QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: mol.106.024737v1 70/4/1184    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lee, K. S. Articles by Lee, Y. C. Search for Related Content PubMed PubMed Citation Articles by Lee, K. S. Articles by Lee, Y. C.

Antioxidant Down-Regulates Interleukin-18 Expression in Asthma

Department of Internal Medicine, Airway Remodeling Laboratory, Research Center for Allergic Immune Diseases, Chonbuk National University Medical School, Jeonju, South Korea (K.S.L., S.R.K., S.J.P., K.H.M., K.Y.L., S.M.J., Y.C.L.); and Department of Internal Medicine, Chonbuk National University Medical School, Jeonju, South Korea (W.H.Y.)

An alteration in the balance between a T-helper type 2 cell (Th2) response and a Th1 response may predispose to the development of bronchial asthma. Interleukin-18 (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. Recent studies have demonstrated that antioxidants are able to reduce airway inflammation and hyperreactivity in animal models of asthma. In this study, we used a C57BL/6 mouse model of allergic asthma to examine the effects of antioxidants on the regulation of IL-18 expression. Our present study with ovalbumin-induced murine model of asthma revealed that ROS production in cells from bronchoalveolar lavage fluids was increased and that administration of L-2-oxothiazolidine-4-carboxylic acid or -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-B (NF-B), activity. These results indicate that antioxidants may reduce IL-18 expression in asthma by inhibiting the activity of NF-B and suggest that ROS regulate the IL-18 expression.

Address correspondence to: Dr. Yong Chul Lee, Department of Internal Medicine, Chonbuk National University Medical School, San 2-20, Geumamdong, Deokjin-gu, Jeonju, Jeonbuk 561-180, South Korea. E-mail: leeyc{at}chonbuk.ac.kr

This article has been cited by other articles:

				C. F. Fortin, T. Ear, and P. P. McDonald Autocrine role of endogenous interleukin-18 on inflammatory cytokine generation by human neutrophils FASEB J, January 1, 2009; 23(1): 194 - 203. [Abstract] [Full Text] [PDF]

				J. J. Ryan, H. R. Bateman, A. Stover, G. Gomez, S. K. Norton, W. Zhao, L. B. Schwartz, R. Lenk, and C. L. Kepley Fullerene Nanomaterials Inhibit the Allergic Response J. Immunol., July 1, 2007; 179(1): 665 - 672. [Abstract] [Full Text] [PDF]