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Glycobiology Advance Access published online on July 21, 2005
Glycobiology, doi:10.1093/glycob/cwj007
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Published by Oxford University Press 2005.
Received May 9, 2005
Revised June 30, 2005
Accepted June 30, 2005

Article

Roles for the Galactose/N-Acetylgalactosamine binding lectin of Entamoeba in parasite virulence and differentiation

Jesse R. Frederick 1 and William A. Petri Jr1*

1 Division of Infectious Diseases, University of Virginia Health System, MR4 Bldg, Room 2115, Charlottesville VA 22908-1340

* To whom correspondence should be addressed.
William A. Petri Jr, E-mail: wap3g{at}virginia.edu


  Abstract

Entamoeba histolytica, an intestinal protozoan parasite, is a major cause of morbidity and mortality in developing countries. The pathology of the disease is caused by the colonization of the large intestine by the amoebic trophozoites, and the invasion of the intestinal epithelium. Some of the trophozoites will eventually differentiate into the infectious cyst form, allowing them to be transmitted out of the bowel and into water supplies in order to be passed from person to person. Both the virulence of the organism as well as the differentiation process relies on a galactose/N-acetyl galactosamine binding lectin that is expressed on the surface of trophozoites. The functional activity of this lectin has been shown to be involved in host cell binding, cytotoxicity, complement resistance, induction of encystation, and generation of the cyst wall. The role of the lectin in both differentiation and virulence suggests that it may be a pivotal molecule that determines the severity of the infection from a commensal state resulting from increased encystation to an invasive state. The lectin-glycan interactions that initiate these diverse processes will be discussed with emphasis on comparing the binding of host ligands and the interactions involved in encystation.

Keywords: Entamoeba/lectin/encystation/amoebiasis.
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