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8 results on '"Margarita Hurtado-Nedelec"'

1. Effects of venoms on neutrophil respiratory burst: a major inflammatory function

Author

Pham My-Chan Dang, Margarita Hurtado-Nedelec, Jamel El-Benna, Marie-Anne Gougerot-Pocidalo, 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), DANG, Pham My-Chan, and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)

Subjects
Neutrophils, Disintegrins, RC955-962, Inflammation, Review, Toxicology, Mastoporan, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, 03 medical and health sciences, chemistry.chemical_compound, Phospholipase A2, Arctic medicine. Tropical medicine, RA1190-1270, medicine, [SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, Phagosome, chemistry.chemical_classification, 0303 health sciences, Reactive oxygen species, PLA2, NADPH oxidase, Innate immune system, biology, Parabutoporin, Chemistry, Superoxide, 030302 biochemistry & molecular biology, ROS, Venom, 3. Good health, Cell biology, Respiratory burst, Infectious Diseases, QL1-991, L-amino acid oxidase, Toxicology. Poisons, biology.protein, Animal Science and Zoology, Parasitology, medicine.symptom, Zoology
Abstract

Neutrophils play a pivotal role in innate immunity and in the inflammatory response. Neutrophils are very motile cells that are rapidly recruited to the inflammatory site as the body first line of defense. Their bactericidal activity is due to the release into the phagocytic vacuole, called phagosome, of several toxic molecules directed against microbes. Neutrophil stimulation induces release of this arsenal into the phagosome and induces the assembly at the membrane of subunits of the NAPDH oxidase, the enzyme responsible for the production of superoxide anion that gives rise to other reactive oxygen species (ROS), a process called respiratory burst. Altogether, they are responsible for the bactericidal activity of the neutrophils. Excessive activation of neutrophils can lead to extensive release of these toxic agents, inducing tissue injury and the inflammatory reaction. Envenomation, caused by different animal species (bees, wasps, scorpions, snakes etc.), is well known to induce a local and acute inflammatory reaction, characterized by recruitment and activation of leukocytes and the release of several inflammatory mediators, including prostaglandins and cytokines. Venoms contain several molecules such as enzymes (phospholipase A2, L-amino acid oxidase and proteases, among others) and peptides (disintegrins, mastoporan, parabutoporin etc.). These molecules are able to stimulate or inhibit ROS production by neutrophils. The present review article gives a general overview of the main neutrophil functions focusing on ROS production and summarizes how venoms and venom molecules can affect this function.

Published
2021

2. Neutrophil Degranulation of Azurophil and Specific Granules

Author

Jamel El-Benna, Samia Bedouhene, Margarita Hurtado-Nedelec, Pham My-Chan Dang, 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 Paris Diderot - Paris 7 (UPD7)

Subjects
0301 basic medicine, biology, Chemistry, Granule (cell biology), Degranulation, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, 3. Good health, Cell biology, 03 medical and health sciences, Azurophilic granule, 030104 developmental biology, 0302 clinical medicine, Specific granule, 030220 oncology & carcinogenesis, Myeloperoxidase, Neutrophil degranulation, biology.protein, Cell activation, ComputingMilieux_MISCELLANEOUS, Phagosome
Abstract

Neutrophils play a pivotal role in innate immunity and in the inflammatory reactions. Upon activation, neutrophils release several toxic molecules directed against microbial pathogens into the phagosome. These molecules include reactive oxygen species (ROS), myeloperoxidase, glucosidases, proteases, and antibacterial peptides. In resting cells these proteins and the enzyme responsible for ROS production (NOX2) are stored inside or at the membranes of different granules called azurophil or primary, specific or secondary, gelatinase or tertiary, and the secretory vesicles. Each granule has a specific density, content, and markers. Myeloperoxidase (MPO) is the azurophil granule marker, and the neutrophil-gelatinase-associated lipocalin (NGAL) is the specific granule marker. After cell activation by different stimuli, granule contents are released into the phagosome or in the extracellular space through a process called degranulation. Also during this process, membrane granules fuse with the phagosome and plasma membrane allowing expression of new markers at the cell surface. The degranulation can be assessed by measuring either the release of different proteins by neutrophils or the expression of granule markers at the plasma membrane. In this chapter, we describe the techniques used to measure degranulation of azurophil and specific neutrophil granules using different approaches such as measurement of MPO enzymatic activity and detection of MPO and NGAL proteins by SDS-PAGE and Western blot.

