O papel da arginase na cisticercose experimental por Taenia crassiceps

• Ano de defesa: 2010
• Autor(a) principal: Moura, Vânia Beatriz Lopes
• Orientador(a): Oliveira, Milton Adriano Pelli de
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Goiás
• Programa de Pós-Graduação: Programa de Pós-graduação em Medicina Tropical e Saúde Publica (IPTSP)
• Departamento: Instituto de Patologia Tropical e Saúde Pública - IPTSP (RG)
• País: Brasil
• Palavras-chave em Português: Colágeno; Taenia crassiceps; Cisticercose; Macrófagos alternativamente ativado
• Palavras-chave em Inglês: Collagen; Taenia crassiceps; Cysticercosis; Alternatively activated macrophages
• Área do conhecimento CNPq: MEDICINA::ANATOMIA PATOLOGICA E PATOLOGIA CLINICA
• Link de acesso: http://repositorio.bc.ufg.br/tede/handle/tede/3266

The role of arginase on experimental cysticercosis induced by Taenia crassiceps Murine infection by Taenia crassiceps cysticerci is used as an experimental model for human and animal cysticercosis. In this infection parasites can be found inside an inflammatory infiltrated enriched with macrophages. These macrophages can be divided in alternatively activated, that express high amount of the arginase enzyme and classically activated (CMø) that express high amount of induced nitric oxide sintase enzyme (iNOS). Arginase uses the substrate L-arginine to produce ornithine favoring the cellular proliferation and collagen synthesis. The iNOS uses the same substrate to synthesize nitric oxide (NO), which is a highly microbicide compound responsible for the cysticerci control. To observe if there is an association between macrophages expressing arginase and an increase of the susceptibility to T. crassiceps, BALB/c mice were infected IP with 10 cysticerci and followed up by 84 days. It was measured the number and stages of the cysticerci, profile of systemic cytokines, profile of the macrophages in inflamed tissue and collagen deposition over the peritoneum. Besides, infected mice were treated with arginase inhibitor or L-arginine and followed up by 56 days. The parasitic load was observed, which increased significantly after the 30th day. At the end of experimental period number of cysticerci was 1022 (±230). The serum interferon- (IFN-) of infected animals was higher than controls at the 28th day after infection and IL-4 at the 42th day. Macrophages were the major cells observed at the infected site, and the polimorphonuclear cells (PMN) picked at the 14th day after the infection, returning to the normal values at the 42th day. Cells carrying the marker CD301, present on AAMø, and high arginase activity increased in the early phase after infection. The presence of collagen in the peritoneum of infected animals decreased until 14th day after the infection, however, in the latest phases the collagen increases and become superior to the control. The treatment with the arginase inhibitor or L-arginine did not alter the profile of the infection; however the arginase inhibitor inhibited the deposition of collagen in the peritoneum. These results suggest that the enzyme arginase does not interfere with the control of the cysticerci during experimental infection with T. crassiceps cysticerci, but it is important for the formation of fibrosis in cysticercosis.