Biomedical subjects

Valérie Marin

Publications and source records attributed to Valérie Marin.

11 recordsLinked to original sources

PubMed2006

Allergic memory of patients sensitized to castor bean after a long stimulation-free period.

We have taken advantage of the temporary exposure of Marseilles population to castor bean seed proteins to follow 26 allergic patients more than 20 years after sensitization. Skin tests, specific immunoglobulin E (IgE) antibody assays, and specific immunoblots were performed. Skin test reactivity to Ricinus Communis and specific IgE concentrations decreased progressively and almost completely disappeared after 20 years. Specific IgE concentration displayed a fairly exponential decrease, with a half-life of 4.7 years. Thus, in the absence of any antigenic stimulation, directly by castor bean, or indirectly by cross-reactivity to other Euphorbiaceae, especially latex, IgE sensitization is bound to disappear.

Aged↗

PubMed2006

Neuromuscular blocking agents decrease inflammatory response in patients presenting with acute respiratory distress syndrome.

OBJECTIVE: To evaluate the effects of neuromuscular blocking agents (NMBAs) on pulmonary and systemic inflammation in patients with acute respiratory distress syndrome ventilated with a lung-protective strategy. DESIGN: Multiple-center, prospective, controlled, and randomized trial. SETTING: One medical and two medical-surgical intensive care units. PATIENTS: A total of 36 patients with acute respiratory distress syndrome (Pao2/Fio2 ratio of < or =200 at a positive end-expiratory pressure of > or =5 cm H2O) were included within 48 hrs of acute respiratory distress syndrome onset. INTERVENTIONS: Patients were randomized to receive conventional therapy plus placebo (n = 18) or conventional therapy plus NMBAs (n = 18) for 48 hrs. Both groups were ventilated with a lung-protective strategy (tidal volume between 4 and 8 mL/kg ideal body weight, plateau pressure of < or =30 cm H2O). MEASUREMENTS AND MAIN RESULTS: Bronchoalveolar lavages and blood samples were performed, before randomization and at 48 hrs, to determine the concentrations of tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, and IL-8. Pao2/Fio2 ratio was evaluated before randomization and at 24, 48, 72, 96, and 120 hrs. A decrease over time in IL-8 concentrations (p = .034) was observed in the pulmonary compartment of the NMBA group. At 48 hrs after randomization, pulmonary concentrations of IL-1beta (p = .005), IL-6 (p = .038), and IL-8 (p = .017) were lower in the NMBA group as compared with the control group. A decrease over time in IL-6 (p = .05) and IL-8 (p = .003) serum concentrations was observed in the NMBA group. At 48 hrs after randomization, serum concentrations of IL-1beta (p = .037) and IL-6 (p = .041) were lower in the NMBA group as compared with the control group. A sustained improvement in Pao2/Fio2 ratio was observed and was reinforced in the NMBA group (p < .001). CONCLUSION: Early use of NMBAs decrease the proinflammatory response associated with acute respiratory distress syndrome and mechanical ventilation.

Cytokines↗

PubMed2005

Severe imbalance of IL-18/IL-18BP in patients with secondary hemophagocytic syndrome.

Hemophagocytic syndrome (HPS) is characterized by an uncontrolled and poorly understood activation of T-helper 1 (Th-1) lymphocytes and macrophages. We studied 20 patients with HPS secondary to infections, autoimmune disease, lymphoma, or cancer and observed that the concentrations of serum interleukin 18 (IL-18), a strong inducer of Th-1 responses, interferon gamma (IFN-gamma) production, and stimulation of macrophages and natural killer (NK) cells were highly increased in HPS but not in control patients. In contrast, concentrations of its natural inhibitor, the IL-18 binding protein (IL-18BP), were only moderately elevated, resulting in a high level of biologically active free IL-18 in HPS (4.6-fold increase compared with controls; P < .001). Free IL-18 but not IL-12 concentrations significantly correlated with clinical status and the biologic markers of HPS such as anemia (P < .001), hypertriglyceridemia, and hyperferritinemia (P < .01) and also with markers of Th-1 lymphocyte or macrophage activation, such as elevated concentrations of IFN-gamma and soluble IL-2 and tumor necrosis factor alpha (TNF-alpha) receptor concentrations. Despite high IL-18 elevation, in vitro NK-cell cytotoxicity was severely impaired in HPS patients, in part due to NK-cell lymphopenia that was observed in a majority of patients but also secondary to an intrinsic NK-cell functional deficiency. We concluded that a severe IL-18/IL-18BP imbalance results in Th-1 lymphocyte and macrophage activation, which escapes control by NK-cell cytotoxicity and may allow for secondary HPS in patients with underlying diseases.

