Galactose-specific adhesin and cytotoxicity of Entamoeba histolytica

Abstract

We examined the molecular mechanisms of the cytotoxicity of Entamoeba histolytica, using the loss of transepithelial electrical resistance (TER) of monolayers of Madin-Darby canine-kidney (MDCK) cells on their incubation with axenic trophozoites of the HM1-IMSS strain. Such loss of TER occurs very early (in 2-5 min) and is caused by the opening of tight junctions and the detachment of cells. We used specific inhibitors for three of the four molecules currently accepted as being responsible for cytotoxicity: galactose-specific adhesin(s), phospholipase A, and cysteine proteinases. We also used inhibitors of calcium channels. Axenic trophozoites of E. histolytica strain HM1-IMSS were preincubated with the different inhibitors for 1 h prior to their coincubation with MDCK-cell monolayers. The only inhibitor that effectively blocked the loss of TER caused by the parasite was galactose. We suggest that in this experimental model, galactose-specific adhesin(s) are essential for amebic cytotoxicity.

Morphometric study of the hepatic lesions experimentally induced in hamsters byEntamoeba disparandE. histolytica

“…There are many molecules involved in the tissue destruction by amoebas (Leippe et al, 1993;Lopez-vancell et al, 2000;Que & Reed, 2000;Aguirre-Garcia et al, 2002), but amoebiasis pathogenesis is still not totally understood. In this context, the development of new strategies for the study of amoebic lesions may identify other functions of E. histolytica virulence, adding data to better understand the disease.…”

“…E. histolytica lytic capacity has been corroborated using a wide range of in vivo and in vitro experimental models. The main types of amoeba products that have been suggested as cell destruction-inducing agents are: adhesins, amoebapores, phospholipase A, phosphatases, collagenases and cysteine proteinases (Leippe et al, 1993;Lopez-Vancell et al, 2000;Que & Reed, 2000; titative study of the necrotic area and the number of immunohistochemically labeled trophozoites in different periods of infection.…”

The EhCPADH112 Complex of Entamoeba histolytica Interacts with Tight Junction Proteins Occludin and Claudin-1 to Produce Epithelial Damage

“…Invasive amoebiasis is characterized by disruption and invasion of the colonic mucosa by E. histolytica trophozoites resulting in colonic ulceration [2], [3], [4]. The concerted activity of E. histolytica proteins, like the EhCPADH112 complex [5], the Gal/GalNAc lectin [6], [7], amoebapores [8] and cysteine proteases [9], [10], [11], lyses enteric cells that are subsequently ingested by trophozoites [12].…”

Evolution of Surgical Treatment of Amebiasis-Associated Colon Perforation

“…7 The trophozoite adheres to the cells of the mucosa by means of a cell surface protein denominated adherence lectin (Ga1/Ga1 NAc), amebopores, protein kinases that degrade extracellular protein and that give rise to disruption of the colonic mucosa, and the epithelial barrier. [15][16][17][18][19] Amebapores are polypeptides that are associated with amebic virulence and comprise poreforming cells in the white cell with cytolytic activity that induce the release of Na + , K + , and Ca + from the soft cell and, finally, cytolysis. 18 The inflammatory response is mediated by amebic phospholipases; however, the response is observed to be potentiated by cytolysis of epithelial and inflammatory cells, which add another proinflammatory mechanism.…”