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A Journal on Angiology

Official Journal of the International Union of Angiology, the International Union of Phlebology and the Central European Vascular Forum
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International Angiology 2016 Feb 12

language: English

Human classical monocytes display unbalanced M1/M2 phenotype with increased atherosclerotic risk and presence of disease

Helen WILLIAMS 1, 2, Gabriel CASSORLA 1, Nicholas PERTSOULIS 1, Vyoma PATEL 1, Mauro VICARETTI 1, 2, Najwa MARMASH 3, Kerry HITOS 4, John P. FLETCHER 1, 2, Heather MEDBURY 1, 2

1 Vascular Biology Research Centre, Department of Surgery, Westmead Hospital, Westmead, Australia; 2 Western Clinical School, University of Sydney, Westmead, Australia; 3 Research and Education Network, WSLHD, Westmead Hospital, Westmead, Australia; 4 Westmead Research Centre for Evaluation of Surgical Outcomes, Department of Surgery, University of Sydney, Westmead Hospital, Westmead, Australia


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.
CONCLUSION: 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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