Interactions of human galectins with Trypanosoma cruzi

We report here the specific interaction between several members of the human galectin family with the three developmental stages of several genetic lineages of the protozoan parasite Trypanosoma cruzi.We provide data of specific and differential binding of human galectin (gal)-1, -3, -4, -7 and -8 t...

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Detalles Bibliográficos
Autores: Pineda, Miguel Ángel, Corvo, Laura, Soto, Manuel, Fresno, Manuel, Bonay, Pedro
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2015
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/139570
Acceso en línea:http://hdl.handle.net/10261/139570
Access Level:acceso abierto
Palabra clave:Trypanosoma cruzi
host cell adhesion
discrete typing units
galectin
Descripción
Sumario:We report here the specific interaction between several members of the human galectin family with the three developmental stages of several genetic lineages of the protozoan parasite Trypanosoma cruzi.We provide data of specific and differential binding of human galectin (gal)-1, -3, -4, -7 and -8 to 14 strains of T. cruzi that belong to the six genetic lineages representing the genetic diversity of the parasite. It is shown that galectins preferentially bind forms present in the host, trypomastigotes and amastigotes, compared with the non-infective epimastigote present on the intestinal tract of the vector, reflecting the changes on glycosylation that occur during the metacyclogenesis and amastigogenesis process. Also, it is evidenced that galectin binding to the parasites promotes binding to the host cells and higher infection rates. In addition, evidence is provided indicating that the intracellular amastigotes may take over the cytosolic pool of some galectins when released to the extracellular medium. Finally, by applying unweighted pair group method analysis to the galectin-binding profile to either cell-derived trypomastigotes or amastigotes,we showthat the differential-binding profile by the host galectins to the six lineages resembles the clustering based in genetic data. Therefore, the differential-binding profile for the six lineages could have implications in the immunopathology of Chagas’ disease, affecting the complex network of immune responses on which galectins mediate, thus providing linkage clues to the notion that different lineages may be related to different clinical forms of the disease.