Entamoeba histolytica: from adherence to enteropathy.

Entamoeba histolytica, a cause of invasive colitis or liver abscess, is responsible for substantial worldwide morbidity and mortality. An understanding of the biochemical basis for the parasite adherence and cytolytic activities and antiamebic host immune response mechanisms are prerequisites for vaccine development. The E. histolytica galactose (Gal) or N-acetyl-D-galactosamine (GalNAc) inhibitable adherence lectin mediates attachment of trophozoites to colonic mucins or mammalian target cells. Amebic cytolysis of target cells requires Gal/GalNAc-lectin-mediated adherence, parasite phospholipase A activity, and maintenance of an acid pH in amebic intracellular vesicles. Cytolytic activity is stimulated by phorbol esters (activators of protein kinase C) and results from an E. histolytica-mediated increase in free Ca++ within the target cell. The Gal/GalNAc adherence lectin is a highly conserved antigen that is universally recognized by human immune sera; patients cured of invasive amebiasis possess antigen-specific cell-mediated immunity effective in vitro against E. histolytica trophozoites. Promising vaccines include the purified adherence lectin, for eliciting an intestinal secretion of IgA antibody to lectin, and additional E. histolytica antigens, which elicit cell-mediated amebicidal responses.