Many airway diseases including COPD, bronchiectasis, bronchiolitis, and cystic fibrosis are characterized by neutrophil infiltration of the airway wall. Likewise, neutrophils are believed to play a fundamental role in acute lung injury (ALI)/ARDS and many of the vasculitides. Considerable observational and experimental data support an association between neutrophils and the severity and progression of the above airways diseases; for example, in COPD neutrophils have been shown to be the most abundant inflammatory cell present in the bronchial wall, bronchial lumen, lung parenchyma, and submucosal glands,1 and the intensity of the airway and blood neutrophilia, in smokers and ex-smokers, correlates with the rate of decline in FEV1.2 In addition, neutrophils have been demonstrated in bronchial biopsy samples obtained taken during the allergen-induced late asthmatic response,3 and a strong association has now been established between airway neutrophilia and severe asthma, corticosteroid-resistant asthma, asthma exacerbations, acute fatal asthma, and certain forms of occupational asthma (see Macdowell and Peters4). Where measured, neutrophil numbers in asthma correlate with markers of neutrophil degranulation, implying that these cells are also activated. While in severe asthma, eosinophils and neutrophils are often found together, neutrophils may gradually replace eosinophils in proportion to the severity and/or duration of the disease, perhaps reflecting the ability of corticosteroids to induce eosinophil apoptosis while inhibiting this process in neutrophils.5 In addition to the direct effects of proteases on airway epithelia, neutrophil elastase has been shown to stimulate transforming growth factor-β release from airway smooth-muscle cells,6 suggesting a potential role in airway remodeling.