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Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
11:20

Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice

Published on: March 2, 2019

Defective macrophage phagocytosis of bacteria in COPD

A E Taylor1, T K Finney-Hayward, J K Quint

  • 1Airways Disease Section, National Heart and Lung Institute, Dovehouse Street, London, UK.

The European Respiratory Journal
|November 10, 2009
PubMed

Insights

Macrophages in chronic obstructive pulmonary disease (COPD) show impaired bacterial clearance. This defective immune response in COPD patients may increase bacterial colonization and exacerbation frequency.

Area of Science:

  • Immunology
  • Pulmonary Medicine
  • Microbiology

Background:

  • Exacerbations of chronic obstructive pulmonary disease (COPD) lead to hospitalizations and disease progression.
  • Bacterial infections contribute to approximately half of COPD exacerbations, suggesting impaired pathogen clearance.
  • Lower airways colonization by bacteria is common in COPD patients.

Purpose of the Study:

  • To investigate whether bacterial clearance by macrophages is defective in COPD.
  • To compare the phagocytic capacity of macrophages from COPD patients with those from healthy smokers and non-smokers.

Main Methods:

  • Assessed phagocytosis of fluorescently labeled beads, Haemophilus influenzae, and Streptococcus pneumoniae by alveolar macrophages and monocyte-derived macrophages (MDM) using fluorimetry and flow cytometry.
  • Measured cell surface receptor expression (TLR2, TLR4, CD163, CD36, mannose receptor) via flow cytometry.
  • Evaluated the impact of medications (budesonide, formoterol, azithromycin) on macrophage phagocytosis.

Main Results:

  • No significant difference in polystyrene bead phagocytosis was observed between MDM from COPD patients, smokers, and non-smokers.
  • MDM from COPD patients exhibited reduced phagocytic responses to S. pneumoniae and H. influenzae compared to non-smokers and smokers.
  • Reduced phagocytosis was not linked to alterations in the expression of tested cell surface receptors or suppressed by common COPD medications.

Conclusions:

  • Macrophage innate immune responses are suppressed in COPD patients.
  • Defective bacterial clearance by macrophages may contribute to bacterial colonization and increased exacerbation frequency in COPD.
  • Targeting macrophage function could be a therapeutic strategy for COPD exacerbations.

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