Published
2020

3. NOX1-derived ROS drive the expression of Lipocalin-2 in colonic epithelial cells in inflammatory conditions

Author

Coralie Pintard, Pham My-Chan Dang, Jean-Claude Marie, Marjan Mojallali, Philippe Lettéron, Margarita Hurtado-Nedelec, Viviana Marzaioli, Marwa Ben Khemis, Yamina Khichane, Nesrine Makhezer, Aurélie Sannier, Asma Tlili, Jamel El-Benna, Dan Liu, Anne-Laure Pelletier, 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 Diderot - Paris 7 (UPD7), Université Paris Descartes - Faculté de Médecine (UPD5 Médecine), Université Paris Descartes - Paris 5 (UPD5), Hôpital Bichat - Claude Bernard, and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)

Subjects
Immunology, Inflammation, Inflammatory bowel disease, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, Proinflammatory cytokine, 03 medical and health sciences, 0302 clinical medicine, Lipocalin-2, NOX1, medicine, Immunology and Allergy, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, 0303 health sciences, NADPH oxidase, Innate immune system, biology, Chemistry, Inflammatory Bowel Disease, ROS, medicine.disease, 3. Good health, 030220 oncology & carcinogenesis, cardiovascular system, biology.protein, Cancer research, Tumor necrosis factor alpha, P22phox, medicine.symptom
Abstract

Inflammatory bowel disease (IBD) is characterized by severe and recurrent inflammation of the gastrointestinal tract, associated with altered patterns of cytokine synthesis, excessive reactive oxygen species (ROS) production, and high levels of the innate immune protein, lipocalin-2 (LCN-2), in the mucosa. The major source of ROS in intestinal epithelial cells is the NADPH oxidase NOX1, which consists of the transmembrane proteins, NOX1 and p22PHOX, and the cytosolic proteins, NOXO1, NOXA1, and Rac1. Here, we investigated whether NOX1 activation and ROS production induced by key inflammatory cytokines in IBD causally affects LCN-2 production in colonic epithelial cells. We found that the combination of TNFα and IL-17 induced a dramatic upregulation of NOXO1 expression that was dependent on the activation of p38MAPK and JNK1/2, and resulted into an increase of NOX1 activity and ROS production. NOX1-derived ROS drive the expression of LCN-2 by controlling the expression of IκBζ, a master inducer of LCN-2. Furthermore, LCN-2 production and colon damage were decreased in NOX1-deficient mice during TNBS-induced colitis. Finally, analyses of biopsies from patients with Crohn's disease showed increased JNK1/2 activation, and NOXO1 and LCN-2 expression. Therefore, NOX1 might play a key role in mucosal immunity and inflammation by controlling LCN-2 expression.

Published
2019

4. NADPH oxidase activation in neutrophils: Role of the phosphorylation of its subunits

Author

Loïc Rolas, Pham My-Chan Dang, Jamel El-Benna, Sahra Amel Belambri, Margarita Hurtado-Nedelec, Houssam Raad, 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 Paris Diderot - Paris 7 (UPD7)

Subjects
0301 basic medicine, Neutrophils, Clinical Biochemistry, Enzyme Activators, Biochemistry, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Bacterial Proteins, Humans, Protein phosphorylation, Phosphorylation, ComputingMilieux_MISCELLANEOUS, chemistry.chemical_classification, Reactive oxygen species, NADPH oxidase, Innate immune system, biology, Superoxide, NADPH Oxidases, General Medicine, Phosphoproteins, Cell biology, Enzyme Activation, 030104 developmental biology, Enzyme, chemistry, 030220 oncology & carcinogenesis, NADPH Oxidase 2, biology.protein, Tetradecanoylphorbol Acetate, P22phox
Abstract

