Search

Your search keyword '"Hurtado-Nedelec, Margarita"' showing total 180 results
Start Over Author "Hurtado-Nedelec, Margarita"
180 results on '"Hurtado-Nedelec, Margarita"'

5. Outcome of SARS-CoV-2 infection is linked to MAIT cell activation and cytotoxicity

Author

Flament, Héloïse, Rouland, Matthieu, Beaudoin, Lucie, Toubal, Amine, Bertrand, Léo, Lebourgeois, Samuel, Rousseau, Camille, Soulard, Pauline, Gouda, Zouriatou, Cagninacci, Lucie, Monteiro, Antoine C., Hurtado-Nedelec, Margarita, Luce, Sandrine, Bailly, Karine, Andrieu, Muriel, Saintpierre, Benjamin, Letourneur, Franck, Jouan, Youenn, Si-Tahar, Mustapha, Baranek, Thomas, Paget, Christophe, Boitard, Christian, Vallet-Pichard, Anaïs, Gautier, Jean-François, Ajzenberg, Nadine, Terrier, Benjamin, Pène, Frédéric, Ghosn, Jade, Lescure, Xavier, Yazdanpanah, Yazdan, Visseaux, Benoit, Descamps, Diane, Timsit, Jean-François, Monteiro, Renato C., and Lehuen, Agnès

Published
2021
Full Text
View/download PDF

7. Is telomere length a predictor of long-term survival in patients with COVID-19 pneumonia?

Author

Bernardinello, Nicol, primary, Crestani, Bruno, additional, Spagnolo, Paolo, additional, Ghanem, Mada, additional, Homps-Legrand, Méline, additional, Morer, Lise, additional, Goletto, Tiphaine, additional, Frija-Masson, Justine, additional, Bancal, Catherine, additional, Hurtado-Nedelec, Margarita, additional, de Chaisemartin, Luc, additional, Debray, Marie Pierre, additional, Neukirch, Catherine, additional, Taillé, Camille, additional, Ba, Ibrahima, additional, Kannengiesser, Caroline, additional, Lainey, Elodie, additional, Abels, Anne, additional, Vankann, Lucia, additional, Beier, Fabian, additional, and Borie, Raphaël, additional

Published
2023
Full Text
View/download PDF

10. Type I interferon signaling in systemic immune cells from patients with alcoholic cirrhosis and its association with outcome

Author

Weiss, Emmanuel, Rautou, Pierre-Emmanuel, Fasseu, Magali, Giabicani, Mikhael, de Chambrun, Marc, Wan, JingHong, Minsart, Charlotte, Gustot, Thierry, Couvineau, Alain, Maiwall, Rakhi, Hurtado-Nedelec, Margarita, Pilard, Nathalie, Lebrec, Didier, Valla, Dominique, Durand, François, de la Grange, Pierre, Monteiro, Renato C., Paugam-Burtz, Catherine, Lotersztajn, Sophie, and Moreau, Richard

Published
2017
Full Text
View/download PDF

14. Blood fibrocytes are associated with severity and prognosis in COVID-19 pneumonia

Author

Ghanem, Mada, Homps-Legrand, Méline, Garnier, Marc, Morer, Lise, Goletto, Tiphaine, Frija-Masson, Justine, Wicky, Paul-Henri, Jaquet, Pierre, Bancal, Catherine, Hurtado-Nedelec, Margarita, de Chaisemartin, Luc, Jaillet, Madeleine, Mailleux, Arnaud, Quesnel, Christophe, Poté, Nicolas, Debray, Marie-Pierre, de Montmollin, Etienne, Neukirch, Catherine, Borie, Raphael, Taillé, Camille, Crestani, Bruno, Covid Cohort Study Group, French, Andréjak, Claire, Physiopathologie et Epidémiologie des Maladies Respiratoires (PHERE (UMR_S_1152 / U1152)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service d'Anesthésie réanimation [CHU Tenon], CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Institut Pasteur [Paris] (IP), Agents infectieux, résistance et chimiothérapie - UR UPJV 4294 (AGIR ), Université de Picardie Jules Verne (UPJV)-CHU Amiens-Picardie, CHU Amiens-Picardie, French COVID cohort study group, ANR-21-CO12-0007,FIBROCO,Implication des fibrocytes circulants dans la physiopathogénie et le pronostic de la pneumopathie sévère au cours du COVID-19(2021), HAL-SU, Gestionnaire, and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)

