Although many studies have characterized polarity of macrophages in chronic obstructive pulmonary disease (COPD), limited information is available regarding cellular phenotypes of circulating monocytes in this condition. This study aimed to determine the influence of cigarette smoking and COPD on the cellular phenotype of circulating monocytes. Thirty-two patients with COPD and 36 healthy volunteers (n = 17 and 19 in nonsmokers and smokers with normal lung functions, respectively) were enrolled in this study. The expression of two cell surface markers, pro-inflammatory-related S100A9 and anti-inflammatory-related CD163, on classical monocytes was analyzed by flow cytometry. The percentage of CD14strongCD16- classical monocytes in circulating monocytes showed no difference among the three groups. The percentage of S100A9+, S100A9+CD163-, and S100A9+CD163+ cells in classical monocytes was significantly increased in COPD patients relative to nonsmoker controls. In contrast, the levels of S100A9-CD163+ cells were significantly decreased in smokers with normal lung functions and in COPD patients relative to that in nonsmokers. Multivariate analyses revealed an independent association between S100A9+ cell rates and COPD (exponent 1.0336, 95% confidence interval [CI] 1.0063-1.0617, p value < 0.05). In Receiver operating characteristic (ROC) analyses, the ratio of S100A9+CD163-/S100A9-CD163+ cells yielded a receiver operating characteristic-area under the curve of 0.719 (95% CI = 0.567-0.871) for discrimination between smokers with normal lung functions and COPD patients. In conclusion, our results demonstrated increased pro-inflammatory phenotypes in circulating classical monocytes in COPD, providing novel insights to elucidate their roles in the pathogenesis of COPD.
Keywords: CD163; S100A9; chronic obstructive pulmonary disease; inflammation; monocytes.