Given this systemic signature of enhanced neutrophil protease activity during COPD exacerbation, established evidence of pathological hypoxia during inflammation, and our previous results demonstrating hypoxia-augmented NE release from GM-CSF (granulocyte–macrophage colony–stimulating factor)–primed neutrophils (2), we next examined the ability of inflammatory mediators relevant to COPD and hypoxia to influence neutrophil degranulation. This evidence concerns the gene CSF2 and chronic obstructive pulmonary disease.