TITLE

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

AUTHOR(S)
Dentener, M. A.; Creutzberg, E. C.; Schols, A. M. W. J.; Mantovani, A.; van't#Veer, C.; Buurman, W. A.; Wouters, E. F. M.
PUB. DATE
September 2001
SOURCE
Thorax;Sep2001, Vol. 56 Issue 9, p721
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background-The 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. Methods-Systemic levels of the anti-inflammatory mediators soluble interleukin 1 receptor II (sIL- 1RII), soluble tumor necrosis factor receptor p55 (sTNF-R55) and sTNF-R75, and of C reactive protein (CRP) and lipopolysaccharide binding protein (LBP) were analyzed 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 FEV1 34% predicted (range 19-51)) during the first 7 days in hospital with an exacerbation of the disease. Results-Patients with stable COPD were characterized by a systemic inflammatory process indicated by an increased leucocyte count (7.2 (4.7-16.4) v 4.8 (3.5-8.3) x 109/1), raised levels of CRP (11.8 (1.1-75.0) v 4.1 (0.6-75.0) μg/ml) and LBP (45.6 (8.1- 200.0) v 27.9 (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) v 4.63 (3.80-5.93) μg/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. Conclusions-These 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.
ACCESSION #
12927263

 

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