吸烟患或未患慢性阻塞性肺疾病患者肺组织中巨噬细胞移动抑制因子表达  

The expression of macrophage migration inhibition factor in pulmonary tissues of smokers with or without chronic obstructive pulmonary disease

作　　者：佘惟槟[1] 刘先胜[1] 倪望[1] 陈仕新[1] 徐永健[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院呼吸与危重症医学科卫生部呼吸疾病重点实验室,武汉430030

出　　处：《中华内科杂志》2012年第11期863-866,共4页Chinese Journal of Internal Medicine

基　　金：2010年度卫生公益性行业科研专项经费项目“慢性呼吸疾病的预防与规范诊治体系建设及适宜技术研究”（201002008,卫科教规划便函[2011]20号）资助

摘　　要：目的通过检测吸烟患或未患慢性阻塞性肺疾病（COPD）患者肺组织中巨噬细胞移动抑制因子（MIF）表达水平，为进一步了解COPD易患机制提供基础研究资料。方法肺组织来源于因肺癌行肺叶切除术的41例患者，分吸烟患COPD组（16例）、吸烟未患COPD组（13例）、无吸烟对照组（12例）3组。所有受试者均于术前1周做肺功能检查[第1秒用力呼气容积（FEV1），用力肺活量（FVC）]，采用实时定量PCR和免疫组化检测肺组织中MIF mRNA和蛋白表达水平，并行相关分析。结果（1）实时定量PCR检测肺组织内MIF mRNA表达水平，吸烟患COPD组（4．87±1．79）高于吸烟未患COPD组（2．16±0．72），而吸烟未患COPD组又高于无吸烟对照组（1．09±0．48；P〈0．01）。（2）免疫组化显示，肺组织内MIF蛋白表达吸光度值吸烟患COPD组（0．277±0．025）高于吸烟未患COPD组（0．199±0．034），而吸烟未患COPD组高于无吸烟对照组（0．130±0．021；P〈0．01）。（3）相关性分析：肺组织内MIF mRNA表达与FEV。占预计值百分比、FEV1／FVC呈负相关（r分别为-0．578、-0．607，P值均〈0．01）。结论吸烟患COPD者肺组织中MIF表达明显增加，且与气流受限程度呈正相关，提示MIF可能在吸烟致COPD发病机制中起重要作用。Objective To investigate the expression of macrophage migration inhibition factor （MIF） in pulmonary tissues of the smokers with and without chronic obstructive pulmonary disease （COPD）. Methods The subjects were assigned into three groups： non-smokers without COPD （control group, n = 12）, smokers without COPD （ smoker group, n = 13 ） and smokers with COPD （ COPD group, n = 16）. The specimens were obtained from lung tissues as far away from cancer focus as possible （ 〉 5 cm）. Real-time quantitative PCR and immunohistochemistry were used to investigate the expression and distribution of MIF in pulmonary tissues. The relationship between the severity of airflow obstruction and the differential expressions of MIF in lung tissues of the smokers with or without COPD was analyzed. Results （ 1 ） MIF mRNA expression in COPD group （ 4. 87±1.79 ） was higher than that in the smoker group （2. 16±0. 72 ; P 〈 0. 01 ）, which was higher than that in the control group （ 1.09±0. 48 ; P 〈 0.01 ）. （2） Immunohistochemistry analysis showed that MIF protein expression in lung tissues of the COPD group （0. 277±20. 025 ） was higher than that in the smokers group （0. 199 ± 0.034; P 〈 0. 01 ）, which was significantly higher than that in control group （0. 130 ± 0. 021 ; P 〈 0. 01 ）. （ 3 ） Correlation analysis of MIF mRNA expression in the lung tissues and pulmonary function parameters of forced expired volume in one second（ FEV1 ） percentage of predicted（ FEV1 pred） and ratio of FEV1 to forced vital capacity （FEV1/FVC） suggested that MIF mRNA expression in the lung tissues was negatively related with FEV1 pred （r =-0.578, P 〈 0.01 ） and FEV1/FVC （r = - 0.607, P 〈 0.01 ）. Conclusions MIF expression significantly increases in the smokers with COPD, and MIF level in the lung is positively correlated with airflow limitation. The results suggest that MIF may play an important role in the pathogenesis of smoking- induced COPD.

关 键 词：肺疾病 慢性阻塞性 巨噬细胞迁移抑制因子 吸烟 

分 类 号：R563.9[医药卫生—呼吸系统]