Search

Your search keyword '"MESH : Chemokines"' showing total 7 results
Start Over Descriptor "MESH : Chemokines"
7 results on '"MESH : Chemokines"'

1. Infection-Mediated Priming of Phagocytes Protects against Lethal Secondary Aspergillus fumigatus Challenge

Author

Oumaïma Ibrahim-Granet, Amélie Savers, Bernhard Ryffel, Marianna Parlato, Gérard Eberl, Grégory Jouvion, Jean-Marc Cavaillon, Orhan Rasid, Matthias Brock, Cytokines et Inflammation, Institut Pasteur [Paris], School of Life Sciences, University of Nottingham, UK ( UON ), Imagine - Institut des maladies génétiques ( IMAGINE - U1163 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Histopathologie humaine et Modèles animaux, Immunologie et Neurogénétique Expérimentales et Moléculaires ( INEM ), Université d'Orléans ( UO ) -Centre National de la Recherche Scientifique ( CNRS ), Développement des Tissus Lymphoïdes, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique ( CNRS ), This work was supported by funding from Institut Pasteur PTR 468 to OIG and AS, and the Transregio 124 'FungiNet' project A3 to AS and MB., University of Nottingham, UK (UON), Imagine - Institut des maladies génétiques (IMAGINE - U1163), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), Centre National de la Recherche Scientifique (CNRS)-Université d'Orléans (UO), Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [Paris], Institut Pasteur [Paris] (IP), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), and BENEDIC, Bénédicte

Subjects
MESH : Bone Marrow, MESH : Spores, Fungal, medicine.medical_treatment, MESH : Cytokines, MESH: Flow Cytometry, Pathology and Laboratory Medicine, Aspergillosis, MESH: Phagocytes, Aspergillus fumigatus, Animal Cells, MESH : Aspergillosis, MESH: Animals, lcsh:Science, skin and connective tissue diseases, Lung, Disease Resistance, Fungal Pathogens, Phagocytes, Innate Immune System, MESH: Cytokines, Flow Cytometry, 3. Good health, [SDV] Life Sciences [q-bio], Aspergillus, Blood, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Aspergillus Fumigatus, Medical Microbiology, Spectrophotometry, Cytokines, MESH: Bone Marrow, Cytophotometry, Cellular Types, MESH : Receptors, Interleukin-8B, Immune Cells, Phagocytosis, Immunology, 030106 microbiology, Microbiology, 03 medical and health sciences, Microbial Pathogens, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, Blood Cells, [ SDV ] Life Sciences [q-bio], Macrophages, lcsh:R, MESH: Host-Pathogen Interactions, Organisms, Biology and Life Sciences, Molecular Development, medicine.disease, Molds (Fungi), Mice, Inbred C57BL, 030104 developmental biology, lcsh:Q, Developmental Biology, 0301 basic medicine, Chemokine, Neutrophils, [SDV]Life Sciences [q-bio], lcsh:Medicine, MESH: Mice, Knockout, Receptors, Interleukin-8B, White Blood Cells, Spectrum Analysis Techniques, Bone Marrow, [ SDV.MP ] Life Sciences [q-bio]/Microbiology and Parasitology, Immune Physiology, Medicine and Health Sciences, MESH : Lectins, C-Type, CXC chemokine receptors, MESH : Host-Pathogen Interactions, Mice, Knockout, Mice, Inbred BALB C, Multidisciplinary, Bone Marrow/immunology/metabolism, biology, MESH: Receptors, Interleukin-8B, Hematology, Spores, Fungal, MESH: Chemokines, Body Fluids, Cytokine, Cell Processes, Host-Pathogen Interactions, MESH : Phagocytes, Aspergillus fumigatus/immunology, Chemokines, Pathogens, Anatomy, MESH: Aspergillus fumigatus, Research Article, MESH : Flow Cytometry, MESH : Lung, MESH: Mice, Inbred BALB C, MESH: Disease Resistance, Mycology, MESH : Mice, Inbred C57BL, Research and Analysis Methods, Immune system, MESH: Mice, Inbred C57BL, MESH: Spores, Fungal, medicine, MESH : Disease Resistance, Animals, Lectins, C-Type, MESH: Lung, MESH : Chemokines, MESH: Aspergillosis, MESH : Mice, Inbred BALB C, Innate immune system, Fungi, Cell Biology, Aspergillosis/immunology/microbiology, biology.organism_classification, Immune System, MESH : Aspergillus fumigatus, physiology, biology.protein, MESH : Mice, Knockout, MESH : Animals, MESH: Lectins, C-Type
Abstract

