engleski

Frequencies and activation of NK cell subsets differ between patients with myocardial infarction in respects to percutaneous coronary intervention

Introduction: Natural killer (NK) cells of CD3- CD56+ phenotype are heterogeneous population containing two distinct subsets based on the cell surface density of CD56 molecule. NK subset of CD56+dim phenotype shows high cytotoxic activities, whereas CD56+bright cells mostly produce cytokines and show regulatory features. Their participation and the role(s) in coronary artery disease in humans are currently insufficient. The aim of our study was to investigate the frequency of NK cell subsets and their activation status measured by cytotoxic mediator perforin in peripheral blood of patients with MI during the first month of rehabilitation period in respect to the application of stent re-vascularisation method. Methods: Peripheral blood samples were taken from patients with ST elevation MI (STEMI) who underwent percutaneous coronary intervention with bare metal stent implantation (25) and patients with non ST elevation MI (NSTEMI) treated just with medicaments (20) on day 7, 14, 21 and 28 after MI. Peripheral blood mononuclear cells (PBMC) were immediately isolated by gradient density centrifugation. Simultaneous intracellular cytolytic mediator perforin and the cell surface CD3 and CD56 molecules were labeled by immunofluorescence and analyzed by flow cytometry. Troponin I concentrations on the 1st hospital day were compared between groups investigated. Results: The frequency of total NK cells gated as CD3- CD56+ events, neither significantly changed in NSTEMI, nor in STEMI patients during rehabilitation period. Mean fluorescence intensity for CD56 molecule significantly differed between CD56+dim and CD56+bright subsets in NSTEMI and STEMI patients at all the time points investigated. The frequency of CD56+dim increased, whereas CD56+bright subset decreased in NSTEMI patients on day 7 and 14 after MI. In the NSTEMI patients, gradual and wavy regression of increased perforin expression was found in both NK subsets. These changes were not noticed in STEMI patients. Conclusions: The reduction of inflammatory reaction that follow the early reperfusion in PCI-treated STEMI patients and prolonged inflammation in NSTEMI patients might represent an important mechanism behind the well established clinical benefits from primary PCI leading toward the introduction of primary PCI in routine NSTEMI treatment.

immune reaction ; myocardial infarction ; NK cells ; perforin ; peripheral blood

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