Subjects
Male, Physiology, CD34, Severity of Illness Index, Gastroenterology, law.invention, 0302 clinical medicine, law, Fibrocyte, Aged, 80 and over, 0303 health sciences, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, medicine.diagnostic_test, Middle Aged, Intensive care unit, 3. Good health, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Cytokines, Female, Research Article, Adult, Pulmonary and Respiratory Medicine, medicine.medical_specialty, CCL2, 03 medical and health sciences, Antigens, CD, Physiology (medical), Internal medicine, Severity of illness, medicine, Humans, COVID-19 pneumonia, Aged, 030304 developmental biology, Serum Amyloid A Protein, Blood Cells, Lung, SARS-CoV-2, business.industry, COVID-19, Cell Biology, medicine.disease, Blood Cell Count, Pneumonia, Bronchoalveolar lavage, fibrocyte, prognosis, Tomography, X-Ray Computed, business, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Increased blood fibrocytes are associated with a poor prognosis in fibrotic lung diseases. We aimed to determine whether the percentage of circulating fibrocytes could be predictive of severity and prognosis during coronavirus disease 2019 (COVID-19) pneumonia. Blood fibrocytes were quantified by flow cytometry as CD45+/CD15−/CD34+/collagen-1+ cells in patients hospitalized for COVID-19 pneumonia. In a subgroup of patients admitted in an intensive care unit (ICU), fibrocytes were quantified in blood and bronchoalveolar lavage (BAL). Serum amyloid P (SAP), transforming growth factor-β1 (TGF-β1), CXCL12, CCL2, and FGF2 concentrations were measured. We included 57 patients in the hospitalized group (median age = 59 yr [23–87]) and 16 individuals as healthy controls. The median percentage of circulating fibrocytes was higher in the patients compared with the controls (3.6% [0.2–9.2] vs. 2.1% [0.9–5.1], P = 0.04). Blood fibrocyte count was lower in the six patients who died compared with the survivors (1.6% [0.2–4.4] vs. 3.7% [0.6–9.2], P = 0.02). Initial fibrocyte count was higher in patients showing a complete lung computed tomography (CT) resolution at 3 mo. Circulating fibrocyte count was decreased in the ICU group (0.8% [0.1–2.0]), whereas BAL fibrocyte count was 6.7% (2.2–15.4). Serum SAP and TGF-β1 concentrations were increased in hospitalized patients. SAP was also increased in ICU patients. CXCL12 and CCL2 were increased in ICU patients and negatively correlated with circulating fibrocyte count. We conclude that circulating fibrocytes were increased in patients hospitalized for COVID-19 pneumonia, and a lower fibrocyte count was associated with an increased risk of death and a slower resolution of lung CT opacities.

Published
2021
Full Text
View/download PDF

15. Cytosolic PCNA interacts with S100A8 and controls an inflammatory subset of neutrophils in COVID-19

Author

de Oliveira Formiga, Rodrigo, primary, Pesenti, Lucie, additional, Ladjemi, Maha Zohra, additional, Frachet, Philippe, additional, Andrieu, Muriel, additional, Many, Souganya, additional, Karunanithy, Vaarany, additional, Bailly, Karine, additional, Dhôte, Théo, additional, Castel, Manon, additional, Rousseau, Christophe, additional, Starick, Marick, additional, da Rocha, Edroaldo Lummertz, additional, Lombardi, Emilia Puig, additional, Granger, Vanessa, additional, Chollet-Martin, Sylvie, additional, De Chaisemartin, Luc, additional, Mouthon, Luc, additional, Spiller, Fernando, additional, Hosmalin, Anne, additional, Hurtado-Nedelec, Margarita, additional, Martin, Clémence, additional, Pène, Frédéric, additional, Burgel, Pierre-Regis, additional, Tourneur, Léa, additional, and Witko-Sarsat, Véronique, additional

Published
2022
Full Text
View/download PDF

17. Gene- and exon-expression profiling reveals an extensive LPS-induced response in immune cells in patients with cirrhosis

Author

Gandoura, Sonia, Weiss, Emmanuel, Rautou, Pierre-Emmanuel, Fasseu, Magali, Gustot, Thierry, Lemoine, Frédéric, Hurtado-Nedelec, Margarita, Hego, Caroline, Vadrot, Nathalie, Elkrief, Laure, Lettéron, Philippe, Tellier, Zéra, Pocidalo, Marie-Anne, Valla, Dominique, Lebrec, Didier, Groyer, André, Monteiro, Renato C., de la Grange, Pierre, and Moreau, Richard

Published
2013
Full Text
View/download PDF

22. Impaired p47phox phosphorylation in neutrophils from p67phox-deficient chronic granulomatous disease patients Short title: p67phox regulates p47phox phosphorylation

