References of "Oury, Cécile"
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See detailSepsis prediction in critically ill patients by platelet activation markers on ICU admission: a prospective pilot study
LAYIOS, Nathalie ULiege; Delierneux, Céline ULiege; Hego, Alexandre ULiege et al

in Intensive Care Medicine Experimental (2017), 5(1), 32

Background: Platelets have been involved in both surveillance and host defense against severe infection. To date, whether platelet phenotype or other hemostasis components could be associated with ... [more ▼]

Background: Platelets have been involved in both surveillance and host defense against severe infection. To date, whether platelet phenotype or other hemostasis components could be associated with predisposition to sepsis in critical illness remains unknown. The aim of this work was to identify platelet markers that could predict sepsis occurrence in critically ill injured patients. Results: This single-center, prospective, observational, 7-month study was based on a cohort of 99 non-infected adult patients admitted to ICUs for elective cardiac surgery, trauma, acute brain injury and post-operative prolonged ventilation and followed up during ICU stay. Clinical characteristics and severity score (SOFA) were recorded on admission. Platelet activation markers, including fibrinogen binding to platelets, platelet membrane P-selectin expression, plasma soluble CD40L, and platelet-leukocytes aggregates were assayed by flow cytometry at admission and 48h later, and also at the time of sepsis diagnosis (Sepsis-3 criteria) and 7 days later for sepsis patients. Hospitalization data and outcomes were also recorded. Of the 99 patients, 19 developed sepsis after a median time of 5 days. SOFA at admission was higher; their levels of fibrinogen binding to platelets (platelet-Fg) and of D-dimers were significantly increased compared to the other patients. Levels 48h after ICU admission were no longer significant. Platelet-Fg % was an independent predictor of sepsis (P = 0.030). By ROC curve analysis cutoff points for SOFA (AUC=0.85) and Platelet-Fg (AUC=0.75) were 8 and 50%, respectively. The prior risk of sepsis (19%) increased to 50% when SOFA was above 8, to 46% when Platelet-Fg was above 50%, and to 87% when both SOFA and Platelet-Fg were above their cutoff values. By contrast, when the two parameters were below their cutoffs, the risk of sepsis was negligible (3.8%). Patients with sepsis had longer ICU and hospital stays and higher death rate. Conclusion: In addition to SOFA, platelet-bound fibrinogen levels assayed by flow cytometry within 24h of ICU admission help identifying critically ill patients at risk of developing sepsis. [less ▲]

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See detailDusp3 deletion in mice promotes experimental lung tumour metastasis in a macrophage dependent manner
Vandereyken, Maud; Jacques, Sophie; Van Overmeire, Eva et al

in PLoS ONE (2017)

Vaccinia-H1 Related (VHR) dual-specificity phosphatase, or DUSP3, plays an important role in cell cycle regulation and its expression is altered in several human cancers. In mouse model, DUSP3 deletion ... [more ▼]

Vaccinia-H1 Related (VHR) dual-specificity phosphatase, or DUSP3, plays an important role in cell cycle regulation and its expression is altered in several human cancers. In mouse model, DUSP3 deletion prevents neo-angiogenesis and b-FGF-induced microvessel out- growth. Considering the importance of angiogenesis in metastasis formation, our study aimed to investigate the role of DUSP3 in tumour cell dissemination. Using a Lewis Lung carcinoma (LLC) experimental metastasis model, we observed that DUSP3-/- mice devel- oped larger lung metastases than littermate controls. DUSP3-/- bone marrow transfer to lethally irradiated DUSP3+/+ mice was sufficient to transfer the phenotype to DUSP3+/+ mice, indicating that hematopoietic cells compartment was involved in the increased tumour cell dissemination to lung tissues. Interestingly, we found a higher percentage of tumour- promoting Ly6Cint macrophages in DUSP3-/- LLC-bearing lung homogenates that was at least partially due to a better recruitment of these cells. This was confirmed by 1) the pres- ence of higher number of the Ly6Bhi macrophages in DUSP3-/- lung homogenates and by 2) the better migration of DUSP3-/- bone marrow sorted monocytes, peritoneal macrophages and bone marrow derived macrophages (BMDMs), compared to DUSP3+/+ monocytes, macrophages and BMDMs, in response to LLC-conditioned medium. Our study demon- strates that DUSP3 phosphatase plays a key role in metastatic growth through a mechanism involving the recruitment of macrophages towards LLC-bearing lungs. [less ▲]

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See detailDual-specificity-phosphatase 3 (DUSP3) deletion promotes liver inflammation and high fat diet-induced hepatocellular carcinoma
Jacques, Sophie ULiege; Arjomand, Arash ULiege; Vandereyken, Maud ULiege et al

Poster (2017, July 24)

Overweight and obesity are considered as risk factors for hepatocellular carcinoma (HCC) development. The mechanisms by which obesity promotes liver inflammation are however poorly understood. We recently ... [more ▼]

