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Copyright ©ERS Journals Ltd 2006
Oxidative stress and redox regulation of lung inflammation in COPD
1 Dept of Environmental Medicine, Division of Lung Biology and Disease, University of Rochester Medical Center, Rochester, NY, USA, 2 Airway Disease Section, National Heart and Lung Institute, Imperial College School of Medicine, London, UK.
CORRESPONDENCE: I. Rahman, Dept of Environmental Medicine, Division of Lung Biology and Disease, University of Rochester Medical Center, MRBX 3.11106, 601 Elmwood Ave., Box 850, Rochester, NY 14642, USA. Fax: 1 5855060239. E-mail: irfan_rahman{at}urmc.rochester.edu
Keywords: Chronic obstructive pulmonary disease, glucocorticoids, glutathione, histone deacetylase, nuclear factor-
B, reactive oxygen species
Received: May 5, 2005
Accepted February 10, 2006
Reactive oxygen species, either directly or via the formation of lipid peroxidation products, may play a role in enhancing inflammation through the activation of stress kinases (c-Jun activated kinase, extracellular signal-regulated kinase, p38) and redox-sensitive transcription factors, such as nuclear factor (NF)-
Emerging evidence suggests the glutathione redox couple may entail dynamic regulation of protein function by reversible disulphide bond formation on kinases, phosphatases and transcription factors. Oxidative stress also inhibits histone deacetylase activity and in doing so further enhances inflammatory gene expression and may attenuate glucocorticoid sensitivity.
The antioxidant/anti-inflammatory effects of thiol molecules (glutathione, N-acetyl-L-cysteine and N-acystelyn, erdosteine), dietary polyphenols (curcumin-diferuloylmethane, cathechins/quercetin and reserveratol), specific spin traps, such as
Thus, oxidative stress regulates both key signal transduction pathways and histone modifications involved in lung inflammation. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in chronic obstructive pulmonary disease are also discussed.
B and activator protein-1. This results in increased expression of a battery of distinct pro-inflammatory mediators. Oxidative stress activates NF-B-mediated transcription of pro-inflammatory mediators either through activation of its activating inhibitor of B-
kinase or the enhanced recruitment and activation of transcriptional co-activators. Enhanced NF-B-co-activator complex formation results in targeted increases in histone modifications, such as acetylation leading to inflammatory gene expression. -phenyl-N-tert-butyl nitrone, a catalytic antioxidant (extracellular superoxide dismutase (SOD) mimetic, SOD mimetic M40419 and SOD, and catalase manganic salen compound, eukarion-8), porphyrins (AEOL 10150 and AEOL 10113) and theophylline have all been shown to play a role in either controlling NF-B activation or affecting histone modifications with subsequent effects on inflammatory gene expression in lung epithelial cells.
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