Het effect van bèta-agonisten en corticosteroïden op de cytokineproductie bij COPD-patiënten

Objective: In this study we investigated whether treatment with beta-agonists and corticosteroids affects the release of cytokines by human macrophages from patients with COPD. Furthermore, we investigated whether cytokines can be used as biomarkers for COPD. Design: In this experimental/observational study we included three groups of subjects: non-smoking healthy volunteers (n = 17), smoking healthy volunteers (n = 9) and smoking patients with COPD (n = 6). Methods: About 30 ml of blood was withdrawn from subjects. We measured the amount of the cytokines IL-8, TNFα and IFNα in serum. Thereafter, monocytes were isolated and exposed to cigarette smoke. The amount of cytokines was measured in the presence of the beta-agonist salbutamol and/or the corticosteroid beta-methasone. Results: IL-8 in serum could not be detected in any subject. In smoking subjects without COPD, TNFα and IFNγ levels were significantly increased compared to non-smoking subjects. In patients with COPD these cytokines could not be observed. Treatment with betamethasone decreased IL-8 production in stimulated monocytes. The combination salbutamol + betamethasone further decreased IL-8 production. Stimulation with cigarette smoke increased TNFα production in non-smoking and smoking volunteers. Treatment with salbutamol + betamethasone resulted in the highest reduction in TNFα production. In patients with COPD TNFα could not be detected. Conclusions: TNFα and IFNγ levels, but not IL-8 levels, in serum can probably be used as biomarkers in smokers to predict the development of COPD in these patients. Treatment with betamethasone decreased cytokine production in smokers and patients with COPD. Whether the combination salbutamol + betamethasone has any further beneficial effect has to be determined in future experiments.