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Induction of colitis in mice with food allergen-specific immune response

机译:食物过敏原特异性免疫应答诱导小鼠的结肠炎

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The pathogenesis of intestinal chronic inflammation is unclear. Food allergy plays an important role in the induction of intestinal inflammation. This study aims to test a hypothesis that food allergy initiates colitis. In this study, BALB/c mice were sensitized to a common food allergen, ovalbumin (OVA) with cholera toxin (CT) as an adjuvant. The colon epithelial barrier function was assessed with Ussing chamber technique. Expression of T cell immunoglobulin mucin domain molecule-4 (TIM4) in dendritic cells was evaluated by flow cytometry, RT-PCR and Western blotting. The results showed that allergen-related colitis was induced in mice as shown by heavy infiltration of inflammatory cells in the colon mucosa, loss of body weight of mice, increases in myeloperoxidase, tumor necrosis factor-α, interleukin-4, OVA-specific IgE in the colon tissue. The colon epithelial barrier function was markedly compromised in colitis group mice, which was mimicked by exposure the colon mucosa to CT in Ussing chamber. High frequency of TIM4(+) dendritic cells was detected in the colon mucosa of colitis mice. Exposure of dendritic cells to CT markedly increased the expression of TIM4. We conclude that IBD-like inflammation can be induced in the mouse colon by the food allergen-related immune response.
机译:肠道慢性炎症的发病机制尚不清楚。食物过敏在肠道炎症诱导中起着重要作用。本研究旨在测试食物过敏发起结肠炎的假设。在本研究中,BALB / C小鼠用霍乱毒素(CT)作为佐剂致敏于常见的食物过敏原,卵蛋白(OVA)。利用USSing室技术评估结肠上皮屏障功能。通过流式细胞术,RT-PCR和Western印迹评估树突细胞中T细胞免疫球蛋白粘液蛋白分子分子-4(TIM4)的表达。结果表明,在小鼠中诱导过敏原相关的结肠炎,如炎性细胞在结肠粘膜中的重渗透,小鼠体重丧失,肌释放酶的丧失增加,肿瘤坏死因子-α,白细胞介素-4,特异性IgE在结肠组织中。结肠炎群小鼠的结肠上皮阻隔功能显着损害,通过暴露结肠粘膜在USSing室中的CON粘膜模仿。在结肠炎小鼠的结肠粘膜中检测到TIM4(+)树突细胞的高频。树突细胞暴露于CT显着增加了TIM4的表达。我们得出结论,可以通过食物过敏原相关的免疫反应在小鼠结肠中诱导IBD样炎症。

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