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Adherence-blocking vaccine for amebiasis.

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The Gal/GalNAc lectin is a candidate vaccine antigen for an amebiasis vaccine due to its mediation of parasite adherence to the human intestine, because partial immunity in humans is associated with a mucosal IgA response against it, and because it is effective as a vaccine against amebic colitis in

Infection and immunity mediated by the carbohydrate recognition domain of the Entamoeba histolytica Gal/GalNAc lectin.

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Entamoeba histolytica causes invasive amebiasis, a major parasitic disease of the developing world, whose primary symptoms are liver abscess and colitis. All strains of E. histolytica express a 260-kDa surface Gal/GalNAc lectin that is antigenically conserved and immunogenic. The lectin is required

Innate and acquired resistance to amebiasis in bangladeshi children.

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Entamoeba histolytica infection and colitis occurred in 55% and 4%, respectively, of a cohort of Bangladeshi preschool children observed for 2 years. DNA typing demonstrated that infecting E. histolytica isolates were genetically diverse. Innate resistance to infection in children was linked to the

Recognition of carbohydrate epitopes specific for electron-dense granule antigens from Entamoeba histolytica by monoclonal antibodies in the cecal content of infected hamsters.

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The pathogenic trophozoites of Entamoeba histolytica produce and secrete electron-dense granules (EDG) containing collagenase, considered a virulence factor. Two monoclonal antibodies (MAbs) (L7.1 and L1.1) anti-EDG antigens were raised. MAb L7.1 has been reported to recognize proteic EDG antigens

Crosstalk between Entamoeba histolytica and the human intestinal tract during amoebiasis.

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The protozoan parasite Entamoeba histolytica is the microbial agent of amoebiasis - an infection that is endemic worldwide and is associated with high morbidity and mortality rates. As the disease develops, virulent E. histolytica deplete the mucus layer, interact with the intestinal epithelium, and

Pathogenic bacteria prime the induction of Toll-like receptor signalling in human colonic cells by the Gal/GalNAc lectin Carbohydrate Recognition Domain of Entamoeba histolytica.

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In mixed intestinal infections with Entamoeba histolytica trophozoites and enteropathogenic bacteria, which are wide-spread in areas of endemic amoebiasis, interaction between the pathogens could be an important factor in the occurrence of invasive disease. It has been reported that exposure of

Entamoeba histolytica: Overexpression of the gal/galnac lectin, ehcp2 and ehcp5 genes in an in vivo model of amebiasis.

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The parasite Entamoeba histolytica causes intestinal amebiasis and amebic liver abscess as its main extraintestinal manifestation. To study the in vivo events related to inflammation and the interactions between hosts and parasites during amebiasis, we designed a novel model of host-parasite

Entamoeba histolytica infection in children and protection from subsequent amebiasis.

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The contribution of amebiasis to the burden of diarrheal disease in children and the degree to which immunity is acquired from natural infection were assessed in a 4-year prospective observational study of 289 preschool children in an urban slum in Dhaka, Bangladesh. Entamoeba histolytica infection

Substructural specificity and polyvalent carbohydrate recognition by the Entamoeba histolytica and rat hepatic N-acetylgalactosamine/galactose lectins.

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Both the Entamoeba histolytica lectin, a virulence factor for the causative agent of amebiasis, and the mammalian hepatic lectin bind to N-acetylgalactosamine (GalNAc) and galactose (Gal) nonreducing termini on oligosaccharides, with preference for GalNAc. Polyvalent GalNAc-derivatized

Unique posttranslational modifications of chitin-binding lectins of Entamoeba invadens cyst walls.

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Entamoeba histolytica, which causes amebic dysentery and liver abscesses, is spread via chitin-walled cysts. The most abundant protein in the cyst wall of Entamoeba invadens, a model for amebic encystation, is a lectin called EiJacob1. EiJacob1 has five tandemly arrayed, six-Cys chitin-binding

Transcriptional and secretory responses of Entamoeba histolytica to mucins, epithelial cells and bacteria.

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Invasive intestinal amebiasis, caused by Entamoeba histolytica, is initiated with attachment of trophozoites to the colonic mucous layer, mucous disruption and/or depletion, and adherence to and cytolysis of host epithelial and inflammatory cells. A current working model of intestinal amebiasis

Adhesion properties of Entamoeba histolytica.

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Trophozoites of Entamoeba histolytica adhere to and phagocytize red blood cells and bacteria. Furthermore, in the initial step of the amoebic infectious process the parasite attaches to intestinal epithelial cells. A lectin (carbohydrate-binding protein) which apparently has a role in the attachment

Antigenic glycans in parasitic infections: implications for vaccines and diagnostics.

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Infections by parasitic protozoans and helminths are a major world-wide health concern, but no vaccines exist to the major human parasitic diseases, such as malaria, African trypanosomiasis, amebiasis, leishmaniasis, schistosomiasis, and lymphatic filariasis. Recent studies on a number of parasites

Multinucleation and Polykaryon Formation is Promoted by the EhPC4 Transcription Factor in Entamoeba histolytica.

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Entamoeba histolytica is the intestinal parasite responsible for human amoebiasis that is a leading cause of death in developing countries. In this protozoan, heterogeneity in DNA content, polyploidy and genome plasticity have been associated to alterations in mechanisms controlling DNA replication

Prevalence and immune response to Entamoeba histolytica infection in preschool children in Bangladesh.

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Entamoeba histolytica infection was present in 5% and E. dispar in 13% of asymptomatic 2-5-year-old children from an urban slum of Dhaka, Bangladesh. Entamoeba dispar-infected children were no more likely than uninfected children to have serum antibodies to lectin. In contrast, all children infected

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