|Topic:||09. COPD, Emphysema, Chronic Bronchitis, Alpha-1 Antitrypsin Deficiency / Adult / Translational Science / Allergy, Immunology and Inflammation (AII)|
|Authors:||A. Morello Gearhart, R. Fernandez-Botran, P. Peyrani, T. Wiemken, A. Reyes, U. Gauhar, H. Rivas-Perez, J. Roman, J.A. Ramirez, R. Cavallazzi; Louisville, KY/US|
Rationale: Chronic obstructive pulmonary disease (COPD) is a condition of lung and systemic inflammation. The role of cytokines in local and systemic inflammation in COPD is not well characterized. This study aimed to compare plasma and brochoalveolar lavage (BAL) fluid cytokine levels in COPD and non-COPD subjects with the intent of better understanding their potential roles in driving local and systemic inflammation.
Methods: This cross-sectional study analyzed data from 65 subjects: 31 with COPD confirmed by spirometry and 34 non-COPD controls. All patients underwent spirometry, plasma sample collection, and bronchoscopy/BAL. Quantitative levels of 21 inflammatory cytokines were measured in the plasma (systemic inflammation) and BAL (lung inflammation) using a multiplex assay.
Results: COPD patients were overall older (median age 59 vs 36; p = <0.001); otherwise, groups were similar in respect to gender, smoking history and comorbidities. COPD subjects had higher plasma levels of 12 measured cytokines (in pg/ml): tumor necrosis factor (TNF)-alpha (6.5 vs 3.7; p = 0.005), interleukin (IL)-8 (5.1 vs 2.9; p = 0.008), IL-21 (1 vs 0.4; p = 0.006), IL-7 (5.9 vs 4.3; p = 0.022), IL-10 (8.5 vs 5.1; p = 0.036), interferon (IFN)-gamma (12.6 vs 9; p = 0.021), IL-12p70 (1.8 vs 0.7; p = 0.025), IL-2 (1.4 vs 0.9; p = 0.014), IL-17A (4.4 vs 1.7; p = 0.026), IL-23 (34.7 vs 11.3; p = 0.026), macrophage inflammatory protein (MIP)-3 alpha (24.4 vs 19.8; p = 0.035), and fractalkine (68.9 vs 34.3; p = 0.011). In contrast, cytokine levels in the BAL fluid of COPD subjects were not elevated compared with controls.
Conclusion: Elevated levels of cytokines were identified in the plasma of COPD subjects when compared to controls, implying a role for systemic inflammation in this condition. In contrast, lung cytokines were not elevated suggesting that inflammation in the setting of COPD may not originate in the lungs, or that BAL fluid is not an optimal source of information when evaluating inflammation in COPD. Although the role of these cytokines remains uncertain, anti-cytokine therapy might modulate inflammation in COPD and perhaps improve outcomes.