Abstract 2249: Mobilization and Activation of Circulating Dendritic Cells in Patients with Acute Myocardial Infarction
Although it is well known that immune-mediated inflammation contributes to the pathophysiology of acute myocardial infarction (AMI), little is known regarding the source and the mechanism for this immune activation. Dendritic cells (DC) are the most potent antigen-presenting cells that play a central role in initiating the primary immune response. DC comprises two distinct functional subsets, myeloid DC (mDC) and plasmacytoid DC (pDC). We hypothesized that the numbers and activities of peripheral blood DC could be altered in patients with AMI.
Methods: To address this question, we examined the temporal change of activation and numbers of peripheral blood mDC and pDC in patients with AMI (n=14) and age-matched control subjects (n=10), using multi-color flowcytometry. We also examined the recruitment of DCs in the hearts from autopsied patients (n=5) by immunohistochemistry using anti-fascin monoclonal antibody.
Results: We found that the numbers of mDC and pDC were lower in patients with AMI compared with normal subjects on admission (p<0.01). The numbers of mDC and pDC were markedly reduced at 3 days after onset of AMI. The numbers of mDC and pDC were restored at 14 days after onset of AMI. Interestingly, the activation markers (CD40, CD83 CCR7) of mDCs and pDCs were significantly upregulated in the AMI patients compared with normal subjects (p<0.01). Recruitment of DCs into the border zone of infarcted lesion was observed in the hearts from autopsied AMI patients (p<0.01).
The peripheral blood mDC and pDC numbers were transiently reduced in patients with AMI.
The activation markers of circulating mDC and pDC were increased in patients with AMI
DC were significantly recruited in border zone of infarcted lesion in the hearts from autopsied AMI patients.
These data suggest that mobilization and activation of DC may play a role in the pathophysiology of cardiac injury during AMI.