Olivier Meilhac

Paris Diderot University, Lutetia Parisorum, Île-de-France, France

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Publications (128)557.95 Total impact

  • Olivier Meilhac
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    ABSTRACT: Besides their well-documented function of reverse transport of cholesterol, high-density lipoproteins (HDLs) display pleiotropic effects due to their antioxidant, antithrombotic, anti-inflammatory and antiapoptotic properties that may play a major protective role in acute stroke, in particular by limiting the deleterious effects of ischaemia on the blood-brain barrier (BBB) and on the parenchymal cerebral compartment. HDLs may also modulate leukocyte and platelet activation, which may also represent an important target that would justify the use of HDL-based therapy in acute stroke. In this review, we will present an update of all the recent findings in HDL biology that could support a potential clinical use of HDL therapy in ischaemic stroke.
    Handbook of experimental pharmacology 01/2015; 224:509-526.
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    ABSTRACT: Objective Previous studies have suggested positive associations between periodontal infection and cardiovascular disease. We aimed to investigate the associations of circulating antibodies against periodontal pathogens with 1-year cardiovascular outcome, as well as the extent of coronary atherosclerosis, plaque vulnerability and lesion remodeling on intravascular ultrasound (IVUS) imaging. Methods Between 2008 and 2011, radiofrequency IVUS imaging of a non-culprit coronary artery was performed in 581 patients who underwent coronary angiography. Immunoglobulin G (IgG) and A (IgA) against Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia and Prevotella intermedia were measured in plasma. Results None of the antibody levels were associated with coronary plaque burden, radiofreqeuncy-IVUS-derived thin-cap fibroatheroma lesion morphology or 1-year incidence of major adverse cardiac events (MACE), which included all-cause mortality, acute coronary syndrome and unplanned coronary revascularization. IgA against A. actinomycetemcomitans, T. forsythia and P. intermedia were inversely associated with extent of positive lesion remodeling (OR for highest versus lowest tertile 0.55, 95%CI 0.35–0.88, p = 0.012; 0.53, 95%CI 0.32–0.87, p = 0.012; and 0.64, 95%CI 0.40–1.02, p = 0.061, respectively). In diabetic patients specifically, IgG against P. gingivalis tended to be associated with coronary plaque burden (p = 0.080), while IgA against P. gingivalis tended to be associated with incident MACE (p = 0.060). Conclusion Plasma IgG and IgA against major periodontal pathogens were not associated with the extent of coronary atherosclerosis (with the exception of a trend in diabetics) nor with coronary plaque vulnerability. IgA against periodontal pathogens were inversely associated with extent of coronary remodeling. Altogether, these results do not add evidence for a substantial role of systemic exposure to periodontal pathogens in coronary artery disease.
    Atherosclerosis 11/2014; 237(1):84–91. · 3.71 Impact Factor
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    ABSTRACT: Objective Epidemiological, biological and clinical links between periodontal and cardiovascular diseases are now well established. Several human studies have detected bacterial DNA corresponding to periodontal pathogens in cardiovascular samples. Intraplaque hemorrhage has been associated with a higher risk of atherosclerotic plaque rupture, potentially mediated by neutrophil activation. In this study, we hypothesized that plaque composition may be related to periodontal pathogens. Methods Carotid culprit plaque samples were collected from 157 patients. Macroscopic characterization was performed at the time of collection: presence of blood, lipid core, calcification and fibrosis. Markers of neutrophil activation released by carotid samples were quantified (myeloperoxidase or MPO, cell-free DNA and DNA-MPO complexes). PCR analysis using specific primers for Porphyromonas gingivalis, Aggregatibacter actinomycetemcommitans, Treponema denticola, Prevotella intermedia and Tannerella forsythia was used to detect DNA from periodontal pathogens in carotid tissues. In addition, bacterial lipopolysaccharide (LPS) and Immunoglobulins G against Tannerella forsythia were quantified in atherosclerotic carotid conditioned medium. Results Intraplaque hemorrhage was present in 73/157 carotid samples and was associated with neutrophil activation, reflected by the release of MPO, cell-free DNA and MPO-DNA complexes. LPS levels were also linked to intraplaque hemorrhage but not with the neutrophil activation markers. Seventy-three percent of the carotid samples were positive for periodontal bacterial DNA. Furthermore, hemoglobin levels were associated with the detection of T. forsythia and neutrophil activation/inflammation markers. Conclusion This study suggests a potential role of periodontal microorganisms, especially T. forsythia, in neutrophil activation within hemorrhagic atherosclerotic carotid plaques.
