Department of Pulmonary Medicine, Allergy and Immunological Diseases, Iwate Medical University School of Medicine, Shiwa, Japan.
Department of Internal Medicine, Takisawa Chuo Hospital, Takisawa, Japan.
COPD. 2020 Oct;17(5):587-594. doi: 10.1080/15412555.2020.1793925. Epub 2020 Sep 23.
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 ( = 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 CD14CD16 classical monocytes in circulating monocytes showed no difference among the three groups. The percentage of S100A9, S100A9CD163, and S100A9CD163 cells in classical monocytes was significantly increased in COPD patients relative to nonsmoker controls. In contrast, the levels of S100A9CD163 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, value < 0.05). In Receiver operating characteristic (ROC) analyses, the ratio of S100A9CD163/S100A9CD163 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.
尽管许多研究已经描述了慢性阻塞性肺疾病（COPD）中巨噬细胞的极性，但关于这种情况下循环单核细胞的细胞表型的信息有限。本研究旨在确定吸烟和 COPD 对循环单核细胞的细胞表型的影响。本研究纳入了 32 名 COPD 患者和 36 名健康志愿者（分别为无吸烟且肺功能正常者 17 名和 19 名，吸烟者且肺功能正常者 16 名）。通过流式细胞术分析经典单核细胞上两种细胞表面标志物，促炎相关 S100A9 和抗炎相关 CD163 的表达。循环单核细胞中 CD14CD16 经典单核细胞的百分比在三组之间没有差异。与非吸烟者对照组相比，COPD 患者中 S100A9、S100A9CD163 和 S100A9CD163 细胞的百分比显著增加。相比之下，在吸烟者且肺功能正常者和 COPD 患者中，S100A9CD163 细胞的水平显著低于非吸烟者。多变量分析显示，S100A9 细胞率与 COPD 之间存在独立关联（指数 1.0336，95%置信区间 [CI] 1.0063-1.0617， 值<0.05）。在接收者操作特征（ROC）分析中，S100A9CD163/S100A9CD163 细胞的比值对区分吸烟者且肺功能正常者和 COPD 患者的受试者工作特征曲线下面积为 0.719（95%CI=0.567-0.871）。总之，我们的结果表明，COPD 患者循环经典单核细胞中促炎表型增加，为阐明其在 COPD 发病机制中的作用提供了新的见解。
