S100A9/CD163 Expression in Circulating Classical Monocytes in Chronic Obstructive Pulmonary Disease
S100A9/CD163 Expression in Circulating Classical Monocytes in Chronic Obstructive Pulmonary Disease
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DOI：
10.1080/15412555.2020.1793925
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发表时间：
2020-09-22
影响因子：
2.2
通讯作者：
Yamauchi, Kohei
中科院分区：
文献类型：
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作者：
Yamashita, Masahiro;Utsumi, Yu;Yamauchi, Kohei
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，但有关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慢性阻塞性肺病对循环单核细胞的细胞表型的影响。 32 名 COPD 患者和 36 名健康志愿者（肺功能正常的非吸烟者和吸烟者分别为 17 名和 19 名）参加了这项研究。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的 S100A9 和抗炎相关的 CD163 的表达。循环单核细胞中CD14(强)CD16(-)经典单核细胞的百分比在三组之间没有差异。与非吸烟者对照相比，COPD 患者经典单核细胞中 S100A9(+)、S100A9(+)CD163(-) 和 S100A9(+)CD163(+) 细胞的百分比显着增加。相比之下，肺功能正常的吸烟者和COPD患者的S100A9(-)CD163(+)细胞水平相对于不吸烟者显着降低。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，p 值 < 0.05）。在受试者工作特征（ROC）分析中，S100A9（+）CD163（-）/S100A9（-）CD163（+）细胞的比率产生了曲线下受试者工作特征面积0.719（95％CI = 0.567-0.871），用于区分肺功能正常的吸烟者和COPD患者。总之，我们的结果表明，慢性阻塞性肺病中循环经典单核细胞的促炎表型增加，为阐明其在慢性阻塞性肺病发病机制中的作用提供了新的见解。摘要 在同时使用炎症相关 S100A9 和抗炎相关 CD163 标记物的流式细胞术分析中，与健康志愿者和肺功能正常的吸烟者相比，从 COPD 患者获得的循环 CD14（强）CD16（-）经典单核细胞显示出炎症表型增加。
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 CD14(strong)CD16(-)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,pvalue < 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. Summary at a glance In flow cytometric analyses simultaneously using inflammatory-related S100A9 and anti-inflammatory-related CD163 markers, circulating CD14(strong)CD16(-)classical monocytes obtained from patients with COPD showed increased inflammatory phenotypes, as compared to healthy volunteers and smokers with normal lung functions.