T辅助细胞17-相关的细胞因子IL-17A和IL-17F在哮喘和COPD的表达
2011/09/08
背景：哮喘和COPD以气道功能失调和炎症为特征。中性粒细胞气道炎症是COPD的常见特征，并在哮喘尤其是重症哮喘中得到认可。研究提示T辅助细胞（Th）17-细胞因子IL-17A和IL-17F与中性粒细胞气道炎症进展有关，但是其在哮喘和COPD的表达尚不肯定。
方法：该研究纳入了30例哮喘患者，10例戒烟的轻中度COPD患者，并以27例未吸烟者和14例吸烟者为对照，观察IL-17A和IL-17F在支气管粘膜下层的表达。检测165例哮喘患者和27例COPD患者痰液IL-17浓度。
结果：粘膜下层IL-17A （细胞/毫米2）的中位数（四分位间距）和健康对照组【0.4（2.8）】比较，在轻中度哮喘患者明显升高【2.1（2.4）】，而在重度哮喘患者未见明显升高( P = 0.04)。与未吸烟对照受试者【0（0）】而不是吸烟对照受试者比较，粘膜下IL-17A+（细胞/毫米2）在COPD患者增加【0.4（2.8）】( P = 0.046)。和健康对照受试者【0.7（1.4）】比较( P = 0.001)，粘膜下层IL-17F+（细胞/毫米2）在重度哮喘【2.1（3.6）】和轻-中度哮喘【1.6（1.0）】升高,但在COPD患者中未见升高。IL-17A和IL-17F两者与增加的中性粒细胞炎症无相关性，但IL-17F和粘膜下嗜酸粒细胞计数相关( r s =0.5, P =0.005)。COPD患者痰液IL-17浓度较哮喘明显增高【2（0-7） pg/mL vs 0 （0-2） pg/mL, P <.0001】，并与使用支气管扩张剂后的FEV1%预计值( r =-0.5, P =0.008)和FEV1/FVC( r = - 0.4, P =0.04)相关。
方法：该研究纳入了30例哮喘患者，10例戒烟的轻中度COPD患者，并以27例未吸烟者和14例吸烟者为对照，观察IL-17A和IL-17F在支气管粘膜下层的表达。检测165例哮喘患者和27例COPD患者痰液IL-17浓度。
结果：粘膜下层IL-17A （细胞/毫米2）的中位数（四分位间距）和健康对照组【0.4（2.8）】比较，在轻中度哮喘患者明显升高【2.1（2.4）】，而在重度哮喘患者未见明显升高( P = 0.04)。与未吸烟对照受试者【0（0）】而不是吸烟对照受试者比较，粘膜下IL-17A+（细胞/毫米2）在COPD患者增加【0.4（2.8）】( P = 0.046)。和健康对照受试者【0.7（1.4）】比较( P = 0.001)，粘膜下层IL-17F+（细胞/毫米2）在重度哮喘【2.1（3.6）】和轻-中度哮喘【1.6（1.0）】升高,但在COPD患者中未见升高。IL-17A和IL-17F两者与增加的中性粒细胞炎症无相关性，但IL-17F和粘膜下嗜酸粒细胞计数相关( r s =0.5, P =0.005)。COPD患者痰液IL-17浓度较哮喘明显增高【2（0-7） pg/mL vs 0 （0-2） pg/mL, P <.0001】，并与使用支气管扩张剂后的FEV1%预计值( r =-0.5, P =0.008)和FEV1/FVC( r = - 0.4, P =0.04)相关。
结论：我们的发现支持Th17细胞因子IL-17A和IL-17F在哮喘和COPD中的重要作用，但是没有证明与中性粒细胞炎症的相关性。
(王刚 四川大学华西医院中西医结合科呼吸组 610041 摘译)
Expression of the T Helper 17-Associated Cytokines IL-17A and IL-17F in Asthma and COPD
Camille D, Mona B, Salman S, Dhananjay D, Vijay M, Paul R, Margaret M, Joanne W, Richard M, Matthew A. Sleeman I, Anderson and Christopher E.
Chest; 2010;138:1140-1147
Background: Asthma and COPD are characterized by airway dysfunction and inflammation. Neutrophilic airway inflammation is a common feature of COPD and is recognized in asthma, particularly in severe disease. The T helper (Th) 17 cytokines IL-17A and IL-17F have been implicated in the development of neutrophilic airway inflammation, but their expression in asthma and COPD is uncertain.
Methods: We assessed IL-17A and IL-17F expression in the bronchial submucosa from 30 subjects with asthma, 10 ex-smokers with mild to moderate COPD, and 27 nonsmoking and 14 smoking control subjects. Sputum IL-17 concentration was measured in 165 subjects with asthma and 27 with COPD.
Results: The median (interquartile range) IL-17A cells/mm 2 submucosa was increased in mild to moderate asthma (2.1 [2.4]) compared with healthy control subjects (0.4 [2.8]) but not in severe asthma ( P = .04). In COPD, IL-17A 1 cells/mm 2 submucosa were increased (0.5 [3.7]) compared with nonsmoking control subjects (0 [0]) but not compared with smoking control subjects ( P = .046). IL-17F 1 cells/mm 2 submucosa were increased in severe asthma (2.7 [3.6]) and mild to moderate asthma (1.6 [1.0]) compared with healthy controls subjects (0.7 [1.4]) ( P = .001) but was not increased in subjects with COPD. IL-17A and IL-17F were not associated with increased neutrophilic inflammation, but IL-17F was correlated with the submucosal eosinophil count ( r s = 0.5, P= .005). The sputum IL-17 concentration in COPD was increased compared with asthma (2 [0-7] pg/mL vs 0 [0-2] pg/mL, P , .0001) and was correlated with post-bronchodilator FEV 1 % predicted ( r = - 0.5, P = .008) and FEV 1 /FVC ( r = - 0.4, P= .04).
Conclusions: Our findings support a potential role for the Th17 cytokines IL-17A and IL-17F in asthma and COPD, but do not demonstrate a relationship with neutrophilic inflammation.
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