Asthma Research Today is a free monthly online journal that collates and summarizes the latest research about Asthma, including details on symptoms, diagnosis, treatment, causes, medications.

Thioredoxin suppresses airway hyperresponsiveness and airway inflammation in asthma.

Ichiki H, Hoshino T, Kinoshita T, Imaoka H, Kato S, Inoue H, Nakamura H, Yodoi J, Young HA, Aizawa H

Department of Internal Medicine 1, Kurume University School of Medicine, Kurume, Japan.

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.

Published 1 August 2005 in Biochem Biophys Res Commun, 334(4): 1141-8.
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