International audience; Phagocytes restrict the germination of Aspergillus fumigatus conidia and prevent the establishment of invasive pulmonary aspergillosis in immunecompetent mice. Here we report that immunecompetent mice recovering from a primary A. fumigatus challenge are protected against a secondary lethal challenge. Using RAGγc knock-out mice we show that this protection is independent of T, B and NK cells. In protected mice, lung phagocytes are recruited more rapidly and are more efficient in conidial phagocytosis and killing. Protection was also associated with an enhanced expression of CXCR2 and Dectin-1 on bone marrow phagocytes. We also show that protective lung cytokine and chemokine responses are induced more rapidly and with enhanced dynamics in protected mice. Our findings support the hypothesis that following a first encounter with a non-lethal dose of A. fumigatus conidia, the innate immune system is primed and can mediate protection against a secondary lethal infection.

Published
2016
Full Text
View/download PDF

2. Coexpression of major histocompatibility complex class II with chemokines and nuclear NFκB p50 in melanoma: a rational for their association with poor prognosis

Author

Olivier Verola, Manuelle Viguier, Frédérique Deshayes, Jessica Lauriol, Dominique Charron, Isabelle Martins, Khaoussou Sylla, Catherine Alcaide-Loridan, Marie-Caroline Dieu-Nosjean, Reem Al-Daccak, Stephanie Ghislin, Institut Jacques Monod (IJM (UMR_7592)), Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Réponses immunes : régulation et développement, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Département de Dermatologie, Université Paris, Service d'anatomo-pathologie [Paris], Université Paris Diderot - Paris 7 (UPD7)-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), CIB-HOG, Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut Jacques Monod ( IJM ), Université Paris Diderot - Paris 7 ( UPD7 ) -Centre National de la Recherche Scientifique ( CNRS ), Université Paris Diderot - Paris 7 ( UPD7 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre de Recherche des Cordeliers ( CRC (UMR_S 872) ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Assistance publique - Hôpitaux de Paris (AP-HP)-Université Paris Diderot - Paris 7 ( UPD7 ) -Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), and Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)

Subjects
Male, MESH: NF-kappa B p50 Subunit, Cancer Research, Chemokine, Skin Neoplasms, MESH : Aged, MESH: NF-kappa B, MESH : Neoplasm Invasiveness, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, MESH: Aged, 80 and over, 0302 clinical medicine, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, MESH : Female, Extracellular Signal-Regulated MAP Kinases, Melanoma, MESH: Extracellular Signal-Regulated MAP Kinases, Aged, 80 and over, MESH: Aged, Regulation of gene expression, MESH : Trans-Activators, 0303 health sciences, MESH : Prognosis, MESH: Middle Aged, Kinase, NF-kappa B, Nuclear Proteins, MESH: Gene Expression Regulation, Neoplastic, MESH : Adult, Middle Aged, Prognosis, MESH: Chemokines, MESH : Extracellular Signal-Regulated MAP Kinases, Gene Expression Regulation, Neoplastic, Oncology, MESH : NF-kappa B, 030220 oncology & carcinogenesis, Disease Progression, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, MESH: Disease Progression, Chemokines, Matrix Metalloproteinase 1, Adult, Proto-Oncogene Proteins B-raf, MESH: Cell Line, Tumor, P50, MESH : Gene Expression Regulation, Neoplastic, MESH: Melanoma, MESH: Trans-Activators, MESH : Male, MESH : Melanoma, [SDV.CAN]Life Sciences [q-bio]/Cancer, Dermatology, Biology, MESH: Prognosis, 03 medical and health sciences, MESH : HLA-DR Antigens, Cell Line, Tumor, Extracellular, medicine, Humans, MESH : Middle Aged, MESH : Chemokines, Neoplasm Invasiveness, MESH : Aged, 80 and over, Protein kinase A, MESH : Proto-Oncogene Proteins B-raf, Aged, 030304 developmental biology, MESH: Proto-Oncogene Proteins B-raf, MESH: Humans, MESH : Matrix Metalloproteinase 1, MESH : Cell Line, Tumor, MESH: Skin Neoplasms, MESH : Humans, MESH : Skin Neoplasms, MESH: Biological Markers, MESH : Nuclear Proteins, NF-kappa B p50 Subunit, MESH: Adult, MESH : Disease Progression, HLA-DR Antigens, MESH: Neoplasm Invasiveness, MESH: HLA-DR Antigens, medicine.disease, MESH: Male, MESH : Biological Markers, MESH: Matrix Metalloproteinase 1, MESH : NF-kappa B p50 Subunit, Tumor progression, Immunology, Trans-Activators, biology.protein, MESH: Nuclear Proteins, MESH: Female, Biomarkers
Abstract

