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由香烟烟雾引起的慢性阻塞性肺疾病(COPD)中白细胞介素(IL)-8 的增加和 IL-17 的减少。

Increased interleukin (IL)-8 and decreased IL-17 production in chronic obstructive pulmonary disease (COPD) provoked by cigarette smoke.

机构信息

The General Hospital of PLA, Beijing 100853, China.

出版信息

Cytokine. 2011 Dec;56(3):717-25. doi: 10.1016/j.cyto.2011.09.010. Epub 2011 Oct 12.

DOI:10.1016/j.cyto.2011.09.010
PMID:21996014
Abstract

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.

摘要

最近,人们注意到白细胞介素-17(IL-17)在 COPD 的发展中起作用。与白细胞介素-8(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 中的机制,我们研究了 COPD 患者不同阶段的 IL-17 和 IL-8 水平,以及 CS 诱导的 COPD 大鼠中 IL-17 和 IL-8 释放的时间过程。本研究共招募了 73 名老年 COPD 患者和 31 名健康志愿者。测量了痰和血浆中的 IL-17 和 IL-8 水平,并计数了不同细胞的数量。建立了一种新的 CS 诱导的大鼠 COPD 模型,以研究 IL-17 和 IL-8 释放和有核细胞积聚的时间过程。结果表明,重度 COPD 患者痰中 IL-8 水平升高 16.5 倍,但 IL-17 水平降低 4.8 倍。虽然 IL-8 与中性粒细胞相关,IL-17 与单核细胞和淋巴细胞相关。同样,CS 大鼠的支气管肺泡灌洗液(BALF)中 IL-8 水平升高,但 IL-17 水平降低。时间过程研究表明,BALF 中 IL-8 的产生增加始于 CS 暴露后 6 周,但 IL-17 的产生减少始于 10 周。总之,COPD 患者中 IL-8 水平的升高主要来自中性粒细胞和巨噬细胞,而 IL-17 水平的降低似乎是由于单核细胞或上皮细胞数量减少或受损所致。增加的 IL-8(促炎细胞因子)分泌和减少的 IL-17(气道的保护性细胞因子)释放都可能导致 COPD 的发展。

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