%0 Journal Article %T Reciprocal Interference of Experimental Dyslipidemia and Food Allergy in the Evolution of Both Diseases %A A. C. Gomes-Santos %A J. L. Gon£¿alves %A T. R. Fonseca %A A. R. Marques %A L. P. A. Dourado %A D. C. Cara %A J. I. Alvarez-Leite %J ISRN Allergy %D 2013 %R 10.1155/2013/545184 %X 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. 1. Introduction Under physiological conditions, interactions of gut mucosa and dietary proteins are associated with induction of oral tolerance. It has been reported that 130¨C190£¿g of protein is absorbed in small intestine daily. Indeed, lack of homeostasis of these immunological activities can cause disorders such as inflammatory bowel disease and food allergies [1, 2]. Food allergies develop because of an adverse immune response to food proteins. IgE-mediated food allergies (type I food allergies) account for the majority of food allergic reactions, and the onset of symptoms can occur immediately after ingestion of the allergen [3, 4]. Food allergies are particularly frequent among children, and the symptoms include vomiting, weight loss, abdominal pain, malabsorption, atopic eczema, urticarial, and angioedema [5]. Epidemiological studies have suggested that there has been a significant increase in the prevalence of allergic %U http://www.hindawi.com/journals/isrn.allergy/2013/545184/