Overweight and obesity are considered as risk factors for hepatocellular carcinoma (HCC) development. The mechanisms by which obesity promotes liver inflammation are however poorly understood. We recently generated a full DUSP3 knockout (KO) mouse. The obtained mice were born normal with no spontaneous phenotype. However, while aging, DUSP3-KO mice became obese and developed hepatosteatosis. The phenotype was exacerbated under high fat diet (HFD). Furthermore, when treated with diethylnitrosamine (DEN) procarcinogen, DUSP3-KO mice developed HCC faster than WT littermates. The combination of DEN with HFD accelerated the onset of HCC development in these mice compared to WT mice. This was associated with increased systemic levels of several metabolites and with hyperphosphorylation of the insulin-like growth factor receptor I. [less ▲]

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See detailPlatelets promote immunosuppression and colorectal tumor formation: inhibition by clopidogrel
Servais, Laurence ULiege; Delierneux, Céline; Wéra, Odile ULiege et al

Poster (2017, July)

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See detailA Highly Durable RNAi Therapeutic Inhibitor of PCSK9
LANCELLOTTI, Patrizio ULiege; Oury, Cécile ULiege

in New England Journal of Medicine (2017), 376

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See detailTargeting of C-type lectin-like receptor 2 or P2Y12 for the prevention of platelet activation by immunotherapeutic CpG oligodeoxynucleotides
Delierneux, Céline ULiege; Donis, Nathalie ULiege; servais, laurence et al

in Journal of Thrombosis and Haemostasis (2017), 15(5), 983-997

Background: Synthetic phosphorothioate-modified CpG oligodeoxynucleotides (CpG ODNs) display potent immunostimulatory properties that are widely exploited in clinical trials of anticancer treatment ... [more ▼]

Background: Synthetic phosphorothioate-modified CpG oligodeoxynucleotides (CpG ODNs) display potent immunostimulatory properties that are widely exploited in clinical trials of anticancer treatment. Unexpectedly, a recent study indicates that CpG ODNs activate human platelets via the immunoreceptor tyrosine-based activation motif (ITAM)-coupled receptor glycoprotein VI. Objective: To further analyze the mechanisms of CpG ODN-induced platelet activation and identify potential inhibitory strategies. Methods: In vitro analyses were performed on human and mouse platelets, and on cell lines expressing platelet ITAM receptors. CpG ODN platelet activating effects were evaluated in a mouse model of thrombosis. Results: We demonstrated platelet uptake of CpG ODNs, resulting in platelet activation and aggregation. The C-type lectin-like receptor 2 (CLEC-2) expressed in DT40 cells bound CpG ODNs. CpG ODN uptake did not occur in CLEC-2-deficient mouse platelets. Inhibition of human CLEC-2 with a blocking antibody inhibited CpG ODN-induced platelet aggregation. CpG ODNs caused CLEC-2 dimerization, and provoked its internalization. They induced dense granule release before the onset of aggregation. Accordingly, pretreating platelets with apyrase, or inhibiting P2Y12 with cangrelor or clopidogrel prevented CpG ODN platelet activating effect. In vivo, intravenously injected CpG ODN interacted with platelets adhered to mouse injured endothelium, and promoted thrombus growth, which was inhibited by CLEC-2 deficiency or by clopidogrel. Conclusions: CLEC-2 and P2Y12 are required for CpG ODN-induced platelet activation and thrombosis and might be targeted to prevent adverse events in patients at risk. [less ▲]

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See detailROLE OF IMAGING IN LEFT ATRIAL APPENDAGE OCCLUSION
LEMPEREUR, Mathieu ULiege; AMINIAN, Adel; DULGHERU, Raluca Elena ULiege et al

in international journal of cardiovascular practice (2017), 2(2), 33-43

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See detailPharmacogenomics screening
Oury, Cécile ULiege; Bours, Vincent ULiege

in Galderisi, Maurizio; Lancellotti, Patrizio; Zamorano Gomez, Jose (Eds.) Anticancer treatments and cardiotoxicity (2017)

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See detailSerum albumin level and hospital mortality in acute non-ischemic heart failure.
ANCION, Arnaud ULiege; Allepaerts, Sophie; Oury, Cécile ULiege et al

in ESC heart failure (2017), 4(2), 138-145

AIMS: Hypoalbuminemia is common in heart failure (HF), especially in elderly patients. It is associated with an increased risk of death. The present study sought to examine the prognostic significance of ... [more ▼]

