title: Effect of 1.8-Cineole in Dermatophagoides pteronyssinus-Stimulated Bronchial Epithelial Cells and Mouse Model of Asthma.
abstract: 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.
authors.affiliation: Laboratory of Allergy and Clinical Immunology, Dongguk University Ilsan Hospital Medical Research Center.
authors.forename: Hyun-Seung
authors.initials: HS
authors.lastname: Lee
authors.forename: Da-Eun
authors.initials: DE
authors.lastname: Park
authors.forename: Woo-Jung
authors.initials: WJ
authors.lastname: Song
authors.forename: Heung-Woo
authors.initials: HW
authors.lastname: Park
authors.forename: Hye-Ryun
authors.initials: HR
authors.lastname: Kang
authors.forename: Sang-Heon
authors.initials: SH
authors.lastname: Cho
authors.forename: Seong-Wook
authors.initials: SW
authors.lastname: Sohn
mesh_terms: D000818:Animals; D001249:Asthma / Q000097:blood / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002460:Cell Line; D002470:Cell Survival; D003511:Cyclohexanols / Q000494:pharmacology* / Q000627:therapeutic use*; D016207:Cytokines / Q000378:metabolism; D040002:Dermatophagoides pteronyssinus; D004195:Disease Models, Animal; D004804:Eosinophils / Q000166:cytology; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism; D000077591:Eucalyptol; D005260:Female; D006801:Humans; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008807:Mice, Inbred BALB C; D039821:Monoterpenes / Q000494:pharmacology* / Q000627:therapeutic use*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D012130:Respiratory Hypersensitivity / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D020545:Respiratory Mucosa / Q000187:drug effects / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D003511:Cyclohexanols; D016207:Cytokines; D039821:Monoterpenes; D051197:Toll-Like Receptor 4; D051057:Proto-Oncogene Proteins c-akt; D048051:p38 Mitogen-Activated Protein Kinases; D000077591:Eucalyptol