Neutrophils are key cells of innate immunity and during inflammation. Upon activation, they produce large amounts of superoxide anion (O2 -. ) and ensuing reactive oxygen species (ROS) to kill phagocytized microbes. The enzyme responsible for O2 -. production is called the phagocyte NADPH oxidase. This is a multicomponent enzyme system that becomes active after assembly of four cytosolic proteins (p47phox , p67phox , p40phox and Rac2) with the transmembrane proteins (p22phox and gp91phox , which form the cytochrome b558 ). gp91phox represents the catalytic subunit of the NADPH oxidase and is also called NOX2. NADPH oxidase-derived ROS are essential for microbial killing and innate immunity; however, excessive ROS production induces tissue injury and prolonged inflammatory reactions that contribute to inflammatory diseases. Thus, NADPH oxidase activation must be tightly regulated in time and space to limit ROS production. NADPH oxidase activation is regulated by several processes such as phosphorylation of its components, exchange of GDP/GTP on Rac2 and binding of p47phox and p40phox to phospholipids. This review aims to provide new insights into the role of the phosphorylation of the NADPH oxidase components, that is gp91phox , p22phox , p47phox , p67phox and p40phox , in the activation of this enzyme.

Published
2018

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

Author

Claire Demongeot, Manuelle Viguier, Jean-Jacques Boffa, Stéphanie Tellier, Margarita Hurtado-Nedelec, Vincent Pestre, Gérard Cheron, Guillaume Burda, Martin Flamant, Héloïse Flament, Jérôme Verine, Alexandre Seidowsky, E Bourrat, Stéphane Decramer, Mathilde de Menthon, Karine Brochard, Karim Bouchireb, Maud Bezier, Evangeline Pillebout, Fabrice Mihout, Martine Bagot, Olivier Fain, Maya Halabi-Tawil, Agnès Jamin, Philippe Remy, Sonia Azib, Vincent Audard, Monique Dehoux, Jacqueline Rivet, Quentin Raimbourg, Denis Viglietti, Alexis Mathian, Laure Champion, Guillaume Bussone, Bertrand Godeau, Eric Daugas, Anne Saussine-Hickman, Antoine Froissart, Eric Thervet, Elisa Funck-Brentano, Alain Robert, Laureline Berthelot, Nathalie Vittoz, Nicolas Limal, Denis Glotz, Georges Deschênes, Isabelle Halphen, Theresa Kwon, Laurence Vrigneaud, Pierre Housset, Sophie Georgin-Lavialle, Florence Cordoliani, Arsene Mekinian, Virginia Sauvaget, Philippe Grimbert, Jean Christophe Mercier, Philippe Vanhille, Véronique Baudouin, François Vrtovsnik, Agathe Raynaud-Simon, Renato C. Monteiro, Jean-David Bouaziz, Leila Tricot, Laurène Dehoux, Melissa Pierre, Alexandre Karras, Laure Dehen, Céline Lebas, Nathalie Bocquet, Marc Fila, Claire Dossier, Thomas Quemeneur, Maryam Piram, Coralie Bloch-Queyrat, Antoine Dossier, David Verhelst, Anne Maisin, Olivier Benveniste, Dominique Farge, Charlotte Fite, Loïc Guillevin, Rémi Salomon, Emmanuelle Vidal-Petiot, Zahir Amoura, Valérie Caudwell, Assia Smail, Philippe Bouvier, Michel Delahousse, Gentiane Monsel, Jonathan M. Chemouny, Hamza Ayari, Anne-Sophie Verhoeven, Centre de Recherche en Transplantation et Immunologie (U1064 Inserm - CRTI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), 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 Néphrologie [Saint-Louis], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service de Néphrologie [Bichat - Claude Bernard], 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), UMR 1599, Centre National de la Recherche Scientifique (CNRS), Service de médecine interne [CHU Pitié-Salpétrière], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Service de néphrologie [CHU Henri Mondor], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Henri Mondor, Service de néphrologie pédiatrique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Robert Debré, Institut Mondor de recherche biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Service de neuropédiatrie et maladies métaboliques [CHU Robert-Debré], Sorbonne Université (SU), Hôpital Saint-Louis, Institut National de l'Environnement