TLR 4 expression on monocyte subsets in myocardial infarction

Background Monocyte toll‐like receptor 4 ( TLR 4) has been implicated in the pathogenesis of atherosclerosis with increased levels in myocardial infarction. The aim of this study was to assess the numbers of TLR 4 + monocytes in each monocyte subset in MI , the expression of TLR 4 and association with markers of monocyte activation, inflammation, myocardial damage and postmyocardial infarction ( MI ) cardiac contractility. Methods Surface expression of TLR 4 and numbers of TLR 4‐expressing monocytes were quantified by flow cytometry of venous blood in 50 patients with ST ‐elevation MI ( STEMI ), 48 with non‐ STEMI ( NSTEMI ) and 40 with stable coronary artery disease ( CAD ). These parameters were measured on days 1, 3, 7 and 30 post‐ MI in STEMI patients. Three monocyte subsets were defined as CD 14 ++ CD 16 − CCR 2 + (Mon1), CD 14 ++ CD 16 + CCR 2 + (Mon2) and CD 14 + CD 16 ++ CCR 2 − (Mon3). Plasma inflammatory cytokines were assessed using cytometric bead arrays. Results There was a significant increase in counts of TLR 4 + Mon1 and Mon2 in STEMI patients and TLR 4 + Mon2 in NSTEMI patients compared with controls with CAD . Monocyte TLR 4 + expression was similar between the groups, and was not changed during follow‐up in STEMI patients. Plasma interleukin‐6 ( IL 6) levels correlated positively with TLR 4 + Mon2 count ( r  = 0.54, P  <   0.001), but negatively with TLR 4 expression on Mon2 ( r  = −0.33, P  =   0.021). Conclusion Following treatment of acute MI , TLR 4 expression by individual monocyte subsets is unchanged. An increase in TLR 4 + Mon1 and Mon2 count in patients with STEMI and TLR + Mon2 count in those with NSTEMI is due to an increase in monocyte subset count and not to changes in TLR 4 expression. Monocyte counts but not TLR 4 expression correlate positively with plasma IL 6 levels. We suggest that TLR 4 expression may not be a reliable marker of monocyte activation in MI .