Received for publication March 21, 2006.
Revised June 30, 2006.
Accepted for publication July 5, 2006.

Antioxidant down-regulates IL-18 expression in asthma

Abstract

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. 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 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 activity of NF-B, and suggest that ROS regulate the IL-18 expression.

Key words: Interleukins, NFkappaB, Oxidative stress/antioxidants, Oxidative stress

This article has been cited by other articles:

				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]