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首页> 外文期刊>Cytokine >Increased interleukin (IL)-8 and decreased IL-17 production in chronic obstructive pulmonary disease (COPD) provoked by cigarette smoke.
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Increased interleukin (IL)-8 and decreased IL-17 production in chronic obstructive pulmonary disease (COPD) provoked by cigarette smoke.

机译：香烟引起的慢性阻塞性肺疾病（COPD）中白介素（IL）-8升高，IL-17产生降低。

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Recently, involvement of IL-17 in development of COPD has been noticed. Unlike IL-8, the role of IL-17 in COPD remains controversial. In order to further understand mechanisms in cigarette smoke (CS) induced COPD, we investigated IL-17 and IL-8 levels in different stages of COPD patients, and time courses of IL-17 and IL-8 release in CS induced COPD rats. A total of 73 elderly patients with COPD and 31 healthy volunteers were recruited in the study. IL-17 and IL-8 levels in the sputum and plasma were measured, and number of differential cells was counted. A newly developed CS induced rat COPD model was employed to study time courses of IL-17 and IL-8 release and nucleated cell accumulation. The results showed that IL-8 levels in the sputum of severe COPD patients were elevated by 16.5-fold, but IL-17 levels were reduced by 4.8-fold. While IL-8 correlated with neutrophils, IL-17 correlated with monocytes and lymphocytes. Similarly, level of IL-8 was increased, but IL-17 was decreased in the bronchoalveolar lavage fluid (BALF) of CS rats. Time course study showed that increased IL-8 production in the BALF initiated at 6 weeks, but decreased IL-17 production started at 10 weeks following CS exposure. In conclusion, increased IL-8 level in COPD patients appears mainly secreted from neutrophils and macrophages, whereas decreased IL-17 level seems resulted from reduced number of monocytes or damaged epithelial cells. Increased IL-8 (a proinflammatory cytokine) secretion and decreased IL-17 (a protective cytokine of airways) release can both contribute to development of COPD.
机译：最近，已经注意到IL-17参与COPD的发展。与IL-8不同，IL-17在COPD中的作用仍存在争议。为了进一步了解香烟烟雾（CS）诱导的COPD的机制，我们调查了COPD患者不同阶段的IL-17和IL-8水平，以及CS诱导的COPD大鼠IL-17和IL-8释放的时程。该研究共招募了73名COPD老年患者和31名健康志愿者。测量痰和血浆中的IL-17和IL-8水平，并计数分化细胞的数量。使用新开发的CS诱导的大鼠COPD模型来研究IL-17和IL-8释放与有核细胞积聚的时程。结果表明，重症COPD患者痰液中的IL-8水平升高了16.5倍，而IL-17水平降低了4.8倍。 IL-8与中性粒细胞相关，而IL-17与单核细胞和淋巴细胞相关。同样，在CS大鼠的支气管肺泡灌洗液（BALF）中，IL-8的水平升高，但IL-17的水平降低。时程研究显示，BALF中CS-8暴露后6周开始增加IL-8的产生，但IL-17产生开始降低。总之，COPD患者的IL-8水平升高主要来自嗜中性粒细胞和巨噬细胞，而IL-17水平降低似乎是由于单核细胞数量减少或受损的上皮细胞所致。 IL-8（促炎性细胞因子）分泌增加和IL-17（气道的保护性细胞因子）释放减少均可以促进COPD的发展。

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