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烘烤花生过敏原 Ara h 3 蛋白对 Caco-2 细胞致敏的影响。

Effect of roasted peanut allergen Ara h 3 protein on the sensitization of Caco-2 cells.

机构信息

School of Life Sciences, Shanghai University, Shanghai, China.

School of Medicine, Shanghai University, Shanghai, China.

出版信息

J Sci Food Agric. 2021 Oct;101(13):5325-5336. doi: 10.1002/jsfa.11180. Epub 2021 Mar 26.

DOI:10.1002/jsfa.11180
PMID:33650104
Abstract

BACKGROUND

Roasted peanut is widely loved as a kind of food with rich taste. However, peanut allergy is one of the major threats to human health, which affects about 5% of children and 1.4-2% of adults in the world.

RESULTS

To evaluate the sensitization mechanism of peanut allergen Ara h 3, Caco-2 cells as the model, which has the similar structure and function to differentiated small intestinal epithelial cells. Compared with Ara h 3-raw (purified from raw peanut) group, more significant results such as the inhibited Caco-2 cell viability and proliferation, the increased secretion of reactive oxygen species (ROS) and the decreased transepithelial electrical resistance were obtained in Ara h 3-roasted (purified from roasted peanut) group. Accordingly, oxidative stress and NF-κB signaling pathway were more imbalanced, which lead to the increased of thymic stromal lymphopoietin (TSLP), interleukin 6 (IL-6), IL-8 and monocyte chemotactic protein 1 (MCP-1). Then, the gene expression of tight junction proteins ZO-1, occludin and JAM-1 were reduced, which proved that the integrity of the Caco-2 monolayer barrier is severely damaged.

CONCLUSION

These finding identify the mechanisms of the allergenicity of roasted peanut allergy proteins are probably associated with intestinal uptake and cytokine dependent allergies. The aggravated allergic reaction might be caused by the increment of TSLP, IL-6, IL-8 and MCP-1 due to the activated NF-κB signaling pathway, and the enhanced transport of Ara h 3-roasted protein by Caco-2 monolayer. © 2021 Society of Chemical Industry.

摘要

背景

烤花生作为一种口感丰富的食品而深受人们喜爱。然而,花生过敏是人类健康的主要威胁之一,影响全球约 5%的儿童和 1.4-2%的成年人。

结果

为了评估花生过敏原 Ara h 3 的致敏机制,我们以 Caco-2 细胞为模型,该细胞具有与分化的小肠上皮细胞相似的结构和功能。与 Ara h 3-raw(从生花生中纯化)组相比,在 Ara h 3-roasted(从烤花生中纯化)组中获得了更显著的结果,例如 Caco-2 细胞活力和增殖受到抑制、活性氧(ROS)分泌增加和跨上皮电阻降低。相应地,氧化应激和 NF-κB 信号通路更加失衡,导致胸腺基质淋巴细胞生成素(TSLP)、白细胞介素 6(IL-6)、IL-8 和单核细胞趋化蛋白 1(MCP-1)增加。然后,紧密连接蛋白 ZO-1、occludin 和 JAM-1 的基因表达减少,这证明了 Caco-2 单层屏障的完整性受到严重破坏。

结论

这些发现表明,烤花生过敏蛋白的变应原性机制可能与肠道摄取和细胞因子依赖的过敏有关。由于 NF-κB 信号通路的激活,TSLP、IL-6、IL-8 和 MCP-1 的增加,以及 Ara h 3-roasted 蛋白通过 Caco-2 单层的增强转运,可能导致过敏反应加剧。 © 2021 英国化学学会。

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