Industriel et des Risques (INERIS), Remodelage et Reparation du Tissu Renal, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Dermatologie [AP-HP Hôpital Saint-Louis], Hopital Saint-Louis [AP-HP] (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Department of dermatology, Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Service Pédiatrique [Toulouse], CHU Toulouse [Toulouse], 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), Centre Hospitalier Sud Francilien, Department of Dermatology, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de dermatologie [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Service de transplantation rénale, Hôpital Foch [Suresnes], AP-HP, Service de Néphrologie Pédiatrique, Hôpital Robert Debré, Paris, Hôpital Bicêtre, Service de Médecine Interne, Centre de Recherche Saint-Antoine (UMRS893), Physiopathologie et Epidemiologie de l'Insuffisance Respiratoire, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de médecine interne, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Jean Verdier [AP-HP], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Service de dermatologie, Service de Physiologie [Bichat-Claude Bernard], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Immunité et cancer (U932), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Biomarqueurs et essais cliniques en Cancérologie et Onco-Hématologie (BECCOH), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Saclay, Physiopathologie des maladies génétiques d'expression pédiatrique, Service de médecine interne [Mondor], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Service de médecine interne et centre de référence des maladies rares [CHU Cochin], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Cochin [AP-HP], Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), AP-HP Hôpital universitaire Robert-Debré [Paris], Service de Néphrologie [CHRU Lille], Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Service de rhumatologie [CHU Saint-Antoine], CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de Département de Néphrologie = Service de Néphrologie et Dialyses [CHU Tenon], CHU Tenon [AP-HP], Service de Pédiatrie Générale et Rhumatologie Pédiatrique, Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Bicêtre, CH Valenciennes, Université Paris Descartes - Paris 5 (UPD5), Gvh et Gvl : Physiopathologie Chez l'Homme et Chez l'Animal, Incidence et Role Therapeutique, Développement et Communication Chimique chez les Insectes (DCCI), Université de Bourgogne (UB)-Centre National de la Recherche Scientifique (CNRS), Service de néphrologie pédiatrique [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Necker - Enfants Malades [AP-HP], Centre de Référence du Sud Ouest des Maladies Rénales Rares, Service de néphrologie adultes [CHU Necker], Service de médecine interne et néphrologie, Centre Hospitalier Henri Duffaut (Avignon), Service de Néphrologie [Valenciennes], Centre Hospitalier de Valenciennes, Service d'anatomo-pathologie [Paris], Paris-Centre de Recherche Cardiovasculaire (PARCC - UMR-S U970), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Henri Mondor [Créteil], Pôle Enfants [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Université de Toulouse (UT)-Université de Toulouse (UT)- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Néphrologie et Dialyses [CHU Tenon], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Tenon [AP-HP], Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), CHU Toulouse [Toulouse]-Hôpital des Enfants, Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), CH Evry-Corbeil, Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre National de la Recherche Scientifique (CNRS)-Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Université Paris Diderot - Paris 7 (UPD7)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), 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 Pierre et Marie Curie - Paris 6 (UPMC), and Hôpital Cochin [AP-HP]

