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

M. A. Dentener, E. C. Creutzberg, A. M W J Schols, A. Mantovani, C. Van't Veer, W. A. Buurman, E. F M Wouters

Research output: Contribution to journalArticle

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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 inflammatory mechanism. Methods - Systemic levels of the 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 (FEV,) 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 characterised by a systemic inflammatory process indicated by an increased leucocyte count (7.2 (4.7-16.4) υ 4.8 (3.5-8.3) × 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) υ 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) υ 4.63 (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. 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.

Original languageEnglish
Pages (from-to)721-726
Number of pages6
JournalThorax
Volume56
Issue number9
DOIs
Publication statusPublished - 2001

Fingerprint

Interleukin-1 Receptors
Chronic Obstructive Pulmonary Disease
Anti-Inflammatory Agents
C-Reactive Protein
Disease Progression
Therapeutics
Tumor Necrosis Factor Receptors
Forced Expiratory Volume
Leukocyte Count
Protein Binding
lipopolysaccharide-binding protein

Keywords

  • Chronic obstructive pulmonary disease
  • Soluble interleukin 1 receptor II
  • Systemic inflammation

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Dentener, M. A., Creutzberg, E. C., Schols, A. M. W. J., Mantovani, A., Van't Veer, C., Buurman, W. A., & Wouters, E. F. M. (2001). Systemic anti-inflammatory mediators in COPD: Increase in soluble interleukin 1 receptor II during treatment of exacerbations. Thorax, 56(9), 721-726. https://doi.org/10.1136/thorax.56.9.721

Systemic anti-inflammatory mediators in COPD : Increase in soluble interleukin 1 receptor II during treatment of exacerbations. / Dentener, M. A.; Creutzberg, E. C.; Schols, A. M W J; Mantovani, A.; Van't Veer, C.; Buurman, W. A.; Wouters, E. F M.

In: Thorax, Vol. 56, No. 9, 2001, p. 721-726.

Research output: Contribution to journalArticle

Dentener, MA, Creutzberg, EC, Schols, AMWJ, Mantovani, A, Van't Veer, C, Buurman, WA & Wouters, EFM 2001, 'Systemic anti-inflammatory mediators in COPD: Increase in soluble interleukin 1 receptor II during treatment of exacerbations', Thorax, vol. 56, no. 9, pp. 721-726. https://doi.org/10.1136/thorax.56.9.721
Dentener, M. A. ; Creutzberg, E. C. ; Schols, A. M W J ; Mantovani, A. ; Van't Veer, C. ; Buurman, W. A. ; Wouters, E. F M. / Systemic anti-inflammatory mediators in COPD : Increase in soluble interleukin 1 receptor II during treatment of exacerbations. In: Thorax. 2001 ; Vol. 56, No. 9. pp. 721-726.
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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 inflammatory mechanism. Methods - Systemic levels of the 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 (FEV,) 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 characterised by a systemic inflammatory process indicated by an increased leucocyte count (7.2 (4.7-16.4) υ 4.8 (3.5-8.3) × 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) υ 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) υ 4.63 (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. 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.",
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T2 - Increase in soluble interleukin 1 receptor II during treatment of exacerbations

AU - Dentener, M. A.

AU - Creutzberg, E. C.

AU - Schols, A. M W J

AU - Mantovani, A.

AU - Van't Veer, C.

AU - Buurman, W. A.

AU - Wouters, E. F M

PY - 2001

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N2 - 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 inflammatory mechanism. Methods - Systemic levels of the 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 (FEV,) 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 characterised by a systemic inflammatory process indicated by an increased leucocyte count (7.2 (4.7-16.4) υ 4.8 (3.5-8.3) × 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) υ 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) υ 4.63 (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. 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.

AB - 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 inflammatory mechanism. Methods - Systemic levels of the 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 (FEV,) 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 characterised by a systemic inflammatory process indicated by an increased leucocyte count (7.2 (4.7-16.4) υ 4.8 (3.5-8.3) × 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) υ 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) υ 4.63 (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. 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.

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