Associação entre alergia alimentar e aterosclerose em camundongos

Detalhes bibliográficos
Ano de defesa: 2007
Autor(a) principal: Ana Cristina Gomes Santos
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de Minas Gerais
UFMG
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://hdl.handle.net/1843/BUOS-9LFMYY
Resumo: Atherosclerosis is a chronic inflammatory disease. Recently, Allergic Rhinitis and Asthma have been linked with enhanced risk for atherosclerosis in humans. Paradoxically, atherosclerosis is a Th1-cell- driven disease while, in allergies, Th2- type cell responses are dominant. To investigate the effect of food allergy in this process and in lipid profile, C57BL/6 and low density lipoprotein receptor deficient mice were fed atherogenic diet. The food allergy was induced in ovalbumin-sensitized mice by the egg-white solution intake. The control group was not sensitized. Allergy was confirmed by the high production of antiovalbumin IgE as well as anti-OVA IgG1 antibodies in both mice strain, without intestinal injury detection. However, LDLr-/- allergic mice had reduced IgE level of oral challenger to the end of the experiment and less aversion compared to C57BL/6 allergic mice. This mice lost abdominal fat while in LDLr-/- was not seen difference. The results suggest that LDLr- /- was more resistant of food allergy model than C57BL/6 mice. C57BL/6 and LDLr-/- sensitized mice had a pro-atherogenic profile associated to HDL reduction. Lipid deposition in thoracic and abdominal aorta, area and composition of atherosclerotic plaque and oxidative stress marker were not affect in LDLr/- allergic mice. In conclusion, the food allergy was able to alter the lipid profile without affecting the oxidative stress and the atherogenesis in C57BL/6 and LDLr-/- mice.