RT Journal Article
SR Electronic
T1 Antioxidant Down-Regulates Interleukin-18 Expression in Asthma
JF Molecular Pharmacology
JO Mol Pharmacol
FD American Society for Pharmacology and Experimental Therapeutics
SP 1184
OP 1193
DO 10.1124/mol.106.024737
VO 70
IS 4
A1 Kyung Sun Lee
A1 So Ri Kim
A1 Seoung Ju Park
A1 Kyung Hoon Min
A1 Ka Young Lee
A1 Sun Mi Jin
A1 Wan Hee Yoo
A1 Yong Chul Lee
YR 2006
UL http://molpharm.aspetjournals.org/content/70/4/1184.abstract
AB 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. The American Society for Pharmacology and Experimental Therapeutics