    Atherosclerosis 10/2014; · 3.71 Impact Factor
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    ABSTRACT: Previous studies have suggested positive associations between periodontal infection and cardiovascular disease. We aimed to investigate the associations of circulating antibodies against periodontal pathogens with 1-year cardiovascular outcome, as well as the extent of coronary atherosclerosis, plaque vulnerability and lesion remodeling on intravascular ultrasound (IVUS) imaging.
    Atherosclerosis 09/2014; 237(1):84-91. · 3.71 Impact Factor
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    ABSTRACT: Abdominal aortic aneurysm (AAA) is a particular form of arterial disease characterized by the dilation of the aortic wall and the presence of an intraluminal thrombus linked to a high proteolytic activity. The aim of this study was to investigate the effect of an elastase inhibitor (AZD9668 from AstraZeneca) on aneurysm progression.
    Journal of Vascular Surgery 08/2014; · 2.98 Impact Factor
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    ABSTRACT: Low levels of low-density lipoprotein-cholesterol (LDL-C) are suspected to be associated with a risk of hemorrhagic transformation after ischemic stroke. We assessed the risk of hemorrhagic transformation after cerebral ischemia/reperfusion in mice with low levels of LDL-C resulting from proprotein convertase subtilisin kexin 9 (PCSK9) deficiency.
    Stroke 08/2014; 45(10). · 6.02 Impact Factor
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    ABSTRACT: Rationale: Several studies report that high-density lipoproteins (HDL) can carry alpha1-antitrypsin (AAT, an elastase inhibitor). Objectives: We aimed at determining whether injection of exogenous HDL, enriched or not in AAT, may have protective effects against pulmonary emphysema. Methods: After tracheal instillation of saline or elastase, mice were randomly treated intravenously with saline, human plasma HDL (75mg ApoA1/kg), HDL-AAT (75mg ApoA1-3.75mgAAT/kg) or AAT alone (3.75mg/kg) at 2, 24, 48 and 72h. Results: We have shown that HDL-AAT reached the lung and prevented the development of pulmonary emphysema by 59.3% at 3 weeks (alveoli mean chord length µm: 22.9±2.8 vs 30.7±4.5 μm, p<0.001) whereas injection of HDL or AAT alone only showed a moderate, non-significant protective effect (28.2±4.2 vs 30.7±5μm, p=0.23; and 27.3±5.66 vs 30.71±4.96 μm, p=0.18, respectively). Indeed, protection by HDL-AAT was significantly higher than that observed with HDL or AAT (p=0.006 and p=0.048, respectively). This protective effect was associated (at 6, 24 and 72 hours) with 1) a reduction in neutrophil and macrophage number in the bronchoalveolar lavage fluid (BALF), 2) decreased concentrations of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-α (TNF-α) in both BALF and plasma, 3) a reduction in matrix metalloproteinase (MMP)-2 and MMP-9 activities, and 4) a reduction in the degradation of fibronectin, a marker of tissue damage. Also, HDL-AAT reduced acute cigarette smoke-induced inflammatory response. Conclusions: i.v. HDL-AAT treatment afforded a better protection against elastase-induced pulmonary emphysema than AAT alone, and may represent a significant development for the management of emphysema associated with AAT deficiency.
    American Journal of Respiratory Cell and Molecular Biology 05/2014; · 4.15 Impact Factor
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    ABSTRACT: Objective To identify circulating biomarkers that originate from atherosclerotic vulnerable plaques and that could predict future cardiovascular events. Methods After a protein enrichment step (combinatorial peptide ligand library approach), we performed a two-dimensional electrophoresis comparative analysis on human carotid plaque protein extracts (fibrotic and hemorrhagic atherosclerotic plaques). In silico analysis of the biological processes was applied on proteomic data. Luminex xMAP assays were used to quantify inflammatory components in carotid plaques. The systemic quantification of proteins originating from vulnerable plaques in blood samples from patients with stable and unstable coronary disease was evaluated. Results A total of 118 proteins are differentially expressed in fibrotic and hemorrhagic plaques, and allowed the identification of three biological processes related to atherosclerosis (platelet degranulation, vascular autophagy and negative regulation of fibrinolysis). The multiplex assays revealed an increasing expression of VEGF, IL-6, IL-8, IP-10 and RANTES in hemorrhagic as compared to fibrotic plaques (p < 0.05). Measurement of protein expressions in plasmas from patients with stable and unstable coronary disease identified a combination of biomarkers, including proteins of the smooth muscle cell integrity (Calponin-1), oxidative stress (DJ-1) and inflammation (IL-8), that allows the accurate classification of patients at risk (p = 0.0006). Conclusion Using tissue protein enrichment technology, we validated proteins that are differentially expressed in hemorrhagic plaques as potential circulating biomarkers of coronary patients. Combinations of such circulating biomarkers could be used to stratify coronary patients.
