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Published on: August 13, 2015
The CD14++CD16+ monocyte subset and monocyte-platelet interactions in patients with ST-elevation myocardial
L D Tapp1, E Shantsila, B J Wrigley
1University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, UK.
Insights
The intermediate monocyte subset (Mon2) uniquely changes after ST-elevation myocardial infarction (STEMI), correlating with cardiac injury markers and predicting left ventricular function. Monocyte-platelet aggregates remain elevated one month post-STEMI.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Hematology
Background:
- Monocytes exhibit subset heterogeneity, influencing myocardial damage and repair.
- The specific roles of human monocyte subsets, particularly CD14++CD16+, in ST-elevation myocardial infarction (STEMI) remain unclear.
- Understanding monocyte dynamics and their interaction with platelets post-STEMI is crucial for assessing cardiac outcomes.
Purpose of the Study:
- To investigate the dynamic changes in three human monocyte subsets (Mon1, Mon2, Mon3) following STEMI.
- To analyze the contribution of these subsets to monocyte-platelet aggregates (MPAs).
- To determine the relationship between monocyte subset behavior, MPAs, and left ventricular ejection fraction (LVEF) post-STEMI.
Main Methods:
- Flow cytometry was used to analyze monocyte subsets and MPAs in STEMI patients, stable coronary artery disease (CAD) patients, and healthy volunteers.
- Measurements were taken at multiple time points (days 1, 3, 7, and 30) after primary percutaneous coronary intervention (PCI).
- Monocyte activation (NFκB pathway), plasma cytokines, troponin levels, and LVEF were assessed and correlated with monocyte subsets and MPAs.
Main Results:
- The intermediate monocyte subset (Mon2) showed significant dynamic changes, increased CD14 and CCR2 expression, and reduced CD16 expression post-STEMI.
- Mon2 subset activity correlated with peak troponin, IL-6, and IL-10 levels, while Mon1 correlated with IL-6.
- Reduced Mon2 CD16 expression on day 1 predicted higher LVEF, and MPA counts remained elevated one month after STEMI.
Conclusions:
- The Mon2 'intermediate' monocyte subset exhibits distinct dynamics and functional characteristics after STEMI, linked to cardiac injury markers and recovery.
- Persistent elevation of MPAs post-STEMI may influence monocyte subset function.
- These findings highlight the importance of monocyte subset analysis in understanding STEMI pathophysiology and predicting cardiac outcomes.
Aim:
Monocytes contribute to both myocardial damage and repair by virtue of subset heterogeneity. The dynamics and functional characteristics of the three human monocyte subsets, including the unique CD14++CD16+ subset, and their contributions to monocyte platelet aggregates (MPAs) following ST-elevation myocardial infarction (STEMI) are unknown. We aimed to examine dynamic changes and relation to left ventricular ejection fraction (LVEF) of the three human monocyte subsets and their aggregates with platelets following STEMI.
Methods:
Three monocyte subsets, CD14++CD16-CCR2+ ('classical', Mon1), CD14++CD16+CCR2+ ('intermediate', Mon2) and CD14+CD16++CCR2- ('non-classical', Mon3), and their contribution to MPAs were analyzed by flow cytometry in 50 patients with STEMI, 40 patients with stable coronary artery disease (CAD) and 40 healthy volunteers. Study parameters were measured within 24 h of primary percutaneous coronary intervention (PCI) (day1) and on days 3, 7 and 30. Monocyte activation was assessed by measuring the nuclear factor κB (NFκB) pathway. LVEF was assessed 6 weeks after STEMI. Correlations between monocyte subsets/MPAs and plasma cytokines and troponin were assessed.
Results:
We observed marked differences in subset dynamics, with a prominent increase in Mon2 (P < 0.0001) but no changes in Mon3. Significant increases in Mon2 CD14 (P = 0.002) and CCR2 (P < 0.0001) expression, and reduction in CD16 expression (P = 0.001) were seen. NFκB pathway activity increased most prominently in Mon2 (P = 0.007). Mon2 count correlated with peak troponin (r = 0.31, P = 0.04) and plasma interleukin (IL)-6 (r = 0.65, P < 0.0001) and IL-10 (r = 0.34, P = 0.017). Mon1 correlated with IL-6 (r = 0.55, P < 0.0001). Reduced Mon2 expression of CD16 on day 1 was independently predictive of higher LVEF (β = -0.37, P = 0.013). The increase in MPA count following STEMI persisted at 1 month.
Conclusion:
The Mon2 'intermediate' subset has unique dynamic and functional characteristics following STEMI and significant correlations with troponin, plasma cytokines and convalescent left ventricular function. The persistent increase in MPA count 30 days after STEMI may affect monocyte subset functional activity.
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