AIMS: Hypoalbuminemia is common in heart failure (HF), especially in elderly patients. It is associated with an increased risk of death. The present study sought to examine the prognostic significance of serum albumin level in the prediction of hospital mortality in patients admitted for acute non-ischemic HF. METHODS AND RESULTS: We examined the association between albumin and hospital mortality in a cohort of 546 patients admitted for acute non-ischemic HF. None of the patients had infectious disease, severe arrhythmias (atrial fibrillation, ventricular tachycardia, ventricular fibrillation), required invasive ventilation, or presented with acute coronary syndrome or primary valvular disease. Thirty-six patients (7%) died during the hospital stay. These patients were significantly older (78 +/- 9 vs. 72 +/- 12 years; P = 0.006), had higher heart rate (P < 0.0001), increased creatinine level (P = 0.01), lower systolic and diastolic blood pressures (P < 0.05), elevated leucocyte count (P = 0.001), and lower albumin levels (31.3 +/- 5.6 g/L vs. 36.9 +/- 4.1 g/L; P < 0.001). With multivariable analysis, age (P = 0.01), heart rate (P < 0.0003), diastolic blood pressure (P < 0.01), leukocyte count (P = 0.009), and serum albumin level (P < 0.0001) emerged as independent predictors of hospital mortality. Hypoalbuminemia (<34 g/L) yielded the best sensitivity (78.8%) and specificity (75%) for predicting hospital death. CONCLUSIONS: Serum albumin level measured at admission can serve as a simple prognostic factor in acute non-ischemic HF. Hypoalbuminemia is associated with increased risk of hospital mortality, especially in elderly patients. [less ▲]

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See detailThe Dual Role of Neutrophils in Inflammatory Bowel Diseases
Wéra, Odile ULiege; Lancellotti, Patrizio ULiege; Oury, Cécile ULiege

in Journal of clinical medicine (2016), 5(12),

Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are characterised by aberrant immunological responses leading to chronic inflammation without tissue regeneration ... [more ▼]

Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are characterised by aberrant immunological responses leading to chronic inflammation without tissue regeneration. These two diseases are considered distinct entities, and there is some evidence that neutrophil behaviour, above all other aspects of immunity, clearly separate them. Neutrophils are the first immune cells recruited to the site of inflammation, and their action is crucial to limit invasion by microorganisms. Furthermore, they play an essential role in proper resolution of inflammation. When these processes are not tightly regulated, they can trigger positive feedback amplification loops that promote neutrophil activation, leading to significant tissue damage and evolution toward chronic disease. Defective chemotaxis, as observed in Crohn's disease, can also contribute to the disease through impaired microbe elimination. In addition, through NET production, neutrophils may be involved in thrombo-embolic events frequently observed in IBD patients. While the role of neutrophils has been studied in different animal models of IBD for many years, their contribution to the pathogenesis of IBD remains poorly understood, and no molecules targeting neutrophils are used and validated for the treatment of these pathologies. Therefore, it is crucial to improve our understanding of their mode of action in these particular conditions in order to provide new therapeutic avenues for IBD. [less ▲]

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See detailP2X1 ion channel is critical for vascular integrity in inflammation
Wéra, Odile ULiege; Delierneux, Céline; Servais, Laurence ULiege et al

Poster (2016, November)

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See detailP2X1 ion channel is critical for vascular integrity in inflammation
Wéra, Odile ULiege; Delierneux, Céline; Hego, Alexandre ULiege et al

Conference (2016, September)

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See detailFunctional analysis of protein tyrosine phosphatases in thrombosis and haemostasis
Rahmouni, Souad ULiege; Hego, Alexandre ULiege; Delierneux, Céline ULiege et al

in Protein Tyrosine Phosphatases: Methods and Protocols (2016)

Platelets are small blood cells derived from cytoplasmic fragments of megakaryocytes and play an essential role in thrombosis and haemostasis. Platelet activation depends on the rapid phosphorylation and ... [more ▼]

Platelets are small blood cells derived from cytoplasmic fragments of megakaryocytes and play an essential role in thrombosis and haemostasis. Platelet activation depends on the rapid phosphorylation and dephosphorylation of key signaling molecules, and a number of kinases and phosphatases have been identified as major regulators of platelet function. However, the investigation of novel signaling proteins has suffered from technical limitations due to the anucleate nature of platelets and their very limited levels of mRNA and de novo protein synthesis. In the past, experimental methods were restricted to the generation of genetically modified mice and the development of specific antibodies. More recently, novel (phospho)proteomic technologies and pharmacological approaches using specific small-molecule inhibitors have added additional capabilities to investigate specific platelet proteins. In this chapter, we report methods for using genetic and pharmacological approaches to investigate the function of platelet signaling proteins. While the described experiments focus on the role of the dual-specificity phosphatase 3 (DUSP3) in platelet signaling, the presented methods are applicable to any signaling enzyme. Specifically, we describe a testing strategy that includes 1) aggregation and secretion experiments with mouse and human platelets, 2) immunoprecipitation and immunoblot assays to study platelet signaling events, 3) detailed protocols to use selected animal models in order to investigate thrombosis and haemostasis in vivo, and 4) strategies for utilizing pharmacological inhibitors on human platelets. [less ▲]

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