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目的观察慢性阻塞性肺疾病(COPD)患者肺泡巨噬细胞分泌的细胞因子的临床意义。方法稳定期COPD患者15例,另有11名健康者作为对照,进行肺功能检查,并经支气管肺泡灌洗获取肺泡巨噬细胞进行培养,测定大肠杆菌内毒素(LPS)刺激前、后上清液中白细胞介素-18(IL-18)I、L-23的浓度;采用直线相关分析IL-18I、L-23与肺功能关系。结果①COPD组患者肺泡巨噬细胞基础值IL-18均较对照组降低(P<0.05);LPS刺激后,COPD组和对照组IL-18均较刺激前升高(P<0.05),但两组之间差异无统计学意义(P>0.05);②COPD组患者肺泡巨噬细胞IL-23基础值均较对照组升高(P<0.05);LPS刺激以后,COPD组和对照组患者IL-23均较刺激前升高(P<0.05),而且两组之间比较差异有统计学意义(P<0.05);③COPD组1 s用力呼气容积/用力肺活量百分比(FEV1/FVC)、FEV1与肺泡巨噬细胞释放IL-23呈负相关(P<0.05)。结论IL-18、IL-23参与了COPD气道炎症反应,而且肺泡巨噬细胞释放的IL-23与FEV1/FVC、FEV1呈负相关,可能是导致气道阻塞的原因之一。
Objective To observe the clinical significance of cytokines secreted by alveolar macrophages in patients with chronic obstructive pulmonary disease (COPD). Methods Fifteen patients with stable COPD and 11 healthy controls were enrolled in this study. Pulmonary function tests were performed. Alveolar macrophages were obtained by bronchoalveolar lavage and cultured. The levels of lipopolysaccharide (LPS) before and after stimulation IL-18, IL-18, IL-18, IL-18 and lung function were determined by linear correlation analysis. Results ① The basal level of IL-18 in alveolar macrophages in COPD group was lower than that in control group (P <0.05). After LPS stimulation, the levels of IL-18 in COPD group and control group were significantly higher than those before stimulation (P <0.05) (P> 0.05) .②The basal levels of IL-23 in alveolar macrophages in COPD group were significantly higher than those in control group (P <0.05). After LPS stimulation, the levels of IL-23 in alveolar macrophages in COPD group and control group were significantly higher than those in control group (P <0.05). ③ The FEV1 / FVC, FEV1 and FEV1 of COPD group were significantly higher than those before stimulation (P <0.05), and the differences between the two groups were statistically significant Alveolar macrophages release IL-23 was negatively correlated (P <0.05). Conclusions IL-18 and IL-23 are involved in airway inflammation in COPD. The negative correlation between IL-23 released from alveolar macrophages and FEV1 / FVC and FEV1 may be one of the reasons leading to airway obstruction.