Author

Belambri, Sahra Amel, Marzaioli, Viviana, Hurtado-Nedelec, Margarita, Pintard, Coralie, Liang, Shiyu, Liu, Yezhou, Boussetta, Tarek, Gougerot-Pocidalo, Marie-Anne, Ye, Richard, Dang, Pham My-Chan, El-Benna, Jamel, DANG, Pham My-Chan, Centre de recherche sur l'Inflammation (CRI (UMR_S_1149 / ERL_8252 / U1149)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Laboratoire d'Excellence INFLAMEX [Paris], Université Sorbonne Paris Cité (USPC), AP-HP - Hôpital Bichat - Claude Bernard [Paris], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
PHAGOCYTES, GRANULOCYTES, AND MYELOPOIESIS, [SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity
Abstract

International audience; Abstract Superoxide production by the phagocyte reduced NAD phosphate (NADPH) oxidase is essential for innate immunity as shown in chronic granulomatous disease (CGD), an immunodeficiency disease resulting from mutations in 1 of its genes. The NADPH oxidase is composed of 2 membrane proteins (gp91phox/NOX2 and p22phox) and 4 cytosolic proteins (p47phox, p67phox, p40phox, and Rac1/2). The phosphorylation of p47phox is required for NADPH oxidase activation in cells. As p47phox and p67phox can form a tight complex in cells, we hypothesized that p67phox could regulate p47phox phosphorylation. To investigate this hypothesis, we used phospho-specific antibodies against 5 major p47phox-phosphorylated sites (Ser304, Ser315, Ser320, Ser328, and Ser345) and neutrophils from healthy donors and from p67phox−/− CGD patients. Results showed that formyl-methionyl-leucyl-phenylalanine and phorbol myristate acetate induced a time- and a concentration-dependent phosphorylation of p47phox on Ser304, Ser315, Ser320, and Ser328 in healthy human neutrophils. Interestingly, in neutrophils and Epstein-Barr virus-transformed B lymphocytes from p67phox−/− CGD patients, phosphorylation of p47phox on serine residues was dramatically reduced. In COSphox cells, the presence of p67phox led to increased phosphorylation of p47phox. In vitro studies showed that recombinant p47phox was phosphorylated on Ser304, Ser315, Ser320, and Ser328 by different PKC isoforms and the addition of recombinant p67phox alone or in combination with p40phox potentiated this process. Thus, p67phox and p40phox are required for optimal p47phox phosphorylation on Ser304, Ser315, Ser320, and Ser328 in intact cells. Therefore, p67phox and p40phox are novel regulators of p47phox-phosphorylation.

Published
2022
Full Text
View/download PDF

26. Identification of secreted phosphoprotein 1 gene as a new rheumatoid arthritis susceptibility gene

Author

Gazal, Steven, Sacre, Karim, Allanore, Yannick, Teruel, Maria, Goodall, Alison H, Tohma, Shigeto, Alfredsson, Lars, Okada, Yukinori, Xie, Gang, Constantin, Arnaud, Balsa, Alejandro, Kawasaki, Aya, Nicaise, Pascale, Amos, Christopher, Rodriguez-Rodriguez, Luis, Chiocchia, Gilles, Boileau, Catherine, Zhang, Jinyi, Vittecoq, Olivier, Barnetche, Thomas, Gay, Miguel A Gonzalez, Furukawa, Hiroshi, Cantagrel, Alain, Le Loët, Xavier, Sumida, Takayuki, Hurtado-Nedelec, Margarita, Richez, Christophe, Chollet-Martin, Sylvie, Schaeverbeke, Thierry, Combe, Bernard, Khoryati, Liliane, Coustet, Baptiste, El-Benna, Jammel, Siminovitch, Katherine, Plenge, Robert, Padyukov, Leonid, Martin, Javier, Tsuchiya, Naoyuki, and Dieudé, Philippe

Published
2015
Full Text
View/download PDF

28. Blood fibrocytes are associated with severity and prognosis in COVID-19 pneumonia

Author

Ghanem, Mada, primary, Homps-Legrand, Meline, additional, Morer, Lise, additional, Goletto, Tiphaine, additional, Frija, Justine, additional, Bancal, Catherine, additional, Hurtado-Nedelec, Margarita, additional, Jaillet, Madeleine, additional, Mailleux, Arnaud, additional, Neukirch, Catherine, additional, Borie, Raphael, additional, Taille, Camille, additional, and Crestani, Bruno, additional

Published
2021
Full Text
View/download PDF

29. Apocynin prevents GM-CSF-induced-ERK1/2 activation and -neutrophil survival independently of its inhibitory effect on the phagocyte NADPH oxidase NOX2

