RT Journal Article SR Electronic T1 Elevated IL-17A in very severe COPD is localized to mast cells and correlates with lung function decline JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP 1722 VO 44 IS Suppl 58 A1 Abraham Roos A1 Leif Bjermer A1 Martin Stampfli A1 Jonas Erjefält YR 2014 UL http://erj.ersjournals.com/content/44/Suppl_58/1722.abstract AB Escalation and progression of chronic obstructive pulmonary disease (COPD) is poorly understood. Interleukin (IL)-17A plays a complex role in immunity and is increased in peripheral lung tissue of mild/moderate COPD and in the bronchial mucosa of severe COPD, suggesting a potential role in pathogenesis. The expression of IL-17A has, however, not been determined in very severe COPD. We hypothesized that the expression of IL-17A is increased in peripheral lung tissue of very severe COPD, and is associated with lung function decline.Automated immunodetection of IL-17A and cell specific markers was performed in lung tissue specimens collected from patients with GOLD stage I-IV COPD, as well as from smoking and never-smoking controls. Expression of immunoreactivity was quantified using digital image analysis.Increased expression of IL-17A was observed in COPD compared to smoking and never-smoking controls, and expression of IL-17A correlated with lung function decline. Further analysis revealed that IL-17A was only significantly elevated in severe-very severe COPD (GOLD III/IV), compared to asymptomatic never-smokers as well as current smokers. While small a proportion of CD3+ T cells expressed IL-17A in very severe COPD, the majority of IL-17A+ cells were identified as tryptase+ mast cells.The increased expression of IL-17A in the peripheral lung of patients with advanced COPD correlates with lung function decline and is suggestive of a potential role in disease progression. Furthermore, IL-17A was foremost localized to mast cells underscoring a role of this cell type in the immunopathology of COPD.