Comparative study of the presence of Trypanosoma cruzi kDNA inflammation and denervation in chagasic patients with and without megaesophagus

Comparative study of the presence of Trypanosoma cruzi kDNA inflammation and denervation in chagasic patients with and without megaesophagus
复制标题

DOI:
10.1017/s0031182005008061
复制
发表时间:
2005-11-01
期刊:
影响因子:
2.4
通讯作者:
Reis, DD
Reis, DD
中科院分区:
医学2区
文献类型:
--
作者:
da Silveira, ABM;Arantes, RME;Reis, DD

文献摘要

被引文献

相似文献

神经病变一直被认为是恰加斯特大食道的标志,但克氏锥虫的作用。而炎症细胞在这一过程中的参与仍然存在争议。在本研究中,我们统计了患有和不患有巨食道的患者食道中的神经元,并进一步检查了这些样本中是否存在寄生虫kDNA和具有细胞溶解潜能的细胞(自然杀伤细胞、细胞毒性淋巴细胞和巨噬细胞)。在100%的食管肥大患者和60%的非食管肥大患者中均存在寄生虫kDNA。在分析神经元数量时,无巨食道患者可分为神经元数量正常组和神经元数量减少组。前一组没有出现任何炎症过程,但有趣的是,所有没有出现神经元数量减少的食管肥大患者在器官中也出现了寄生虫kDNA和炎症过程。我们进一步观察到,肌肠丛区细胞毒性细胞的数量与神经元的数量呈负相关。这些数据共同有力地表明,chagasic巨型食道的慢性病变可能是免疫介导机制的结果,这种机制持续到感染的慢性阶段,并且依赖于寄生虫在宿主组织中的持久性。
Neuronal lesions have been considered the hallmark of chagasic megaesophagus, but the role of Trypanosoma cruzi. and the participation of the inflammatory cells in this process are still debated. In the present study we counted neurons in the oesophagus from patients with and without megaesophagus and further examined these samples for the presence of parasite kDNA and cells with cytolytic potential (Natural Killer cells, cytotoxic lymphocytes and macrophages). The presence of parasite kDNA was demonstrated in 100% of cases with megaesophagus and in 60% of patients without megaesophagus. When analysed for the number Of neurons, the patients without megaesophagus could be classified into 2 groups, as having normal or a decreased number of neurons. The former group did not show any inflammatory process, but interestingly, all patients without megaesophagus presenting decreased number of neurons also presented both parasite kDNA and inflammatory process in the organ. We further observed that the numbers of cytotoxic cells in the myenteric plexus region inversely correlate with the number of neurons. These data together strongly Suggest that chronic lesions in chagasic megaesophagus might be a consequence of immune-mediated mechanisms, that last until the chronic phase of infection, and are dependent on the persistence of parasite in the host's tissue.