Subjects
0301 basic medicine, Immunoglobulin A, Adult, Male, medicine.medical_specialty, IgA Vasculitis, Urinary system, 030232 urology & nephrology, Antigen-Antibody Complex, Gastroenterology, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Internal medicine, medicine, Humans, Prospective Studies, 10. No inequality, Prospective cohort study, ComputingMilieux_MISCELLANEOUS, Aged, Transplantation, Proteinuria, Nephritis, biology, business.industry, Middle Aged, medicine.disease, Prognosis, 3. Good health, 030104 developmental biology, IgA vasculitis, ROC Curve, Nephrology, biology.protein, Female, medicine.symptom, Vasculitis, business, Biomarkers, Systemic vasculitis, Glomerular Filtration Rate
Abstract

Background Henoch-Schonlein 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

Published
2017

6. NOX5 and p22phox are 2 novel regulators of human monocytic differentiation into dendritic cells

Author

Jean-Claude Marie, Pham My-Chan Dang, Coralie Pintard, Renato C. Monteiro, Margarita Hurtado-Nedelec, Viviana Marzaioli, Jamel El-Benna, Asma Tlili, Marie-Anne Gougerot-Pocidalo, DANG, Pham My-Chan, 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), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service d'hématologie et immunologie, 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), Université Paris Diderot - Paris 7 (UPD7)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
0301 basic medicine, MAPK/ERK pathway, Immunology, Inflammation, Mitochondrion, Models, Biological, Biochemistry, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, Monocytes, stat, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Immune system, medicine, Humans, Enzyme Inhibitors, [SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity, ComputingMilieux_MISCELLANEOUS, Membrane Glycoproteins, biology, NF-kappa B, Membrane Proteins, NADPH Oxidases, Cell Differentiation, Dendritic Cells, Free Radical Scavengers, Cell Biology, Hematology, Phenotype, Mitochondria, 3. Good health, Cell biology, 030104 developmental biology, NADPH Oxidase 5, chemistry, 030220 oncology & carcinogenesis, Mitochondrial Membranes, NADPH Oxidase 2, biology.protein, P22phox, medicine.symptom, Reactive Oxygen Species, Nicotinamide adenine dinucleotide phosphate, Protein Binding, Signal Transduction
Abstract

Dendritic cells (DCs) are a heterogeneous population of professional antigen-presenting cells and are key cells of the immune system, acquiring different phenotypes in accordance with their localization during the immune response. A subset of inflammatory DCs is derived from circulating monocytes (Mo) and has a key role in inflammation and infection. The pathways controlling Mo-DC differentiation are not fully understood. Our objective was to investigate the possible role of nicotinamide adenine dinucleotide phosphate reduced form oxidases (NOXs) in Mo-DC differentiation. In this study, we revealed that Mo-DC differentiation was inhibited by NOX inhibitors and reactive oxygen species scavengers. We show that the Mo-DC differentiation was dependent on p22phox, and not on gp91phox/NOX2, as shown by the reduced Mo-DC differentiation observed in chronic granulomatous disease patients lacking p22phox. Moreover, we revealed that NOX5 expression was strongly increased during Mo-DC differentiation, but not during Mo-macrophage differentiation. NOX5 was expressed in circulating myeloid DC, and at a lower level in plasmacytoid DC. Interestingly, NOX5 was localized at the outer membrane of the mitochondria and interacted with p22phox in Mo-DC. Selective inhibitors and small interfering RNAs for NOX5 indicated that NOX5 controlled Mo-DC differentiation by regulating the JAK/STAT/MAPK and NFκB pathways. These data demonstrate that the NOX5-p22phox complex drives Mo-DC differentiation, and thus could be critical for immunity and inflammation.

Published
2017

7. Protective role of mouse IgG1 in cryoglobulinaemia; insights from an animal model and relevance to human pathology

Author

Margarita Hurtado-Nedelec, Héloïse Flament, Sanae Ben Mkaddem, Renato C. Monteiro, François Vrtovsnik, Eric Daugas, Jonathan M. Chemouny, Laureline Berthelot, CHU Pontchaillou [Rennes], 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 Diderot - Paris 7 (UPD7), Immunité et cancer (U932), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de recherche biomédicale Bichat-Beaujon (CRB3), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), UMR 1599, Centre National de la Recherche Scientifique (CNRS), Service de Néphrologie [Bichat - Claude Bernard], 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), Centre de Recherche en Transplantation et Immunologie (U1064 Inserm - CRTI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM), and Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris]-Université Paris Diderot - Paris 7 (UPD7)

Subjects
0301 basic medicine, chemical and pharmacologic phenomena, Immunoglobulin D, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, Immunoglobulin G, 03 medical and health sciences, Mice, Immune system, Gammopathy, Medicine, Animals, Humans, Receptor, ComputingMilieux_MISCELLANEOUS, Transplantation, biology, Effector, business.industry, Phenotype, 3. Good health, Disease Models, Animal, 030104 developmental biology, Cryoglobulinemia, [SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunology, Nephrology, Immunology, biology.protein, Antibody, business
Abstract

