Overexpression of CD163, CD204 and CD206 on alveolar macrophages in the lungs of patients with severe chronic obstructive pulmonary disease

PLoS One. 2014 Jan 30;9(1):e87400. doi: 10.1371/journal.pone.0087400. eCollection 2014.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Antigens, CD / genetics*
  • Antigens, CD / metabolism
  • Antigens, Differentiation, Myelomonocytic / genetics*
  • Antigens, Differentiation, Myelomonocytic / metabolism
  • Female
  • Humans
  • Lectins, C-Type / genetics*
  • Lectins, C-Type / metabolism
  • Lung / pathology*
  • Macrophages, Alveolar / metabolism
  • Macrophages, Alveolar / pathology*
  • Male
  • Mannose Receptor
  • Mannose-Binding Lectins / genetics*
  • Mannose-Binding Lectins / metabolism
  • Matrix Metalloproteinase 9 / genetics
  • Matrix Metalloproteinase 9 / metabolism
  • Middle Aged
  • Pulmonary Alveoli / metabolism
  • Pulmonary Alveoli / pathology*
  • Pulmonary Disease, Chronic Obstructive / genetics*
  • Pulmonary Disease, Chronic Obstructive / metabolism
  • Pulmonary Disease, Chronic Obstructive / pathology
  • Receptors, Cell Surface / genetics*
  • Receptors, Cell Surface / metabolism
  • Scavenger Receptors, Class A / genetics*
  • Scavenger Receptors, Class A / metabolism
  • Severity of Illness Index
  • Smoking / genetics
  • Smoking / metabolism
  • Smoking / pathology

Substances

  • Antigens, CD
  • Antigens, Differentiation, Myelomonocytic
  • CD163 antigen
  • Lectins, C-Type
  • MSR1 protein, human
  • Mannose Receptor
  • Mannose-Binding Lectins
  • Receptors, Cell Surface
  • Scavenger Receptors, Class A
  • Matrix Metalloproteinase 9

Supplementary concepts

  • Pulmonary Disease, Chronic Obstructive, Severe Early-Onset

Grants and funding

This work was supported by a grant to the Respiratory Failure Research Group from the Ministry of Health, Labour and Welfare, Japan (T.H.), a Grant-in-Aid for Scientific Research (C) (no. 25461201: T.H.) from the Ministry of Education, Science, Sports, and Culture of Japan, Kato Memorial Fund for Incurable Diseases Research (Tokyo, Japan) (T.H.), Kaibara Morikazu Medical Science Promotion Foundation (HI), Allergy Foundation (T.H. and H.I.) and Takeda Science Foundation (Tokyo, Japan) (H.I.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.