The change in the quantity of macrophages and their stabilin-1 + M2 subpopulation in the myocardium in patients during early postinfarction period

Abstract

Investigation of the role of macrophages and their functional plasticity in reparative process accompanying myocardial infarction (MI) and postinfarction cardiac remodeling is the relevant issue of current medical science. The purpose of the study: to investigate CD68+ and stabilin-1 +-macrophage infiltration and its dynamics in patients with MI in comparison with intact myocardium. The study included patients with fatal MI type 1 (n=41). All patients were divided into 4 groups depending on the onset of death (group 1, n=13, patients who died during the first 24 hours of MI; group 2, n=11, patients who died within 24-72 hours of MI; group 3, n=9, patients who died on days 4-10; and group 4, n=8, patients who died 11-28 days after MI). The control group included patients (n=9) who died due to fatal trauma and who did not suffer from cardiovascular pathology. For evaluation of functional immunopheno-type of macrophages we used immunohistochemistry. We counted cells expressing on their surface a common macrophages marker - CD68 and specific marker of regulatory M2 macrophages that demonstrates an anti-inflammatory activity - stabilin-1 in the infarct area, peri-infarct area, and non-infarct area. In comparison with the intact myocardium (control group) the number of CD68+-macrophages in the infarct area, periinfarct area, and non-infarct area increased from the first day of disease and peaked on day 4-10. The quantity of stabilin-1 + macrophages in all zones investigated during the acute phase of MI was lower than in the intact myocardium and increased on day 4-10 in the infarct area. Furthermore, in the non-infarct zone the quantity of stabilin-1 +-macrophages was lower than its quantity in the control group both during the acute phase and the regenerative phase of MI. The data obtained indicate the participation of stabilin-1 + macrophages in process of postinfarction myocardial healing and the development of the inflammatory immune response in the myocardium during the acute phase of MI and its maintaining at late stages of the disease.