    Atherosclerosis 04/2014; 233(2):551–558. · 3.71 Impact Factor
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    ABSTRACT: Previous proteomics experiments have demonstrated that several proteins are differentially expressed in vulnerable human carotid plaques compared with stable plaques. This study aims to investigate the prognostic value of 13 such circulating biomarkers in patients with coronary artery disease. Between 2008 and 2011, 768 patients who underwent coronary angiography for acute coronary syndrome or stable angina pectoris were included in a prospective biomarker study. Plasma concentrations of 13 biomarkers were measured in 88 patients who experienced a major adverse cardiovascular event (MACE) within 1 year and 176 control patients without MACE who were matched on age, sex, and number of diseased coronary vessels. MACE comprised all-cause mortality, acute coronary syndrome, unplanned coronary revascularization, and stroke. After adjustment for established cardiovascular risk factors, osteoglycin (OGN; odds ratio per SD increase in ln-transformed OGN, 1.53; 95% confidence interval, 1.11-2.11; P=0.010) and neutrophil gelatinase-associated lipocalin/matrix metalloproteinase 9 (NGAL/MMP9; odds ratio per SD increase in ln-transformed NGAL/MMP9, 1.37; 95% confidence interval, 1.01-1.85; P=0.042) complex were independently associated with MACE during follow-up. These associations were independent of C-reactive protein levels. Adding OGN or NGAL/MMP9 to a model containing conventional risk factors did not significantly improve discriminatory power (OGN: area under receiver operating characteristic curve, 0.75 versus 0.67; NGAL/MMP9: 0.73 versus 0.67) but did significantly improve risk reclassification (OGN: net reclassification index=0.29; 95% confidence interval, 0.05-0.53; P<0.019; NGAL/MMP9: net reclassification index=0.44; 95% confidence interval, 0.20-0.69; P<0.001). Circulating OGN and NGAL/MMP9 complex are promising biomarkers that are expressed in vulnerable atherosclerotic plaques and may have incremental value for prediction of MACE within 1 year after coronary angiography.
    Arteriosclerosis Thrombosis and Vascular Biology 03/2014; · 6.34 Impact Factor
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    ABSTRACT: Iron deposits are observed in tissue of abdominal aortic aneurysm (AAA) patients, although the underlying mechanisms are not completely elucidated. Therefore we explored circulating markers of iron metabolism in AAA patients, and tested if they could serve as biomarkers of AAA. Increased red blood cell (RBC)-borne iron retention and transferrin, transferrin receptor and ferritin expression was observed in AAA tissue compared to control aorta (immunohistochemistry and western blot). In contrast, decreased circulating iron, transferrin, mean corpuscular haemoglobin concentration (MCHC) and haemoglobin concentration, along with circulating RBC count, were observed in AAA patients (aortic diameter >3 cm, n=114) compared to controls (aortic diameter <3 cm, n=88) (ELISA), whereas hepcidin concentrations were increased in AAA subjects (MS/MS assay). Moreover, iron, transferrin and haemoglobin levels were negatively, and hepcidin positively, correlated with aortic diameter in AAA patients. The association of low haemoglobin with AAA presence or aortic diameter was independent of specific risk factors. Moreover, MCHC negatively correlated with thrombus area in another cohort of AAA patients (aortic diameter 3-5 cm, n=357). We found that anaemia was significantly more prevalent in AAA patients (aortic diameter >5 cm, n=8,912) compared to those in patients with atherosclerotic aorto-iliac occlusive disease (n=17,737) [adjusted odds ratio=1.77 (95% confidence interval: 1.61;1.93)]. Finally, the mortality risk among AAA patients with anaemia was increased by almost 30% [adjusted hazard ratio: 1.29 (95% confidence interval: 1.16;1.44)] as compared to AAA subjects without anaemia. In conclusion, local iron retention and altered iron recycling associated to high hepcidin and low transferrin systemic concentrations could lead to reduced circulating haemoglobin levels in AAA patients. Low haemoglobin levels are independently associated to AAA presence and clinical outcome.
