Table of Contents
ISRN Allergy
Volume 2013, Article ID 545184, 7 pages
Research Article

Reciprocal Interference of Experimental Dyslipidemia and Food Allergy in the Evolution of Both Diseases

1Department of Food, Faculty of Pharmacy, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
2Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Avenida Antônio Carlos 6627, Pampulha, 30161-970 Belo Horizonte, MG, Brazil
3Department of Morphology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil

Received 23 April 2013; Accepted 19 May 2013

Academic Editors: A. Lorentz, C. Pereira, and B. Xu

Copyright © 2013 A. C. Gomes-Santos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Food allergies have been shown to reduce serum triacylglycerol, glucose, cholesterol, and free fatty acid levels in mice. In turn, dyslipidemias, especially dyslipidemias presenting with low levels of HDL cholesterol, are important risk factors for the development of atherosclerosis. However, the consequences of food allergies on dyslipidemia and atherosclerosis have not been fully investigated. Methods. Food allergy was induced using an egg white solution (EWS) in ovalbumin- (OVA-) sensitized C57BL/6 and low-density lipoprotein receptor knockout mice (LDLr−/−) for 5 weeks and was confirmed by the high production of anti-OVA IgE and IgG1 antibodies in both mouse strains. Results. The allergic C57BL/6 mice exhibited EWS aversion that was associated with less visceral fat and high levels of anti-Ova IgE antibodies after 5 weeks of EWS intake compared to controls. However, LDLr−/− allergic mice showed reduced anti-Ova IgE levels that were similar to the nonsensitized group. The LDLr−/− allergic mice also demonstrated a reversal of food aversion and sustained visceral fat after 5 weeks of allergy. Although HDL cholesterol levels were reduced in both sensitized mouse strains, lipid deposition in thoracic and abdominal aorta as well as area and composition of atherosclerotic plaques as unaffected by chronic ingestion of EWS. Conclusion. LDLr−/− mice develop an attenuated food allergy, as they showed a reversal of food aversion and lower IgE production after 5 weeks of induced allergy. The development of atherosclerosis, in turn, was not accelerated in the allergic LDLr−/− group despite the more atherogenic lipid profile.