당질스테로이드를 이용한 진균에 의한 비강상피세포의 활성화 억제

당질스테로이드·Alternaria·비강상피세포·Protease-activated receptor. Background and Objectives:Airway epithelial cells contribute to the pathogenesis of air disease by their interaction with inhalant pathogenic extracts. Airborne fungi interact with nasal epithelial cell and enhance the production of inflammatory...

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Veröffentlicht in:Journal of rhinology 2006, 13(1), , pp.32-36
1. Verfasser: 신승헌
Format: Artikel
Sprache:kor
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Zusammenfassung:당질스테로이드·Alternaria·비강상피세포·Protease-activated receptor. Background and Objectives:Airway epithelial cells contribute to the pathogenesis of air disease by their interaction with inhalant pathogenic extracts. Airborne fungi interact with nasal epithelial cell and enhance the production of inflammatory cytokines. Glucocorticosteroids (GCs) have been used therapeutically for nasal polyps and allergic disease with potent anti-inflammatory effects. The purpose of this study was to investigate the inhibitory effect of GCs on fungi induced nasal epithelial cell activation. Materials and Methods:The epithelial cells of nasal polyps were obtained from patients and stimulated with Alternaria. To evaluate the anti-inflammatory effects of GCs, Alternaria was pretreated with GCs (triamcinolone, dexamethasone, and budesonide) and cultured with epithelial cells. Interleukin-8 (IL-8) and granulocyte-macrophage colony stimulating factor (GM-CSF) were measured to determine the activation of epithelial cells. Reverse transcriptase-polymerase chain reaction (RT-PCR) test for protease-activated receptors (PARs) mRNA expression in nasal epithelial cells were performed. Results:Alternaria enhanced the production of IL-8 and GM-CSF from nasal epithelial cells. GCs inhibited the activation of nasal epithelial cells, but the PAR2 and PAR3 mRNA expression were not suppressed by GCs. Conclusion:These data suggest that GCs inhibit the production of chemical mediators by Alternaria, but anti-inflammatory effect of GCs are not associated with PARs. KCI Citation Count: 0
ISSN:1229-1498
2384-4361