“…IL-6 is a cytokine that mediates the inflammatory response, which is increased in AECOPD and is correlated with exacerbation frequency and lung function decline[ 21 ]; (2) The change in the level of tumor necrosis factor-alpha (TNF-α) in serum from baseline to the end of treatment, as measured by the ELISA method (R&D Systems, Inc., United States). TNF-α is a pro-inflammatory cytokine that induces the production of other inflammatory mediators, which is elevated in AECOPD and linked with the airway inflammation and the oxidative stress[ 22 ]; (3) Change in the level of CRP in the sputum from baseline to the end of treatment, as measured using the immunoturbidimetric method (model: AU5800, Beckman Coulter, Inc., United States). CRP in sputum reflects local inflammation in the airways, which is increased in AECOPD and is associated with bacterial infection and sputum characteristics[ 23 ]; (4) The change in the IL-6 and TNF-α levels in sputum from baseline to the end of treatment, as measured using the ELISA method (R&D Systems, Inc., United States); and (5) The change in lung ventilation function parameters from baseline to the end of treatment, including FEV1, FVC, and peak expiratory flow (PEF), were measured using a spirometer (model: SP-10, Contec Medical Systems Co., Ltd., China), according to the American Thoracic Society/European Respiratory Society guidelines[ 24 ].…”