Oxidative and Nitrosative Stress and Histone Deacetylase-2 Activity in Exacerbations of COPD.

Chest
Joseph FootittSebastian L Johnston

Abstract

Respiratory virus infections are commonly associated with COPD exacerbations, but little is known about the mechanisms linking virus infection to exacerbations. Pathogenic mechanisms in stable COPD include oxidative and nitrosative stress and reduced activity of histone deacetylase-2 (HDAC2), but their roles in COPD exacerbations is unknown. We investigated oxidative and nitrosative stress (O&NS) and HDAC2 in COPD exacerbations using experimental rhinovirus infection. Nine subjects with COPD (Global Initiative for Chronic Obstructive Lung Disease stage II), 10 smokers, and 11 nonsmokers were successfully infected with rhinovirus. Markers of O&NS-associated cellular damage, and inflammatory mediators and proteases were measured in sputum, and HDAC2 activity was measured in sputum and bronchoalveolar macrophages. In an in vitro model, monocyte-derived THP-1 cells were infected with rhinovirus and nitrosylation and activity of HDAC2 was measured. Rhinovirus infection induced significant increases in airways inflammation and markers of O&NS in subjects with COPD. O&NS markers correlated with virus load and inflammatory markers. Macrophage HDAC2 activity was reduced during exacerbation and correlated inversely with virus load, infla...Continue Reading

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Citations

Dec 19, 2015·Expert Review of Respiratory Medicine·Neil C Thomson
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Jul 29, 2021·American Journal of Respiratory and Critical Care Medicine·Faisal KamalGeorge B Hanna

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Methods Mentioned

BETA
enzyme-linked immunosorbent assay
Immunoprecipitation
biopsies

Software Mentioned

GraphPad
GraphPad Prism

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