Neutrophil degranulation responses in exacerbators and non-exacerbators of COPD

Introduction Neutrophilic inflammation, particularly from proteinases such as neutrophil elastase is implicated in the pathogenesis of COPD (Thorax 2006; 61: 250). We compared unstimulated and stimulated production of neutrophil elastase in people suffering >2 exacerbations, needing oral steroids or hospital attendance in the last 12 months and those having no exacerbations. Methods Subjects: people with COPD (Stage 3-4), prescribed optimal medical therapy and all ex-smokers (eCO<10ppm). Unstimulated and stimulated (bacterial lipopolysaccharide; 840-15, Sigma, UK) neutrophil-specific elastase production was determined with a commercially available enzyme-linked immunosorbent assay (Merck, Germany) from plasma and spontaneous sputum. Results Clinical characteristics and neutrophil-specific elastase concentrations   Frequent exacerbators (N = 36) Non-exacerbators (N = 20) p-value Age (years) 66 ± 8 70 ± 8 0.16 FEV1% predicted 44 ± 17 43 ± 17 0.89 Unstimulated plasma elastase μg/L 433 ± 643 695 ± 854 0.09 Stimulated plasma elastase μg/L 2674 ± 1465 3452 ± 2462 0.37 Unstimulated sputum elastase μg/L 21 ± 31 66 ± 107 0.08 Stimulated sputum elastase μg/L 37 ± 43 13 ± 32 0.02 Data presented as mean ± standard deviation Conclusion Frequent exacerbators have heightened elastase release in response to bacterial stimulation in sputa and a tendency for lower neutrophil-specific elastase concentration at rest in both plasma and sputa compared to non-exacerbators.