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

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  • Hitoshi Tajima
    Toxicology Division Institute of Environmental Toxicology Ibaraki Japan
  • Risako Tajiki‐Nishino
    Toxicology Division Institute of Environmental Toxicology Ibaraki Japan
  • Yuko Watanabe
    Toxicology Division Institute of Environmental Toxicology Ibaraki Japan
  • Keigo Kurata
    Institute of Tokyo Environmental Allergy, ITEA Inc. Tokyo Japan
  • Tomoki Fukuyama
    Toxicology Division Institute of Environmental Toxicology Ibaraki Japan

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<jats:title>Abstract</jats:title><jats:p>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.</jats:p>

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