Abstract

We have previously reported that the lungs of patients with very severe chronic obstructive pulmonary disease (COPD) contain significantly higher numbers of alveolar macrophages than those of non-smokers or smokers. M1 and M2 macrophages represent pro- and anti-inflammatory populations, respectively. However, the roles of M1 and M2 alveolar macrophages in COPD remain unclear. Immunohistochemical techniques were used to examine CD163, CD204 and CD206, as M2 markers, expressed on alveolar macrophages in the lungs of patients with mild to very severe COPD (Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage I (mild) n = 11, II (moderate) n = 9, III (severe) n = 2, and IV (very severe) n = 16). Fifteen smokers and 10 non-smokers were also examined for comparison. There were significantly higher numbers of alveolar macrophages in COPD patients than in smokers and non-smokers. The numbers and percentages of CD163+, CD204+ or CD206+ alveolar macrophages in patients with COPD at GOLD stages III and IV were significantly higher than in those at GOLD stages I and II, and those in smokers and non-smokers. In patients with COPD, there was a significant negative correlation between the number of CD163+, CD204+ or CD206+ alveolar macrophages and the predicted forced expiratory volume in one second. Overexpression of CD163, CD204 and CD206 on lung alveolar macrophages may be involved in the pathogenesis of COPD.

Highlights

  • Chronic obstructive pulmonary disease (COPD) is an important pulmonary inflammatory disease for which the prevalence and associated mortality rates have been predicted to rise

  • The present study demonstrated that CD163+, CD204+ and CD206+ macrophages were abundant in the lungs of ex-smokers with sever and very severe COPD (GOLD stage III/IV)

  • There was a negative correlation between the number of CD163+, CD204+ or CD206+ cells and %FEV1.0 in COPD patients

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Summary

Introduction

Chronic obstructive pulmonary disease (COPD) is an important pulmonary inflammatory disease for which the prevalence and associated mortality rates have been predicted to rise. Smoking is recognized as the largest risk factor for COPD, and quitting smoking is thought to be important for prevention and control of COPD [1,2]. There is no effective treatment for COPDrelated pulmonary inflammation. We have previously demonstrated persistent and severe inflammation of small airways in the lungs of ex-smokers with very severe COPD. The number of macrophages in the lungs of patients with very severe COPD was increased [3]. Increased numbers of CD8+ T-cells, alveolar macrophages and neutrophils are characteristic pathological features of the lungs in COPD [4,5]. The effects of smoking on macrophage phenotypes in COPD are incompletely understood

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