Análise dos corpúsculos lipídicos em macrófagos humanos infectados pela Cepa Y do Trypanosoma cruzi e submetidos ao tratamento com a droga benzonidazol

• Ano de defesa: 2012
• Autor(a) principal: Patricia Pereira Silva
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Corpúsculos lipídicos; Benzonidazol; Macrófagos humanos; Cepa Y; Trypanosoma cruzi; Tripanossoma cruzi; Macrófagos; Biologia celular
• Link de acesso: http://hdl.handle.net/1843/BUOS-972KG3

Chagas disease, still considered uncontrollable dimensions is due to the contact between the protozoan Trypanosoma cruzi with host cells definitive, especially the cells of the mononuclear phagocyte system, where they multiply and subsequently infect new cells. However, there is no literature about the lipid bodies in human macrophages infected in vitro with the Y strain of T. cruzi, followed by a treatment with the drug benznidazole. The objectives of this study are to describe the occurrence and possible diameter ultrastructural changes in lipid bodies infected with T. cruzi and treated with benznidazole. To this end, cells were analyzed using bright field microscopy, using osmium tetroxide as specific staining for lipid body, and fluorescence labeling of lipid bodies with BODIPY®. The human macrophage lipid bodies were also analyzed by the transmission electron microscopy. The results showed the infected macrophages with a typical euchromatic nuclei, projections and cytoplasmic organelles such as the endoplasmic reticulum, Golgi apparatus, mitochondria and lipid bodies, organelles described as structural markers of inflammation. These organelles were slightly rounded with typical variation in its osmiofilia. Besides showing interaction, for example, with the smooth endoplasmic reticulum, demonstrating its dynamic and heterogeneous characteristic, the lipid bodies were also found increased in numbers and its diameter. It is highlighted, however, that the group of macrophages infected with Y strain and treated with benznidazole although have shown the same cell activation signals described above showed a reduction in the number of lipid bodies, possibly in response to the treatment with the drug. We conclude from our results, that similar to macrophages of other species lipid bodies were responsive to cellular-parasite interaction in human infection, and provide possible inferences to new treatment strategies and studies mechanisms of new drugs reaction.