Department of Morphology, ICB, Universidade Federal de Minas Gerais, CEP 31.270-901, Brazil.
Hum Pathol. 2010 Apr;41(4):528-34. doi: 10.1016/j.humpath.2009.05.018. Epub 2009 Dec 11.
Chagas disease is caused by infestation with the parasite Trypanosoma cruzi, and some patients who are serologically positive develop chronic megaesophagus, whereas others are symptom-free. Gastrointestinal form of Chagas disease involves an inflammatory invasion of the enteric plexuses and degeneration of enteric neurons and previous works related that enteroglial cells would be involved in enteric inflammatory responses. Because of this, the aims of this study were to determine the relation of enteroglial cells with the denervation process in chagasic patients with and without megaesophagus and seronegative individuals. Our results indicated that the innervation of the esophageal muscle was substantially reduced in patients with megaesophagus, but asymptomatic seropositive subjects were not different to seronegative controls. Besides, patients with megaesophagus had significant decreased of enteroglial cells labeled with S-100 and glial fibrillary acidic protein, whereas patients without megaesophagus presented an increased of both labels. We believe that enteroglial cells would operate a mechanism of defense in the enteric nervous system against the Trypanosoma cruzi infection, which could prevent the organ denervation and preserve the esophagus function.
恰加斯病是由寄生虫克氏锥虫感染引起的,一些血清学阳性的患者会发展为慢性巨食管,而另一些则无症状。胃肠道形式的恰加斯病涉及肠丛的炎症浸润和肠神经元的变性,先前的研究表明肠胶质细胞可能参与肠炎症反应。基于此,本研究旨在确定有和无巨食管的恰加斯病患者以及血清阴性个体的肠胶质细胞与去神经过程的关系。我们的结果表明,巨食管患者的食管肌肉神经支配明显减少,但无症状的血清阳性患者与血清阴性对照组没有区别。此外,巨食管患者的 S-100 和神经胶质纤维酸性蛋白标记的肠胶质细胞显著减少,而无巨食管患者的这两种标记物增加。我们认为,肠胶质细胞可能在肠道神经系统中对克氏锥虫感染产生一种防御机制,从而防止器官去神经支配并维持食管功能。