Efeitos do TNF-á sobre a infecção de células da glia com Trypanosoma cruzi

• Ano de defesa: 2015
• Autor(a) principal: Reinaldo Atila Franca Cordeiro
• 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
• Link de acesso: http://hdl.handle.net/1843/BUBD-A34HP7

Chagas disease, caused by Trypanosoma cruzi protozoan parasite, is a serious public health problem in Latin America. Early in infection, T. cruzi induces an intense inflammatory response that involves increased IL-12 and TNF- production by dendritic cells and macrophages, and IFN- by natural killer (NK) cells. This response plays a crucial role in the pathogenesis of the disease. In patients under the age of two years and in immunosuppressed adults, T. cruzi can cause damage to the CNS. The proliferation of astrocytes and microglia is a common response to injury in the CNS. The fact that TNF- increases the susceptibility of epithelial cells to infection with T. cruzi seems to indicate that the interaction of the parasite with the host cell depends on numerous factors, including the microenvironment in which it is inserted. Thus, it becomes important to evaluate the effects of TNF- on astrocyte and microglia invasion. Both cells were isolated from rat brains and were infected with the strain Y or the clone Col1.7G2 6 hours after treatment with 20 ng/ml of TNF-. Astrocytes treated with TNF- showed a significant increase in the percentage of cells infected with T. cruzi Y strain, 2 and 24 hours after infection, in comparison to untreated astrocytes. These cells also showed a significant increase in the number of parasites /100 cells 2 hours after infection. In turn, Col1.7G2-infected astrocytes showed no differences in these parameters after treatment with TNF-. Microglia treated with 20ng / ml TNF- for 6 hours prior to infection with T. cruzi Y strain showed a significant increase in the proportion of infected cells compared to untreated ones. On the other hand, infection of these cells with the T. cruzi Col1.7G2 clone resulted in no differences in these parameters after treatment with TNF-. Our results indicate that TNF- acts differently on astrocytes and microglia infection with T. cruzi. Our results also show that different T. cruzi populations might interact in a different way with the target cell.