A wheat-based, diabetes-promoting diet induces a Th1-type cytokine bias in the gut of NOD mice
A wheat-based, diabetes-promoting diet induces a Th1-type cytokine bias in the gut of NOD mice
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DOI：
10.1016/s1043-4666(02)00486-6
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发表时间：
2003-02-07
期刊：
影响因子：
3.8
通讯作者：
Kolb, H
中科院分区：
文献类型：
--
作者：
Flohé, SB;Wasmuth, HE;Kolb, H
饮食抗原是1型糖尿病发病机制中的候选环境因素。在非肥胖糖尿病（NOD）小鼠（1型糖尿病的动物模型）中，基于谷物的饮食促进疾病发展，而基于水解蛋白质或非致糖尿病蛋白质的饮食具有保护作用。测试了致糖尿病饮食调节肠道中细胞因子平衡的假设。NOD小鼠喂食NTP-2000（主要是基于小麦的无乳饮食）或Prosobee（基于大豆蛋白分离物的半纯化低过敏性饮食）或Prosobee加酪蛋白（乳蛋白组分）。通过半定量RT-PCR测定小肠和派尔集合淋巴结中IFN-γ、IL-10、TNF-α、TGF-β和诱导型NO合酶的mRNA水平。与Prosobee喂养的动物相比，喂食基于谷物的NTP-2000饮食的小鼠表达了更高水平的Th 1型和促炎标志物IFN-γ、TNF-α和诱导型NO合酶mRNA。反调节细胞因子IL-10和TGF-β的表达不受影响。这导致喂食NTP-2000后肠道细胞因子平衡向T辅助细胞1型的显著偏倚。肠道相关Peyer集合淋巴结中细胞因子mRNA水平不受影响。因此，通过饮食调节肠道免疫反应性可能有助于NOD小鼠的疾病发展。(C)2003爱思唯尔科技有限公司版权所有。
Dietary antigens are candidate environmental factors in the pathogenesis of type 1 diabetes. In the non-obese diabetic (NOD) mouse, an animal model of type 1 diabetes, cereal-based diets promote disease development, whereas the diets based on hydrolysed proteins or non-diabetogenic proteins are protective. The hypothesis that diabetogenic diets modulate the cytokine balance in the gut was tested. NOD mice were fed with NTP-2000 (mainly a wheat-based milk-free diet) or Prosobee (a semi-purified hypoallergenic diet based on soy protein isolate) or Prosobee plus casein (milk protein fraction). The mRNA levels of IFN-gamma, IL-10, TNF-alpha, TGF-beta, and inducible NO synthase in the small intestine and the Peyer's patches were determined by semi-quantitative RT-PCR. Mice fed on the cereal-based NTP-2000 diet expressed higher levels of the Th1-type and pro-inflammatory markers IFN-gamma, TNF-alpha, and inducible NO synthase mRNA compared to the Prosobee-fed animals. The expression of the counterregulatory cytokines IL-10 and TGF-beta was unaffected. This resulted in a significant bias of the intestinal cytokine balance towards T helper cell type 1 after feeding NTP-2000. The cytokine mRNA levels in the gut-associated Peyer's patches were not affected. Thus, modulation of gut immunoreactivity by diet may contribute to disease development in NOD mice. (C) 2003 Elsevier Science Ltd. All rights reserved.