Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by chronic irreversible inflammation and progressive decline in lung function. While smoking and other environmental agents (e.g., air pollutants) are common causes of COPD, the major challenges in managing this condition are the persistent inflammation and functional deterioration which are not reversed by removal of precipitating agents (e.g., smoking cessation) or treatment with anti-inflammatory agents. We hypothesized that the reactivation of latent CMV infection may trigger expansion of pro-inflammatory CD28null T cells and hence promote sysmetic inflammation in patients with COPD. This study presents novel data showing increased levels of CMV-reactive IgM and IgG in COPD patients compared to controls. This paralleled observed increases in markers of sytemic inflammation ex vivo and proportions of circulating CD28null T cells. This mechanism may explain the persistent inflammation in COPD patients.

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