Leukocyte and leukocyte subset counts reveal compensatory mechanisms in coronary heart disease

BackgroundLeukocyte number in the circulation plays a central role in inflammatory diseases, such as coronary heart disease (CHD). Increased counts are correlated with the intensity of the peri-infarction inflammatory response and adverse outcomes. We investigated leukocyte and leukocyte subset counts in dyslipidaemia patients and their relationship with LDL oxidation.MethodsDyslipidaemia patients (207) were selected for blood counts and LDL-C testing. The level of HNP-1and myeloperoxidase in subsets of leukocytes and their relationship with LDL oxidation were compared between 24 CHD patients and 24 normal controls.ResultsIn dyslipidaemia patients, total leukocyte and neutrophil counts increased with LDL-C (p = 0.001). Monocyte counts showed the opposite trend (p = 0.001). Although serum HNP-1 levels were not different between CHD patients and normal controls (p = 0.558), neutrophil HNP-1 mRNA levels were 2.13-fold greater than those of normal controls. However, monocyte HNP-1 mRNA levels were lower (p = 0.005). The distribution of myeloperoxidase in monocytes and neutrophils is different, myeloperoxidase locates mainly in the cytoplasm of monocytes, on the cell membrane of neutrophils.ConclusionsLeukocyte and leukocyte subset counts may correlate with LDL-C levels and LDL oxidation. The monocyte–neutrophil interaction reveals a potential compensatory mechanism associated with LDL oxidation in CHD that may be a prognostic factor of CHD.

► We found that monocytes and neutrophils have functional cross-talk in CHD.
► We first demonstrate that neutrophils compensate for monocytes in LDL oxidation.
► We combine the clinical research and experimental research to reveal the mechanism.
► HNP-1 and MPO in monocyte and neutrophil are associated with the mechanism.
► The compensatory mechanism may be a novel clue for early clinical diagnosis of CHD.