Strait et al. described a novel mouse model of cryoglobulinaemia by challenging mice deficient in the immunoglobulin (Ig)G1 subclass (γ1(-) mice) with goat anti-mouse IgD [5]. The phenotype of wild-type mice was not remarkable, whereas γ1(-) mice developed IgG3 anti-goat IgG cryoglobulins as well as severe and lethal glomerulonephritis. Renal phenotype could not be rescued in γ1(-) mice by the deletion of C3, fragment crystalline γ receptor (FcγR) or J chain. On the other hand, early injection of IgG1, IgG2a or IgG2b inhibited the pathogenic effects of IgG3 in an antigen-dependent manner even in the absence of the FcγRIIb, an anti-inflammatory receptor. The authors concluded that the pathogenic role of IgG3 and the protective characteristic of IgG1 in this model were not explained by their abilities to bind to FcRs or effector molecules but are rather due to structural discrepancies enhancing the precipitation properties/solubility of IgG3/IgG1-containing immune complexes. The present article aims to discuss the current knowledge on IgG biology and the properties of IgGs explaining their differential propensity to acquire cryoglobulin activity.

Published
2016

8. Anvillea garcinii extract inhibits the oxidative burst of primary human neutrophils

Author

Margarita Hurtado-Nedelec, Viviana Marzaioli, Dalila Bendjeddou, Jamel El Benna, Jean-Claude Marie, Hanane Boukemara, 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), Dysfonctionnements Immunitaires [AP-HP Hôpital Bichat, Paris], AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Nord Val de Seine, Département de Biologie [Guelma, Algeria], Laboratoire de Biologie, eau et Environnement [Guelma, Algeria], Université du 8 Mai 1945 [Guelma, Algérie]-Université du 8 Mai 1945 [Guelma, Algérie], and BMC, BMC

Subjects
0301 basic medicine, Phagocyte, Neutrophils, Anvillea garcinii, [SDV]Life Sciences [q-bio], Asteraceae, Cell Degranulation, 03 medical and health sciences, 0302 clinical medicine, Africa, Northern, medicine, Humans, Cells, Cultured, Protein kinase C, chemistry.chemical_classification, Inflammation, Reactive oxygen species, Plants, Medicinal, NADPH oxidase, biology, Plant Extracts, business.industry, Cytochrome c, General Medicine, Zygophyllum gaetulum, North Africa, Molecular biology, 3. Good health, Respiratory burst, [SDV] Life Sciences [q-bio], Oxidative Stress, 030104 developmental biology, medicine.anatomical_structure, Complementary and alternative medicine, chemistry, 030220 oncology & carcinogenesis, Myeloperoxidase, Immunology, Leukocytes, Mononuclear, biology.protein, Neutrophil degranulation, business, Research Article
Abstract

Background Anvillea garcinii Coss. & Durieu (Anv) plant is used as a traditional North African medicine against several diseases associated with inflammation. At inflammatory sites, reactive oxygen species (ROS) produced in excess by activated phagocyte NADPH oxidase (NOX2) can accentuate inflammatory responses. Thus, we investigated if Anv-water soluble polysaccharides could modulate primary human neutrophil oxidative burst in vitro. Methods Human neutrophils were isolated from fresh whole blood and O2 .- generation was measured by cytochrome c reduction assays. Western blots were used to analyse the translocation of PKC, p47phox (a key component of NOX2 activity) to neutrophil plasma membrane. Also, myeloperoxidase (MPO) release in the extracellular medium was studied by western blots. Flow cytometric analysis was used to detect CD11b membrane expression. Results Water soluble polysaccharides from Anv dose-dependently inhibited N-formyl-methionyl-leucyl-phenylalanine (fMLF)- and phorbol myristate acetate (PMA)-induced O2 .- generation by human neutrophils. Moreover, Anv-polysaccharides strongly inhibited PMA-induced PKCβ and p47phox translocation to membranes and p47phox phosphorylation on Ser328, a main PKC target. In contrast, polysaccharides extract from Zygophyllum gaetulum plant, which is also used as a traditional North African medicine against inflammatory diseases, was ineffective on this PKCβ-p47phox pathway. Further, Anv inhibited important neutrophil degranulation markers corresponding to myeloperoxidase (MPO) release and CD11b membrane expression. Conclusion The process of down-regulating NADPH oxidase by polysaccharides extracts from Anv provides new insights into the mechanism of Anv’s anti-inflammatory actions. Electronic supplementary material The online version of this article (doi:10.1186/s12906-016-1411-7) contains supplementary material, which is available to authorized users.

Published
2015

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