    Thrombosis and Haemostasis 03/2014; 112(1). · 5.76 Impact Factor
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    ABSTRACT: In this work, we describe an approach of detecting biomarkers by Surface Plasmon Resonance imaging (SPRi) technique in real samples. Two C-Reactive Protein (CRP)-antibody immobilization methods were used: The first method was based on direct physisorption of CRP-antibody onto gold surface; the second one was based on oriented CRP-antibody with protein G intermediate layer. The two developed immunosensors were tested against CRP antigen in phosphate buffer saline solution with the SPRi technique. The response of the developed immunosensors was reproducible and stable. The detection limit of 10 pg∙mL−1 and 50 pg∙mL−1 CRP-antigen was observed with and without protein G respectively with this technique. Moreover, the developed SPRi immunosensor was used for CRP-antigen detection in human plasma. A detection limit of 5 ng∙mL−1 and 10 ng∙mL−1 was obtained with and without protein G respectively. These obtained results were compared to those obtained with QCM (Quartz Crystal Microbalance) and Enzyme-Linked Immunosorbent Assay (ELISA) techniques.
    Journal of Biomaterials and Nanobiotechnology 01/2014; 5:153-158.
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    ABSTRACT: Objective Hemostasis interrupts bleeding from disrupted blood vessels by activating platelet aggregation and coagulation. A similar mechanism termed thrombosis generates obstructive thrombi inside diseased arteries. As a consequence of this similarity, current antithrombotic agents increase the risk of bleeding. Atherosclerotic plaques produce significant amounts of prostaglandin E2 (PGE2) which activates its receptor EP3 on platelets and aggravates atherothrombosis. We investigated whether blocking EP3 could dissociate atherothrombosis from hemostasis.Methods and ResultsInhibiting in vivo the receptor EP3 for PGE2 with the blocking agent DG-041 reduced murine thrombosis triggered by local delivery of arachidonic acid or ferric chloride on healthy arteries. Importantly, it also reduced thrombosis triggered by scratching murine atherosclerotic plaques. PGE2 was not produced at the bleeding site after tail clipping. Consistently, blocking EP3 did not alter murine tail, liver or cerebral hemostasis. Furthermore, blocking EP3 reduced murine pulmonary embolism and intensified platelet inhibition by clopidogrel leaving tail bleeding times unchanged. Human atherosclerotic plaques produced PGE2, which facilitated platelet aggregation in human blood and rescued function of P2Y12-blocked platelets. Finally, in healthy patients DG-041 reduced platelet aggregation, but did not significantly alter the cutaneous bleeding time at doses up to 8-times the dose that inhibited the facilitating effect of PGE2 on platelets. In mice, blocking EP3 inhibited atherothrombosis without affecting hemostasis and intensified efficiency of conventional antiplatelet treatment without aggravating the bleeding risk. In patients, blocking EP3 should improve the prevention of cardiovascular diseases which is currently limited by the risk of bleeding.
    Cardiovascular Research 12/2013; · 5.81 Impact Factor
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    ABSTRACT: In this work, we study the electrochemical properties of protein layer grafted on gold electrode for C-reactive protein detection. Two CRP-antibody immobilization methods were used: the first method is based on direct physisorption of CRP-antibody onto the gold surface and the second method is based on oriented CRP-antibody with protein G intermediate layer. The two developed immunosensors were tested against CRP antigen in phosphate buffer saline solution and in human plasma. The electrochemical characterization of each immobilized layers was achieved by cyclic voltammetry and impedance spectroscopy. The morphology of the deposited biomolecules was observed by Atomic Force Microscopy and the roughness was measured. Moreover, contact angle measurement was used for wettability studies. The response of the developed immunosensors was reproducible, rapid, and highly stable and a detection limit of 100 fg/mL and 10 pg/mL antigen was observed with and without protein G respectively. The developed immunosensors was used for CRP detection in human plasma.
    Talanta 11/2013; 116:84–90. · 3.50 Impact Factor
  • B. Lapergue, O. Meilhac
    Archives des Maladies du Coeur et des Vaisseaux - Pratique 10/2013; 2013(221):34–36.
