Imperial College London
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DrSarahEssilfie-Quaye

Faculty of Medicine, National Heart & Lung Institute

Equality, Diversity and Inclusion Research Fellow.
 
 
 
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Contact

 

+44 (0)20 7594 2857s.essilfie-quaye Website

 
 
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Location

 

Faculty BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Footitt:2016:10.1378/chest.14-2637,
author = {Footitt, J and Mallia, P and Durham, AL and Ho, WE and Trujillo-Torralbo, MB and Telcian, AG and Del, Rosario A and Chang, C and Peh, HY and Kebadze, T and Aniscenko, J and Stanciu, L and Essilfie-Quaye, S and Ito, K and Barnes, PJ and Elkin, SL and Kon, OM and Wong, WS and Adcock, IM and Johnston, SL},
doi = {10.1378/chest.14-2637},
journal = {Chest},
pages = {62--73},
title = {Oxidative and Nitrosative Stress and Histone Deacetylase-2 Activity in Exacerbations of COPD.},
url = {http://dx.doi.org/10.1378/chest.14-2637},
volume = {149},
year = {2016}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - BACKGROUND: 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. METHODS: 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. RESULTS: 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, inflammatory markers, and nitrosative stress. Sputum macrophage HDAC2 activity pre-infection was inversely associated with sputum virus load and inflammatory markers during exacerbation. Rhinovirus infection of monocytes induced nitrosylation of HDAC2 and reduced HDAC2 activity; inhibition of O&NS inhibited rhinovirus-induced inflammatory cytokines. CONCLUSIONS: O&NS, airways inflammation, and impaired HDAC2 may be important mechanisms of virus-induced COPD exacerbations. Therapies targeting these mechanisms offer potential new treatments for COPD exacerbations.
AU  - Footitt,J
AU  - Mallia,P
AU  - Durham,AL
AU  - Ho,WE
AU  - Trujillo-Torralbo,MB
AU  - Telcian,AG
AU  - Del,Rosario A
AU  - Chang,C
AU  - Peh,HY
AU  - Kebadze,T
AU  - Aniscenko,J
AU  - Stanciu,L
AU  - Essilfie-Quaye,S
AU  - Ito,K
AU  - Barnes,PJ
AU  - Elkin,SL
AU  - Kon,OM
AU  - Wong,WS
AU  - Adcock,IM
AU  - Johnston,SL
DO  - 10.1378/chest.14-2637
EP  - 73
PY  - 2016///
SN  - 1931-3543
SP  - 62
TI  - Oxidative and Nitrosative Stress and Histone Deacetylase-2 Activity in Exacerbations of COPD.
T2  - Chest
UR  - http://dx.doi.org/10.1378/chest.14-2637
UR  - http://hdl.handle.net/10044/1/30043
VL  - 149
ER  -
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