Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock

LPS Differentially Affects Expression of CD14 and CCR2 in Monocyte Subsets of Post-STEMI Patients with Hyperglycemia.

Abstract

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 C-C 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 microg/mL for 4 hours) 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.