TY - JOUR T1 - Interleukin-18 levels in induced sputum of stable and exacerbated COPD patients JF - European Respiratory Journal JO - Eur Respir J VL - 44 IS - Suppl 58 SP - P848 AU - Ingvild Haaland AU - Marianne Aanerud AU - Solveig Tangedal AU - Louise J. Persson AU - Per S. Bakke AU - Tomas M. Eagan Y1 - 2014/09/01 UR - http://erj.ersjournals.com/content/44/Suppl_58/P848.abstract N2 - Background: The pro-inflammatory cytokine Interleukin-18 (IL-18) is increased in blood and sputum from COPD patients, and may be further upregulated through inflammasome activation during acute exacerbations of COPD (AECOPD). The role of IL-18 in AECOPD is however largely unknown.Aims:In this study, we aimed to compare levels of soluble IL-18 in induced sputum between healthy controls and stable COPD patients, between COPD patients with high and low exacerbation frequency, and between stable COPD and AECOPD.Methods: Induced sputum samples were collected from 43 healthy individuals, 253 stable COPD patients and 56 patients during AECOPD. Patients were recruited from Bergen COPD Cohort Study and Bergen COPD Exacerbation Study (aged 40-76, GOLD stage II-IV). IL-18 levels were measured by a bead-based immunoassay.Results: Induced sputum IL-18 levels were significantly higher in stable COPD patients compared to healthy controls (mean 11.3 vs 3.3 pg/ml; p<0.01), and in GOLD stage IV compared to II (mean 30.7 vs 8.5 pg/ml; p<0.01). Patients with frequent exacerbations (≥2/year) expressed higher IL-18 levels than low frequency exacerbators (<2/year), both in stable COPD (mean 15.8 vs 10.3 pg/ml) and AECOPD (mean 12.6 vs 9.3 pg/ml), although differences were not statistically significant. Finally, there was no difference in IL-18 levels between COPD patients at the stable state and during AECOPD (mean 11.3 vs 10.0 pg/ml; p=0.5).Conclusions: IL-18 is increased in induced sputum of COPD patients, with a tendency to elevated levels in patients with frequent exacerbations. The lack of difference in IL-18 levels between stable and exacerbated COPD suggests that AECOPD mechanisms are independent of IL-18 activation. ER -