Modulation of tachykinin and cytokine release in patients with coronary disease undergoing percutaneous revascularization

Paroli, Marino; Mariani, Paola; Accapezzato, Daniele; D’Alessandro, Mariadomenica; Russo, Claudio Di; Bifolco, Maura; Sirinian, Maria Isabella; Fedele, Francesco; Bruno, Guglielmo; Sardella, Gennaro

doi:10.1016/j.clim.2004.03.021

Cited by 14 publications

(10 citation statements)

References 32 publications

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“…The largest amount of data are available with regards to IL-1 and IL-6, both in animal models with ACS [34,35] and in humans [36][37][38], whereas evidences on TNF are contrasting: Pudil et al did not find any release of TNF in subjects with ACS [38], while other authors showed increased TNF levels during ACS [36,37,39]. In a paper by Fichtlscherer et al., enrolling patients with endothelial dysfunction, higher levels of IL-10 were demonstrated in subjects with a less compromised endothelial reserve [40], while lower concentrations were found in patients with ACS [21,41]. There are fewer data regarding IL-2, IL-18, and IFN [39], particularly during the first 24 h of ACS.…”

Section: Discussionmentioning

confidence: 89%

Inflammatory Cytokines Imbalance in the Very Early Phase of Acute Coronary Syndrome: Correlations with Angiographic Findings and In-Hospital Events

et al. 2010

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The aim of this study is to investigate the release of some inflammatory cytokines (Cks) during the very early phase (first 24 h) of acute coronary syndrome (ACS). Twenty-six consecutive subjects admitted to coronary care unit with ACS underwent serial blood sampling in order to evaluate concentrations of interleukin (IL)-2, IL-10, IL-18, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ. Blood samples were taken within 6 h after onset of chest pain (T₀), at 12 h (T₁), and at 24 h (T₂). Patients were thus divided into four groups comparing pro-inflammatory Ck release (IL-2, TNF-α, and IFN-γ) and anti-inflammatory activity (IL-10). Clinical features, risk factors, incidence of adverse events, and coronary angiography findings were compared with Ck activation. Ck levels were significantly increased if compared with baseline. Subjects with marked inflammatory response showed a higher incidence of left anterior descending coronary disease (IL-2, p < 0.001; TNF-α and IFN-γ, p < 0.05) and more often incurred early complications (IL-2, p < 0.05; IFN-γ, p < 0.001). A correlation was detectable between IL-18 levels and myocardial enzyme release (creatine kinase, r = 0.47; lactate dehydrogenase, r = 0.54; troponin I, r = 0.58; p < 0.05). TNF-α levels were associated with a worse prognosis at follow-up (Log rank, p < 0.05). A Ck activation characterizes the early phase of ACS. Early inflammatory reaction seems to correlate with coronary disease and adverse events.

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Section: Discussionmentioning

confidence: 89%

Inflammatory Cytokines Imbalance in the Very Early Phase of Acute Coronary Syndrome: Correlations with Angiographic Findings and In-Hospital Events

et al. 2010

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“…Inflammatory mechanisms have been indicated to play a pivotal role in neointimal formation and restenosis. The pleiotropic pro-inflammatory cytokine IFN-γ has been implicated in the pathogenic processes of restenosis (11)(12)(13). However, IFN-γ has been shown to both promote (11) and inhibit (14) injury-mediated neointimal formation, and therefore warrants further investigation.…”

Section: A B Cmentioning

confidence: 99%

“…Activation of IFN-γ signalling in neointimal SMCs was indicated in 37 of the 223 differentially expressed genes in atherectomy specimens of patients with restenosis, determined by a transcriptome study (13). Furthermore, elevated circulating IFN-γ has been detected within 15 min following stent implantation, in both chronic and acute coronary syndrome patients undergoing angioplasty, suggesting that modulation of IFN-γ release plays a role in inflammatory complications of angioplasty during/following stenting (12). Animal studies concerning the role of IFN-γ on injury-mediated models of neointimal formation have yielded (11), and exogenous IFN-γ treatment (14) reduced injury-induced neointimal formation in rats.…”

Section: Introductionmentioning

confidence: 98%

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Interferon-γ deficiency reduces neointimal formation in a model of endoluminal endothelial injury combined with atherogenic diet

