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Interaction of cholera toxin with three life-cycle stages of Schistosoma mansoni: adult worm, egg and cercaria

Journal article
Authors Aliasghar Akhiani
A. M. Deelder
Jan-Eric Månsson
Lars-Åke Nilsson
Published in Scand J Immunol
Volume 65
Issue 1
Pages 48-53
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Biomedicine, Department of Microbiology and Immunology
Pages 48-53
Language en
Keywords Animals, Antigens, Helminth/*immunology, Cholera Toxin/immunology/*metabolism, Cross Reactions, Fluorescent Antibody Technique, Gangliosides/analysis, Glycoproteins/*immunology, Helminth Proteins/*immunology, Life Cycle Stages, Mice, Schistosoma mansoni/growth & development/*metabolism
Subject categories Microbiology in the medical area


We have previously reported that there is an immunological cross-reactivity between Schistosoma mansoni and cholera toxin (CT). In this study, using an immunofluorescence technique with anti-CT antibody, we provide further evidence for this cross-reactivity by demonstrating an antigen, localized in the tegument of S. mansoni adult worms which is cross-reactive with a CT antigen. Anti-CT antibodies also reacted with structures in S. mansoni cercariae and eggs. Additionally, CT itself was found to bind strongly to the gut of the adult worm, gut cells of cercaria and the egg shell. The binding of CT to the parasite was blocked when parasite sections were incubated with CT which had been incubated with the ganglioside GM1. Lipid extraction and isolation of gangliosides demonstrated the presence of GM1 in adult worms. For further analysis of CT-binding structures, the possible interaction of CT with two major schistosome gut antigens, circulating cathodic antigen (CCA) and circulating anodic antigen (CAA), was studied. We found that CT blocked the binding of anti-CCA antibody to the gut of adult worms and that anti-CCA blocked the binding of CT to the worm gut. These findings indicate that CT binds to CCA present in the gut of the parasite and thus has, in addition to GM1, a second binding specificity.

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