Increased expression of CD4+IL-17+ cells in the lung tissue of patients with stable chronic obstructive pulmonary disease (COPD) and smokers.
Increased expression of CD4+IL-17+ cells in the lung tissue of patients with stable chronic obstructive pulmonary disease (COPD) and smokers.
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DOI：
10.1016/j.intimp.2012.10.018
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发表时间：
2013
影响因子：
5.6
通讯作者：
Jianquan Zhang;Shuyuan Chu;X. Zhong;Qi-fang Lao;Zhiyi He;Yi Liang
中科院分区：
文献类型：
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作者：
Jianquan Zhang;Shuyuan Chu;X. Zhong;Qi-fang Lao;Zhiyi He;Yi Liang
CD 4 +IL-17+细胞在控制免疫和炎症反应中具有重要作用。本研究的作者假设这些细胞可能参与慢性阻塞性肺疾病（COPD）的发病机制。为了表征非吸烟者、肺功能正常的吸烟者和COPD患者的肺泡壁、小气道和肌性肺动脉中的CD 4 +IL-17+细胞的频率，使用双重免疫荧光染色评估10个非吸烟者的外周肺组织中的CD 4 + IL-17+细胞数量，并且使用实时定量PCR测量IL-17和IL-21表达，10名吸烟者肺功能正常，10名吸烟者COPD稳定。在肺泡壁，CD 4 +IL-17+细胞的数量增加，COPD患者与非吸烟者相比，正常吸烟者与非吸烟者相比。COPD患者小气道内CD 4 +IL-17+细胞数高于正常吸烟者和非吸烟者。肺组织中CD 4 +IL-17+细胞的表达与病理改变呈正相关。在小气道中，CD 4 +IL-17+细胞的数量与气流受限呈正相关。COPD患者和正常吸烟者肺组织中IL-17 mRNA水平均高于非吸烟者。肺组织中增加的CD 4 +IL-17+细胞数量涉及肺部的慢性炎症，并且与COPD患者和无气道限制的吸烟者中的肺损伤加重平行。这些发现有助于更好地理解COPD中CD 4+细胞相关的发病机制。
CD4+IL-17+cells have an important role in controlling immune and inflammatory reactions. The authors of the present study hypothesize that these cells may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). To characterize the frequency of CD4+IL-17+cells in the lung alveolar walls, small airways and muscular pulmonary arteries of nonsmokers, smokers with normal lung function and COPD patients, CD4+IL-17+cell number was assessed using double immunofluorescence staining, and IL-17 and IL-21 expression were measured using real-time quantitative PCR in the peripheral lung tissues of 10 nonsmokers, 10 smokers with normal lung function and 10 smokers with stable COPD. In the lung alveolar walls, the number of CD4+IL-17+cells was increased in COPD patients compared with nonsmokers and in normal smokers compared with nonsmokers. In the small airways, the CD4+IL-17+cell numbers were higher in COPD patients than in normal smokers and nonsmokers. A positive correlation was observed between CD4+IL-17+cell expression and pathological changes in the lung tissue. In the small airways, the number of CD4+IL-17+cells was positively correlated with airflow limitations. The IL-17 mRNA levels in lung tissues were increased in COPD patients and normal smokers compared with nonsmokers. Increased CD4+IL-17+cell number in lung tissue is involved in chronic inflammation of the lungs and parallels lung injury aggravation in COPD patients and in smokers without airway limitations. These findings contribute to a better understanding of CD4+cell-related pathogenesis in COPD.