The expression of macrophage migration inhibition factor in pulmonary tissues of smokers with or without chronic obstructive pulmonary disease / 中华内科杂志

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 groupsnon-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 (＞ 5cm).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 (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 smokinginduced COPD.