C57BL/6 α-1,3-Galactosyltransferase Knockout Mouse as an Animal Model for Experimental Chagas Disease

Edward Valencia Ayala, Gisele Rodrigues Da Cunha, Maira Araujo Azevedo, Maritza Calderon, Juan Jimenez, Ana Paula Venuto, Ricardo Gazzinelli, Raúl Jesus Ynocente Lavalle, Angela Giovana Vidal Riva, Robert Hincapie, M. G. Finn, Alexandre F. Marques

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

3 Citas (Scopus)

Resumen

The leading animal model of experimental Chagas disease, the mouse, plays a significant role in studies for vaccine development, diagnosis, and human therapies. Humans, along with Old World primates, alone among mammals, cannot make the terminal carbohydrate linkage of the α-Gal trisaccharide. It has been established that the anti-α-Gal immune response is likely to be a critical factor for protection against Trypanosoma cruzi (T. cruzi) infection in humans. However, the mice customarily employed for the study of T. cruzi infection naturally express the α-Gal epitope and therefore do not produce anti-α-Gal antibodies. Here, we used the C57BL/6 α-1,3-galactosyltransferase knockout (α-GalT-KO) mouse, which does not express the α-Gal epitope as a model for experimental Chagas disease. We found the anti-α-Gal IgG antibody response to an increase in α-GalT-KO mice infected with Arequipa and Colombiana strains of T. cruzi, leading to fewer parasite nests, lower parasitemia, and an increase of INF-Î, TNF-α, and IL-12 cytokines in the heart of α-GalT-KO mice compared with α-GalT-WT mice on days 60 and 120 postinfection. We therefore agree that the C57BL/6 α-GalT-KO mouse represents a useful model for initial testing of therapeutic and immunological approaches against different strains of T. cruzi.

Idioma originalInglés
Páginas (desde-hasta)1807-1815
Número de páginas9
PublicaciónACS Infectious Diseases
Volumen6
N.º7
DOI
EstadoPublicada - 10 jul 2020

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Copyright © 2020 American Chemical Society.

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