International audience; The constitutive expression of major histocompatibility complex class II (MHC II) molecules in melanoma is highly unusual and has been associated with unfavorable clinical outcome and higher metastatic dissemination. This association remains poorly understood and therefore, in this study we looked to whether it is caused by intracellular events that promote tumor progression. We previously reported that MHC II expression in melanoma cells requires active mitogen-activated protein kinase/extracellular signal-related kinase. However, our comparative and molecular analyses of a panel of melanoma cell lines herein provide clear evidence that mitogen-activated protein kinase/extracellular signal-related kinase is not sufficient for HLA-DR expression. We found that the expression of HLA-DR in these tumors rather coincides with the expression of CXCL-1 and CXCL-8 chemokines, both known to be expressed in tumors that invade early and are related to invasive stages of melanoma. The expression of HLA-DR also nicely paralleled that of the nuclear NFkappaB p50 subunit, regulating the expression of these chemokines in melanoma and previously correlated with poor prognosis of melanoma patients, although we provide evidence that NFkappaB is not directly regulating MHC II expression level. The molecular basis for class II transactivator and HLA-DR expression in melanoma therefore remains unsolved, but our findings linking together the expression of HLA-DR, of chemokines involved in invasiveness, and of nuclear NFkappaB p50 strongly support the content that MHC II may be a marker of invasive primary melanoma, and could explain the long-standing association of MHC II expression with overall poor prognosis and unfavorable clinical outcome.

