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LPS differentially affects expression of CD14 and CCR2 in monocyte subsets of Post-STEMI patients with hyperglycemia
Anson M Blanks1, Lauren N Pedersen1, Heather L Caslin2
1Department of Kinesiology and Health Sciences, College of Humanities and Sciences, Virginia Commonwealth University, Richmond, VA 23284, United States.
Insights
Individuals with impaired glucose tolerance post-STEMI show heightened monocyte activation. This may impede myocardial healing and increase heart failure risk.
Area of Science:
- Immunology
- Cardiology
- Metabolism
Background:
- Monocyte subsets are crucial for myocardial wound healing after ST-segment elevation myocardial infarction (STEMI).
- CC chemokine receptor type 2 (CCR2) mediates monocyte migration, while CD14 is involved in inflammatory activation.
- Understanding monocyte responses in relation to glucose levels post-STEMI is vital for predicting healing outcomes.
Purpose of the Study:
- To investigate the impact of ex-vivo lipopolysaccharide (LPS) activation on monocyte subset CD14 and CCR2 expression.
- To compare these effects in post-STEMI patients with normal versus elevated random blood glucose levels.
Main Methods:
- Monocytes were isolated from post-STEMI patients categorized into normal glucose (NG) and impaired glucose (IG) groups.
- Cells were analyzed for CD14 and CCR2 expression before and after LPS activation (1 µg/mL for 4 hours).
Main Results:
- Intermediate monocytes from IG individuals exhibited lower CD14 expression compared to NG, a difference sustained post-LPS activation.
- The normal glucose group demonstrated a greater reduction in classical monocyte CCR2 expression after LPS activation, creating a significant difference between groups.
Conclusions:
- Impaired glucose tolerance in post-STEMI patients is associated with an exaggerated pro-inflammatory monocyte response.
- This heightened activation may compromise myocardial repair processes, potentially increasing the risk of chronic heart failure.
Aims:
Following ST-segment elevation myocardial infarction (STEMI), recruitment and activation of monocytes [classical (CD14++CD16-CCR2++), intermediate (CD14++CD16+CCR2+), non-classical (CD14LowCD16++CCR2Low)] are needed for myocardial wound healing. Monocyte surface receptor CC chemokine receptor type 2 (CCR2) is responsible for monocyte chemotaxis to sites of inflammation and the lipopolysaccharide (LPS)-binding protein co-receptor, CD14, is involved in pro-inflammatory monocyte activation. The purpose of this investigation was to determine the effects of ex-vivo LPS activation on monocyte subset CD14 and CCR2 expression in post-STEMI individuals with normal and elevated random blood glucose.
Methods:
Post-STEMI subjects were identified as normal random glucose (NG, <98 mg/dL, n = 13) or impaired random glucose (IG, ≥98 mg/dL, n = 26) and monocytes were analyzed for non-activated and LPS-activated (1 µg/mL for 4 h) CCR2 and CD14 expression.
Results:
Non-activated intermediate monocytes from IG showed decreased CD14 expression when compared to NG, which was maintained following LPS-activation. The NG group showed a larger absolute reduction in classical CCR2 expression, leading to a significant difference between NG and IG following LPS-activation.
Conclusion:
Results suggest a heightened response to pro-inflammatory activation in IG following STEMI, which may impair or delay post-STEMI myocardial healing, and thus increase the incidence of chronic heart failure. NIH 1R34HL121402.
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