Avaliação de modelos de infecção visceral causada por Leishmania (Leishmania) chagasi em camundongos BALB/c: detecção do parasita no parênquima cerebral dos animais

• Ano de defesa: 2010
• Autor(a) principal: Dulcilene Mayrink de Oliveira
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Neurociências; Parasitologia; Leishmaniose visceral
• Link de acesso: http://hdl.handle.net/1843/BUBD-8AGDYX

The leishmaniasis are diseases that present a high incidence in Brazil. In the Latin America, one of its classic and serious forms of the disease, visceral leishmaniasis (VL), is caused by the Leishmania chagasi specie. Among the clinical manifestations of VL, those that involvethe central nervous system (CNS) are poor or its not diagnosed properly. There are reports of the invasion of the parasite through leucocyte migration into the CNS. The use of murine models to the study of the L. chagasi infection has been done for different evaluations of immune response and the effectiveness of antigens candidates; however, the different evaluation periods used, as well as the parasite inoculums and the several infection routes don't allow the definition of an ideal model of study for the evolution of the visceral disease, compromising the efficiency of the evaluation of vaccinate antigens. The present work hasfor objective to evaluate different models (infection routes and inoculums size) of visceral disease caused by L. chagasi in BALB/c mice. Mice were infected with 103, 105 or 107 parasites for the subcutaneous route or 107 parasites for intravenous route. The parasite burden was determined in the spleen, liver, lymph nodes, brain and in the bone marrow of theanimals; 15, 30, 45 and 60 days after challenge. PCR was used for the detection of the parasite in the brain of the infected animals. The profile of the cellular and humoral responses was evaluated by production of IFN-ã, IL-4, IL-10 and of specific-parasite IgG1 and IgG2a antibodies, in the different periods of time. In the results, was verified that the parasiteburden found in the analyzed organs was directly proportional to the size of the parasites inoculum and it progressed with the chronicity of the infection; the detection of DNA of L. chagasi in the cerebral parenchyma of the mice, 15 days after the challenge, evidenced the involvement of this organ in the visceralization of the parasite and allowed to infer theexistence of the systemic compromising of the animal, even in the acute phase of the infection. A direct correlation among the parasitic load in the different evaluated organs, a production of IL-4, IL-10 and pecific-parasite IgG1 antibodies was observed in the experimental groups infected with 105 and, specially, 107 parasites. Therefore, our conclusion showed that the murine model of infection using 107 parasites and the subcutaneous route was that in which a more severe infection was observed in the evaluated animals, in all periods of time evaluated.