Published
2009
Full Text
View/download PDF

3. L14. Immunomodulatory properties of apoptotic cells

Author

Philippe Saas, Sylvain Perruche, Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC ( HOTE GREFFON ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Etablissement français du sang [Bourgogne-France-Comté] ( EFS [Bourgogne-France-Comté] ) -Université de Franche-Comté ( UFC ), Laboratoire d'Excellence : Lipoprotéines et Santé : prévention et Traitement des maladies Inflammatoires et du Cancer ( LabEx LipSTIC ), Institut National de la Recherche Agronomique ( INRA ) -Université Montpellier 2 - Sciences et Techniques ( UM2 ) -Université Paris-Sud - Paris 11 ( UP11 ) -École pratique des hautes études ( EPHE ) -Institut Gustave Roussy ( IGR ) -Centre Hospitalier Régional Universitaire de Nancy ( CHRU Nancy ) -Université de Bourgogne ( UB ) -Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand ( CHU Dijon ) -Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc ( CRLCC - CGFL ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Fédération Francophone de la Cancérologie Digestive, FFCD-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-France-Comté] ( EFS [Bourgogne-France-Comté] ) -Centre National de la Recherche Scientifique ( CNRS ) -Centre Hospitalier Régional Universitaire [Besançon] ( CHRU Besançon ) -Université de Franche-Comté ( UFC ), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (HOTE GREFFON), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-France-Comté] (EFS [Bourgogne-France-Comté])-Université de Franche-Comté (UFC), Laboratoire d'Excellence : Lipoprotéines et Santé : prévention et Traitement des maladies Inflammatoires et du Cancer (LabEx LipSTIC), Institut National de la Recherche Agronomique (INRA)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université Paris-Sud - Paris 11 (UP11)-École pratique des hautes études (EPHE)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc (CRLCC - CGFL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-France-Comté] (EFS [Bourgogne-France-Comté])-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire [Besançon] (CHRU Besançon)-Université de Franche-Comté (UFC)-Université de Montpellier (UM), Saas, Philippe, Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Institut National de la Recherche Agronomique (INRA)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université Paris-Sud - Paris 11 (UP11)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-Université de Montpellier (UM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté]), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université de Montpellier (UM), and Université de Franche-Comté (UFC)-Etablissement français du sang [Bourgogne-France-Comté] (EFS [Bourgogne-France-Comté])-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
MESH: Inflammation, MESH: Signal Transduction, Cell Transplantation, Neutrophils, medicine.medical_treatment, Apoptosis, MESH: T-Lymphocyte Subsets, Pharmacology, MESH: Neutrophils, T-Lymphocytes, Regulatory, MESH : Neutrophils, MESH : T-Lymphocytes, Regulatory, 0302 clinical medicine, T-Lymphocyte Subsets, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, MESH: Animals, MESH : Antigen-Presenting Cells, MESH: Desensitization, Immunologic, MESH: Phagocytosis, ComputingMilieux_MISCELLANEOUS, Desensitization (medicine), MESH : Macrophages, 0303 health sciences, Phagocytes, tolerance, MESH: Dendritic Cells, MESH: Antigen-Presenting Cells, MESH : Immune Tolerance, General Medicine, MESH: Chemokines, MESH: Cell Transplantation, [SDV.IMM]Life Sciences [q-bio]/Immunology, Chemokines, Inflammation Mediators, medicine.symptom, Signal Transduction, TGF-β, MESH: Immune Tolerance, [SDV.IMM] Life Sciences [q-bio]/Immunology, MESH: Inflammation Mediators, MESH: Immunomodulation, Antigen-Presenting Cells, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, Inflammation, Immunomodulation, MESH : Inflammation Mediators, 03 medical and health sciences, MESH: Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, Cell transplantation, Text mining, Phagocytosis, MESH : Phagocytosis, Immune Tolerance, medicine, Animals, Humans, MESH : Chemokines, 030304 developmental biology, MESH : Immunomodulation, MESH : Signal Transduction, MESH: Humans, MESH : Inflammation, business.industry, Macrophages, MESH: T-Lymphocytes, Regulatory, MESH: Apoptosis, MESH : Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, MESH : Humans, MESH: Macrophages, Dendritic Cells, MESH : T-Lymphocyte Subsets, MESH : Cell Transplantation, Desensitization, Immunologic, inflammation, MESH : Dendritic Cells, MESH : Desensitization, Immunologic, MESH : Animals, business, MESH : Apoptosis, 030215 immunology
Abstract

International audience

Published
2013
Full Text
View/download PDF

4. Variable beta-glucans production by different states of Eurotium amstelodami explains differences in inflammatory responses in airway cells

Author

Stéphane Bretagne, Sandrine Roussel, Anne-Pauline Bellanger, Bénédicte Rognon, Laurence Millon, Françoise Botterel, Gabriel Reboux, Laboratoire Chrono-environnement ( LCE ), Université Bourgogne Franche-Comté ( UBFC ) -Centre National de la Recherche Scientifique ( CNRS ) -Université de Franche-Comté ( UFC ), Laboratoire de Parasitologie-Mycologie, Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), Service de parasitologie [Mondor], Laboratoire Chrono-environnement - CNRS - UBFC (UMR 6249) (LCE), Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), and Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)

