesis of a part of giant cell myocarditis. However, evidence for autoimmunity has rarely been demonstrated in clinical investigations. In this study, we have demonstrated a new animal model of autoimmune myocarditis characterized by the appearance of multinucleated giant cells. Lewis rats were immunized twice with human cardiac myosin fraction in complete Freund''s adjuvant. Cardiac myosin fraction was prepared from the ventricular muscle of human hearts. Three weeks after the first immunization, acute and severe myocarditis was elicited in all rats. This myocarditis was characterized by massive pericardial effusion, enlargement of the heart, and gray discoloration of the cardiac muscle. Microscopically, there was marked cellular infiltration consisting of mononuclear cells, neutrophils, fibroblasts, and a considerable number of multinucleated giant cells. Extensive myocardial necrosis was also present. The heart weights increased from the third week to the fourth week and then gradually decreased. The titer of anti-myosin antibodies began to elevate from the second week and remained high until the sixth week. In the sixth week, inflammation became smoldering and the multinucleated giant cells disappeared. These findings indicate that the cardiac myosin fraction contains myocarditogenic antigen and that giant cell myocarditis can be induced by autoimmune involvement. To our knowledge, this is the first report of experimental giant cell myocarditis, which is closely similar to human giant cell myocarditis in its histology and clinical course.