Influência da infecção por Leishmania major no perfil lipídico e aterogênese em camundongos deficientes em apoE

• Ano de defesa: 2006
• Autor(a) principal: Luciana Rodrigues Fernandes
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Bioquímica e Imunologia; Bioquímica; Leishmania; Aterosclerose
• Link de acesso: http://hdl.handle.net/1843/BUOS-9M8JGC

Atherosclerosis is a chronic inflammatory disease that affects arterial walls, mainly induced by disturbances on lipid metabolism, characterized by the presence of cells and fibrotic elements in large and medium arteries. Besides traditional risk factors, infectious agents are also related to atherosclerosis. Some consistent studies showed the involvement of virus, bacteria and, recently, protozoan in atherogenesis. Leishmania major infection induces a pro-inflammatory immune response (Th1 profile) in resistant animals. Different from infection with other parasites, L. major elicits a local and self-limited disease in C57BL/6 resistant mice. The aim of the present work was investigate the possible effects of L. major infection on lipid metabolism and on the development of atherosclerosis. For that, ApoE- / - deficient mice were distributed in control and L. major infected groups. Our results showed that L. major infected mice presented an increase in serum total cholesterol as well as in atherogenic and nonatherogenic fractions, associated to the decrease of serum and hepatic triglycerides levels. Concerning atherogenesis, L. major infected group showed an increase in atherosclerotic lesion when compared to the control group. The increase in lesion area was associated to higher levels of inflammatory cells in the lesion site of infected mice. Collagen quantif ication was similar in both groups. Specific L. major DNA was detected in the heart of infected mice, highlighting the possibility of infected-macrophages recruitment to the atherosclerotic lesion area. The visceral form of the disease was discarded, as confirmed by the absence of L. major in spleen and liver. We suggested that the migration of activated macrophages to the lesion site aggravated the inflammatory status and contributed for the atherosclerosis development. In conclusion, infection caused by L. major in apoE- / - mice, although not showing an important inflammatory systemic response, was able to alter the lipid profile and accelerate atherogenesis in these animals.