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目的探讨支气管哮喘(简称哮喘)和慢性阻塞性肺疾病(COPD)患者诱导痰中基质金属蛋白酶9(MMP-9)和基质金属蛋白酶抑制剂1(TIMP-1)的水平及其与炎性细胞数、肺功能的关系。方法分别选择14例缓解期哮喘患者(哮喘组)、12例稳定期 COPD 患者(COPD 组)和10名健康对照者(健康对照组)进行肺功能测定和用诱导痰检查方法对痰炎性细胞进行分类计数,并用酶联免疫吸附试验(ELISA)法测定诱导痰上清液中白细胞介素4(IL-4)、MMP-9和 TIMP-1浓度。结果哮喘组患者诱导痰中嗜酸粒细胞、中性粒细胞分别为0.181±0.067、0.30±0.07,健康对照组为0.007±0.005、0.26±0.06,COPD 组为0.042±0.017、0.50±0.10,3组细胞间比较差异有统计学意义(F 值分别为4.32、4.13,P 均<0.05)。哮喘组、COPD 组、健康对照组间诱导痰中 IL-4浓度分别为(19±7)×10~(-3)g/L、(14±6)×10~(-3)g/L、(11±4)×10~(-3)g/L,3组诱导痰中 IL-4浓度比较差异无统计学意义(F=1.56,P 均>0.05),且分别与嗜酸粒细胞、中性粒细胞和第一秒用力呼气容积占预计值百分比(FEV_1占预计值%)无相关(r 分别为0.33、0.11、0.19、0.25、0.39、0.40、0.21、0.35、0.17,P 均>0.05)。哮喘组和 COPD 组诱导痰中 MMP-9、TIMP-1浓度分别为(15.9±6.0)g/L、(13.4±5.1)g/L、(19.8±8.5)g/L、(16.7±7.6)g/L,健康对照组分别为(1.8±1.1)g/L、(1.3±0.9)g/L,两组MMP-9、TIMP-1浓度比较差异有统计学意义(F 值分别为2.99、4.22,P 均<0.05)。哮喘组 MMP-9浓度与嗜酸粒细胞呈正相关(r=0.71,P<0.05);COPD 组 MMP-9浓度与中性粒细胞呈正相关(r=0.59,P<0.05),但与 FEV_1占预计值%和第一秒用力呼气容积/用力肺活量(FEV_1/FVC)无相关(r 分别为0.22、0.16、0.25、0.30,P 均>0.05)。哮喘组和 COPD 组 TIMP-1浓度均与嗜酸粒细胞和中性粒细胞无相关(r 分别为0.27、0.31、0.20、0.35,P 均>0.05),但与 FEV_1占预计值%呈负相关(r 分别为-0.58、-0.62,P 均<0.05)。哮喘组和 COPD 组诱导痰中 MMP-9/TIMP-1比值分别为0.8±0.7、0.8±0.6,两组比较差异无统计学意义(F=1.78,P>0.05),但与健康对照组(1.5±0.6)比较差异有统计学意义(F=3.70,P<0.05),且与 FEV_1占预计值%呈正相关(r 分别为0.56、0.61,P 均<0.05)。结论哮喘组和 COPD 组患者诱导痰中 MMP-9/TIMP-1比值的失衡与气道炎症和气流受限有关,这种失衡在哮喘和 COPD 细胞外基质的重塑和气流受限的发病机制中发挥重要作用。
Objective To investigate the levels of matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in sputum induced by bronchial asthma (COPD) and chronic obstructive pulmonary disease (COPD) Number of lung function. Methods 14 patients with remission asthma (asthma group), 12 patients with stable COPD (COPD group) and 10 healthy controls (healthy control group) were selected for pulmonary function test and sputum test for sputum inflammatory cells The numbers of IL-4, MMP-9 and TIMP-1 in the induced sputum supernatant were determined by enzyme-linked immunosorbent assay (ELISA). Results The numbers of induced eosinophils and neutrophils in asthmatic patients were 0.181 ± 0.067,0.30 ± 0.07, 0.007 ± 0.005 and 0.26 ± 0.06 respectively in healthy controls and 0.042 ± 0.017 and 0.50 ± 0.10 in COPD patients There was significant difference between groups (F = 4.32, 4.13, P <0.05 respectively). The levels of IL-4 in induced sputum in asthmatic group, COPD group and healthy control group were (19 ± 7) × 10 ~ (-3) g / L and (14 ± 6) × 10 ~ (-3) g / L (11 ± 4) × 10 ~ (-3) g / L, there was no significant difference in sputum IL-4 concentration between the three groups (F = 1.56, P all> 0.05) , Neutrophils and forced expiratory volume in the first second as a percentage of predicted value (FEV_1 accounted for the expected value%) had no correlation (r were 0.33,0.11,0.19,0.25,0.39,0.40,0.21,0.35,0.17, P > 0.05). The levels of MMP-9 and TIMP-1 in induced sputum of asthma group and COPD group were (15.9 ± 6.0) g / L, (13.4 ± 5.1) g / L and (19.8 ± 8.5) g / g / L and (1.8 ± 1.1) g / L and (1.3 ± 0.9) g / L respectively in the healthy control group. There was significant difference between the two groups in the concentrations of MMP-9 and TIMP- 4.22, P <0.05). The concentration of MMP-9 in asthma group was positively correlated with eosinophil (r = 0.71, P <0.05). The MMP-9 concentration in COPD group was positively correlated with neutrophil (r = 0.59, Predicted% did not correlate with FEV 1 / FVC in the first second (r = 0.22, 0.16, 0.25, 0.30, P> 0.05). The levels of TIMP-1 in asthma group and COPD group were all correlated with eosinophils and neutrophils (r = 0.27,0.31,0.20,0.35, P> 0.05), but negatively correlated with FEV 1 (r were -0.58, -0.62, P <0.05). The ratios of MMP-9 / TIMP-1 in induced sputum in asthmatic group and COPD group were 0.8 ± 0.7 and 0.8 ± 0.6 respectively, with no significant difference between the two groups (F = 1.78, P> 0.05) 1.5 ± 0.6) (F = 3.70, P <0.05), and had a positive correlation with the predicted value of FEV_1 (r = 0.56,0.61, all P <0.05). Conclusions The imbalance of MMP-9 / TIMP-1 ratio in sputum induced by asthma and COPD patients is associated with airway inflammation and limited air flow. This imbalance plays an important role in the remodeling of asthma and COPD extracellular matrix and the pathogenesis of airflow limitation In the play an important role.