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首页> 外文期刊>Infection and immunity >Pathology Affects Different Organs in Two Mouse Strains Chronically Infected by a Trypanosoma cruzi Clone: a Model for Genetic Studies of Chagas’ Disease
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Pathology Affects Different Organs in Two Mouse Strains Chronically Infected by a Trypanosoma cruzi Clone: a Model for Genetic Studies of Chagas’ Disease

机译：病理学影响两个受克鲁斯锥虫克隆慢性感染的小鼠品系中的不同器官：南美锥虫病遗传研究的模型

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Chagas’ disease is a chronic infection caused by Trypanosoma cruzi and represents an important public health burden in Latin America. Frequently the disease evolves undetectable for decades, while in a significant fraction of the affected individuals it culminates in death by heart failure. Here, we describe a novel murine model of the chronic infection with T. cruzi using a stable clone isolated from a human patient (Sylvio X10/4). The infection in the C3H/HePAS mouse strain progresses chronically and is mainly characterized by intense cardiac inflammatory lesions that recapitulate the chronic cardiac pathology observed in the human disease. Moderate striated muscle lesions are also present in C3H/HePAS mice. Viable parasites are detected and recovered from the chronic heart lesions of C3H/HePAS mice, supporting the current notion that development of heart pathology in Chagas’ disease is related to parasite persistence in the inflamed tissue. By contrast, in infected A/J mice, chronic inflammatory lesions are targeted to the liver and the skeletal muscle, while pathology and parasites are undetectable in the heart. The phenotypic analysis of F1 (A/J × C3H/HePAS) and F2 (A/J × C3H/HePAS) mice suggests that the genetic predisposition to develop the inflammatory lesions caused by T. cruzi (Sylvio X10/4 clone) is heterogeneous because the heart and liver pathology segregate in the F2 generation. These findings raise the hypothesis that the pathology heterogeneity observed in humans with Chagas’ disease (absence and presence of cardiac or digestive chronic lesions) may be attributable to host genetic factors.
机译：恰加斯病是由克鲁斯锥虫引起的慢性感染，在拉丁美洲代表着重要的公共卫生负担。这种疾病经常演变成几十年来无法发现，而在相当一部分受影响的个体中，它最终因心力衰竭而死亡。在这里，我们描述了一种新型的 T慢性感染的鼠模型。使用从人类患者身上分离的稳定克隆（Sylvio X10 / 4）。 C3H / HePAS小鼠品系中的感染是慢性进展的，其主要特征是强烈的心肌炎性病变，概括了人类疾病中观察到的慢性心脏病。 C3H / HePAS小鼠中也存在中度条纹肌损伤。从C3H / HePAS小鼠的慢性心脏病变中检出并回收了活的寄生虫，这支持了目前的观念，即恰加斯病中心脏病理的发展与发炎组织中的寄生虫持久性有关。相比之下，在感染的A / J小鼠中，慢性炎性病变的目标是肝脏和骨骼肌，而心脏中无法检测到病理和寄生虫。 F 1 （A / J×C3H / HePAS）和F 2 （A / J×C3H / HePAS）小鼠的表型分析表明，遗传易感性T引起的炎性病变。 Cruzi （Sylvio X10 / 4克隆）之所以异质，是因为心脏和肝脏病理在F 2 世代中分离。这些发现提出了一个假说，即在南美锥虫病患者中观察到的病理异质性（缺乏或存在心脏或消化系统慢性病变）可能归因于宿主遗传因素。

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