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首页> 外文期刊>COPD: Journal of Chronic Obstructive Pulmonary Disease >Expression of interleukin (IL)-10, IL-17A and IL-22 in serum and sputum of stable chronic obstructive pulmonary disease patients
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Expression of interleukin (IL)-10, IL-17A and IL-22 in serum and sputum of stable chronic obstructive pulmonary disease patients

机译：稳定型慢性阻塞性肺疾病患者血清和痰中白介素（IL）-10，IL-17A和IL-22的表达

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摘要

Interleukin (IL)-17A, IL-22 and IL-10 have been implicated in the development of chronic obstructive pulmonary disease (COPD), but their expression in COPD is uncertain. Here we investigate the expression of IL-17A, IL-22 and IL-10 in the serum and sputum of COPD patients. Blood samples and induced sputum samples were collected from 94 patients with COPD, 23 healthy smokers, and 22 healthy control non-smokers. IL-17A, IL-22 and IL-10 were measured by enzyme-linked immunosorbent assay (ELISA). We found that: 1) serum and sputum IL-17A were higher in COPD compared to healthy smokers and non-smokers; 2) serum IL-17A increased with COPD stages, it was inversely correlated with percentage of forced expiratory volume in the first second (FEV1%) reference and positively correlated with C-reactive protein (CRP), Sputum IL-17A levels in the severe COPD patients were positively correlated with sputum neutrophils, and reversely correlated with sputum macraphages (p < 0.01); 3) serum and sputum IL-22 were significantly higher in COPD and healthy smokers than those in the non-smoker group, sputum IL-22 was similar in severe COPD (stage III and IV), which were higher than those in the other groups (p < 0.05); and, 4) serum and sputum IL-10 were similiar in COPD and healthy smokers, which were decreased compared to non-smokers. These data suggest that the increased level of IL-17A in serum and sputum plays important roles in the pathogenesis of COPD. The increased sputum IL-22 might also play important roles in the pathogenesis of COPD, while IL-10 secretion might be not only affected by COPD but also by cigarette smoke.
机译：白介素（IL）-17A，IL-22和IL-10与慢性阻塞性肺疾病（COPD）的发生有关，但它们在COPD中的表达尚不确定。在这里，我们研究了COPD患者血清和痰中IL-17A，IL-22和IL-10的表达。从94名COPD患者，23名健康吸烟者和22名健康对照非吸烟者中采集血液和痰标本。通过酶联免疫吸附测定（ELISA）测量IL-17A，IL-22和IL-10。我们发现：1）与健康吸烟者和非吸烟者相比，COPD中的血清和痰IL-17A更高。 2）血清IL-17A随COPD分期而增加，与重度第一秒钟呼气量百分比（FEV1％）成反比，与C反应蛋白（CRP），重度痰中IL-17A呈正相关。 COPD患者与痰中性粒细胞呈正相关，而与痰中的巨噬细胞呈负相关（p <0.01）。 3）COPD和健康吸烟者的血清和痰IL-22显着高于非吸烟组，重度COPD（III和IV期）的痰IL-22相似，高于其他组（p <0.05）; 4）COPD和健康吸烟者的血清和痰液IL-10相似，与非吸烟者相比有所降低。这些数据表明，血清和痰中IL-17A水平升高在COPD的发病机制中起重要作用。痰液中IL-22的增加也可能在COPD的发病机理中起重要作用，而IL-10的分泌不仅可能受到COPD的影响，而且还受到香烟烟雾的影响。

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