| Revista: | The journal of venomous animals and toxins including tropical diseases |
| Base de datos: | PERIÓDICA |
| Número de sistema: | 000298909 |
| ISSN: | 1678-9199 |
| Autores: | Picka, M.C.M1 Calvi, S.A Lima, C.R.G Santos, I.A.T Marcondes-Machado, J |
| Instituciones: | 1Universidade Estadual Paulista "Julio de Mesquita Filho", Faculdade de Medicina de Botucatu, Botucatu, Sao Paulo. Brasil |
| Año: | 2005 |
| Periodo: | Dic |
| Volumen: | 11 |
| Número: | 4 |
| Paginación: | 540-556 |
| País: | Brasil |
| Idioma: | Inglés |
| Tipo de documento: | Artículo |
| Enfoque: | Experimental, aplicado |
| Resumen en inglés | Acute infection by Toxoplasma gondii leads to suppression of cell-mediated immunity, facilitating chronic infection. One of the causes of immunosuppression is Interleukin-10 (IL-10) production. Glucan is used to stimulate phagocytosis. Our objective was to study IL-10 induction in male BALB/c mice with acute T. gondii BTU-2 strain infection, glucan immunostimulation, and sulfadiazine treatment. Animals were distributed into 7 groups: G1: infected with T. gondii; G2: infected with T. gondii and treated with sulfadiazine; G3: infected with T. gondii and immunostimulated with glucan; G4: infected with T. gondii, immunostimulated with glucan, and treated with sulfadiazine; G5: imunostimulated with glucan; G6: treated with saline; and G7: treated with sulfadiazine. IL-10 levels were determined by ELISA; the highest levels were found in G2, G3 and G4, and the lowest in G1 (p<0.001). Groups G1 to G5 and G7 had substantially higher levels than G6 (p<0.001). In this study, the highest IL-10 levels were found in groups treated with glucan |
| Disciplinas: | Medicina |
| Palabras clave: | Medicina experimental, Parasitología, Inmunología, Toxoplasmosis, Interleucina 10, Glucano, Respuesta inmune, Sulfadiazina, Toxoplasma gondii |
| Keyword: | Medicine, Experimental medicine, Parasitology, Immunology, Toxoplasmosis, Interleukin 10, Glucan, Immune response, Sulfadiazine, Toxoplasma gondii |
| Texto completo: | Texto completo (Ver HTML) |