Author

El Benna, Jamel, Pintard, Coralie, Ben Khemis, Marwa, Liu, Dan, Dang, Pham My-Chan, Hurtado-Nedelec, Margarita, El-Benna, Jamel, Lab Excellence Inflamex (CRI INSERM U1149 - Bichat Medical Faculty), Université Paris Diderot - Paris 7 (UPD7), Centre de recherche sur l'Inflammation (CRI (UMR_S_1149 / ERL_8252 / U1149)), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)

Subjects
inorganic chemicals, 0301 basic medicine, Phagocyte, Cell Survival, Neutrophils, Apoptosis, Biochemistry, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, Antioxidants, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, medicine, Humans, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, Cells, Cultured, ComputingMilieux_MISCELLANEOUS, Pharmacology, chemistry.chemical_classification, Reactive oxygen species, Phagocytes, NADPH oxidase, biology, Kinase, Degranulation, Acetophenones, Granulocyte-Macrophage Colony-Stimulating Factor, NADPH Oxidases, 3. Good health, Cell biology, Enzyme Activation, 030104 developmental biology, medicine.anatomical_structure, chemistry, 030220 oncology & carcinogenesis, Apocynin, cardiovascular system, biology.protein, [SDV.IMM]Life Sciences [q-bio]/Immunology, Reactive Oxygen Species, circulatory and respiratory physiology
Abstract

Neutrophils are key cells in innate immunity and inflammation. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is known to enhance many neutrophil functions such as reactive oxygen species (ROS) production, degranulation and cell survival via the activation of the ERK1/2 pathway. ERK1/2 pathway activation is redox sensitive and could be modulated by ROS. In order to investigate whether NADPH oxidase NOX2-derived ROS could contribute to GM-CSF-induced ERK1/2 phosphorylation, we tested the effect of two selective NOX2 inhibitors, diphenylene iodonium (DPI) and apocynin. Results showed that, while both DPI and apocynin strongly inhibited neutrophil ROS production, only apocynin, but not DPI, inhibited GM-CSF-induced ERK1/2 phosphorylation, suggesting that ROS are not involved in this process. Apocynin did not affect GM-CSF-induced p38MAPKinase phosphorylation, another redox sensitive kinase. Interestingly, apocynin inhibited GM-CSF-induced MEK1/2 and AKT phosphorylation without affecting fMLF-induced phosphorylation of these proteins. GM-CSF is known to inhibit neutrophils apoptosis and to promote cell survival via the AKT-ERK1/2 pathway. In this regard, we found that apocynin also inhibited GM-CSF-induced anti-apoptotic effect in neutrophils. These results suggest that NADPH oxidase NOX2-derived ROS are not involved in GM-CSF-induced ERK1/2 phosphorylation and that apocynin inhibits GM-CSF-induced ERK1/2 phosphorylation pathway independently of its inhibitory action on NADPH oxidase NOX2. Thus, apocynin can exert an anti-inflammatory effect not only by limiting neutrophil ROS production but also by decreasing neutrophil survival at inflammatory site.

Published
2020
Full Text
View/download PDF

31. Innate immune deficiencies in patients with COVID-19

Author

Peyneau, Marine, primary, Granger, Vanessa, additional, Wicky, Paul-Henri, additional, Khelifi-Touhami, Dounia, additional, Timsit, Jean-François, additional, Lescure, François-Xavier, additional, Yazdanpanah, Yazdan, additional, Tran-Dihn, Alexy, additional, Montravers, Philippe, additional, Monteiro, Renato C., additional, Chollet-Martin, Sylvie, additional, Hurtado-Nedelec, Margarita, additional, and de Chaisemartin, Luc, additional

Published
2021
Full Text
View/download PDF

33. Correction: Cytosolic PCNA interacts with p47phox and controls NADPH oxidase NOX2 activation in neutrophils

Author

Ohayon, Delphine, primary, De Chiara, Alessia, additional, My-Chan Dang, Pham, additional, Thieblemont, Nathalie, additional, Chatfield, Simon, additional, Marzaioli, Viviana, additional, Burgener, Sabrina Sofia, additional, Mocek, Julie, additional, Candalh, Céline, additional, Pintard, Coralie, additional, Tacnet-Delorme, Pascale, additional, Renault, Gilles, additional, Lagoutte, Isabelle, additional, Favier, Maryline, additional, Walker, Francine, additional, Hurtado-Nedelec, Margarita, additional, Desplancq, Dominique, additional, Weiss, Etienne, additional, Benarafa, Charaf, additional, Housset, Dominique, additional, Marie, Jean-Claude, additional, Frachet, Philippe, additional, El-Benna, Jamel, additional, and Witko-Sarsat, Véronique, additional