Subjects
MESH: Inflammation, MESH : Cell Line, Chemokine, MESH : Spores, Fungal, beta-Glucans, MESH : beta-Glucans, MESH : Cytokines, MESH: Eurotium, Conidium, Immunology and Allergy, MESH : Fungal Proteins, [SDV.MP.MYC]Life Sciences [q-bio]/Microbiology and Parasitology/Mycology, [ SDV.MP.MYC ] Life Sciences [q-bio]/Microbiology and Parasitology/Mycology, MESH : Eurotium, 0303 health sciences, Fungal protein, MESH: Cytokines, biology, MESH: beta-Glucans, General Medicine, Spores, Fungal, MESH: Chemokines, MESH : Epithelial Cells, MESH : Air Pollution, Indoor, MESH: Epithelial Cells, Air Pollution, Indoor, Cytokines, Proteoglycans, MESH: Fungal Proteins, medicine.symptom, Chemokines, Microbiology (medical), Hypha, Hyphae, Inflammation, Fungus, Pathology and Forensic Medicine, Microbiology, Cell Line, Fungal Proteins, 03 medical and health sciences, MESH: Hyphae, MESH: Spores, Fungal, Eurotium, medicine, Humans, MESH : Chemokines, Interleukin 8, 030304 developmental biology, A549 cell, MESH: Humans, MESH : Inflammation, 030306 microbiology, fungi, MESH : Humans, Epithelial Cells, biology.organism_classification, MESH: Cell Line, Immunology, biology.protein, MESH : Hyphae, MESH: Air Pollution, Indoor
Abstract

International audience; Eurotium amstelodami, a mold frequently identified in housing and farm air samples, is a suspected cause of respiratory diseases such as allergic alveolitis, atopic asthma, and organic dust toxic syndrome. This fungus is present in the air in three different states (ascospores, conidia, and hyphae). The aim of this study was to test in vitro the differential inflammatory response of airway cells exposed to 1,3 betaglucanase-treated protein extract (BGPE), from E. amstelodami ascospores, conidia, and hyphae. Confluent cells from the A549 cell line were inoculated with calibrated BGPE issued from the three fungal forms. The levels of eight cytokines and chemokines involved in inflammatory responses were measured after 8 h of exposure. Beta-d-glucan (BDG) was quantified in total fungal extract as well as in the BGPE from the three fungal states. Hyphal BGPE were the only ones to induce a marked inflammatory response and they contain higher quantities of BDG. The present study adds to the growing body of evidence that beta-glucan from fungal hyphae play a crucial role in respiratory diseases.

Published
2011
Full Text
View/download PDF

5. Stimulation of angiogenesis resulting from cooperation between macrophages and MDA-MB-231 breast cancer cells: proposed molecular mechanism and effect of tetrathiomolybdate

Author

Linda-Louise Pritchard, Ulrich Joimel, Hong Li, Rémi Varin, Emmanuel Blot, Claudine Soria, Lionel Cazin, Caroline Gest, Marc Laurent, Jeannette Soria, Jean-Pierre Vannier, Jérôme Alexandre, Micro-Environnement et Régulation Cellulaire Intégrée (MERCI), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU), Laboratoire d'Oncologie Médicale, Université Paris Descartes - Paris 5 (UPD5)-Hôtel Dieu de Paris, Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Paris Descartes - Paris 5 (UPD5)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Génomique fonctionnelle de la prolifération et différenciation cellulaire, Université Paris-Sud - Paris 11 (UP11)-Institut André Lwoff (IAL)-Centre National de la Recherche Scientifique (CNRS), We are grateful to the comité de l'Eure de la Ligue contre le Cancer and to the Association Ti'toine, for financing the fellowship of Ulrich Joimel. We thank the Groupement des Entreprises Francaises dans la Lutte contre le Cancer (GEFLUC) Rouen Normandie and the comité de Seine-Maritime de la Ligue contre le Cancer, who generously supported this work by a program grant from the Cancer Research Campaign., Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), BMC, Ed., Micro-Environnement et Régulation Cellulaire Intégrée ( MERCI ), Université de Rouen Normandie ( UNIROUEN ), Normandie Université ( NU ) -Normandie Université ( NU ), Université Paris Descartes - Paris 5 ( UPD5 ) -Hôtel Dieu de Paris, Centre de Recherche des Cordeliers ( CRC (UMR_S 872) ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), and Université Paris-Sud - Paris 11 ( UP11 ) -Institut André Lwoff (IAL)-Centre National de la Recherche Scientifique ( CNRS )

