4.7 Article

Immunophenotyping of Monocyte Migration Markers and Therapeutic Effects of Selenium on IL-6 and IL-1β Cytokine Axes of Blood Mononuclear Cells in Preoperative and Postoperative Coronary Artery Disease Patients

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MDPI
DOI: 10.3390/ijms24087198

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selenium; post-cardiotomy syndrome; coronary artery disease; pro-inflammatory cytokines and monocytes

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Multivessel coronary artery disease (CAD) is characterized by chronic vascular inflammation and occlusion in the coronary arteries. This study aimed to investigate the inflammation levels and cytokine production in preoperative and postoperative CAD patients, and to intervene with selenium to reduce inflammation. It was found that postoperative CAD patients had higher levels of pro-inflammatory cytokines and CCR1(high) monocytes. In vitro intervention with selenium demonstrated mitigating effects on IL-6/STAT-3 axis and reduced IL-1 beta production and caspase-1 activity. However, selenium had no obvious effect on the TNF-alpha/NF-kappa B axis. Overall, selenium could be used to reduce systemic inflammation and protect bypass grafts during the post-surgical period.
Multivessel coronary artery disease (CAD) is characterized by underlying chronic vascular inflammation and occlusion in the coronary arteries, where these patients undergo coronary artery bypass grafting (CABG). Since post-cardiotomy inflammation is a well known phenomenon after CABG, attenuation of this inflammation is required to reduce perioperative morbidity and mortality. In this study, we aimed to phenotype circulating frequencies and intensities of monocyte subsets and monocyte migration markers, respectively, and to investigate the plasma level of inflammatory cytokines and chemokines between preoperative and postoperative CAD patients and later, to intervene the inflammation with sodium selenite. We found a higher amplitude of inflammation, postoperatively, in terms of CCR1(high) monocytes and significantly increased pro-inflammatory cytokines, IL-6, IL-8, and IL-1RA. Further, in vitro intervention with selenium displayed mitigating effects on the IL-6/STAT-3 axis of mononuclear cells derived from postoperative CAD patients. In addition, in vitro selenium intervention significantly reduced IL-1 beta production as well as decreased cleaved caspase-1 (p20) activity by preoperative (when stimulated) as well as postoperative CAD mononuclear cells. Though TNF-alpha exhibited a positive correlation with blood troponin levels in postoperative CAD patients, there was no obvious effect of selenium on the TNF-alpha/NF-kappa B axis. In conclusion, anti-inflammatory selenium might be utilized to impede systemic inflammatory cytokine axes to circumvent aggravating atherosclerosis and further damage to the autologous bypass grafts during the post-surgical period.

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