Pacheco Judith, Shibayama Mineko, Campos Rafael, Beck David L, Houpt Erick, Petri William A, Tsutsumi Víctor
Department of Experimental Pathology, Center for Research and Advanced Studies, National Polytechnic Institute, Cinvestav-IPN, Av. IPN 2508, Col. San Pedro Zacatenco, Mexico, D.F. 07360, Mexico.
Parasitol Int. 2004 Mar;53(1):35-47. doi: 10.1016/j.parint.2003.10.005.
The Gal/GalNAc lectin of Entamoeba histolytica trophozoites plays an important role in adhesion. The distribution and final destiny of the lectin during the interaction with host cells are poorly understood. Using monoclonal and polyclonal antibodies against the lectin we studied by immunocytochemistry the in vitro and in vivo interaction of E. histolytica trophozoites with human and hamster hepatocytes. We also analyzed the presence and distribution of the lectin in a mouse model of intestinal amoebiasis. In all cases, trophozoites were highly labeled by anti-lectin antibodies. Cultured human and hamster hepatocytes in contact with, or localized at the vicinity of parasites were also labeled by anti-lectin antibodies. Most of the labeled hepatocytes showed variable degrees of cell damage. Hepatocytes distantly localized from the parasites were also stained with the anti-lectin antibodies. Immunolabeling of tissue sections from different stages of the development of experimental amoebic liver abscess in hamsters showed inflammatory foci containing lectin-labeled trophozoites, hepatocytes, and sinusoidal and inflammatory cells. Lectin-containing hepatocytes had vacuolated cytoplasm with some nuclei with a condensed appearance. Damaged intestinal epithelium also was labeled with anti-lectin antibodies in a mouse model of intestinal amoebiasis. Electron microscopy of axenically cultured trophozoites using gold-labeled monoclonal and polyclonal anti-lectin antibody showed that plasma membrane, vacuole membranes and areas of cell cytosol were labeled. Higher deposits of gold particles in plasma membrane suggestive of cell secretion were observed. Our results demonstrated that Gal/GalNAc lectin was bound and captured by different target cells, and that host cells containing the lectin showed signs of cell damage. The contribution of lectin transfer to host cells in adherence and cell injury remains to be determined.
溶组织内阿米巴滋养体的半乳糖/ N - 乙酰半乳糖胺凝集素在黏附中起重要作用。人们对该凝集素在与宿主细胞相互作用过程中的分布及最终归宿了解甚少。我们使用针对该凝集素的单克隆抗体和多克隆抗体，通过免疫细胞化学方法研究了溶组织内阿米巴滋养体与人和仓鼠肝细胞在体外及体内的相互作用。我们还分析了该凝集素在肠道阿米巴病小鼠模型中的存在及分布情况。在所有情况下，滋养体均被抗凝集素抗体高度标记。与寄生虫接触或位于其附近的培养的人和仓鼠肝细胞也被抗凝集素抗体标记。大多数被标记的肝细胞显示出不同程度的细胞损伤。远离寄生虫的肝细胞也被抗凝集素抗体染色。对仓鼠实验性阿米巴肝脓肿不同发育阶段组织切片的免疫标记显示，炎症灶中含有凝集素标记的滋养体、肝细胞、窦状隙细胞和炎性细胞。含有凝集素的肝细胞胞质有空泡，一些细胞核外观浓缩。在肠道阿米巴病小鼠模型中，受损的肠上皮也被抗凝集素抗体标记。使用金标记的单克隆和多克隆抗凝集素抗体对无菌培养的滋养体进行电子显微镜观察显示，质膜、液泡膜和细胞胞质区域被标记。在质膜中观察到较高的金颗粒沉积，提示细胞分泌。我们的结果表明，半乳糖/ N - 乙酰半乳糖胺凝集素被不同的靶细胞结合并捕获，并且含有该凝集素的宿主细胞显示出细胞损伤的迹象。凝集素转移对宿主细胞黏附和细胞损伤的作用仍有待确定。
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