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Home-Based Prescribed Pulmonary Exercise in Patients with Stable Chronic Obstructive Pulmonary Disease
Published on: August 24, 2019
Cytokines and statin therapy in chronic obstructive pulmonary disease patients
Marevic Sanja1, Petrik Jozsef2, Popovic Grle Sanja3
1a Department of Medical Biochemistry and Hematology , University Hospital for Infectious Diseases ''Dr. Fran Mihaljevic'' , Zagreb , Croatia.
Abstract:
Cytokines are biological response modifiers involved in the pathophysiology of chronic obstructive pulmonary disease (COPD). This study investigated the potential use of cytokines as disease severity biomarkers in COPD patients and the possible effect of statin therapy on cytokine expression. Possible associations between cytokines, body mass index (BMI) and smoking have also been studied. Cytokines IFN-γ, IL-2, IL-12 p70, TNF-α, TNF-β, IL-4, IL-5, IL-6, IL-10, IL-1β and IL-8 were measured in the plasma of 100 clinically stable COPD patients using a fluorescent bead immunoassay on a flow cytometer. When patients were grouped according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage (A-D), no significant differences in cytokine concentrations were found (p > .05). Significantly decreased concentrations of IL-1β, IL-2, IL-4, IL-8, IL-10, IL-12p70 and TNF-α were found in COPD patients receiving statin therapy in comparison with COPD patients not receiving statin therapy (p < .05). COPD patients with increased BMI (>25) had decreased IL-2 (p=.038), IL-8 (p = .039) and IL-10 (p = .005) concentrations compared to normal BMI (20-25) patients. Current COPD smokers had increased concentrations of IL-5 (p = .037) compared to former COPD smokers. Hierarchical cluster analysis showed several patterns of measured cytokines in serum of patients with stable COPD. Statin therapy is associated with decreased expression of selected Th1 and Th2 cytokines in COPD, and this effect could be of relevance in COPD patients with increased cardiovascular risk. Concentrations of Th1 and Th2 cytokines in plasma cannot be used as biomarkers of disease severity or progression of COPD.
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