There is a growing consensus that the balance between the persistence of infection and the host immune response is crucial for chronification of Chagas heart disease. Extrapolation for chagasic megacolon is hampered because research in humans and animal models that reproduce intestinal pathology is lacking. The parasite-host relationship and its consequence to the disease are not well-known. Our model describes the temporal changes in the mice intestine wall throughout the infection, parasitism, and the development of megacolon. It also presents the consequence of the infection of primary myenteric neurons in culture with Trypanosoma cruzi (T. cruzi). Oxidative neuronal damage, involving reactive nitrogen species induced by parasite infection and cytokine production, results in the denervation of the myenteric ganglia in the acute phase. The long-term inflammation induced by the parasite's DNA causes intramuscular axonal damage, smooth muscle hypertrophy, and inconsistent innervation, affecting contractility. Acute phase neuronal loss may be irreversible. However, the dynamics of the damages revealed herein indicate that neuroprotection interventions in acute and chronic phases may help to eradicate the parasite and control the inflammatory-induced increase of the intestinal wall thickness and axonal loss. Our model is a powerful approach to integrate the acute and chronic events triggered by T. cruzi, leading to megacolon.

越来越多的共识认为，感染持续性和宿主免疫反应之间的平衡对于查加斯（Chagas）心脏病的发病率至关重要。由于缺乏在人类和动物模型中复制肠道病理的研究，因此无法对chagasic megacolon进行外推。寄生虫与宿主的关系及其对疾病的后果尚不为人所知。我们的模型描述了小鼠肠道壁在整个感染，寄生和巨结肠形成过程中的时间变化。它还显示了原代肌层神经元在培养过程中感染的后果。克氏锥虫 （克鲁斯）。氧化性神经元损害，包括由寄生虫感染和细胞因子产生引起的反应性氮物种，导致在急性期神经节神经节的神经失活。寄生虫的DNA引起的长期炎症会引起肌内轴突损伤，平滑肌肥大和神经支配不一致，从而影响收缩力。急性期神经元丢失可能是不可逆的。但是，本文揭示的损伤动态表明，急性和慢性期的神经保护干预措施可能有助于根除寄生虫并控制炎症诱导的肠壁厚度增加和轴突损失。我们的模型是整合由以下情况触发的急性和慢性事件的有效方法克鲁斯，导致大冒号。