title: [The expression of macrophage migration inhibition factor in pulmonary tissues of smokers with or without chronic obstructive pulmonary disease].
abstract: 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 ± 0.025) 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 (FEV(1)) percentage of predicted (FEV(1) pred)and ratio of FEV(1) to forced vital capacity (FEV(1)/FVC) suggested that MIF mRNA expression in the lung tissues was negatively related with FEV(1) pred (r = -0.578, P < 0.01) and FEV(1)/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.
authors.affiliation: Key Laboratory of Chinese Ministry of Public Health, Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
authors.forename: Wei-bin
authors.initials: WB
authors.lastname: She
authors.forename: Xian-sheng
authors.initials: XS
authors.lastname: Liu
authors.forename: Wang
authors.initials: W
authors.lastname: Ni
authors.forename: Shi-xin
authors.initials: SX
authors.lastname: Chen
authors.forename: Yong-jian
authors.initials: YJ
authors.lastname: Xu
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D019746:Intramolecular Oxidoreductases / Q000378:metabolism*; D008168:Lung / Q000378:metabolism*; D008263:Macrophage Migration-Inhibitory Factors / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism*; D012907:Smoking / Q000378:metabolism*
chemical_list: D008263:Macrophage Migration-Inhibitory Factors; D019746:Intramolecular Oxidoreductases; C515598:MIF protein, human