Transient reduction and activation of circulating dendritic cells in patients with acute myocardial infarction

Abstract

BackgroundDendritic cells (DCs) are highly potent professional antigen-presenting cells that play a central role in initiating the primary immune response. Accumulating evidence suggests that immune-mediated inflammation plays an important role in the pathophysiology of AMI, but the mechanism that triggers such immune responses is unknown. MethodsUsing multi-color flow-cytometry, we determined the numbers of circulating myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) in patients with AMI (n=26) or stable angina pectoris (SAP) (n=19), and in age-matched control subjects (n=19). The DC activation markers CD40 and CD83 were also measured. ResultsOn admission, circulating mDC and pDC counts were significantly lower in AMI patients compared to control subjects and SAP patients (mDC, P<0.01; pDC, P<0.05). The activation markers of mDCs in AMI patients were significantly higher and returned to the levels of control subjects or SAP patients 3days after AMI (mDC, P<0.05; pDC, P<0.05). Reductions of circulating mDC and pDC numbers were restored 7days after the onset of AMI. Furthermore, we found that the recovery of the circulating DC numbers 14days after AMI was correlated with the alterations of creatine kinase-MB (CK-MB) (mDC, r=0.48, P<0.05; pDC, r=0.52, P<0.01) and brain natriuretic peptide (BNP) (mDC, r=0.53, P<0.01; pDC, r=0.51, P<0.01). ConclusionOur findings suggest that the transient reduction and activation of circulating DCs may play important roles in the pathophysiology of myocardial injury after AMI.