Background and objective: Alveolar macrophages (AM) play an important role in the pathogenesis of COPD, and their numbers are significantly increased in patients with COPD. We previously demonstrated that expression of the transcription factor, MafB, was upregulated in AM of mice exposed to cigarette smoke. The aim of this study was to investigate whether the expression of MafB is associated with the degree of airflow limitation (AFL) in smokers.
Methods: Lung tissue specimens were obtained from male patients undergoing resection of small peripheral lung tumours. The patients were classified into three groups according to smoking index and FEV1 /FVC: (i) non-smokers or non-heavy ex-smokers without AFL (FEV1 /FVC ≥ 0.7, smoking index ≤ 400) (n=8); (ii) heavy current smokers without AFL (FEV1 /FVC ≥ 0.7, smoking index ≥ 800) (n=8); and (iii) heavy current smokers with AFL (FEV1 /FVC < 0.6, smoking index ≥ 800) (n=8). The intensity of immunostaining for MafB in AM was quantified by image analysis.
Results: Immunostaining for MafB was significantly enhanced in AM of smokers with AFL compared with AM of subjects without AFL. Smoking index, FEV1/FVC and FEF(25-75%) (% predicted) were significantly correlated with the intensity of MafB immunostaining. Multiple linear regression analysis revealed that FEV1 % was also an independent negative predictor of the intensity of MafB immunostaining.
Conclusions: The degree of immunostaining for MafB in AM was correlated with the degree of AFL in smokers. MafB may be involved in the pathophysiology of COPD.
© 2010 The Authors. Respirology © 2010 Asian Pacific Society of Respirology.