Early Expression of FcγRI (CD64) on Monocytes of Cardiac Surgical Patients and Higher Density of Monocyte Anti‐Inflammatory Scavenger CD163 Receptor in “On‐Pump” Patients

Abstract

Objective. Activation of innate immunity cells is inseparably linked to cardiac surgical operation. The aim of this study was to assess the kinetics in the expression of receptor for Fc part of IgG, FcγRI (CD64), and scavenger receptor CD163 on peripheral blood cells of cardiac surgical patients and to examine the effect of cardiac bypass as a separable influence on the systemic acute inflammatory response. Methods. Forty patients, twenty in each group, were randomly assigned to CABG surgery performed either with “on-pump” or without “off-pump” cardiopulmonary bypass. Standardized quantitative flow cytometry method was used to determine the expression of surface markers. Results. The density of CD64 molecule on monocytes reached maximum on the 1st postoperative day (P<.001) whereas the peak for CD64 molecule expression on granulocytes was postponed to the 3rd postoperative day (P<.001). The expression of CD163 scavenger molecule on monocytes reached maximum on the 1st postoperative day (P<.001). The density of CD163 molecule on monocytes on the 1st postoperative day is significantly higher in “on-pump” patients in comparison with “off-pump” patients (P<.001). Conclusion. In cardiac surgical patients the expression of activation marker FcγR1 (CD64) on monocytes is increased earlier in comparison with granulocytes in both “on-pump” and “off-pump” patients. The expression of scavenger molecule CD163 on monocytes is significantly higher in “on-pump” patients.

Kinetic of monocytes Fcγ receptors in patients after coronary artery bypass

“…We could not fine a statistically difference in monocyte CD64 dynamics pattern by a subgroup of patients (n=8), who developed postoperatively SIRS associated with infections. These results correspond well with earlier report [5], and indicate that activation of CD64 on monocytes is a more unspecific phenomenon than "de novo" synthesis of this receptor on neutrophils. It also confirms the conclusion that in the presence of proinflammatory stimuli the upregulation of CD64 on monocytes and neutrophils at least are regulated by different mechanisms [11].…”

“…All three receptors have been investigated by leukocytes in different study design by different patient's groups. The key goal was either to identify patients at the risk of development of overwhelming inflammatory response or to implicate the causative agent of such a response, for example, bacterial infection [5][6][7]. In a previous study we found neutrophil CD64 expression to be a specific marker for the detection of bacterial infections after a major surgical trauma [8].…”

Scavenger Receptor CD163 and Its Biological Functions

“…It represents a new class of macrophage specific biomarkers relevant to the detection of coronary artery disease, transplantation, atherosclerosis, rheumatoid arthritis, lysosomal Gaucher storage diseases and cancer, cardiac surgery patient respectively (4,15).…”

“…In many of this diseases, the patients are extensively exposed to a large amounts of free heme/hemoproteins due to intravascular haemolysis and tissues damage; CD163 represents a highly efficient system to remove potentially toxic an pro inflammatory hemoglobin from the circulation and local sites of inflammation; for this reason is considered to be a prognostic marker in different diseases; mainly in inflammation (15).…”

Current Evidence of On-Pump Versus Off-Pump Coronary Artery By-Pass Surgery

“…Randomized comparisons between CCABG and OPCAB shows the CCABG patients to have increased serum-levels of a multitude of different substances including tumor necrosis factor-alpha, interleukins 6 and 8, selectin, c-reactive protein, intracellular adhesion molecule -1, and vascular endothelial growth factor (39,(67)(68)(69)(70)(71)(72). Also, the expression of a scavenger molecule on monocytes is significantly higher in "on-pump" patients (73). It has been proposed that this inflammatory over-activation can be harmful and lead to organ failure and infections.…”