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    ABSTRACT: Abdominal aortic aneurysm (AAA) is a particular form of atherothrombotic disease characterized by the dilation of the aortic wall and the presence of an intraluminal thrombus (ILT). The objective of the present study was to evaluate the pro-oxidant properties of the ILT and to characterize the anti-oxidant capacity of high-density lipoproteins (HDLs).Methods and ResultsOur results show that both ILT, adventitia and plasma from AAA patients contained high concentrations of lipid and protein oxidation products. Mediators produced within or released by the thrombus and the adventitia were shown to induce reactive oxygen species (ROS) production by cultured aortic smooth muscle cells (AoSMCs) and to trigger the onset of apoptosis (an increase in mitochondrial membrane potential). Iron chelation Hemoglobin depletion limited these effects. Both concentration and functionality of HDLs were altered in AAA patients. Plasma levels of Apo A-I were lower and small HDL subclasses were decreased in AAA patients. Circulating HDLs in AAA patients displayed an impaired capacity to inhibit copper-induced low-density lipoprotein oxidation and AoSMC ROS production. Western blot analyses of HDLs demonstrated that myeloperoxidase is associated with HDL particles in AAA patients. The ILT and adventitia are is a source of pro-oxidant products, in particular hemoglobin, which may impact on the wall stability/rupture in AAA. In addition, HDLs from AAA patients exhibit an impaired anti-oxidant activity. In this context, restoring HDL functionality may represent a new therapeutic option in AAA.
    Cardiovascular Research 08/2013; · 5.81 Impact Factor
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    ABSTRACT: In the past 10 years, the LDL receptor inhibitor proprotein convertase subtilisin kexin type 9 (PCSK9) has emerged as a validated target for lowering plasma LDL cholesterol levels. Here we review the most recent reports on PCSK9 out of a total of 500 publications published in print or online before March 2013 and indexed on PubMed. All published in 2012, phase I and II clinical trials demonstrate that fully human monoclonal antibodies targeting PCSK9 dramatically reduce LDL-C and enable patients to reach their target goals, without severe or serious safety issues. This review summarizes the discovery of PCSK9, its original mode of action as a secreted inhibitor of the LDL receptor, as well as its genetic regulation by statins. We then focus on the major results from the 2012 phase I and II PCSK9 inhibitor clinical trials. We also review the recent in-vivo studies demonstrating the potential cardiovascular benefits of long-term PCSK9 inhibition and discuss its potential side-effects.
    Current opinion in lipidology 06/2013; · 5.80 Impact Factor
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    ABSTRACT: OBJECTIVE: To identify proteins related to intraluminal thrombus biological activities that could help to find novel pathological mechanisms and therapeutic targets for human abdominal aortic aneurysm (AAA). APPROACH AND RESULTS: Tissue-conditioned media from patients with AAA were analyzed by a mass spectrometry-based strategy using liquid chromatography coupled to tandem mass spectrometry. Global pathway analysis by Ingenuity software highlighted the presence of several circulating proteins, among them were proteins from the complement system. Complement C3 concentration and activation were assessed in plasma from AAA patients (small AAA, AAA diameter=3-5 cm and large AAA, AAA diameter >5 cm), showing decreased C3 levels and activation in large AAA patients. No association of a combination of single-nucleotide polymorphisms in complement genes between large and small AAA patients was observed. Intense extracellular C3 inmunostaining, along with C9, was observed in AAA thrombus. Analysis of C3 in AAA tissue homogenates and tissue-conditioned media showed increased levels of C3 in AAA thrombus, as well as proteolytic fragments (C3a/C3c/C3dg), suggesting its local deposition and activation. Finally, the functional role of local complement activation in polymorphonuclear (PMN) cell activation was tested, showing that C3 blockade by anti-C3 antibody was able to decrease thrombus-induced neutrophil chemotaxis and reactive oxygen species production. CONCLUSIONS: A decrease of systemic C3 concentration and activity in the later stages of AAA associated with local complement retention, consumption, and proteolysis in the thrombus could induce PMN chemotaxis and activation, playing a detrimental role in AAA progression.
