Thioredoxin suppresses airway hyperresponsiveness and airway inflammation in asthma

Biochem Biophys Res Commun. 2005 Sep 9;334(4):1141-8. doi: 10.1016/j.bbrc.2005.07.007.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Asthma / chemically induced
  • Asthma / immunology
  • Asthma / pathology*
  • Asthma / prevention & control*
  • Female
  • Injections, Intraperitoneal
  • Mice
  • Mice, Inbred BALB C
  • Ovalbumin
  • Pneumonia / chemically induced
  • Pneumonia / immunology
  • Pneumonia / pathology*
  • Pneumonia / prevention & control*
  • Respiratory Hypersensitivity / chemically induced
  • Respiratory Hypersensitivity / immunology
  • Respiratory Hypersensitivity / pathology
  • Respiratory Hypersensitivity / prevention & control
  • Thioredoxins / administration & dosage*
  • Treatment Outcome

Substances

  • Thioredoxins
  • Ovalbumin