Published
2019
Full Text
View/download PDF

35. Cytosolic PCNA interacts with p47phox and controls NADPH oxidase NOX2 activation in neutrophils

Author

Ohayon, Delphine, primary, De Chiara, Alessia, additional, Dang, Pham My-Chan, additional, Thieblemont, Nathalie, additional, Chatfield, Simon, additional, Marzaioli, Viviana, additional, Burgener, Sabrina Sofia, additional, Mocek, Julie, additional, Candalh, Céline, additional, Pintard, Coralie, additional, Tacnet-Delorme, Pascale, additional, Renault, Gilles, additional, Lagoutte, Isabelle, additional, Favier, Maryline, additional, Walker, Francine, additional, Hurtado-Nedelec, Margarita, additional, Desplancq, Dominique, additional, Weiss, Etienne, additional, Benarafa, Charaf, additional, Housset, Dominique, additional, Marie, Jean-Claude, additional, Frachet, Philippe, additional, El-Benna, Jamel, additional, and Witko-Sarsat, Véronique, additional

Published
2019
Full Text
View/download PDF

37. Intérêt du dosage des chaînes légères libres dans le cadre de gammapathies monoclonales et d'autres hémopathies malignes et maladies auto-immunes.

Author

Verebi, Camille, Talbot, Alexis, Gendron, Nicolas, and Hurtado-Nedelec, Margarita

Abstract

Résumé: Les chaînes légères des immunoglobulines sont qualifiées de libres lorsqu'elles ne sont pas liées à des chaînes lourdes pour former une immunoglobuline entière. La quantification de ces chaînes légères libres dans le sérum est recommandée par la Haute autorité de santé pour le diagnostic et le suivi du myélome multiple à chaînes légères, pauci- ou non sécrétant et de l'amylose AL. Plus récemment, l'Organisation mondiale de la santé a inclus ce dosage dans les critères pronostiques des gammapathies monoclonales de signification indéterminée. Cependant, la littérature met en évidence de plus en plus d'indications potentielles à ce dosage au cours des gammapathies monoclonales mais aussi des hémopathies malignes telles que les hémopathies lymphoïdes, et certaines pathologies auto-immunes telles que le diabète, la polyarthrite rhumatoïde, le lupus érythémateux disséminé, la sclérose en plaques ou encore le syndrome de Gougerot-Sjögren. Immunoglobulin light chains are called free when they are not linked with heavy chains to form a whole immunoglobulin. Quantification of free light chains is a part of the French national authority for health guidelines for diagnostic and follow-up of light chain, oligo or non-secretory myeloma and AL amyloidosis. Most recently, the World health organisation had included free light chains quantification in prognostic criteria for monoclonal gammopathy of undetermined significance. However the literature bring to light some other potential indications of this analysis in the exploration of monoclonal gammopathy, also in lymphoid malignancies and some autoimmune diseases such as diabetes, rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis and Sjögren syndrome [ABSTRACT FROM AUTHOR]

Published
2020
Full Text
View/download PDF

38. Macrophage Polarization Favors Epithelial Repair During Acute Respiratory Distress Syndrome*

Author

Garnier, Marc, primary, Gibelin, Aude, additional, Mailleux, Arnaud A., additional, Leçon, Véronique, additional, Hurtado-Nedelec, Margarita, additional, Laschet, Jamila, additional, Trebbia, Grégoire, additional, Neuville, Mathilde, additional, Tanaka, Sébastien, additional, Crestani, Bruno, additional, Dehoux, Monique, additional, and Quesnel, Christophe, additional

Published
2018
Full Text
View/download PDF

40. Aspergillus-induced pneumonia in adult without obvious immunodeficiency: test the burst!

Author

Flament, Héloïse, primary, Granger, Vanessa, additional, Vezinet, Corinne, additional, Marzaioli, Viviana, additional, Kannengiesser, Caroline, additional, de Chaisemartin, Luc, additional, Hurtado-Nedelec, Margarita, additional, Litvinova, Elena, additional, Messika, Jonathan, additional, Adam, Nicolas, additional, Gougerot-Pocidalo, Marie-Anne, additional, Dang, Pham My-Chan, additional, Monteiro, Renato, additional, el Benna, Jamel, additional, Langeron, Olivier, additional, Chollet-Martin, Sylvie, additional, and Monsel, Antoine, additional

Published
2018
Full Text
View/download PDF

41. Additional file 1: of Anvillea garcinii extract inhibits the oxidative burst of primary human neutrophils

Author

Boukemara, Hanane, Hurtado-Nedelec, Margarita, Marzaioli, Viviana, Bendjeddou, Dalila, Benna, Jamel El, and Marie, Jean-Claude