    Arteriosclerosis Thrombosis and Vascular Biology 05/2013; · 6.34 Impact Factor
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    ABSTRACT: Epidemiological data indicate an association between periodontitis and obesity. The biological mechanisms of this relationship remain unclear. A cross-sectional study was conducted to evaluate the relationship between periodontitis and the common systemic inflammatory markers in 32 morbidly obese patients recruited in a Clinical Nutrition department. Periodontal condition was evaluated using pocket depth (PD) measurement, a classical clinical marker of ongoing periodontitis. Major periodontal risk factors were recorded (age, gender, diabetes and smoking status), as well as plasma levels of inflammatory markers (CRP, orosomucoid, IL-6) and adipokines (adiponectin, leptin). All patients included in the sample exhibited evidence of periodontitis, 16 of whom were diagnosed as having severe disease. Adjusted logistic regression analysis indicated that the severity of periodontitis was associated with the plasma level of orosomucoid (p<0.04) after adjustment for age, gender and smoking. Our study thus suggests that the severity of periodontitis, in morbidly obese patients, is associated with the increase of orosomucoid levels.
    PLoS ONE 03/2013; 8(3):e57645. · 3.53 Impact Factor
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    ABSTRACT: High density lipoproteins (HDLs) represent a family of particles characterized by the presence of apolipoprotein A-I (apoA-I) and by their ability to reverse transport cholesterol from peripheral tissues back to the liver. In addition to this function, HDLs display pleiotropic effects including antioxidant, anti-apoptotic, anti-inflammatory, anti-thrombotic or anti-proteolytic properties that account for their protective action on endothelial cells (ECs). Vasodilatation via production of nitric oxide (NO) is also a hallmark of HDL action on ECs. ECs express receptors for apoA-I/HDLs that mediate intracellular signalling and potentially participate in the internalization of these particles. In this review, we will detail the different effects of HDLs on the endothelium in normal and pathological conditions with a particular focus on the potential use of HDL therapy to restore endothelial function and integrity.
    British Journal of Pharmacology 03/2013; · 5.07 Impact Factor
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    ABSTRACT: Infective endocarditis (IE) remains a life-threatening infectious disease with high morbidity and mortality. The objectives of the present study are to assess host proteolytic activities of the vegetations and their cytotoxic potential in a rat model of experimental IE. Rats were infected with a strain of Enterococcus faecalis of particularly low virulence and weak protease expression.We tested the presence of proteases released by infiltrated leukocytes (matrix metalloproteinases and elastase) or produced in situ within the septic vegetation, such as those linked to the fibrinolytic system (plasmin, plasminogen activators). We also assessed the tissue damage induced by the infective thrombus in vitro and ex vivo.The model of IE was characterized by larger and more extensive vegetations in infected versus non-septic rats and an intense neutrophil infiltrate interfacing with the injured underlying tissue. Neutrophil extracellular DNA was shown to trap bacteria and to produce increased levels of cell-free DNA in plasma. Matrix metalloproteinase 9, elastase and plasminogen activators were increased in septic vs non-septic vegetations (as shown by zymography and immuno-histology). Finally, proteolysis of the extracellular matrix and apoptosis were shown to be associated with host proteases. Bacteria exhibited no detectable proteolytic activity or direct cytotoxic effects. Bacterial membranes/dead bacteria were sufficient to induce leukocyte recruitement and activation that could promote vegetation formation and growth. Our results suggest that despite the lack of bacterial proteases, the continuous attractant signals coming from bacterial colonies may lead to a chronic and deleterious aggression toward myocardial/valvular tissues by host proteases.
    Infection and immunity 03/2013; · 4.16 Impact Factor

Publication Stats

2k Citations
557.95 Total Impact Points


  • 2009–2014
    • Paris Diderot University
      Lutetia Parisorum, Île-de-France, France
  • 2004–2013
    • Universidad Autónoma de Madrid
      • Departamento de Inmunología
      Madrid, Madrid, Spain
  • 2003–2011
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
  • 2010
    • Instituto de Investigación Sanitaria
      Madrid, Madrid, Spain
    • University of Paris-Est
      Centre, France
    • Université René Descartes - Paris 5
      • Faculté de chirurgie dentaire
      Paris, Ile-de-France, France
  • 2006–2010
    • Fundación Jiménez Díaz
      • Servicio de Nefrología e Hipertensión
      Madrid, Madrid, Spain
  • 2002–2009
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 2000–2002
    • Emory University
      • Department of Gynecology and Obstetrics
      Atlanta, GA, United States
  • 1998
    • Institut Louis Bachelier
      Lutetia Parisorum, Île-de-France, France
  • 1997–1998
    • Paul Sabatier University - Toulouse III
      • Faculté de médecine Rangueil
      Toulouse, Midi-Pyrenees, France