Oral-tolerance induction in diet-induced obese mice

被引:9
|
作者
Mito, Natsuko
Kaburagi, Tomoko
Yoshino, Haruka
Imai, Atsuko
Sato, Kazuto
机构
[1] Natl Inst Hlth & Nutr, Div Appl Food Res, Shinjuku Ku, Tokyo 1628636, Japan
[2] Japan Womens Univ, Dept Food & Nutr, Div Clin Nutr, Bunkyo Ku, Tokyo 1128681, Japan
关键词
oral tolerance; intestinal immune system; diet-induced obese mice;
D O I
10.1016/j.lfs.2006.03.015
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Objective: It is known that immune functions are altered in various ways by obesity. However, changes in the intestinal immune system resulting from obesity remain poorly understood. Oral tolerance is a system that suppresses antigen specific immune responses to orally administrated antigens. The intestinal immune system is intimately associated with the oral tolerance system, that acts to prevent allergic and inflammatory diseases. In this study we investigated the effect of obesity on induction of oral tolerance to ovalbumin (OVA) in an animal model of obesity. Research methods and procedures: Obese mice induced by a high fat diet and control mice were allowed free access for 3 days to a 1%-ovalbumin (OVA) solution in drinking water. After continuous feeding of the antigen, all the mice were immunized by two intraperitoneal injections of OVA administered 7 days apart. Results: In the control mice, induction of oral tolerance caused an increase in antigen specific IgG1 levels and a decrease in IgG2a levels. In contrast, the IgG1/IgG2a ratio was reversed in obese mice. OVA-specific IL-2 production was suppressed by antigen feeding in both the control and obese mice; however, suppression of OVA-specific IL-10 was observed only in the control mice. Although OVA-specific IgA and IgM were not affected by antigen feeding, the obese groups of mice had significantly lower titers of antibodies. Discussion: These findings suggest that obesity may affect induction of oral tolerance following antigen feeding and that these changes may be related to the inflammatory reaction. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:1056 / 1061
页数:6
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