Department of Pathology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, S.P., Brazil.
Microbes Infect. 2012 Jan;14(1):59-68. doi: 10.1016/j.micinf.2011.08.010. Epub 2011 Aug 31.
Chronic Chagas cardiomyopathy evolves over a long period of time after initial infection by Trypanosoma cruzi. Similarly, a cardiomyopathy appears later in life in muscular dystrophies. This study tested the hypothesis that dystrophin levels are decreased in the early stage of T. cruzi-infected mice that precedes the later development of a cardiomyopathy. CD1 mice were infected with T. cruzi (Brazil strain), killed at 30 and 100 days post infection (dpi), and the intensity of inflammation, percentage of interstitial fibrosis, and dystrophin levels evaluated. Echocardiography and magnetic resonance imaging data were evaluated from 15 to 100 dpi. At 30 dpi an intense acute myocarditis with ruptured or intact intracellular parasite nests was observed. At 100 dpi a mild chronic fibrosing myocarditis was detected without parasites in the myocardium. Dystrophin was focally reduced or completely lost in cardiomyocytes at 30 dpi, with the reduction maintained up to 100 dpi. Concurrently, ejection fraction was reduced and the right ventricle was dilated. These findings support the hypothesis that the initial parasitic infection-induced myocardial dystrophin reduction/loss, maintained over time, might be essential to the late development of a cardiomyopathy in mice.
慢性恰加斯心肌病在初次感染克氏锥虫后经过很长一段时间才会发展。同样，在肌肉营养不良症中，也会在生命后期出现心肌病。本研究检验了这样一个假设，即在随后发生心肌病之前，感染克氏锥虫的小鼠早期的肌营养不良蛋白水平会降低。将 CD1 小鼠感染克氏锥虫（巴西株），在感染后 30 天和 100 天处死，并评估炎症强度、间质纤维化百分比和肌营养不良蛋白水平。从 15 天到 100 天检测心脏超声心动图和磁共振成像数据。在 30 天观察到强烈的急性心肌炎，伴有破裂或完整的细胞内寄生虫巢。在 100 天检测到轻度慢性纤维化性心肌炎，心肌中无寄生虫。在 30 天，肌营养不良蛋白在心肌细胞中呈局灶性减少或完全丢失，这种减少一直持续到 100 天。同时，射血分数降低，右心室扩张。这些发现支持这样一种假设，即初始寄生虫感染诱导的心肌肌营养不良蛋白减少/缺失，随着时间的推移得以维持，可能对小鼠晚期心肌病的发展至关重要。
