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Activation of aryl hydrocarbon receptor by benzo[a]pyrene increases interleukin 33 expression and eosinophil infiltration in a mouse model of allergic airway inflammation.

苯并 [a] 芘激活芳香烃受体增加变应性气道炎症小鼠模型白细胞介素 33 表达和嗜酸性粒细胞浸润。

  • 影响因子:3.14
  • DOI:10.1002/jat.4017
  • 作者列表:"Tajima H","Tajiki-Nishino R","Watanabe Y","Kurata K","Fukuyama T
  • 发表时间:2020-06-18
Abstract

:We recently demonstrated that benzo[a]pyrene (BaP), the aryl hydrocarbon receptor (AhR) ligand, directly contributes to aggravation of cutaneous allergy in a mouse model of allergic dermatitis. The present study aimed to determine whether BaP-induced AhR activation results in development of airway inflammation. Initially, the potential for a direct relationship between BaP-induced AhR activation and airway inflammation was investigated in vivo, using a mouse model of type 2 helper T cell (Th2) hapten toluene-2,4-diisocyanate (TDI)-induced airway inflammation. Mice were orally administered BaP at 48, 24, and 4 h before the final allergen challenge. Oral administration of BaP showed a significant increase in lung inflammation and eosinophil infiltration. While expression of Th2 cytokines such as interleukin 4 (IL-4) and IL-13 was not affected by exposure to BaP, AhR activation significantly increased IL-33 expression. To confirm the in vivo results, in vitro experiments were performed using the human eosinophilic leukemia cell line (EOL-1), human bronchial epithelial cell line (BEAS-2B), and human lung adenocarcinoma epithelial cell line (A549). Results indicated that pre-treatment with BaP increased expression of IL-8 in house dust mite-activated EOL-1, BEAS-2B, and A549 cells. In addition, IL-33 levels in BEAS-2B cells were significantly increased after BaP exposure. Our findings indicated that BaP-induced AhR activation is involved in the pro-inflammatory response in respiratory allergy, and that this effect may be mediated by increased IL-33 expression and eosinophil infiltration.

摘要

: 我们最近证明,芳基烃受体 (AhR) 配体苯并 [a] 芘 (BaP) 直接有助于过敏性皮炎小鼠模型皮肤过敏的加重。本研究旨在确定 BaP 诱导的 AhR 激活是否导致气道炎症的发生。最初,使用 2 型辅助性 T 细胞 (Th2) 半抗原甲苯-2 的小鼠模型,在体内研究了 BaP 诱导的 AhR 活化与气道炎症之间直接关系的潜力,4-二异氰酸酯 (TDI) 诱导的气道炎症。小鼠在最终过敏原激发前 48 、 24 和 4 h 经口给予 BaP。口服 BaP 表现为肺部炎症和嗜酸性粒细胞浸润明显增加。而 Th2 细胞因子如白细胞介素 4 (IL-4) 和 IL-13 的表达不受暴露于 BaP 的影响,AhR 激活显著增加 IL-33 表达。为了证实体内结果,使用人嗜酸性粒细胞白血病细胞系 (EOL-1) 、人支气管上皮细胞系 (BEAS-2B) 进行体外实验,和人肺腺癌上皮细胞系 (A549)。结果表明,BaP 预处理可增加屋尘螨活化 IL-8 、 EOL-1 和 A549 细胞中 BEAS-2B 的表达。此外,BaP 暴露后 IL-33 细胞中 BEAS-2B 水平显著升高。我们的研究结果表明,BaP 诱导的 AhR 激活参与了呼吸道过敏的促炎症反应,这种作用可能是通过增加 IL-33 表达和嗜酸性粒细胞浸润介导的。

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影响因子:3.94
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DOI:10.1016/j.taap.2019.114847
作者列表:["Bernstein DM","Toth B","Rogers RA","Kling DE","Kunzendorf P","Phillips JI","Ernst H"]

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影响因子:4.04
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DOI:10.1042/BST20191010
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