Adolescent↗

PubMed2005

Vascular cell adhesion molecule-1 (VCAM-1) plays a central role in the pathogenesis of severe forms of vasculitis due to hepatitis C-associated mixed cryoglobulinemia.

BACKGROUND/AIMS: To better characterize the molecules involved in leukocyte tissue infiltration during hepatitis C-mixed cryoglobulinemia (HCV-MC)-associated vasculitis. METHODS: The involvement of ELAM, ICAM-1 and VCAM-1 was evaluated in 36 patients with HCV-MC vasculitis using three different approaches: concentrations of soluble forms by specific ELISA, tissue expression by immunohistochemistry on patients nerve biopsies, endothelial expression by FACS analysis, on cells activated in vitro by cryoprecipitates purified from HCV-MC patients. RESULTS: Concentrations of sVCAM-1 were significantly elevated in the serum of HCV-MC patients compared to HCV patients without MC, the highest concentrations being found in severe vasculitis. VCAM-1 expression was detected on blood vessels from nerve biopsies performed in patients with severe vasculitis. When added to endothelial cells in vitro, HCV-MC patients cryoprecipitate induced VCAM-1 but also ELAM and ICAM-1 expression possibly through a mechanism due to the C1q complement fraction interaction with endothelial cells, since C1q was consistently present in the cryoprecipitates. CONCLUSIONS: VCAM-1 is mainly involved in the pathogenesis of HCV-MC-associated severe vasculitis and may be a potential interesting therapeutic target.

Adult↗

PubMed2005

The endothelial cholesterol efflux is promoted by the high-density lipoprotein anionic peptide factor.

The prevention of atherosclerosis depends on the high-density lipoprotein (HDL) capacity to stimulate the efflux of unesterified cholesterol (UC). We tested here the effects of 2 HDL apolipoproteins, apo A-I and the 7-kd anionic peptide factor (APF), on the UC efflux by human endothelial ECV 304 cells in culture. Apolipoprotein A-I (10 micromol/L) or APF (3.5 micromol/L) in lipid-free forms or small particles (13 nm with apo A-I or 19 nm with APF) were incubated in the presence of [4-14C]UC. The phosphatidylcholines (PCs) were present either at a low level (0.35 mmol/L with apo A-I or 0.20 mmol/L with APF) or at a high level (1 mmol/L with apo A-I). We also tested either large 53-nm bile lipoprotein complex-like particles (3.5 micromol/L APF [13 microg/500 microL]) with a high PC level (0.65 mmol/L) or a 9-residue synthetic peptide (13 microg/500 microL), derived from the NH2-terminal domain of HDL3-APF, in a lipid-free or low-lipidated (0.20 mmol/L PCs) form. A control was developed in absence of the added compounds. A rapid [4-14C]UC efflux mediated by APF added in free form or in 19-nm complexes was 2.2- to 2.3-fold higher than that mediated by apo A-I in free form or in 13-nm particles (P < .05). The level of this high APF-related efflux was comparable with that obtained with the 12-nm native HDLs (10 micromol/L apo A-I) or free PCs (1 mmol/L). The increase in the UC efflux was much more limited (1.4-fold) in the presence of the 53-nm APF/high-PC particles, but it was higher than that mediated by apo A-I. In addition, the efflux mediated by the synthetic peptide, in lipid-free or low-lipidated form, constituted the major part of that related to the full-length APF. Thus, all these particles are very active HDL components, able to act as cholesterol acceptors. Interestingly, we further showed a new anti-atherogenic property of APF as well as its metabolic importance and clinical relevance. By its involvement in the first step of the reverse cholesterol transport, APF could reduce the risk of cardiovascular disease.

