Ventura-Juárez J, Campos-Rodríguez R, Rodríguez-Martínez H A, Rodríguez-Reyes A, Martínez-Palomo A, Tsutsumi V
Department of Experimental Pathology, Center for Research and Advanced Studies, National Polytechnic Institute, Mexico, D.F.
Parasitol Res. 1997;83(5):510-4. doi: 10.1007/s004360050289.
Liver invasion by amebas with production of amebic liver abscess (ALA) is the most common extraintestinal lesion produced by the protozoan parasite Entamoeba histolytica. This hepatic damage is characterized by the presence of extensive tissue necrosis. However, little is known about the parasite and host factors involved in the process of tissue damage. During the early establishment of amebas in the liver parenchyma as well as during the extension of the tissue necrosis, parasites interact with sinusoidal endothelial cells. As a consequence of ameba-endothelial cell interactions, the latter can be activated and express proinflammatory factors that could be related to tissue destruction. We studied by immunohistochemistry the localization of antigenic molecules of E. histolytica trophozoites and of molecules such as intercellular adhesion molecule 1 (ICAM-1), ICAM-2, and von willebrand factor in activated endothelial cells of human ALA, which could be related to the pathophysiological mechanisms of tissue destruction in amebiasis.
阿米巴侵袭肝脏并形成阿米巴肝脓肿（ALA）是原生动物寄生虫溶组织内阿米巴最常见的肠外病变。这种肝脏损伤的特征是存在广泛的组织坏死。然而，对于组织损伤过程中涉及的寄生虫和宿主因素知之甚少。在阿米巴在肝实质中早期定植以及组织坏死扩展过程中，寄生虫与窦状内皮细胞相互作用。由于阿米巴与内皮细胞的相互作用，后者可被激活并表达可能与组织破坏有关的促炎因子。我们通过免疫组织化学研究了溶组织内阿米巴滋养体抗原分子以及细胞间粘附分子1（ICAM-1）、ICAM-2和血管性血友病因子等分子在人类ALA活化内皮细胞中的定位，这些分子可能与阿米巴病组织破坏的病理生理机制有关。
