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Updated: Mar 2, 2026
Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
COPD monocytes demonstrate impaired migratory ability
Arjun K Ravi1,2, Jonathan Plumb3, Rosemary Gaskell3
1NIHR Respiratory and Allergy Clinical Research Facility, Manchester Academic Health Science Centre, University Hospital South Manchester NHS Foundation Trust, University of Manchester, Manchester, UK. ARavi@meu.org.uk.
Background:
Increased lung macrophage numbers in COPD may arise from upregulation of blood monocyte recruitment into the lungs. CCR5 is a monocyte chemokine receptor regulated by interleukin-6 (IL-6); the concentration of CCR5 ligands are known to be elevated in COPD lungs. The objective of this study was to investigate mechanisms of monocyte recruitment to the lung in COPD, including the role of CCR5 signalling.
Methods:
Ninety one COPD patients, 29 smokers (S) and 37 non-smokers (NS) underwent sputum induction, plasma sampling (to measure IL-6 and soluble IL-6 receptor [sIL-6R] by immunoassay), monocyte characterization (by flow cytometry) and monocyte isolation for cell migration and quantitative polymerase chain reaction studies. Lung tissue was used for immunohistochemistry.
Results:
Plasma IL-6 and sIL-6R levels were increased in COPD. Greater proportions of COPD CD14++CD16+ monocytes expressed CCR5 compared to controls. Monocyte stimulation with IL-6 and sIL-6R increased CCR5 gene expression. COPD monocytes demonstrated impaired migration towards sputum supernatant compared to NS (% migration, 4.4 vs 11.5, respectively; p < 0.05). Pulmonary microvessels showed reduced monocyte recruitment (% marginated cells) in COPD compared to NS, (9.3% vs 83.1%, respectively). The proportion of replicating Ki67+ alveolar macrophages was reduced in COPD compared to NS. All alveolar macrophages from COPD and S expressed the anti-apoptosis marker BCL2; this protein was not present in non-smokers or COPD ex-smokers.
Conclusion:
COPD monocytes show decreased migratory ability despite increased CCR5 expression. Increased COPD lung macrophage numbers may be due to delayed apoptosis.
Insights
Chronic obstructive pulmonary disease (COPD) monocytes exhibit reduced migration despite higher CCR5 receptor expression. Increased lung macrophages in COPD may result from delayed cell death, not just recruitment.
Area of Science:
- Immunology
- Respiratory Medicine
- Cell Biology
Background:
- Increased lung macrophage numbers in Chronic Obstructive Pulmonary Disease (COPD) may stem from enhanced blood monocyte recruitment.
- Chemokine receptor 5 (CCR5) is a key monocyte receptor regulated by interleukin-6 (IL-6), with elevated CCR5 ligand concentrations observed in COPD lungs.
Purpose of the Study:
- To investigate the mechanisms of monocyte recruitment to the lungs in COPD.
- To elucidate the specific role of CCR5 signaling in COPD pathogenesis.
Main Methods:
- Study involved 91 COPD patients, 29 smokers, and 37 non-smokers undergoing sputum induction and plasma sampling.
- Monocyte characterization, migration assays, quantitative PCR, and immunohistochemistry were performed on lung tissue.
Main Results:
- COPD patients showed increased plasma IL-6 and soluble IL-6 receptor (sIL-6R) levels.
- COPD monocytes exhibited higher CCR5 expression but impaired migration towards sputum supernatant compared to non-smokers.
- Pulmonary microvessel monocyte recruitment was reduced in COPD, and alveolar macrophages showed delayed apoptosis (BCL2 expression).
Conclusions:
- COPD monocytes display reduced migratory capacity despite elevated CCR5 expression.
- Increased lung macrophage populations in COPD may be attributed to delayed apoptosis rather than solely increased recruitment.
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