2014
DOI: 10.1038/cmi.2014.24
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Effect of everolimus on the immunomodulation of the human neutrophil inflammatory response and activation

Abstract: The primary cause of mortality at 5 years following a cardiac transplantation is the development of atherosclerosis, termed coronary allograft vasculopathy (CAV). This pathology is characterized by diffused intimal hyperplasia and emanates from coronary arterial injuries caused by immune inflammatory cells. Neutrophils play an important role in this inflammatory process; however, their potential participation in the pathogenesis of CAV is poorly understood. Despite their essential contribution to the preventio… Show more

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Cited by 50 publications
(45 citation statements)
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“…Because neutrophils are able to release numerous mediators, including pro-inflammatory (IL-1α/β; -6; -7; -8; -9; -16), pro-inflammatory/angiogenic (tumor growth factor TGF-α; vascular endothelial growth factor VEGF), and anti-inflammatory mediators (IL-1 receptor antagonist (IL-1RA), TGF-β), they likely play a pivotal yet not well characterized role in the initiation and the development of CAV [28] . Previous studies have demonstrated the potential deleterious role of neutrophils during myocardial reperfusion immediately after CTx in rodents, notably via neutrophil activated αMβ2 integrin complexes (CD11b/CD18) [29,30] .…”
Section: The Pathogenesis Of Cav: An Inflammatory Perspectivementioning
confidence: 99%
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“…Because neutrophils are able to release numerous mediators, including pro-inflammatory (IL-1α/β; -6; -7; -8; -9; -16), pro-inflammatory/angiogenic (tumor growth factor TGF-α; vascular endothelial growth factor VEGF), and anti-inflammatory mediators (IL-1 receptor antagonist (IL-1RA), TGF-β), they likely play a pivotal yet not well characterized role in the initiation and the development of CAV [28] . Previous studies have demonstrated the potential deleterious role of neutrophils during myocardial reperfusion immediately after CTx in rodents, notably via neutrophil activated αMβ2 integrin complexes (CD11b/CD18) [29,30] .…”
Section: The Pathogenesis Of Cav: An Inflammatory Perspectivementioning
confidence: 99%
“…The use of sirolimus (SIR) has been proposed as a substitute for CNIs in cardiac transplant patient based on its role in renal function preservation and prevention of chronic allograft vasculopathy [76][77][78] . In fact, SIR, can prevent vascular remodeling and neointimal proliferation, two key components of CAV, by inhibiting smooth muscle cell (SMC) and fibroblast proliferation [7,28,[79][80][81][82][83][84][85][86] . SIR has been shown to reduce the incidence of acute rejection among renal-transplant recipients and to prevent CAV in animals [87] .…”
Section: Mtor and Mtor Inhibitorsmentioning
confidence: 99%
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“…To evaluate the potential role of immunosuppression in the prevention of CAV in heart transplant recipients, Vitiello et al 8 evaluated the effect of different routinely used immunosuppressive drugs (ID) cyclosporine A (CsA), tacrolimus (TAC), mycophenolic acid (MPA), sirolimus (SIR) or everolimus (EVE) on neutrophil response. 8 First, they assessed the capacity of selected pro-inflammatory agonists NFormyl-Met-Leu-Phe, bacterial lipopolysaccharide (LPS), TNF-a or control vehicle (phosphate-buffered saline) to induce the release of cytokines by human neutrophils.…”
mentioning
confidence: 99%
“…8 First, they assessed the capacity of selected pro-inflammatory agonists NFormyl-Met-Leu-Phe, bacterial lipopolysaccharide (LPS), TNF-a or control vehicle (phosphate-buffered saline) to induce the release of cytokines by human neutrophils. They observed that treatment with these agonists induced the release of vascular endothelial growth factor (VEGF), IL-1 receptor antagonist (IL-1RA) and IL-8 by neutrophils, and the most potent effect was evoked by LPS.…”
mentioning
confidence: 99%