Human amebic liver abscess: expression of intercellular adhesion molecules 1 and 2 and of von Willebrand factor in endothelial cells |
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Authors: | J Ventura-Juárez R Campos-Rodríguez H A Rodríguez-Martínez A Rodríguez-Reyes A Martínez-Palomo V Tsutsumi |
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Institution: | (1) Department of Experimental Pathology, Center for Research and Advanced Studies, National Polytechnic Institute, Av. IPN No. 2508, Mexico, D.F. CP.07300 Mexico; Fax: 52 (5) 747-71-07, MX;(2) Department of Biochemistry, School of Medicine, National Polytechnic Institute, Mexico, MX;(3) Unit of Pathology, Faculty of Medicine, General Hospital of Mexico and National Autonomous University of Mexico, Mexico, MX;(4) Interdisciplinary Center for Health Sciences, National Polytechnic Institute, Mexico, MX |
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Abstract: | 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.
Received: 11 November 1996 / Accepted: 18 December 1996 |
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