Abstract

Dose-effect of Anvillea garcinii (Anv), Zygophyllum gaetulum (Zyg) and aspirin (Asp) on human neutrophils ROS production. Human neutrophils were incubated with increasing concentration of Anv (38–300 μg/mL), Zyg (38–300 μg/mL) or Asp (62–500 μg/mL) 15 min before stimulation with A) fMLF (10−6 M) or B) PMA (100ng/ mL). ROS was measured by luminol-amplified chemiluminescence and data are expressed as percentage to control (fLMF or PMA alone). All results are means ± SEM of three or more separate experiments. (DOC 35 kb)

Published
2016
Full Text
View/download PDF

42. Reply to the comment of Brinster et al. 'Acquired hemophilia, rheumatoid arthritis, and TNFα antagonists'

Author

Gazal, Steven, Sacré, Karim, Allanore, Yannick, Teruel, Maria, Goodall, Alison, Tohma, Shigeto, Alfredsson, Lars, Okada, Yukinori, Xie, Gang, Constantin, Arnaud, Balsa, Alejandro, Kawasaki, Aya, Nicaise, Pascale, Amos, Christopher, Rodríguez-Rodríguez, Luis, Chiocchia, Gilles, Boileau, Catherine, Zhang, Jinyi, Barnetche, Thomas, Gonzalez-Gay, Miguel, Furukawa, Hiroshi, Cantagrel, Alain, Le Loët, Xavier, Sumida, Takayuki, Hurtado-Nedelec, Margarita, Richez, Christophe, Chollet-Martin, Sylvie, Schaeverbeke, Thierry, Combe, Bernard, Khoryati, Liliane, Coustet, Baptiste, El-Benna, Jammel, Siminovitch, Katherine, Plenge, Robert, Padyukov, Leonid, Martin, Javier, Tsuchiya, Naoyuki, Devauchelle-Pensec, Valérie, Gottenberg, Jacques-Eric, Jousse-Joulin, Sandrine, Berthelot, Jean-Marie, Perdriger, Aleth, Hatron, Pierre Yves, Puéchal, Xavier, Le Guern, Véronique, Sibilia, Jean, Chiche, Laurent, Goëb, Vincent, Larroche, Claire, Fauchais, Anne-Laure, Hayem, Gilles, Morel, Jacques, Zarnitsky, Charles, Dubost, Jean Jacques, Dieudé, Philippe, Pers, Jacques Olivier, Cornec, Divi, Seror, Raphaele, Mariette, Xavier, Nowak, Emmanuel, Saraux, Alain, Banse, Christopher, Vittecoq, Olivier, Levesque, Hervé, Université Paris Diderot - Paris 7 (UPD7), Centre de recherche sur l'Inflammation (CRI (UMR_S_1149 / ERL_8252 / U1149)), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service de rhumatologie [CHU Cochin], CHU Cochin [AP-HP]-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Spanish National Research Council (CSIC), Department of Cardiovascular Sciences [Leicester], University of Leicester, University of Tsukuba, Centre for Occupational and Environmental Medicine, Stockholm County Council, Broad Institute of MIT and Harvard (BROAD INSTITUTE), Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston], University of Toronto, School of Informatics [Edimbourg], University of Edinburgh, University Hospital La Paz, Madrid, Service d'Immunologie, Hôpital Bichat-Claude Bernard, Assistance Publique-Hôpitaux de Paris (AP-HP)-Assistance Publique-Hôpitaux de Paris (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-PRES Sorbonne Paris Cité, Dartmouth College [Hanover], Rheumatology Service, Hospital Clínico San Carlos, Physiopathologie et Pharmacologie Clinique de la Douleur (LPPD), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de cardiologie, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris]-Université Paris Diderot - Paris 7 (UPD7), Hôpital Pellegrin, CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, Kyushu University [Fukuoka], Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse], Protéines de défense des réponses immune et inflammatoire : identification, régulation et rôles physiopathologiques, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU), Université Paris-Sud - Paris 11 (UP11), Service de rhumatologie, CHU Bordeaux [Bordeaux], Hôpital Lapeyronie [Montpellier] (CHU), Service de Rhumatologie, Département Hospitalo-Universitaire (DHU), Merck & Co. Inc, Karolinska Institutet [Stockholm], Institute of Parasitology and Biomedicine (IPB - GRANADA), Lymphocyte B et Auto-immunité (LBAI), Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO), Immuno-Rhumatologie Moléculaire, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre hospitalier universitaire de Nantes (CHU Nantes), CHU Pontchaillou [Rennes], Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), CHU Saint-Antoine [APHP], Service de rhumatologie [Strasbourg], CHU Strasbourg-Hôpital de Hautepierre [Strasbourg], Hôpital Européen [Fondation Ambroise Paré - Marseille], Service de rhumatologie [Rouen], CHU Rouen, Normandie Université (NU)-Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU), Internal Medicine, Paris, Service de Médecine interne A et polyclinique médicale [CHU Limoges], CHU Limoges, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Ambroise Paré, Département de Rhumatologie[Montpellier], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Lapeyronie, Service de Rhumatologie - CH Le Havre, CH Le Havre, Département rhumatologie, CHU Clermont-Ferrand, Service de rhumatologie [Bichat], Immunologie et Pathologie (EA2216), Université de Brest (UBO)-IFR148, CHU Cochin [AP-HP], CHU Le Kremlin-Bicêtre (Rheumatology Department), Department of Rheumatology, CIC Brest, Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital de la Cavale Blanche, Institute for Research and Innovation in Biomedicine (IRIB), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université de Tsukuba = University of Tsukuba, Université Paris Diderot - Paris 7 (UPD7)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Strasbourg (UNISTRA), CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de rhumatologie [CHU Rouen], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Ambroise Paré [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Normandie Université (NU)-Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Cochin [AP-HP], Lymphocytes B, Autoimmunité et Immunothérapies (LBAI), Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-LabEX IGO Immunothérapie Grand Ouest-Institut Brestois Santé Agro Matière (IBSAM), and Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
musculoskeletal diseases, medicine.medical_specialty, congenital, hereditary, and neonatal diseases and abnormalities, Etiology, MESH: Etanercept/adverse effects, [SDV]Life Sciences [q-bio], education, MESH: Arthritis, Rheumatoid/drug therapy, TNFα antagonists, Hemophilia A, Etanercept, Arthritis, Rheumatoid, Rheumatology, hemic and lymphatic diseases, medicine, Humans, MESH: Hemophilia A/chemically induced, Rheumatoid arthritis, skin and connective tissue diseases, MESH: Humans, business.industry, Biotherapy, MESH: Antirheumatic Agents/adverse effects, Joint bone, medicine.disease, Dermatology, Surgery, Acquired hemophilia, Antirheumatic Agents, [SDV.IMM]Life Sciences [q-bio]/Immunology, Tumor necrosis factor alpha, Female, business, MESH: Female
Abstract

