호흡기 상피세포에서 IL-1b에 의해 유발되는 MUC2/MUC5AC 유전자 발현 및 점액분비에 있어서 Budesonide의 억제작용

김용대; 조중석; 장근영; 신재흔; 송시연; 윤석근

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자료유형: 학술저널

저자정보: 김용대 조중석 장근영 신재흔 송시연 윤석근

저널정보: 대한이비인후과학회 대한이비인후-두경부외과학회지 대한이비인후과학회지 두경부외과학 제45권 제9호

발행연도: 2002.1

수록면: 873 - 877 (5page)

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Background and Objectives：Mucus hypersecretion is a hallmark of many respiratory inflammatory diseases such as asthma, bronchitis and sinusitis. While the current therapeutic pharmacological approaches to reducing mucus hypersecretion are limited, clinical studies have suggested that glucocorticoids reduce mucus secretion in patients with airway disease. However, the effect of glucocorticoids on mucus hypersecretion is not clear. Recently, we observed that IL-1β induces MUC2 gene expression and mucin secretion in a previous experiment. This study was designed to investigate the effects of budesonide on the IL-1β-mediated MUC2/5AC genes expression and mucin secretion. Materials and Method：We observed the steady state mRNA level of MUC2/5AC genes using RT-PCR and mucin protein using immunoassay method in cultured human airway NCI-H292 epithelial cells. Results：Budesonide attenuated IL-1β-mediated MUC2/5AC gene expression as well as mucin secretion. The attenuated effect of budesonide was in a dose-dependent pattern. This attenuated effect of budesonide was blocked by glucocorticoid receptor antagonist, RU-486. Conclusion：This result suggests that budesonide suppresses the IL-1β-mediated MUC2/5AC genes expression and mucin secretion via blockage of glucocorticoid receptor. (Korean J Otolaryngol 2002;45:873-7)

#Interleukin-1β·MUC2·MUC5AC·점액· Budesonide. #Interleukin-1b·MUC2·MUC5AC·Mucin·Budesonide.

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