Gomes-Santos A C, Gonçalves J L, Fonseca T R, Marques A R, Dourado L P A, Cara D C, Alvarez-Leite J I
Department of Food, Faculty of Pharmacy, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil ; Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Avenida Antônio Carlos 6627, Pampulha, 30161-970 Belo Horizonte, MG, Brazil.
ISRN Allergy. 2013 Jun 6;2013:545184. doi: 10.1155/2013/545184. Print 2013.
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.
背景。食物过敏已被证明可降低小鼠血清中的三酰甘油、葡萄糖、胆固醇和游离脂肪酸水平。反过来，血脂异常，尤其是表现为高密度脂蛋白胆固醇水平低的血脂异常，是动脉粥样硬化发展的重要危险因素。然而，食物过敏对血脂异常和动脉粥样硬化的影响尚未得到充分研究。方法。在卵清蛋白（OVA）致敏的C57BL/6和低密度脂蛋白受体敲除小鼠（LDLr(-/-)）中，使用蛋清溶液（EWS）诱导食物过敏5周，并通过两种小鼠品系中抗OVA IgE和IgG1抗体的高产量来证实。结果。与对照组相比，过敏的C57BL/6小鼠在摄入EWS 5周后表现出对EWS的厌恶，这与较少的内脏脂肪和高水平的抗Ova IgE抗体有关。然而，LDLr(-/-)过敏小鼠的抗Ova IgE水平降低，与未致敏组相似。LDLr(-/-)过敏小鼠在过敏5周后也表现出食物厌恶的逆转和内脏脂肪的持续存在。尽管两种致敏小鼠品系的高密度脂蛋白胆固醇水平均降低，但慢性摄入EWS并未影响胸主动脉和腹主动脉中的脂质沉积以及动脉粥样硬化斑块的面积和组成。结论。LDLr(-/-)小鼠发生的食物过敏减弱，因为它们在诱导过敏5周后表现出食物厌恶的逆转和较低的IgE产生。尽管脂质谱更易致动脉粥样硬化，但过敏的LDLr(-/-)组中动脉粥样硬化的发展并未加速。
