C57BL/6 α-1,3-Galactosyltransferase Knockout Mouse as an Animal Model for Experimental Chagas DiseaseClick to copy article linkArticle link copied!
- Edward Valencia AyalaEdward Valencia AyalaLaboratório de Imunologia e Genômica de Parasitos, Departamento de Parasitologia, Instituto de Ciências Biológicas/ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais 31270901, BrazilInstituto de Investigación, Centro de Investigación en Inmunología e Infectología, Facultad de Medicina Humana, Universidad de San Martin de Porres, Lima 15000, PerúMore by Edward Valencia Ayala
- Gisele Rodrigues da CunhaGisele Rodrigues da CunhaLaboratório de Imuno-Proteômica e Biologia de Parasitos, Departamento de Parasitologia, Instituto de Ciências Biológicas/ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais 31270901, BrazilMore by Gisele Rodrigues da Cunha
- Maira Araujo AzevedoMaira Araujo AzevedoLaboratório de Imuno-Proteômica e Biologia de Parasitos, Departamento de Parasitologia, Instituto de Ciências Biológicas/ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais 31270901, BrazilMore by Maira Araujo Azevedo
- Maritza CalderonMaritza CalderonLaboratorio de Investigación en Enfermedades Infecciosas and Laboratorio de Biología Molecular, Facultad de Ciencias y Filosofía, Universidad Peruana Cayetano Heredia, Lima 15000, PerúMore by Maritza Calderon
- Juan JimenezJuan JimenezLaboratorio de Parasitología en Fauna Silvestre y Zoonosis, Facultad de Ciencias Biológicas, Universidad Nacional Mayor de San Marcos, Lima 15000, PerúMore by Juan Jimenez
- Ana Paula VenutoAna Paula VenutoLaboratório de Imuno-Proteômica e Biologia de Parasitos, Departamento de Parasitologia, Instituto de Ciências Biológicas/ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais 31270901, BrazilMore by Ana Paula Venuto
- Ricardo GazzinelliRicardo GazzinelliInstituto de Pesquisa Rene Rachou, Fundacao Oswaldo Cruz, Belo Horizonte, Minas Gerais 30190-009, BrazilPlataforma de Medicina Translacional, Fundacao Oswaldo Cruz, Belo Horizonte, Minas Gerais 30190-009, BrazilMore by Ricardo Gazzinelli
- Raúl Jesus Ynocente LavalleRaúl Jesus Ynocente LavalleLaboratorio de Parasitología en Fauna Silvestre y Zoonosis, Facultad de Ciencias Biológicas, Universidad Nacional Mayor de San Marcos, Lima 15000, PerúMore by Raúl Jesus Ynocente Lavalle
- Angela Giovana Vidal RivaAngela Giovana Vidal RivaInstituto de Investigación, Centro de Investigación en Inmunología e Infectología, Facultad de Medicina Humana, Universidad de San Martin de Porres, Lima 15000, PerúLaboratorio de Investigación en Enfermedades Infecciosas and Laboratorio de Biología Molecular, Facultad de Ciencias y Filosofía, Universidad Peruana Cayetano Heredia, Lima 15000, PerúMore by Angela Giovana Vidal Riva
- Robert HincapieRobert HincapieSchool of Chemistry and Biochemistry, School of Biological Sciences, Georgia Institute of Technology, Atlanta, Georgia 30332 United StatesMore by Robert Hincapie
- M. G. FinnM. G. FinnSchool of Chemistry and Biochemistry, School of Biological Sciences, Georgia Institute of Technology, Atlanta, Georgia 30332 United StatesMore by M. G. Finn
- Alexandre F. Marques*Alexandre F. Marques*Email: [email protected] or [email protected]Laboratório de Imuno-Proteômica e Biologia de Parasitos, Departamento de Parasitologia, Instituto de Ciências Biológicas/ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais 31270901, BrazilMore by Alexandre F. Marques
Abstract
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-γ, 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.
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