Abstract

Chronic obstructive pulmonary disease (COPD) is an inflammatory condition with constantly increasing mortality rates. Interleukin (IL)-33 and its decoy receptor, soluble suppression of tumorigenicity 2 (sST2), play a central role in the inflammatory response during infection. sST2 was suggested as a factor in the pathogenesis of COPD and emerged as a predictor of mortality in other non-communicable diseases. The role of sST2 as a predictor of mortality remains unclear in COPD yet. In this cohort study, we measured circulating concentrations of IL-33 and sST2 in the serum of patients with stable COPD (n = 59), patients with acute exacerbation of COPD (n = 29) and smoking (n = 20) and non-smoking controls (n = 20), using commercially available ELISAs, and investigated the prognostic role of sST2 in stable COPD. sST2 levels were significantly higher in COPD patients and smokers compared with non-smoking controls. We identified systolic blood pressure, forced expiratory volume in 1 s (FEV1% predicted), neutrophil count, lactate dehydrogenase and pack-years index as independent predictors of sST2 levels. During a median follow-up time of 10.6 years, 28 patients (47.5%) died. sST2 was an independent predictor of all-cause mortality in patients with COPD with a hazard ratio of 2.9 (95% CI 1.1–8.4, p = 0.035) per one standard deviation after adjustment for age, sex, pack-years, FEV1% predicted and C-reactive protein (CRP). sST2 concentrations are associated with severity of disease and long-term outcome in patients with COPD.

Highlights

  • Chronic obstructive pulmonary disease (COPD) is associated with a chronic inflammatory process of the lungs

  • Significant differences were observed in heart rate, C-reactive protein (CRP) and neutrophil count with the highest levels found during acute exacerbation (Table 1)

  • In COPD, we found significantly increased levels of suppression of tumorigenicity 2 (sST2) and lower levels of IL-33 when compared with healthy controls

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Summary

Introduction

Chronic obstructive pulmonary disease (COPD) is associated with a chronic inflammatory process of the lungs. In contrast to other non-communicable diseases, COPD-related mortality is constantly increasing over decades [1,2]. Well-established predictors of mortality in COPD comprise exacerbations [4,5], infections with inflammatory host response [6,7,8] and, most notably, comorbidities [9,10]. Both inflammatory host response [11] and comorbidities such as heart failure (HF) and coronary artery disease (CAD) revealed augmented expressions of interleukin (IL)-33 and soluble suppression of tumorigenicity 2 (sST2) [12,13]

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