• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Oral-tolerance induction in diet-induced obese mice.
【24h】

Oral-tolerance induction in diet-induced obese mice.

机译：饮食诱导的肥胖小鼠的口服耐受诱导。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

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.
机译：目的：众所周知，肥胖会以多种方式改变免疫功能。但是，肥胖引起的肠道免疫系统变化仍然知之甚少。口服耐受性是抑制对口服施用的抗原的抗原特异性免疫反应的系统。肠道免疫系统与口腔耐受系统密切相关，可预防过敏性和炎症性疾病。在这项研究中，我们调查了肥胖症对肥胖动物模型中对卵白蛋白（OVA）的口服耐受性诱导的影响。研究方法和程序：高脂饮食诱导的肥胖小鼠和对照小鼠在饮用水中可自由摄取1％卵清蛋白（OVA）溶液3天。连续饲喂抗原后，通过两次腹膜内注射间隔7天的OVA免疫所有小鼠。结果：在对照组小鼠中，口服耐受性的诱导导致抗原特异性IgG1水平升高，而IgG2a水平降低。相反，肥胖小鼠中IgG1 / IgG2a比例相反。在对照组和肥胖小鼠中，通过抗原喂养抑制了OVA特异性IL-2的产生;然而，仅在对照小鼠中观察到OVA特异性IL-10的抑制。尽管OVA特异性IgA和IgM不受抗原喂养的影响，但肥胖的小鼠组的抗体滴度明显较低。讨论：这些发现表明肥胖症可能会影响抗原喂养后对口腔耐受的诱导，并且这些变化可能与炎症反应有关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号