Comment on:- Acquired hemophilia possibly induced by etanercept in a patient with rheumatoid arthritis. [Joint Bone Spine. 2015]- Acquired hemophilia, rheumatoid arthritis, and TNFα antagonists: Comment on the article "Acquired hemophilia possibly induced by etanercept in a patient with rheumatoid arthritis" by Banse et al., Joint Bone Spine 2015;82:200-2. [Joint Bone Spine. 2015]; International audience; Correspondance

Published
2015
Full Text
View/download PDF

45. Type I interferon signaling in systemic immune cells from patients with alcoholic cirrhosis and its association with outcome.

Author

Weiss, Emmanuel, Rautou, Pierre-Emmanuel, Fasseu, Magali, Giabicani, Mikhael, de Chambrun, Marc, Wan, JingHong, Minsart, Charlotte, Gustot, Thierry, Couvineau, Alain, Maiwall, Rakhi, Hurtado-Nedelec, Margarita, Pilard, Nathalie, Lebrec, Didier, Valla, Dominique, Durand, François, de la Grange, Pierre, Monteiro, Renato C, Paugam-Burtz, Catherine, Lotersztajn, Sophie, Moreau, Richard, Weiss, Emmanuel, Rautou, Pierre-Emmanuel, Fasseu, Magali, Giabicani, Mikhael, de Chambrun, Marc, Wan, JingHong, Minsart, Charlotte, Gustot, Thierry, Couvineau, Alain, Maiwall, Rakhi, Hurtado-Nedelec, Margarita, Pilard, Nathalie, Lebrec, Didier, Valla, Dominique, Durand, François, de la Grange, Pierre, Monteiro, Renato C, Paugam-Burtz, Catherine, Lotersztajn, Sophie, and Moreau, Richard

Abstract

In immune cells, constitutively and acutely produced type I interferons (IFNs) engage autocrine/paracrine signaling pathways to induce IFN-stimulated genes (ISGs). Enhanced activity of IFN signaling pathways can cause excessive inflammation and tissue damage. We aimed to investigate the poorly known ISG expression in systemic immune cells from patients with decompensated alcoholic cirrhosis and its association with outcome., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2016

