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恰加斯病中的巨结肠:炎症细胞、肠神经和神经胶质细胞的研究

Megacolon in Chagas disease: a study of inflammatory cells, enteric nerves, and glial cells.

作者信息

da Silveira Alexandre Barcelos Morais, Lemos Elenice M, Adad Sheila J, Correa-Oliveira Rodrigo, Furness John B, D'Avila Reis Débora

机构信息

Department of Morphology, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, CEP: 31270-901 Pampulha, Belo Horizonte, Minas Gerais, Brazil.

出版信息

Hum Pathol. 2007 Aug;38(8):1256-64. doi: 10.1016/j.humpath.2007.01.020. Epub 2007 May 8.

Abstract

After acute infestation with the Chagas disease parasite, Trypanosoma cruzi, some patients who are serologically positive develop chronic megacolon and megaesophagus, whereas others are symptom-free. Chagas disease with gastrointestinal involvement involves an inflammatory invasion of the enteric plexuses and degeneration of enteric neurons. It is known that glial cells can be involved in enteric inflammatory responses. The aims were to determine the nature of any difference in lymphocytic invasion, enteric neurons, and enteric glial cells in seropositive individuals with and without megacolon. We have compared colonic tissue from serologically positive individuals with and without symptoms and from seronegative controls. Subjects with megacolon had significantly more CD-57 natural killer cells and TIA-1 cytotoxic lymphocytes within enteric ganglia, but numbers of CD-3 and CD-20 immunoreactive cells were not significantly elevated. The innervation of the muscle was substantially reduced to about 20% in megacolon, but asymptomatic seropositive subjects were not different to seronegative controls. Glial cell loss occurred equally in symptomatic and unaffected seropositive subjects, although the proportion with glial fibrillary acidic protein was greater in seropositive, nonsymptomatic subjects. Development of megacolon after acute infection with T cruzi is associated with maintained invasion of enteric ganglia with cytotoxic T cells and loss of muscle innervation, but changes in glial cell numbers are not associated with progression of enteric neuropathy.

摘要

在被恰加斯病寄生虫克氏锥虫急性感染后,一些血清学呈阳性的患者会发展为慢性巨结肠和巨食管,而其他患者则没有症状。伴有胃肠道受累的恰加斯病涉及肠神经丛的炎性浸润和肠神经元的变性。已知神经胶质细胞可参与肠道炎症反应。目的是确定有和没有巨结肠的血清阳性个体在淋巴细胞浸润、肠神经元和肠神经胶质细胞方面的任何差异的性质。我们比较了有症状和无症状的血清阳性个体以及血清阴性对照的结肠组织。患有巨结肠的受试者肠神经节内的CD-57自然杀伤细胞和TIA-1细胞毒性淋巴细胞明显更多,但CD-3和CD-20免疫反应性细胞的数量没有显著增加。巨结肠患者肌肉的神经支配大幅减少至约20%,但无症状血清阳性受试者与血清阴性对照没有差异。神经胶质细胞丢失在有症状和未受影响的血清阳性受试者中同样发生,尽管血清阳性、无症状受试者中胶质纤维酸性蛋白阳性的比例更高。急性感染克氏锥虫后巨结肠的发展与细胞毒性T细胞对肠神经节的持续浸润和肌肉神经支配的丧失有关,但神经胶质细胞数量的变化与肠道神经病变的进展无关。

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