Neurocisticercose Intraventricular experimental: Análise da resposta inflamatória

• Autor(a) principal: SILVA, Hidelberto Matos
• Data de Publicação: 2011
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da UFG
• dARK ID: ark:/38995/0013000007xfs
• Texto Completo: http://repositorio.bc.ufg.br/tede/handle/tde/1806
• topic: Taenia crassiceps; neurocisticercose; resposta inflamatória; Taenia crassiceps; neurocysticercosis; inflammatory response; CNPQ::CIENCIAS DA SAUDE::MEDICINA

Neurocysticercosis (NCC) is caused by Taenia solium cysticercus and is the main cerebral infection caused by a parasite which can produce seizures and hydrocephaly. Besides the considerable economic losses it is also responsible for over than 50 thousand annual deaths. The use of experimental models has become a good method to the study of human cysticercosis in several organs including the central nervous system. The most used parasite is T. crassiceps cysticerci due to its rapid cycle of development and the antigenic similarity to T. solium and its intraperitoneal model is the most diffused. The inoculation of Mesocestoides corti cysticerci is the most common model of NCC used. Objectives: present a new experimental model to NCC studies by using T. crassiceps cysticerci inoculated into four different mice lineages (BALB/c, BALB/c KO-IL-4, C57BL/6 e C57BL/6 KO-IFNγ) and evaluate the inflammatory response of these animals to the infection during 7, 30, 60 and 90 days after the infection (DAI). This new model showed itself useful into reproducing the disease in animals resulting into lesions and alterations similar to the ones found in humans and without significant damages in the control groups, which enables the study. We observed that BALB/c mice are the less resistant to the infection, presenting greater ventriculomegaly, inflammatory response with the prevalence of acute phase cells and late destruction of the cysticerci when compared to C57BL/6 mice. The latter showed inflammation with prevalence of mononuclear cells and greater efficiency in the destruction of the parasites. When comparing the inflammatory response of conventional BALB/c mice to KO-IL-4 ones it was possible to observe that the absence of IL-4 induces greater parasitism which favors the cysticerci survival, less intensity of the inflammatory response, ventriculomegaly and perivasculitis. Both lineages destroyed the cysticerci at the end of the late phase of the inflammation process. When comparing the inflammatory response of conventional C57BL/6 mice to KO-IFNγ ones, the presence of IFNγ induced greater ventriculomegaly, chronification of the inflammation, microgliosis and precocious destruction of the cysticerci. In the absence of IFNγ the inflammatory response showed less intensity and late destruction of the cysticerci.