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Updated: Mar 25, 2026
Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Human classical monocytes display unbalanced M1/M2 phenotype with increased atherosclerotic risk and presence of
Helen Williams1,2, Gabriel Cassorla3, Nicholas Pertsoulis3
1Vascular Biology Research Centre, Department of Surgery, Westmead Hospital, Westmead, Australia - helen.williams@sydney.edu.au.
Insights
Atherosclerosis patients exhibit altered monocyte subsets, with increased intermediate monocytes and a more inflammatory M1 macrophage profile. These changes correlate with disease risk and likely drive atherosclerotic progression.
Area of Science:
- Immunology
- Cardiovascular Research
Background:
- Monocyte and macrophage subsets are implicated in atherosclerosis.
- Intermediate monocytes and M1 macrophages are elevated in cardiovascular disease and unstable plaques.
- Functional and phenotypic alterations of these subsets require further investigation.
Purpose of the Study:
- To investigate functional and phenotypic alterations in monocyte subsets in atherosclerotic patients.
- To compare M1 and M2 marker expression on monocyte subsets between patients and controls.
Main Methods:
- Whole blood flow cytometry was employed.
- Expression of M1 (CD86) and M2 (CD163) markers on monocyte subsets was analyzed.
- Comparison between atherosclerotic patients and healthy controls.
Main Results:
- Atherosclerotic patients displayed a more inflammatory monocyte profile.
- This profile included increased intermediate monocyte proportions and a higher CD86/CD163 ratio on classical monocytes.
- Elevated serum M1-related chemokines were observed in patients.
- A higher CD86/CD163 ratio correlated with atherosclerotic risk factors in controls.
Conclusions:
- Monocyte subsets exhibit functional and phenotypic changes in cardiovascular disease.
- These alterations are likely contributors to atherosclerotic progression.
Background:
Specific monocyte and macrophage subsets have been implicated in atherosclerosis, with intermediate monocytes proportionally elevated in cardiovascular disease and M1 macrophages abundant in unstable atherosclerotic plaques. While several studies have shown altered proportions of these subsets in atherosclerosis, studies examining functional and phenotypic subset alterations remain scarce.
Methods:
We used whole blood flow cytometry to investigate the expression of M1 (CD86) and M2 (CD163) markers on monocyte subsets of atherosclerotic patients and controls.
Results:
Atherosclerotic patients had a more inflammatory monocyte profile than controls, indicated by increased intermediate subset proportions, a higher classical monocyte CD86/CD163 ratio, and elevated serum M1-related chemokines. A more inflammatory profile appeared to correlate with atherosclerotic risk, as in controls classical monocyte CD86/CD163 ratio was negatively correlated with HDL and apolipoprotein A1, and positively correlated with interleukin-1β.
Conclusions:
We conclude that monocyte subsets show functional and phenotypic changes in cardiovascular disease and such changes are likely to contribute to atherosclerotic progression.
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