吸烟对COPD稳定期患者血清IL-6、IL-18、CC16水平及营养状况的影响

摘要

目的 探讨吸烟对慢性阻塞性肺疾病(COPD)稳定期患者血清IL-6、IL-18、Clara细胞分泌蛋白(CC16)水平及营养状况的影响.方法 收集COPD稳定期患者200例(COPD组)和同期体检健康者100例(对照组)的病史资料、微型营养评定(MNA)结果并对所有受试者行肺功能检查;用酶联免疫吸附试验(ELISA)检测受试者血清IL-6、IL-18、CC16水平.根据受试者的吸烟史,选取COPD组中吸烟者作为COPD吸烟亚组;对照组中吸烟者作为正常吸烟亚组,未吸烟者作为正常未吸烟亚组.在COPD吸烟亚组中根据吸烟指数(SI)进一步分为SI<400亚组与SI≥400亚组,对吸烟COPD稳定期患者的SI、MNA值与血清IL-6、IL-18、CC16进行Spearman相关性分析.结果 COPD组与对照组受试者性别构成比、年龄、吸烟指数等差异无统计学意义(P均>0.05);COPD组第1秒用力呼气容积(FEV 1)、FEV 1占用力肺活量的百分比(FEV 1/FVC)%、CC16浓度、MNA值均低于对照组,而血清IL-6、IL-18水平均高于对照组,P均<0.01.与正常未吸烟亚组相比,正常吸烟亚组、COPD吸烟亚组血清IL-6、IL-18水平均升高,而CC16水平降低;COPD吸烟亚组血清IL-6、IL-18水平高于正常吸烟亚组,而CC16水平低于正常吸烟亚组,差异均有统计学意义(P均<0.05).SI≥400亚组血清IL-6、IL-18水平高于SI<400亚组,而CC16水平及MNA值均低于SI<400亚组,以上差异均有统计学意义(P均<0.05).相关性分析结果显示,吸烟COPD稳定期患者的SI与血清IL-6、IL-18水平呈正相关(r分别为0.443、0.338,P均<0.01),与CC16水平呈负相关(r=-0.423,P<0.01);SI与MNA值呈负相关(r=-0.304,P<0.05);MNA值与血清IL-6、IL-18水平均呈负相关(r分别为-0.485、-0.291,P均<0.05),而与CC16水平无相关性(r=0.111,P=0.289).结论 吸烟可致COPD稳定期患者血清IL-6、IL-18水平升高、CC16水平降低,能增加COPD患者发生营养不良的风险,且与吸烟量有正相关关系.%Objective To explore the effects of smoking on the serum levels of interleukin-6 (IL-6),IL-18,Clara cell secretory protein 16 (CC16),and nutritional status in stable chronic obstructive pulmonary disease (COPD)patients. Meth-ods Data of 200 patients (COPD group)and 100 healthy persons (control group)were collected,and the results of Mini Nutritional Assessment (MNA)were performed,the lung function for all subjects were tested. The serum levels of IL-6,IL-18,and CC16 in the two groups were detected by ELISA. According to the smoking history,smokers in the COPD group were selected as the COPD smoking subgroup,and the control group were divided into the normal smoking subgroup and nonsmok-ing subgroup. According to the smoking index (SI),the COPD smoking subgroup was further divided into SI <400 subgroup and SI ≥ 400 subgroup. Spearman correlation analysis was applied to analyze the correlations of SI and MNA with the serum levels of IL-6,IL-18,and CC16 in patients with stable phase of smoking COPD. Results There were no significant differ-ences in age,gender,and smoking index between the COPD group and the control group (all P >0. 05). Compared with thecontrol group,the forced expiratory volume in one second (FEV 1 )%,FEV 1 / forced vital capacity (FVC)%,serum CC16 level,and the MNA values were decreased and the serum IL-6 and IL-18 levels were increased significantly in the COPD group (all P <0. 01). Compared with the normal nonsmoking subgroup,the serum levels of IL-6 and IL-18 were increased significantly and the serum CC16 level was decreased in the COPD and the normal smoking subgroups. Compared with the normal smoking subgroup,the serum levels of IL-6 and IL-18 were increased significantly and the serum CC16 level was de-creased in the COPD smoking subgroup (all P <0. 05). Compared with the SI <400 subgroup,the serum levels of IL-6 and IL-18 were increased significantly and the serum CC16 level and the MNA values were decreased in the SI ≥ 400 subgroup (all P <0. 05). Correlation analysis showed that SI in patients with stable phase of smoking COPD was positively correlated with the serum levels of IL-6 and IL-18 (r =0. 443,0. 338;both P <0. 01),and negatively correlated with the serum CC16 level (r = -0. 423,P <0. 01). SI was negatively correlated with the MNA values (r = -0. 304,P <0. 05);the MNA val-ues were negatively correlated with the serum levels of IL-6 and IL-18 (r = -0. 485,-0. 291;both P <0. 05),but were not correlated with the serum CC16 level (r =0. 111,P =0. 289). Conclusions Smoking could increase the serum levels of IL-6 and IL-18 and decrease the serum CC16 level in stable COPD patients,and smoking could increase the risk of malnutrition in COPD patients which has a positive correlation with smoking capacity.