Tavakoli

Harris

Sullivan

et al. 2012

International Journal of Molecular Medicine

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Abstract. Interferon (IFN)-γ has been implicated in restenosis, however its precise role in the pathophysiology of neointimal formation following angioplasty is unclear, as it has been shown to both promote and inhibit neointimal formation. Dietary-induced hypercholesterolemia enhances injurymediated neointimal formation, associated with increased systemic inflammation and serum IFN-γ. This study examined the effect of IFN-γ gene deficiency ( -/-) on neointimal formation in a mouse model of endothelial injury combined with an atherogenic diet. Neointimal formation was induced via endoluminal endothelial injury of the common iliac arteries of IFN-γ -/-and wild-type (WT) C57Bl/6 mice. Histopathological analysis of the arteries was performed at 3 and 6 weeks postsurgery. IFN-γ -/-mice demonstrated a significant reduction in neointimal formation at the 3-week time point, compared to their WT counterpart. No significant differences in plasma lipid profile and the extent of re-endothelialization were detected between IFN-γ -/-and WT mice, suggesting that the effect of IFN-γ on neointimal formation is due to injury-mediated vessel neointimal responses. In support of the histopathological findings, immunohistochemical analysis revealed a significant reduction in vessel infiltrating macrophages, and neointimal PDGF-B expression, vascular smooth muscle cell composition and cellular proliferation in the IFN-γ -/-mice, in comparison to their corresponding WT group at the 3-week time point. In conclusion, the IFN-γ-mediated pathway plays an important role in inflammatory responses and proliferative effects following injury, suggesting that modulation of the IFN-γ pathway would be beneficial in controlling neointimal formation and restenosis. IntroductionRestenosis is a common and serious complication associated with re-vascularisation by percutaneous coronary angioplasty, with considerable clinical implications (1). Inflammatory-mediated mechanisms following endothelial injury and/or stent placement are thought to play a pivotal role in restenosis (1). Moreover, injury-induced proliferation and/migration of vascular smooth muscle cells (VSMCs) is an important contributor to neointimal hyperplasia and in-stent restenosis (2,3). However, the precise underlying molecular mechanism(s) of restenosis are not entirely understood.The pro-inflammatory cytokine interferon (IFN)-γ exhibits many biological functions including; mediation of inflammatory responses and immunomodulatory effects (4,5). IFN-γ is secreted from a variety of cells such as T helper cell type 1 (Th1) lymphocytes, activated macrophages, VSMCs and natural killer cells, and its expression has been demonstrated in atherosclerotic lesions (4,6). IFN-γ affects major cell types within the lesion and displays a complex role in vascular lesion development and progression (4). The biological effects of IFN-γ include; stimulating the differentiation of monocytes to macrophages, activation of macrophages and T-lymphocytes (4), and increasing the expression of platelet-derived...

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“…[5][6][7][8][9] Cytokines such as interferon gamma (IFN-γ) and tumour necrosis factor alpha (TNF-α) increase pro-inflammatory activity during and following PCI and might therefore be related to long-term complications after an intervention. 10 Patients with T2DM display increased plasma levels of inflammatory markers, and deteriorating glycaemic control is associated with particularly sensitive to this complication. This has not, however, been fully explored in controlled clinical trials.…”

Section: Introductionmentioning

confidence: 99%

The predictive value of inflammatory activity and markers of the adipo-insular axis on restenosis in patients with type 2 diabetes

Hage

Grip

Malmberg

et al. 2011

Diabetes and Vascular Disease Research

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Aims: Patients with type 2 diabetes (T2DM) have a high restenosis rate after percutaneous coronary intervention (PCI). This study investigated whether markers of inflammation and the adipo-insular axis associated with T2DM and poor metabolic control were able to predict restenosis after PCI in T2DM patients. Methods and results:The predictive value of traditional and non-traditional risk markers, including IL-1β, IL-6, TNF-α, hsCRP, interferon gamma, leptin, IGF-I, insulin, proinsulin and NT-proBNP, was investigated in 82 patients with T2DM. A re-angiography 6 months after the index percutaneous coronary intervention (PCI) revealed that 43% of the patients had a restenosis. In a multiple regression analysis, the only independent predictors of restenosis were fasting glucose before the PCI and previous myocardial infarction (odds ratio [OR] 1.44, 95% confidence interval [CI] 1.07-1.92; p = 0.015 and OR 8.00, 95% CI 2.49-25.67; p ≤ 0.001, respectively). None of the other markers remained as significant predictors. Conclusion: Fasting glucose prior to the PCI was an independent predictor of restenosis in patients with T2DM while analyses of a variety of markers related to inflammation and the adipo-insular axis did not add any further information.

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Modulation of tachykinin and cytokine release in patients with coronary disease undergoing percutaneous revascularization

Cited by 14 publications

References 32 publications

Inflammatory Cytokines Imbalance in the Very Early Phase of Acute Coronary Syndrome: Correlations with Angiographic Findings and In-Hospital Events

Inflammatory Cytokines Imbalance in the Very Early Phase of Acute Coronary Syndrome: Correlations with Angiographic Findings and In-Hospital Events

Interferon-γ deficiency reduces neointimal formation in a model of endoluminal endothelial injury combined with atherogenic diet

The predictive value of inflammatory activity and markers of the adipo-insular axis on restenosis in patients with type 2 diabetes

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