Effect of 1.8-Cineole in Dermatophagoides pteronyssinus-Stimulated Bronchial Epithelial Cells and Mouse Model of Asthma

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  • Lee Hyun-Seung
    Laboratory of Allergy and Clinical Immunology, Dongguk University Ilsan Hospital Medical Research Center
  • Park Da-Eun
    Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center
  • Song Woo-Jung
    Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center
  • Park Heung-Woo
    Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center
  • Kang Hye-Ryun
    Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center
  • Cho Sang-Heon
    Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center
  • Sohn Seong-Wook
    Laboratory of Allergy and Clinical Immunology, Dongguk University Ilsan Hospital Medical Research Center Department of Internal Medicine, Dongguk University Ilsan Hospital

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  • Effect of <i>1.8-Cineole</i> in <i>Dermatophagoides pteronyssinus</i>-Stimulated Bronchial Epithelial Cells and Mouse Model of Asthma

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1.8-Cineole (eucalyptol) is a phytoncide, a volatile organic compound derived from plants. Phytoncides are known to have an anti-inflammatory effect. However, the effects of 1.8-cineole in house dust mite (HDM)-stimulated bronchial epithelial cells are poorly understood. The objective of this study was to assess the effect of 1.8-cineole in HDM-stimulated bronchial epithelial cells and in the HDM-induced murine asthma model. The purpose of the present study is to evaluate the anti-inflammatory effects and mechanism of 1.8-cineole action in HDM-induced airway inflammation. Human bronchial epithelial cells (HBECs) were cultured with Dermatophagoides pteronyssinus (Der p) and 1.8-cineole. Cytokine protein levels, phosphorylation of protein kinases, and intracellular Toll-like receptor 4 (TLR4) expressions were measured. In the murine model, BALB/C mice were sensitized with Der p and were exposed to Der p via intranasal route during the challenge period. 1.8-Cineole was given by inhalation 6 h before the each challenge. Treatment with 1.8-cineole inhibited the Der p-induced cytokine protein expression, phosphorylation of p38 mitogen-activated protein kinase (MAPK) and Akt and intracellular TLR4 expression in HBECs. In the Der p-induced mouse model, airway hyper-responsiveness (AHR) and the number of eosinophils in bronchoalveolar lavage fluid (BALF) was also significantly reduced by 1.8-cineole treatment. The treatment of 1.8-cineole inhibited the increased production of interleukin (IL)-4, IL-13 and IL-17A in BALF after Der p challenge. These results suggest that 1.8-cineole suppresses Der p-induced IL-8, IL-6 and granulocyte macrophage-colony stimulating factor (GM-CSF) production in HBECs. Finally, we confirmed that 1.8-cineole decreases AHR and eosinophilic airway inflammation in Der p-induced asthma mice.

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