Adherence and cytotoxicity of Entamoeba histolytica or how lectins let parasites stick around

• Published in: Infection and immunity 1994-08, Vol.62 (8), p.3045-3050
• Main Authors: MCCOY, J. J, MANN, B. J, PETRI, W. A
• Format: Article
• Language: English
• Subjects: Acetylgalactosamine - physiology; Adhesiveness; Animals; Biological and medical sciences; Complement System Proteins - immunology; Entamoeba histolytica; Entamoeba histolytica - immunology; Entamoeba histolytica - pathogenicity; Fundamental and applied biological sciences. Psychology; Galactose - physiology; Invertebrates; Lectins - chemistry; Lectins - physiology; Life cycle. Host-agent relationship. Pathogenesis; Protozoa; Protozoan Vaccines - immunology
• ISSN: 0019-9567; 1098-5522
• DOI: 10.1128/iai.62.8.3045-3050.1994

The enteric protozoan parasite Entamoeba histolytica is one of the most potent cytotoxic cells known, named by Schaudinn in 1903 for its ability to destroy human tissues (53). Infection occurs when the cyst form of the parasite is ingested with contaminated food or water. After excysting to form the trophozoite in the small intestine, the amebae can colonize the bowel lumen, invade through the intestinal epithelium to cause colitis or liver abscess, or form cysts that are excrete with the stool to start a new round of infection (28). Parasite recognition of glycoconjugates plays an important role in the pathogenesis of amebiasis. Killing of host cells by E. histolytica trophozoites in vitro occurs only upon direct contact, which is mediated by an amebic adhesin which recognizes N- and O-linked oligosaccharides (9, 35, 36, 49). This adhesin is specifically inhibited by millimolar concentrations of galactose and N-acetyl-D-galactosamine (Gal/GalNAc) (36). Avoidance of lysis by the complement membrane attack complex is also mediated by this lectin. Here we discuss recent advances in the understanding of this novel amebic adhesin.