首页 | 本学科首页   官方微博 | 高级检索  
   检索      


Thioredoxin suppresses airway hyperresponsiveness and airway inflammation in asthma
Authors:Ichiki Hiroko  Hoshino Tomoaki  Kinoshita Takashi  Imaoka Haruki  Kato Seiya  Inoue Hiromasa  Nakamura Hajime  Yodoi Junji  Young Howard A  Aizawa Hisamichi
Institution:Department of Internal Medicine 1, Kurume University School of Medicine, Kurume, Japan.
Abstract:Thioredoxin (TRX) is a 12-kDa redox (reduction/oxidation)-active protein that has a highly conserved site (-Cys-Gly-Pro-Cys-) and scavenges reactive oxygen species. Here we examined whether exogenously administered TRX modulated airway hyperresponsiveness (AHR) and airway inflammation in a mouse asthma model. Increased AHR to inhaled acetylcholine and airway inflammation accompanied by eosinophilia were observed in OVA-sensitized mice. Administration of wild-type but not 32S/35S mutant TRX strongly suppressed AHR and airway inflammation, and upregulated expression of mRNA of several cytokines (e.g., IL-1alpha, IL-1beta, IL-1 receptor antagonist, and IL-18) in the lungs of OVA-sensitized mice. In contrast, TRX treatment at the time of OVA sensitization did not improve AHR or airway inflammation in OVA-sensitized mice. Thus, TRX inhibited the asthmatic response after sensitization, but did not prevent sensitization itself. TRX and redox-active protein may have clinical benefits in patients with asthma.
Keywords:Asthma  Thioredoxin  Redox  Airway hyperresponsiveness  Airway inflammation  IL-1  IL-18
本文献已被 ScienceDirect PubMed 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号