吸烟者和慢性阻塞性肺疾病（COPD）的小气道壁和管腔中M1 / M2巨噬细胞表型异常。,Scientific Reports

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吸烟者和慢性阻塞性肺疾病（COPD）的小气道壁和管腔中M1 / M2巨噬细胞表型异常。
Scientific Reports ( IF 3.8 ) Pub Date : 2017-Oct-17 , DOI: 10.1038/s41598-017-13888-x
Mathew Suji Eapen , Philip M. Hansbro , Kielan McAlinden , Richard Y. Kim , Chris Ward , Tillie-Louise Hackett , Eugene H. Walters , Sukhwinder Singh Sohal

我们通过对人类小气道组织，支气管肺泡灌洗液（BAL）和COPD实验鼠模型的综合研究，探讨了COPD发病机制中巨噬细胞表型的潜在失调。我们评估了健康对照，正常肺功能吸烟者（NLFS）和COPD受试者的人气道组织和BAL。小气道和BAL细胞均用抗CD68的总巨噬细胞和抗CD163的M2以及抗iNOS的M1巨噬细胞进行了免疫组织化学染色。多重ELISA检测BAL细胞因子。评估了可比较的香烟烟雾诱导的实验性COPD小鼠模型的相关mRNA谱。我们发现，与对照组相比，NLFS和COPD小气道中促炎性M1的增加与M2巨噬细胞的倒数相对应，而在病理组之间则保持不变。然而，腔巨噬细胞在NLFS和COPD受试者中均表现出显性的M2表型。随着NLFS和COPD中CCL22，IL-4，IL-13和IL-10的增加，BAL细胞因子偏向M2谱。COPD的小鼠模型显示了M2标记mRNA的相似增加。我们的发现表明，COPD患者粘膜和管腔区域的巨噬细胞转换异常，这与细胞因子的平衡密切相关。COPD中巨噬细胞表型的有益治疗性细胞因子操纵可能存在潜力。我们的发现表明，COPD患者粘膜和管腔区域的巨噬细胞转换异常，这与细胞因子的平衡密切相关。COPD中巨噬细胞表型的有益治疗性细胞因子操纵可能存在潜力。我们的发现表明，COPD患者粘膜和管腔区域的巨噬细胞转换异常，这与细胞因子的平衡密切相关。COPD中巨噬细胞表型的有益治疗性细胞因子操纵可能存在潜力。

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Abnormal M1/M2 macrophage phenotype profiles in the small airway wall and lumen in smokers and chronic obstructive pulmonary disease (COPD).

We explore potential dysregulation of macrophage phenotypes in COPD pathogenesis through integrated study of human small airway tissue, bronchoalveolar lavage (BAL) and an experimental murine model of COPD. We evaluated human airway tissue and BAL from healthy controls, normal lung function smokers (NLFS), and COPD subjects. Both small airways and BAL cells were immunohistochemically stained with anti-CD68 for total macrophages and with anti-CD163 for M2, and anti-iNOS for M1 macrophages. Multiplex ELISA measured BAL cytokines. Comparable cigarette smoke-induced experimental COPD mouse model was assessed for relevant mRNA profiles. We found an increase in pro-inflammatory M1s in the small airways of NLFS and COPD compared to controls with a reciprocal decrease in M2 macrophages, which remained unchanged among pathological groups. However, luminal macrophages showed a dominant M2 phenotype in both NLFS and COPD subjects. BAL cytokine skewed towards an M2 profile with increase in CCL22, IL-4, IL-13, and IL-10 in both NLFS and COPDs. The mouse-model of COPD showed similar increase in mRNA for M2 markers. Our finding suggests abnormal macrophage switching in both mucosal and luminal areas of COPD patients, that strongly associated with cytokine balance. There may be potential for beneficial therapeutic cytokine manipulation of macrophage phenotypes in COPD.

更新日期：2017-10-17

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