Cell & Molecular Biology Program Event
Mr. James Nolin
Cellular and Molecular Biology
University of Vermont
Redox-based control of inflammatory signaling in airway epithelial cells
Tuesday January 29th, 2013
Asthma is a chronic inflammatory disease affecting over 300 million people worldwide. An emerging player in the pathogenesis of asthma is the pro-inflammatory cytokine, Interleukin-17 (IL-17).
Stimulation of airway epithelial cells with IL-17 induces NF-kB activity, contributing to the production of pro-inflammatory mediators, resulting in abundant inflammation in the airways. Recent discoveries in our laboratory have demonstrated the importance of the enzyme Glutaredoxin 1 (Grx1) and the redox-dependent post-translational modification, S-glutathionylation, in controlling downstream IL-17-induced gene expression. Under physiological conditions, Grx1 acts to deglutathionylate NF-?B, restoring functional activity. Knockdown of Grx1 leads to a decrease in pro-inflammatory mediator production as well as an increase in S-glutathionylation.
Taken together, our data suggest a novel mode of regulation in IL-17-induced inflammation.