Apoproteins↗

PubMed2005

Comparison of prone positioning and high-frequency oscillatory ventilation in patients with acute respiratory distress syndrome.

OBJECTIVE: Both prone position and high-frequency oscillatory ventilation (HFOV) have the potential to facilitate lung recruitment, and their combined use could thus be synergetic on gas exchange. Keeping the lung open could also potentially be lung protective. The aim of this study was to compare physiologic and proinflammatory effects of HFOV, prone positioning, or their combination in severe acute respiratory distress syndrome (ARDS). DESIGN: : Prospective, comparative randomized study. SETTING: A medical intensive care unit. PATIENTS: Thirty-nine ARDS patients with a Pao2/Fio2 ratio <150 mm Hg at positive end-expiratory pressure > or =5 cm H2O. INTERVENTIONS: After 12 hrs on conventional lung-protective mechanical ventilation (tidal volume 6 mL/kg of ideal body weight, plateau pressure not exceeding the upper inflection point, and a maximum of 35 cm H2O; supine-CV), 39 patients were randomized to receive one of the following 12-hr periods: conventional lung-protective mechanical ventilation in prone position (prone-CV), HFOV in supine position (supine-HFOV), or HFOV in prone position (prone-HFOV). MEASUREMENTS AND MAIN RESULTS: Prone-CV (from 138 +/- 58 mm Hg to 217 +/- 110 mm Hg, p < .0001) and prone-HFOV (from 126 +/- 40 mm Hg to 227 +/- 64 mm Hg, p < 0.0001) improved the Pao2/Fio2 ratio whereas supine-HFOV did not alter the Pao2/Fio2 ratio (from 134 +/- 57 mm Hg to 138 +/- 48 mm Hg). The oxygenation index ({mean airway pressure x Fio2 x 100}/Pao2) decreased in the prone-CV and prone-HFOV groups and was lower than in the supine-HFOV group. Interleukin-8 increased significantly in the bronchoalveolar lavage fluid (BALF) in supine-HFOV and prone-HFOV groups compared with prone-CV and supine-CV. Neutrophil counts were higher in the supine-HFOV group than in the prone-CV group. CONCLUSIONS: Although HFOV in the supine position does not improve oxygenation or lung inflammation, the prone position increases oxygenation and reduces lung inflammation in ARDS patients. Prone-HFOV produced similar improvement in oxygenation like prone-CV but was associated with higher BALF indexes of inflammation. In contrast, supine-HFOV did not improve gas exchange and was associated with enhanced lung inflammation.

Adult↗

PubMed2005

Anionic peptide factor/phosphatidylcholine particles promote the inhibition of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells.

OBJECTIVE: High-density lipoproteins (HDLs) have significant cardiovascular benefits by retarding the progression of atherosclerosis. One of the mechanisms is the inhibition by HDLs of the vascular cell adhesion molecule-1 (VCAM-1) expression in endothelial cells. Our objective was to test the effect on VCAM-1 expression by the human umbilical vein endothelial cells (HUVEC) of a minor HDL2 and HDL3 apolipoprotein, the anionic peptide factor (APF). The peptide has previously been found to develop some beneficial effects against atherosclerosis, i.e. by promoting the cholesterol efflux from endothelial cells. METHODS: We examined the effects of two HDL apolipoproteins A-I and APF, either in presence or absence of phosphatidylcholines (PCs), or free PCs, on the expression of VCAM-1 by HUVEC. The cells were stimulated with either the tumor necrosis factor-alpha (TNFalpha, 500 pg/ml) or the calcium bound to heparin (10 microg Ca2+/ml, 50 microg heparin/ml). RESULTS: In the presence of TNFalpha, only the free PCs (0.25 and 1 mM) developed an inhibitory effect (up to 50%). In the absence of TNFalpha and in the presence of calcium bound to heparin, either the lipid-free APF (3.5 microM) or the APF/PC complexes (1:57 molar ratio) or the free PCs (0.25 mM) exhibited a substantial inhibitory effect (72, 71 and 42%, respectively). CONCLUSION: Our present findings suggest for the first time that one of the mechanisms of the antiatherogenic action of APF involves the inhibition of VCAM-1 expression by HUVEC. The peptide, through its phospholipid-binding and its calcium antagonist abilities, appears to confer on the HDLs a protective effect against the early cellular event of the inflammatory process.

