Antioxidant down-regulates interleukin-18 expression in asthma

Sun Lee Kyung, Ri Kim So, Ju Park Seoung, Kyung-Hoon Min, Young Lee Ka, Mi Jin Sun, Hee Yoo Wan, Chul Lee Yong

Research output: Contribution to journalArticle

33 Citations (Scopus)

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. 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 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-κB (NF-κB), activity. These results indicate that antioxidants may reduce IL-18 expression in asthma by inhibiting the activity of NF-κB and suggest that ROS regulate the IL-18 expression.

Original languageEnglish
Pages (from-to)1184-1193
Number of pages10
JournalMolecular Pharmacology
Volume70
Issue number4
DOIs
Publication statusPublished - 2006 Sep 28
Externally publishedYes

    Fingerprint

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

Cite this

Kyung, S. L., So, R. K., Seoung, J. P., Min, K-H., Ka, Y. L., Sun, M. J., Wan, H. Y., & Yong, C. L. (2006). Antioxidant down-regulates interleukin-18 expression in asthma. Molecular Pharmacology, 70(4), 1184-1193. https://doi.org/10.1124/mol.106.024737