Subjects
Lipopolysaccharides, Chemokine, Cancer Research, MESH : Coculture Techniques, Angiogenesis, MESH : Cytokines, medicine.medical_treatment, Fluorescent Antibody Technique, Angiogenesis Inhibitors, Apoptosis, Chick Embryo, MESH : Lipopolysaccharides, MESH : Breast Neoplasms, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, 0302 clinical medicine, MESH : Chick Embryo, MESH : Female, Interferon gamma, MESH: Animals, MESH : Culture Media, Conditioned, MESH: Fluorescent Antibody Technique, Cells, Cultured, MESH : Macrophages, MESH: Angiogenesis Inhibitors, MESH: Molybdenum, 0303 health sciences, MESH: Cytokines, biology, Neovascularization, Pathologic, MESH: Culture Media, Conditioned, MESH: Enzyme-Linked Immunosorbent Assay, hemic and immune systems, MESH: Chick Embryo, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, MESH: Chemokines, MESH : Enzyme-Linked Immunosorbent Assay, Recombinant Proteins, MESH : Molybdenum, Endothelial stem cell, MESH: Interferon-gamma, Recombinant, Interleukin 10, Cytokine, Oncology, 030220 oncology & carcinogenesis, Cytokines, Tumor necrosis factor alpha, Female, Chemokines, medicine.drug, Research Article, MESH: Cells, Cultured, Macrophage colony-stimulating factor, Breast Neoplasms, Enzyme-Linked Immunosorbent Assay, [SDV.CAN]Life Sciences [q-bio]/Cancer, lcsh:RC254-282, MESH: Coculture Techniques, 03 medical and health sciences, Interferon-gamma, [SDV.CAN] Life Sciences [q-bio]/Cancer, MESH : Cells, Cultured, MESH : Angiogenesis Inhibitors, medicine, Genetics, Animals, Humans, MESH : Chemokines, 030304 developmental biology, Molybdenum, MESH : Interferon-gamma, Recombinant, MESH: Humans, business.industry, Macrophages, MESH: Apoptosis, MESH : Humans, MESH : Neovascularization, Pathologic, MESH: Macrophages, Coculture Techniques, MESH : Fluorescent Antibody Technique, Culture Media, Conditioned, Immunology, Cancer research, biology.protein, MESH : Animals, MESH: Lipopolysaccharides, business, MESH: Neovascularization, Pathologic, MESH: Female, MESH : Apoptosis, MESH: Breast Neoplasms
Abstract

Background Infiltration by macrophages (Mφ) indicates a poor prognosis in breast cancers, in particular by inducing angiogenesis. Our study aimed 1) to investigate the mechanism by which cooperation between Mφ and aggressive breast cancer cells (MDA-MB-231) induces angiogenesis; 2) to examine the effect of tetrathiomolybdate (TM) on this angiogenic activity. Methods Mφ coincubated with MDA-MB-231 were used as a model to mimic the inflammatory microenvironment. Angiogenesis induced by the culture media was tested in the chick chorioallantoic membrane (CAM). Mφ phenotype was evaluated by 1) expression of the M1 marker CD80, and secretion of interleukin 10 (IL-10), an M2 marker; 2) capacity to secrete Tumour Necrosis Factor α (TNFα) when stimulated by lipopolysaccharide/interferon γ (LPS/IFNγ); 3) ability to induce MDA-MB-231 apoptosis. To explore the molecular mechanisms involved, cytokine profiles of conditioned media from MDA-MB-231, Mφ and the coculture were characterised by an antibody cytokine array. All experiments were carried out both in presence and in absence of TM. Results Incubation of Mφ with MDA-MB-231 induced a pro-angiogenic effect in the CAM. It emerged that the angiogenic activity of the coculture is due to the capacity of Mφ to switch from M1 Mφ towards M2, probably due to an increase in Macrophage Colony Stimulating Factor. This M1-M2 switch was shown by a decreased expression of CD80 upon LPS/IFNγ stimulation, an increased secretion of IL-10, a decreased secretion of TNFα in response to LPS/IFNγ and an inability to potentiate apoptosis. At the molecular level, the angiogenic activity of the coculture medium can be explained by the secretion of CXC chemokines/ELR+ and CC chemokines. Although TM did not modify either the M2 phenotype in the coculture or the profile of the secreted chemokines, it did decrease the angiogenic activity of the coculture medium, suggesting that TM inhibited angiogenic activity by interfering with the endothelial cell signalling induced by these chemokines. Conclusions Cooperation between Mφ and MDA-MB-231 transformed M1 Mφ to an angiogenic, M2 phenotype, attested by secretion of CXC chemokines/ELR+ and CC chemokines. TM inhibited this coculture-induced increase in angiogenic activity, without affecting either Mφ phenotype or cytokine secretion profiles.