Cells, Cultured↗

PubMed2003

IL-6: a regulator of the transition from neutrophil to monocyte recruitment during inflammation.

The origin of the Toll-like family of receptors pre-dates the evolutionary split between the plant and animal kingdoms. These receptors are remarkably conserved across the taxonomic kingdoms and have fundamental roles in triggering immune responses. How they trigger such responses, and how these mechanisms arose in evolution, is a topic of extensive debate. We postulate a surveillance model: these receptors "keep watch" for both endogenous and exogenous molecules that indicate tissue inquiry, infection and remodeling. Furthermore, we suggest that the first Toll-like family receptors that arose in evolution might have acted in both development and immunity by recognizing the degradation of endogenous macromolecules.

Animals↗

PubMed2002

[Mechanisms of fever].

Fever represents a normal and adaptative response developed in case of host aggression, notably by infectious agents, and is part of a large defense system, the acute phase response. Fever mediators are mainly derived from the host cells and are pyrogenous cytokines such as interleukin-1, tumour necrosis factor alpha, interleukin-6 or interferons which act at the hypothalamus level via prostaglandin E2. Although fever has been conserved through evolution, its beneficial effects in humans are not well-established.

Acute Disease↗

PubMed2002

Chemotactic agents induce IL-6Ralpha shedding from polymorphonuclear cells: involvement of a metalloproteinase of the TNF-alpha-converting enzyme (TACE) type.

Interleukin (IL)-6 transsignaling plays a pivotal role in the shift from neutrophil to monocyte recruitment at the inflammatory site. Release of neutrophil IL-6 receptor-alpha (IL-6Ralpha, CD126) in its soluble form is a key step of IL-6 transsignaling, however, its physiological inducers are poorly known. Here, we observed that the neutrophil chemoattractants IL-8, C5a complement fraction, platelet activating factor, leukotriene B4 and N-formyl-methionyl-leucyl-phenylalanine rapidly decreased IL-6Ralpha membrane expression and increased soluble IL-6Ralpha concentrations in the neutrophil supernatants, consistent with a shedding process. IL-6Ralpha shedding involved a TNF-alpha-converting enzyme-type metalloproteinase since it was partly decreased in the presence of a specific inhibitor, but not cathepsin G since PMSF or alpha1 antichymotrypsin had no effect. Neutrophil IL-6Ralpha shedding may be a common feature of neutrophilic infiltrates in various inflammatory situations, allowing IL-6 transsignaling, decreasing neutrophil infiltration and in the meantime favoring monocyte recruitment, thus the initiation of an immune response and subsequently the resolution of inflammation.

ADAM Proteins↗

PubMedDate not supplied

Correlation between invasiveness of colorectal tumor cells and adhesive potential under flow.

BACKGROUND: Tumor cell adhesiveness is involved in metastatic dissemination, and adhesive behavior may be different under static and dynamic conditions. MATERIALS AND METHODS: Patients undergoing primary colorectal cancer excision were tested for: i) serum concentration of sE-selectin, sICAM-1 and sVCAM-1, ii) expression of CD18, CD29d and E-cadherin on tumor cells and iii) efficiency of tumor cell adhesion to ECV304 monolayers under flow and resistance to detachment by shear. RESULTS: Twenty out of 31 patients were free of detectable relapse 12 months later. Relapsing and non-relapsing patients had similar levels of soluble adhesion molecules. E-cadherin was detected on tumor cells from three non-relapsing patients, but no relapsing one. Unexpectedly, significant CD18 labeling was found on two relapsing patients and one non-relapsing patient. Cells from relapsing patients displayed significantly increased (p < 0.05 two-sided, p < 0.025 one-sided) capacity to adhere to test monolayers under flow. CONCLUSION: Cancer invasion is related to tumor cell adhesiveness, and the flow chamber provides a practical way of measuring adhesive parameters with a potential value for relapse prediction.

Antigens, CD↗