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The effects of inhaled and oral corticosteroids on serum inflammatory biomarkers in COPD: an exploratory studyDepartment of Medicine (Respiratory Division), University of British Columbia and the Providence Heart and Lung Institute at St. Paul's Hospital (James Hogg iCAPTURE Center), Vancouver, BC, Canada
Department of Medicine (Respiratory Division), University of British Columbia and the Providence Heart and Lung Institute at St. Paul's Hospital (James Hogg iCAPTURE Center), Vancouver, BC, Canada
Discovery Medicine, High Throughput Biology and Data Exploration Sciences, GlaxoSmithKline R&D, King of Prussia, Pennsylvania, US
Discovery Medicine, High Throughput Biology and Data Exploration Sciences, GlaxoSmithKline R&D, King of Prussia, Pennsylvania, US
Discovery Medicine, High Throughput Biology and Data Exploration Sciences, GlaxoSmithKline R&D, King of Prussia, Pennsylvania, US
Discovery Medicine, High Throughput Biology and Data Exploration Sciences, GlaxoSmithKline R&D, King of Prussia, Pennsylvania, US
Department of Medicine (Respiratory Division), University of British Columbia and the Providence Heart and Lung Institute at St. Paul's Hospital (James Hogg iCAPTURE Center), Vancouver, BC, Canada, dsin{at}mrl.ubc.ca Background: Several studies suggest that inhaled and oral corticosteroids repress systemic inflammation in chronic obstructive pulmonary disease (COPD). However, the cytokines that may respond to these medications are unclear. Method: We used data from 41 patients with a history of stable moderate COPD (average age 64 years) who were randomised to inhaled fluticasone (500 µg twice daily from a Diskus inhaler), oral prednisone (30 mg daily) or placebo for 2 weeks. Using a multiplexed array system, different serum cytokines that have been implicated in COPD pathogenesis were measured. Results: We found that compared with placebo, inhaled fluticasone significantly reduced levels of soluble tumour necrosis factor receptor-2 (sTNF-R2) by 24% (95% CI, 7—38%; p = 0.01), monocyte chemoattractant protein-1 by 20% (95% CI, 5—32%; p = 0.01), interferon gamma inducible CXCL10 (IP-10) by 43% (95% CI, 3—66%; p = 0.04), and soluble L-selectin levels by 15% (95% CI, 1—28%; p = 0.04). Compared with placebo, oral prednisone reduced levels of sTNF-R2 by 26% (95% CI, 15—36%; p < 0.001), L-selectin by 22% (95% CI, 8—34%; p = 0.004), intercellular adhesion molecule-1 by 31% (95% CI, 9—48%; p = 0.01), pulmonary and activation-regulated chemokine (PARC) by 18% (95% CI, 2—32%; p = 0.03) and IP-10 by 40% (95% CI, 0—64%; p = 0.05). sTNF-R2, L-selectin and IP-10 were significantly reduced by both oral and inhaled corticosteroids. The other cytokines were not significantly repressed by either oral or inhaled corticosteroids. Conclusions: In summary, inhaled and oral corticosteroids significantly repressed a selected number of systemic cytokines in patients with stable, moderate COPD; most of the steroid-responsive cytokines appear to be chemoattractants.
Key Words: Biomarker • COPD • corticosteroids • fluticasone • prednisone
This version was published on April
1, 2009 Therapeutic Advances in Respiratory Disease, Vol. 3, No. 2,
73-80 (2009) |
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