Abstract
The present study aims to investigate the immunomodulatory effects of essential oil from Chamaecyparis obtusa (EOCO) in an ovalbumin (OVA)-induced allergic rhinitis (AR) mouse model. BALB/c mice were intraperitoneally sensitized and stimulated with OVA. From day 22 to 35, 0.01% and 0.1% ECOC was intranasally administered 1 h before OVA stimulation. Nasal symptoms, as well as serum total and OVA-specific immunoglobulin (Ig) E levels, were measured. Interleukin (IL)-4, IL-10, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α levels in nasal lavage fluid (NLF) and their production by activated splenocytes were measured. Histological changes in the sinonasal mucosa were evaluated through hematoxylin and eosin and periodic acid-Schiff staining procedure. Th cytokines and their transcription factor mRNA expressions were determined using reverse-transcription polymerase chain reaction. Intranasal EOCO administration significantly suppressed allergic symptoms, OVA-specific IgE level, sinonasal mucosal inflammatory cell infiltration, and mucus-producing periodic acid-Schiff (PAS) positive cell count. EOCO also significantly inhibited IL-4, IL-10, and TNF-α levels in NLF and activated splenocytes. Th2 and Treg related cytokines and their transcription factors in sinonasal mucosa were significantly suppressed through intransal EOCO instillation. In conclusion, repetitive EOCO intranasal instillation showed anti-inflammatory and anti-allergic effects by suppressing nasal symptoms and inhibiting the production and expression of inflammatory mediators in the OVA-induced AR mouse model.
Highlights
Allergic rhinitis (AR) is the inflammation of the nasal mucosa induced by a specific immunoglobulin
Most AR treatment modalities are focused on symptomatic control with palliative effects, and allergic immunotherapy is the only potential curative therapy that influences the immunopathologic mechanism in developing nasal mucosal hypersensitivity [2]
Inflammatory mainlybytriggered by inflammatory mediators, such IL-4; as IL-6; and several other inflammatory mediators produced by inflammatory cells, such as mast cells, histamine; IL-4; IL-6; and several other inflammatory mediators produced by inflammatory cells, eosinophils, basophils, and T lymphocytes
Summary
Allergic rhinitis (AR) is the inflammation of the nasal mucosa induced by a specific immunoglobulin. E (IgE)-mediated hypersensitivity reaction against inhaled allergens, which involves Th2 immune responses. Immunologic interactions between epithelial cells, lymphocytes, mast cells, interleukin (IL)-4, IL-5, IL-13, and thymic stromal lymphopoietin (TSLP) are involved in AR [1]. Most AR treatment modalities are focused on symptomatic control with palliative effects, and allergic immunotherapy is the only potential curative therapy that influences the immunopathologic mechanism in developing nasal mucosal hypersensitivity [2]. Essential oils are volatile compounds produced by plants as a protective mechanism against harmful insects and microorganisms. Several essential oils contain active substances that exert anti-fungal, anti-oxidative, and anti-gastropathic activity [3,4].
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