Systemic anti-inflammatory mediators in COPD: increase in soluble interleukin 1 receptor II during treatment of exacerbations

Abstract

BACKGROUNDThe aim of this study was to test the hypothesis that the chronic inflammatory process present in chronic obstructive pulmonary disease (COPD) is due to a defective endogenous anti-inflammatory mechanism.METHODSSystemic levels of the anti-inflammatory mediators soluble interleukin 1 receptor II (sIL-1RII), soluble tumour necrosis factor receptor p55 (sTNF-R55) and sTNF-R75, and of C reactive protein (CRP) and lipopolysaccharide binding protein (LBP) were analysed in 55 patients with stable COPD (median forced expiratory volume in one second (FEV1) 34% predicted (range 15–78)) and compared with levels in 23 control subjects. In addition, changes in these mediators were studied in 13 patients with COPD (median FEV134% predicted (range 19–51)) during the first 7 days in hospital with an exacerbation of the disease.RESULTSPatients with stable COPD were characterised by a systemic inflammatory process indicated by an increased leucocyte count (7.2 (4.7–16.4)v4.8 (3.5–8.3) × 109/l), raised levels of CRP (11.8 (1.1–75.0)v4.1 (0.6–75.0) μg/ml) and LBP (45.6 (8.1–200.0)v27.9 (14.1–71.5) μg/ml), and moderate increases in both sTNF-Rs. In contrast, the sIL-1RII level did not differ between patients and controls (4.53 (2.09–7.60)v4.63 (3.80–5.93) ng/ml). During treatment of disease exacerbations, systemic levels of both CRP (at day 3) and LBP (at day 7) were significantly reduced compared with day 1, whereas sIL-1RII levels increased.CONCLUSIONSThese data suggest an imbalance in systemic levels of pro- and anti-inflammatory mediators in patients with stable COPD. The increase in the anti-inflammatory mediator sIL-1RII during treatment of exacerbations may contribute to the clinical improvement.