Cossio P M, Bustuoabad O, Paternó E, Iotti R, Casanova M B, Podestá M R, Bolomo N, Arana R M, de Pasqualini C D
Clin Immunol Immunopathol. 1984 Nov;33(2):165-75. doi: 10.1016/0090-1229(84)90071-0.
The Swiss mouse is considered a satisfactory model for experimental chronic chagasic myocarditis and there is some evidence of an immunopathologic mechanism in the development of this disease. To further support this conjecture, 45-day-old albino Swiss mice (40 animals) were immunized with homologous heart in complete Freund's adjuvant. As controls, 20 animals were likewise inoculated with allogeneic testis, as "non-related" antigen. Three mice from the former group died suddenly at 19-21 days postinoculation while the survivors were sacrificed at 60 days for serum samples, and histologic analysis of the heart and skeletal muscle. Electrocardiographic records were taken at Days 0, 30, and 60 postinoculation. Of myocardium-inoculated animals and testis-inoculated mice 33/37 (89%) and 1/20 (5%), respectively, exhibited myocarditis (P less than 0.001). Histologic lesions were highly reminiscent of those observed in chronic experimental Chagas' disease of Swiss mice. Antimuscle antibodies were seen, by indirect immunofluorescence employing cryostat sections, in 30/33 (91%) of the former group and in 3/20 (15%) of the latter (P less than 0.001), some of which recognized a surface antigen of primary cultured fetal rat myocardiocytes. Mice inoculated with myocardium also exhibited electrocardiographic abnormalities consisting in QRS interval widening. Results show that following an autoimmune experimental design the main features of chronic chagasic myocarditis may be reproduced in the Swiss mouse. This agrees with the likely role of an immunopathologic mechanism in heart damage due to Trypanosoma cruzi infection.
瑞士小鼠被认为是实验性慢性恰加斯性心肌炎的理想模型，并且有证据表明免疫病理机制在该疾病的发展中起作用。为进一步支持这一推测，将45日龄的白化瑞士小鼠（40只）用完全弗氏佐剂中的同源心脏进行免疫。作为对照，20只动物同样接种异基因睾丸，作为“非相关”抗原。前一组中有3只小鼠在接种后19 - 21天突然死亡，而存活的小鼠在60天时被处死以获取血清样本，并对心脏和骨骼肌进行组织学分析。在接种后第0、30和60天进行心电图记录。接种心肌的动物和接种睾丸的小鼠中，分别有33/37（89%）和1/20（5%）表现出心肌炎（P小于0.001）。组织学病变与瑞士小鼠慢性实验性恰加斯病中观察到的病变高度相似。通过使用冰冻切片的间接免疫荧光法，在前一组的33/33（91%）和后一组的3/20（15%）中发现了抗肌肉抗体（P小于0.001），其中一些抗体识别原代培养的胎鼠心肌细胞的表面抗原。接种心肌的小鼠还表现出心电图异常，表现为QRS间期增宽。结果表明，按照自身免疫实验设计，慢性恰加斯性心肌炎的主要特征可以在瑞士小鼠中重现。这与免疫病理机制在克氏锥虫感染导致心脏损伤中可能发挥的作用相一致。
