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实验性肠道侵袭性阿米巴病的超微结构

Ultrastructure of experimental intestinal invasive amebiasis.

作者信息

Martínez-Palomo A, Tsutsumi V, Anaya-Velazquez F, Gonzalez-Robles A

机构信息

Center for Research and Advanced Studies, National Polytechnical Institute, Mexico City, Mexico.

出版信息

Am J Trop Med Hyg. 1989 Sep;41(3):273-9.

PMID:2552849
Abstract

The morphological features of early intestinal ulcerations induced in rodents with axenic cultures of Entamoeba histolytica were studied by scanning and transmission electron microscopy. Amebas did not attach to the luminal surface of the mucosa except at interglandular regions, where parasites penetrated apparently through pseudopodial movement. Once in the lamina propria, trophozoites multiplied and destroyed mucosal components. Damage extended laterally through the mucosa, but progression to deeper layers of the intestinal wall was prevented by the muscularis mucosae, which acted as a partial barrier. This was eventually breached at focal points where amebas invaded the submucosa. Electron microscopy clearly showed the lysis of abundant polymorphonuclear neutrophil leukocytes (PMNs) by the amebas at the periphery of intestinal ulcerations as well as the lack of bacteria at these sites. This study demonstrates that recruitment and destruction of inflammatory cells following intestinal amebic invasion may take place in the absence of bacterial multiplication. The observations provide histological support to the hypothesis that lysis of PMNs by trophozoites participates in the genesis of amebic intestinal lesions.

摘要

利用扫描电子显微镜和透射电子显微镜研究了用溶组织内阿米巴无菌培养物在啮齿动物中诱导产生的早期肠道溃疡的形态学特征。除了在腺间区域外,阿米巴原虫不会附着在粘膜腔表面,在这些区域,寄生虫显然通过伪足运动穿透。一旦进入固有层,滋养体就会繁殖并破坏粘膜成分。损伤通过粘膜横向扩展,但粘膜肌层起到了部分屏障的作用,阻止了损伤向肠壁更深层发展。最终,在阿米巴原虫侵入粘膜下层的局部点,这一屏障被突破。电子显微镜清楚地显示,在肠道溃疡周边,阿米巴原虫裂解了大量多形核中性粒细胞(PMN),并且这些部位没有细菌。这项研究表明,肠道阿米巴侵袭后炎症细胞的募集和破坏可能在没有细菌繁殖的情况下发生。这些观察结果为滋养体裂解PMN参与阿米巴肠道病变发生的假说提供了组织学支持。

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