title: Systemic anti-inflammatory mediators in COPD: increase in soluble interleukin 1 receptor II during treatment of exacerbations.
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 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(1)) 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 FEV(1) 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) v 4.8 (3.5-8.3) x 10(9)/l), raised levels of CRP (11.8 (1.1-75.0) v 4.1 (0.6-75.0) microg/ml) and LBP (45.6 (8.1-200.0) v 27.9 (14.1-71.5) microg/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) 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.
authors.affiliation: Department of Pulmonology and Surgery, Maastricht University, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), 6202 AZ Maastricht, The Netherlands. Mieke.Dentener@pul.unimaas.nl
authors.forename: M A
authors.initials: MA
authors.lastname: Dentener
authors.forename: E C
authors.initials: EC
authors.lastname: Creutzberg
authors.forename: A M
authors.initials: AM
authors.lastname: Schols
authors.forename: A
authors.initials: A
authors.lastname: Mantovani
authors.forename: C
authors.initials: C
authors.lastname: van't Veer
authors.forename: W A
authors.initials: WA
authors.lastname: Buurman
authors.forename: E F
authors.initials: EF
authors.lastname: Wouters
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000032:analysis; D002352:Carrier Proteins; D002908:Chronic Disease; D002373:Cyclic AMP Receptor Protein / Q000032:analysis; D004268:DNA-Binding Proteins / Q000032:analysis; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D008173:Lung Diseases, Obstructive / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D017472:Receptors, Interleukin-1 / Q000378:metabolism*; D053574:Receptors, Interleukin-1 Type II; D018124:Receptors, Tumor Necrosis Factor / Q000032:analysis; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D015398:Signal Transduction; D014157:Transcription Factors; D014797:Vital Capacity / Q000502:physiology
chemical_list: D015703:Antigens, CD; D002352:Carrier Proteins; D002373:Cyclic AMP Receptor Protein; D004268:DNA-Binding Proteins; D017472:Receptors, Interleukin-1; D053574:Receptors, Interleukin-1 Type II; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014157:Transcription Factors; C085968:UBP1 protein, human