http://www.cnr.it/ontology/cnr/individuo/prodotto/ID23720
Post-reperfusion changes of monocyte function in coronary blood after extracorporeal circulation (Articolo in rivista)
- Type
- Label
- Post-reperfusion changes of monocyte function in coronary blood after extracorporeal circulation (Articolo in rivista) (literal)
- Anno
- 2005-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1002/cyto.b.20049 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Sbrana S.; Bevilacqua S.; Buffa M.; Spiller D.; Parri M.S.; Gianetti J.; De Filippis R.; Clerico A. (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
- In: \" Cytometry Part B (Clinical Cytometry)\"65B,2005,14-21 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Laboratory of Hematology and Flow Cytometry, CNR Institute of Clinical Physiology, Massa, Italy
Cardiac Surgery Department, CNR Institute of Clinical Physiology, Massa, Italy (literal)
- Titolo
- Post-reperfusion changes of monocyte function in coronary blood after extracorporeal circulation (literal)
- Abstract
- 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)-1b, IL-6, IL-8, IL-10, and tumor necrosis factor-
a (TNF-a).
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-a (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-1b 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-a
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. (literal)
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