Introduction:
COPD is a progressive inflammatory lung disease with multiple systemic complications, including pulmonary hypertension and cardiovascular disease (independent of smoking status). Airway neutrophilia correlates with disease severity and neutrophil elastase has been implicated in COPD pathogenesis, but precise mechanisms of tissue damage are unknown. Inflamed COPD airways are profoundly hypoxic, and this tissue hypoxia may synergise with inflammatory cytokines to promote a destructive neutrophil phenotype with enhanced potential for tissue damage.