Post‐reperfusion changes of monocyte function in coronary blood after extracorporeal circulation

Background Neutrophil and mononuclear cell functional changes represent a hallmark of inflammation during cardiopulmonary bypass and cardiovascular surgery. Knowledge of mechanisms underlying monocyte functional modulation in coronary blood may be useful to develop protective interventions that can...

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Published in:Cytometry. Part B, Clinical cytometry Clinical cytometry, 2005-05, Vol.65B (1), p.14-21
Main Authors: Sbrana, Silverio, Bevilacqua, Stefano, Buffa, Manuela, Spiller, Dario, Parri, Maria Serena, Gianetti, Jacopo, De Filippis, Rossella, Clerico, Aldo
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Antigens, Surface - biosynthesis
cardiopulmonary bypass
Cell Adhesion
coronary blood
Coronary Circulation
Enzyme-Linked Immunosorbent Assay
Female
Flow Cytometry
Gene Expression Regulation
Heart Arrest - blood
Humans
Interleukins - biosynthesis
Leukocytes, Mononuclear - cytology
Male
Middle Aged
monocyte
Monocytes - cytology
Monocytes - pathology
Neutrophils - cytology
platelet
Platelet Activation
Reperfusion
Reperfusion Injury - prevention & control
Respiratory Burst
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Summary:Background Neutrophil and mononuclear cell functional changes represent a hallmark of inflammation during cardiopulmonary bypass and cardiovascular surgery. Knowledge of mechanisms underlying monocyte functional modulation in coronary blood may be useful to develop protective interventions that can limit ischemia/reperfusion injury. Methods Samples of 13 patients were drawn from venous coronary sinus before cardioplegic arrest and after reperfusion. The following parameters were studied: surface molecules expression (CD18, CD11b, CD44, CD162, CD15s, CD80, CD86, CD16, CD49d, CD29, CD25, HLA‐DR, Toll‐like receptor‐4 [TLR‐4], CXCR1, CCR2, CCR5, CX3CR1), oxidative burst response, monocyte‐platelet conjugates (using antibodies against CD45, CD14, CD41a), and platelet activation (CD62P, PAC‐1). Enzyme‐linked immunosorbent assays were performed to measure levels of interleukin (IL)‐1β, IL‐6, IL‐8, IL‐10, and tumor necrosis factor‐α (TNF‐α). Results Coronary reperfusion down‐modulated monocyte molecules expression, especially for CD18 (P = 0.048), CD44 (P = 0.0035), CD49d (P = 0.0029), CD29 (P = 0.032), HLA‐DR (P < 0.0001), TLR‐4 (P = 0.0109), CCR2 (P = 0.0184), CCR5 (P = 0.0396), and CX3CR1 (P < 0.0001). A marginal increase (P = 0.062) of a normalized adhesion index between monocytes and platelets was observed at reperfusion. No variations were detected for the monocyte oxidative burst and platelet activation. Increased levels of IL‐6 (P = 0.013), TNF‐α (P = 0.0272), and IL‐10 (P = 0.0008) were measured after cardioplegia. Conclusions The lack of CD11b and CD25 variations and of the oxidative burst exclude monocyte activation at reperfusion. The high after‐cardioplegia level of IL‐10, the decreased expression of HLA‐DR and TLR‐4, and the absence of IL‐1β and IL‐8 suggest an IL‐10–mediated functional depression of monocyte, including their adhesive and migratory capacities. The lack of an after‐cardioplegia orientation toward IL‐10 producing a “macrophage‐like” CD14+/CD16+ phenotype might mean that myocardial infiltrating lymphocytes are the main source of IL‐10. Moreover, the increased after‐cardioplegia levels of IL‐6 and TNF‐α might be due to myocardial and endothelial activations. The increased adhesion index between monocyte and platelets, without receptor variations, suggests a monocyte membrane modification induced by extracorporeal circulation. © 2005 Wiley‐Liss, Inc.
ISSN:1552-4949
1552-4957
DOI:10.1002/cyto.b.20049