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정치량 ( Chi Ryang Chung ),홍윤경 ( Yun Kyung Hong ),김소영 ( So Young Kim ),최영훈 ( Yung Hun Choi ),나영균 ( Young Gyun Na ),박승용 ( Seung Yong Park ),황정환 ( Heong Hwan Hwang ),문희 ( Hee Moon ),오호준 ( Ho Jun Oh ),이석 ( 전북대학교 의과학연구소 2005 全北醫大論文集 Vol.29 No.2
Background: An alteration in the balance between a T-helper type 2 cell (Th2) response and a T-helper type 1 cell (Th1) response may predispose to the development of bronchial asthma. IL-18 has an ability to promote both Th1 and Th2 responses depending on the surrounding cytokine environment. Reactive oxygen species (ROS) play a crucial role in the pathogenesis of airway inflammation and hyperresponsiveness. Objective: An aim of the present study was to determine the effect of ROS on the regulation of IL-18 expression. Methods: We used a C57BL/6 mouse model of allergic asthma to examine effects of antioxidants on the regulation of IL-18 expression. Our present study with ovalbumin (OVA)- induced murine model of asthma revealed that ROS production in cells from bronchoalveolar lavage (BAL) fluids was increased, and that administration of L-2-oxothiazolidine-4-carboxylic acid (OTC) or α-lipoic acid reduced the increased levels of ROS, the increased expression of IL-18 protein and mRNA, airway inflammation, and bronchial hyperresponsiveness. Our results also showed that antioxidants down-regulated a transcription factor, nuclear factor-kB (NF-kB) activity. Conclusion: These results indicate that antioxidants may inhibit LL-18 expression in asthma by inhibiting activity of NF-kB, and suggest that ROS regulate the LL-18 expression.