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S100A9/CD163 Expression in Circulating Classical Monocytes in Chronic Obstructive Pulmonary Disease
Masahiro Yamashita1, Yu Utsumi1, Kohei Yamauchi1,2
1Department of Pulmonary Medicine, Allergy and Immunological Diseases, Iwate Medical University School of Medicine, Shiwa, Japan.
COPD
|September 23, 2020
Summary
This study reveals that circulating monocytes in chronic obstructive pulmonary disease (COPD) exhibit increased pro-inflammatory markers, S100A9. These findings offer new insights into the cellular mechanisms driving COPD development.
Area of Science:
- Immunology
- Pulmonology
- Cell Biology
Background:
- While macrophage polarization in chronic obstructive pulmonary disease (COPD) is studied, circulating monocyte phenotypes remain less understood.
- Cigarette smoking is a primary risk factor for COPD, influencing immune cell function.
Purpose of the Study:
- To investigate the impact of cigarette smoking and COPD on the cellular phenotype of circulating classical monocytes.
- To analyze the expression of S100A9 (pro-inflammatory) and CD163 (anti-inflammatory) markers on monocytes.
Main Methods:
- Flow cytometry was used to analyze cell surface markers on classical monocytes from 32 COPD patients and 36 healthy controls (smokers and non-smokers).
- Expression levels of S100A9 and CD163 were quantified.
- Multivariate and Receiver Operating Characteristic (ROC) analyses were performed.
Main Results:
- COPD patients showed a significant increase in S100A9+ classical monocytes compared to non-smoker controls.
- The proportion of S100A9-CD163+ monocytes was decreased in smokers and COPD patients.
- The ratio of S100A9+CD163-/S100A9-CD163+ cells showed diagnostic potential for differentiating COPD from smokers.
Conclusions:
- Circulating classical monocytes in COPD patients display an enhanced pro-inflammatory phenotype.
- These findings contribute to understanding the role of monocyte subsets in COPD pathogenesis.
- S100A9 expression on monocytes may serve as a potential biomarker in COPD.
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