Chamaecyparis obtusa Essential Oil Inhibits House Dust Mite Induced Nasal Epithelial Cell Activation and Immune Responses

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  • Shin Seung-Heon
    Department of Otorhinolaryngology-Head and Neck Surgery, School of Medicine, Catholic University of Daegu
  • Ye Mi-Kyung
    Department of Otorhinolaryngology-Head and Neck Surgery, School of Medicine, Catholic University of Daegu
  • Chae Mi-Hyun
    Department of Otorhinolaryngology-Head and Neck Surgery, School of Medicine, Catholic University of Daegu
  • Lee Dong-Won
    Department of Otorhinolaryngology-Head and Neck Surgery, School of Medicine, Catholic University of Daegu

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  • <i>Chamaecyparis obtusa</i> Essential Oil Inhibits House Dust Mite Induced Nasal Epithelial Cell Activation and Immune Responses

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<p>Essential oils extracted from plants contain protective volatile compounds and are known to processes antibacterial, antifungal, anti-oxidative, and anti-inflammatory effects. This study was conducted to explore the immunomodulatory effects of essential oil extracted from Chamaecyparis obtusa (EOCO) on house dust mite-induced mucosal inflammation. Cultured primary nasal epithelial cells were stimulated with Dermatophagoides pteronyssinus (DP), and Dermatophagoides farina (DF) for 48 h. The production of interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP) was measured by enzyme-linked immunosorbent assay, and the expression levels of nuclear factor (NF)-κB, activator protein (AP)-1, and mitogen-activated protein kinase (MAPK) were determined by western blot analysis. To examine the effect of EOCO on the production of chemical mediators and the expression of transcription factors, epithelial cells were pretreated with EOCO for 1 h before stimulation. Peripheral blood mononuclear cells (PBMCs) were cultured in nasal epithelial cell conditioned media (NECM) for 72 h, after which the levels of IL-5, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α were measured. DP and DF enhanced the production of IL-25, IL-33, and TSLP, and EOCO pretreatment inhibited their production from nasal epithelial cells. EOCO pretreatment also significantly suppressed the expression of NF-κB and AP-1. NECM induced the production of IL-5, IFN- γ, and TNF-α from PBMCs, and only TNF-α production was significantly inhibited by EOCO pretreatment. EOCO pretreatment inhibited the DP and DF induced nasal epithelial cell derived cytokine production and TNF-α production from PBMCs. These results indicate the potential value of EOCO in the treatment of airway inflammatory or immunological diseases.</p>

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