PT - JOURNAL ARTICLE AU - Svetlana Soodaeva AU - Igor Klimanov AU - Timur Li AU - Marina Boldina AU - Larisa Postnikova AU - Nailja Kubysheva TI - Production of proinflammation cytokines and mean pulmonary arterial pressure in COPD DP - 2013 Sep 01 TA - European Respiratory Journal PG - P643 VI - 42 IP - Suppl 57 4099 - http://erj.ersjournals.com/content/42/Suppl_57/P643.short 4100 - http://erj.ersjournals.com/content/42/Suppl_57/P643.full SO - Eur Respir J2013 Sep 01; 42 AB - Background: Proinflammation cytokines play a role in neutrophilic inflammation in the airway and induce pulmonary fibrosis in COPD.The aim of the study was to analyse the levels of TNF-α, IL-17, IL-18 in the sera of patients with COPD in order to evaluate the role of TNF-α, IL-17, IL-18 production in the pulmonary hypertension of patients with COPD.Methods: In total, 42 COPD patients (37 males and 5 females) 61.2 ± 8,6 years old and 10 healthy volunteers were monitored. COPD severity: GOLD I stage - 8%; II stage - 12%; III stage - 7%; IV stage - 15%. TNF-α, IL-17 and IL-18 levels were measured by immunoassay in serum. The mean pulmonary arterial pressure (mPAP) was detected by Doppler-echocardiography.Results: Levels of TNF-α, IL-17 and IL-18 in serum were significantly higher in COPD patients compared to healthy controls. The progressing increase of inflammation biomarkers concentrations in blood in COPD patients combined with stages of COPD. TNF-α serum levels in COPD IV stage patients were higher than patients with COPD I stage (3.25±0.14 pg/ml vs. 1.34±0.07 pg/ml; p<0.001). IL-17 and IL-18 blood concentrations in COPD IV stage patients were higher than COPD GOLD I stage (3.81±0.17 pg/ml vs. 2.38±0.04 pg/ml; p<0.01 and 198.4±24.9 pg/ml vs. 146.1±13.7 pg/ml; p=0.04). In COPD patients, there was a significant (p<0.001) positive correlation between serum level of IL-17, TNF-α and mPAP (rsp=0.61; p<0.0001), IL-18 and mPAP (rsp=0.68; p<0.0001). Conclusions: Our results may indicate that an increased cytokines serum levels (TNF-α, IL-17 and IL-18) may induce of pulmonary hypertension in COPD.