This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tsutsumi, V. Articles by Martinez-Palomo, A. Search for Related Content PubMed PubMed Citation Articles by Tsutsumi, V. Articles by Martinez-Palomo, A.

American Journal of Pathology, Vol 130, 112-119, Copyright © 1988 by American Society for Investigative Pathology

REGULAR ARTICLES

Inflammatory reaction in experimental hepatic amebiasis. An ultrastructural study

V Tsutsumi and A Martinez-Palomo
Section of Experimental Pathology, Centro de Investigacion del I.P.N., Mexico, D.F. Mexico.

One of the hallmarks of tissue necrosis produced by the human protozoan parasite Entamoeba histolytica, the causative agent of human amebiasis, appeared to be the lack of inflammatory reaction to the invading trophozoites. Recent evidence suggests, however, that inflammatory cells do appear during early stages of amebic destructive lesions and that they contribute to the establishment of foci of tissue necrosis in intestinal and liver lesions. The present analysis of the fine- structural changes that take place during early stages of amebic liver abscesses induced in hamsters after the intraportal inoculation of axenic amebas has shown that large numbers of polymorphonuclear leukocytes (PMNs) are recruited around invading amebas. These leukocytes lyse as a consequence of contact-mediated damage induced by the trophozoites. Amebas were also capable of ingesting apparently intact PMNs. Macrophages and eosinophils were also recruited at the foci of inflammation. At all times examined, trophozoites of Entamoeba histolytica survived in spite of being in close contact with PMNs or degranulating eosinophils. The ultrastructural observations have also shown the lack of direct contact between amebas and liver parenchymal cells during the initial stages of the focal liver necrosis induced by the parasite, therefore supporting the view that hepatic damage may be effected indirectly through lysis of inflammatory cells. The results also provide a basis for the understanding of the induction of experimental protective immunity against invasive amebiasis, a process which seems to be mostly dependent on cellular mechanisms.

This article has been cited by other articles:

				D. R. Boettner, C. D. Huston, J. A. Sullivan, and W. A. Petri Jr. Entamoeba histolytica and Entamoeba dispar Utilize Externalized Phosphatidylserine for Recognition and Phagocytosis of Erythrocytes Infect. Immun., June 1, 2005; 73(6): 3422 - 3430. [Abstract] [Full Text] [PDF]

				C. D. Huston, D. R. Boettner, V. Miller-Sims, and W. A. Petri Jr. Apoptotic Killing and Phagocytosis of Host Cells by the Parasite Entamoeba histolytica Infect. Immun., February 1, 2003; 71(2): 964 - 972. [Abstract] [Full Text] [PDF]