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首页> 外文期刊>Clinical and experimental allergy : >Modulation of mucosal immunity in a murine model of food-induced intestinal inflammation.
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Modulation of mucosal immunity in a murine model of food-induced intestinal inflammation.

机译：食物诱导的肠道炎症的鼠模型中黏膜免疫的调节。

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BACKGROUND: Hypersensitivity or uncontrolled responses against dietary antigens can lead to inflammatory disorders like food allergy and current models reflect a variety of causes but do not reveal the detailed modulation of gut immunity in response to food antigens after breakdown in mucosal tolerance. OBJECTIVE: To develop and characterize a murine model for food-induced intestinal inflammation and to demonstrate the modulation of gut immune response by dietary allergenic antigens. METHODS: C57BL/6 mice were sensitized with peanut proteins, challenged with peanut seeds and their sera and gut segments were collected for subsequent analyses. RESULTS: Sensitization and challenged with peanut seeds led to alterations in gut architecture with inflammatory response characterized by oedema in lamina propria and cell infiltrate composed mainly by eosinophils, mast cells, phagocytes, natural killer and plasma cells, together with low percentage of gammadelta+ and CD4+CD25+Foxp3+ cells in Peyer's patches. These animals also presented high levels of specific IgE and IgG1 in sera and modulation of mucosal immunity was mediated by increased expression of GATA-3, IL-4, IL-13 and TNF-alpha in contrast to low IFN-gamma in the gut. CONCLUSION: A murine model for food-induced intestinal inflammation was characterized in which modulation of gut immunity occurs by peanut antigens in consequence of T-helper type 2 (Th2) allergic response and failure of regulatory mechanisms necessary for mucosa homeostasis, resembling food allergy. This work shed some light on the understanding of the pathogenesis of gastrointestinal disorders and intolerance in the gut and supports the development of therapies for food-related enteropathies like food allergy, focusing on gut-specific immune response.
机译：背景：对饮食抗原的超敏反应或不受控制的反应可导致炎症性疾病，如食物过敏，目前的模型反映了多种原因，但在粘膜耐受性下降后并未揭示对食物抗原的肠道免疫的详细调节。目的：建立和表征鼠源性食物引起的肠道炎症的鼠模型，并证明饮食中的过敏原抗原对肠道免疫应答的调节作用。方法：用花生蛋白致敏C57BL / 6小鼠，用花生种子攻击，并收集其血清和肠道片段进行后续分析。结果：花生种子敏化和攻击导致肠道结构改变，炎症反应以固有层水肿为特征，细胞浸润主要由嗜酸性粒细胞，肥大细胞，吞噬细胞，自然杀伤细胞和浆细胞组成，γ-δ+和CD4含量低Peyer贴片中的+ CD25 + Foxp3 +细胞。这些动物在血清中还表现出高水平的特异性IgE和IgG1，与肠道中低IFN-γ相比，GATA-3，IL-4，IL-13和TNF-α的表达增加介导了粘膜免疫的调节。结论：鼠类食物诱发肠道炎症的模型的特征在于，由于2型T辅助（Th2）过敏反应和粘膜稳态所需的调节机制失效，花生抗原调节了肠道免疫，类似于食物过敏。这项工作为了解胃肠道疾病和肠道不耐受的发病机理提供了一些启示，并支持针对与食物有关的肠病（如食物过敏）的治疗方法的开发，重点在于肠道特异性免疫反应。

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