49. Value of biomarkers for predicting immunoglobulin A vasculitis nephritis outcome in an adult prospective cohort.

Author

Berthelot, Laureline, Jamin, Agnès, Viglietti, Denis, Chemouny, Jonathan M, Ayari, Hamza, Pierre, Melissa, Housset, Pierre, Sauvaget, Virginia, Hurtado-Nedelec, Margarita, and Vrtovsnik, François

Subjects
IMMUNOGLOBULIN A, VASCULITIS, NEPHRITIS, BIOLOGICAL tags, GLOMERULAR filtration rate
Abstract

Background Henoch–Schönlein purpura, more recently renamed immunoglobulin A vasculitis (IgAV), is a systemic vasculitis characterized by IgA deposits. The current markers used to assess IgAV inaccurately evaluate the risk of nephritis occurrence and its long-term outcomes. The current study assessed biomarkers of nephritis outcomes. Methods This French multicentre prospective study enrolled 85 adult patients at the time of disease onset. Patients were assessed for clinical and biological parameters and re-examined after 1 year. Immunoglobulins, cytokines, IgA glycosylation, IgA complexes and neutrophil gelatinase-associated lipocalin (NGAL) concentrations were assessed in blood and urine. Results We identified 60 patients with IgAV-related nephritis (IgAV-N) and 25 patients without nephritis (IgAV-woN). At the time of inclusion (Day 1), the serum levels of galactose-deficient IgA1 (Gd-IgA1) and urinary concentrations of IgA, IgG, IgM, NGAL, interleukin (IL)-1β, IL-6, IL-8, IL-10, IgA–IgG and IgA–sCD89 complexes were higher in the IgAV-N patients than in the IgAV-woN patients (P < 0.005 for all comparisons). After follow-up (1 year), 22 patients showed a poor outcome. Among the tested markers, urine IgA at disease onset adequately reclassified the risk of poor outcome over conventional clinical factors, including estimated glomerular filtration rate, proteinuria and age (continuous net reclassification improvement = 0.72, P = 0.001; integrated discrimination improvement = 0.13, P = 0.009) in IgAV patients. Conclusions Taken together, these results showed that serum Gd-IgA1 and urinary IgA, IgG, IgM, NGAL, IL-1β, IL-6, IL-8, IL-10, IgA–IgG and IgA–sCD89 complexes were associated with nephritis in IgAV patients. Urinary IgA level may improve patient risk stratification for poor outcome. [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
View/download PDF

50. Phosphorylation of p47phox is required for receptor-mediated NADPH oxidase/NOX2 activation in Epstein-Barr virus-transformed human B lymphocytes

Author

Belambri, Sahra Amel, Hurtado-Nedelec, Margarita, Senator, Abderrahmane, Makni-Maalej, Karama, Fay, Michèle, Gougerot-Pocidalo, Marie-Anne, Marie, Jean-Claude, Dang, Pham My-Chan, and El-Benna, Jamel

Subjects
urogenital system, cardiovascular system, Original Article, hormones, hormone substitutes, and hormone antagonists, circulatory and respiratory physiology
Abstract

The phagocyte NADPH oxidase (NOX2) is known to be expressed in Epstein-Barr virus (EBV)-transformed human B lymphocytes. Phosphorylation of the NOX2 cytosolic subunit p47phox is required for phorbol myristate acetate (PMA)-induced NOX2 activation in EBV-transformed B lymphocytes, however the role of this process in receptor-mediated NOX2 activation is not known. Here, we used pansorbin which acts by cross linking cell surface IgG and transfected cells with mutated p47phox to address if the phosphorylation of this subunit is required for receptor-mediated NOX2 activation. We show that pansorbin induced NOX2 activation in a time and concentration-dependent manner, albeit at levels only of 20% of those induced by PMA. GF109203X, a PKC selective inhibitor, inhibited pansorbin as well as PMA-induced NOX2 activation. Using specific anti-phospho serine antibodies we showed that pansorbin induced p47phox phosphorylation on Ser304, 315, 320, 328, and 345 and kinetics of these phosphorylations preceed NOX2 activation. To determine whether the phosphorylation of p47phox is required for pansorbin-induced NOX2 activation, we transfected EBV-transformed lymphocytes deficent in p47phox with a plasmid expressing wild type p47phox or p47phox with all the phosphorylated serines mutated to alanines, p47phoxS(303-379)A. Results show that pansorbin-induced NOX2 activation was greatly decreased in lymphocytes expressing the mutant as compared to the wild-type p47phox. These results show that pansorbin induced p47phox phosphorylation on multiple sites in EBV-transformed B lymphocytes and this process is required for pansorbin-induced NADPH oxidase activation in these cells.

Published
2012

Catalog

Books, media, physical & digital resources
See catalog results