PT  - JOURNAL ARTICLE
AU  - Abraham Roos
AU  - Leif Bjermer
AU  - Martin Stampfli
AU  - Jonas Erjefält
TI  - Elevated IL-17A in very severe COPD is localized to mast cells and correlates with lung function decline
DP  - 2014 Sep 01
TA  - European Respiratory Journal
PG  - 1722
VI  - 44
IP  - Suppl 58
4099  - http://erj.ersjournals.com/content/44/Suppl_58/1722.short
4100  - http://erj.ersjournals.com/content/44/Suppl_58/1722.full
SO  - Eur Respir J2014 Sep 01; 44
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.