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Oxidative-and-Nitrosative-Stress-and-Histone-Deace
Oxidative-and-Nitrosative-Stress-and-Histone-Deace
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Pdf Summary
The study investigates oxidative and nitrosative stress (O&NS) and histone deacetylase-2 (HDAC2) activity in chronic obstructive pulmonary disease (COPD) exacerbations, using an experimental model involving rhinovirus infection. The research reveals that rhinovirus infection significantly increases airway inflammation and O&NS markers in COPD patients, correlating these with viral load and inflammatory mediators. Additionally, macrophage HDAC2 activity decreased during exacerbations, inversely associated with viral load, inflammation, and nitrosative stress. The study also demonstrated that rhinovirus infection of monocytes induced nitrosylation of HDAC2, reducing its activity, highlighting potential therapeutic targets for COPD exacerbations.<br /><br />Nine COPD patients, ten smokers, and eleven nonsmokers were inoculated with rhinovirus, and various markers were measured pre- and post-infection. The research documented a significant increase in airway inflammation and O&NS markers post-infection in COPD subjects compared to control groups. Increased O&NS markers aligned with virus load and inflammation, while macrophage HDAC2 activity reduced, associating inversely with these factors. Furthermore, the in vitro model indicated that inhibiting O&NS lowered rhinovirus-induced inflammatory cytokines, suggesting therapeutic potential in targeting O&NS and impaired HDAC2 in managing COPD exacerbations.<br /><br />The findings underscore significant pathogenic mechanisms of COPD exacerbations involving O&NS, inflammation, and HDAC2 impairment, offering prospects for developing new therapies aimed at these processes. Future treatments could enhance HDAC2 activity, potentially improving the efficacy of corticosteroids and addressing corticosteroid resistance. However, studies with larger cohorts, including subjects with varying COPD severity, are necessary to reinforce these insights. The study emphasizes a detailed understanding of COPD exacerbations' molecular pathways, imperative for innovating effective preventive and therapeutic strategies.
Keywords
COPD
oxidative stress
nitrosative stress
HDAC2 activity
rhinovirus infection
airway inflammation
viral load
macrophage
therapeutic targets
corticosteroid resistance
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