Published
2010
Full Text
View/download PDF

6. Inhibition of prolyl hydroxylase domain proteins promotes therapeutic revascularization

Author

Jacques Pouysségur, Amandine Ginouvès, Bernard I. Levy, Micheline Duriez, Jean-Sébastien Silvestre, Edurne Berra, José Vilar, Alice Recalde, Yasmine Zouggari, Céline Loinard, Clément Cochain, Institut de signalisation, biologie du développement et cancer (ISBDC), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Paris-Centre de Recherche Cardiovasculaire (PARCC - UMR-S U970), 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), Institut de signalisation, biologie du développement et cancer ( ISBDC ), Université Nice Sophia Antipolis ( UNS ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -Centre National de la Recherche Scientifique ( CNRS ), Paris-Centre de Recherche Cardiovasculaire ( PARCC - U970 ), Hôpital Européen Georges Pompidou [APHP] ( HEGP ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Laboratoire de génétique et biologie cellulaire ( LGBC ), Université de Versailles Saint-Quentin-en-Yvelines ( UVSQ ) -École pratique des hautes études ( EPHE ) -Centre National de la Recherche Scientifique ( CNRS ), Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de génétique et biologie cellulaire (LGBC), and Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-École pratique des hautes études (EPHE)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Vascular Endothelial Growth Factor A, MESH: Inflammation, MESH: Signal Transduction, Pathology, MESH : RNA, Messenger, Angiogenesis, Small hairpin RNA, Neovascularization, Mice, 0302 clinical medicine, Ischemia, Medicine, MESH: Animals, MESH: Gene Silencing, [SDV.BDD]Life Sciences [q-bio]/Development Biology, MESH : Macrophages, 0303 health sciences, MESH : Neovascularization, Physiologic, MESH : Procollagen-Proline Dioxygenase, MESH: Hindlimb, MESH: Chemokines, Cell biology, Hindlimb, Femoral Artery, medicine.anatomical_structure, 030220 oncology & carcinogenesis, MESH : Vascular Endothelial Growth Factor A, medicine.symptom, Chemokines, Cardiology and Cardiovascular Medicine, MESH : Gene Therapy, MESH: Neovascularization, Physiologic, MESH: Nitric Oxide Synthase Type III, Plasmids, Signal Transduction, MESH: Femoral Artery, MESH: Procollagen-Proline Dioxygenase, medicine.medical_specialty, MESH : Hypoxia-Inducible Factor 1, alpha Subunit, Nitric Oxide Synthase Type III, Procollagen-Proline Dioxygenase, MESH : Femoral Artery, Neovascularization, Physiologic, MESH : Mice, Inbred C57BL, MESH : Nitric Oxide Synthase Type III, MESH: Hypoxia-Inducible Factor 1, alpha Subunit, Hypoxia-Inducible Factor-Proline Dioxygenases, 03 medical and health sciences, Downregulation and upregulation, MESH : Ischemia, MESH: Mice, Inbred C57BL, MESH: Plasmids, Physiology (medical), MESH : Mice, MESH : Gene Silencing, Gene silencing, Animals, MESH : Chemokines, [ SDV.BDD ] Life Sciences [q-bio]/Development Biology, Gene Silencing, RNA, Messenger, Transcription factor, MESH: Mice, 030304 developmental biology, MESH: RNA, Messenger, MESH : Signal Transduction, Inflammation, Messenger RNA, MESH : Hindlimb, MESH : Inflammation, business.industry, Monocyte, Macrophages, MESH: Vascular Endothelial Growth Factor A, MESH: Macrophages, Genetic Therapy, Hypoxia-Inducible Factor 1, alpha Subunit, Mice, Inbred C57BL, MESH : Plasmids, MESH : Animals, MESH: Gene Therapy, MESH: Ischemia, business
Abstract

Background— The hypoxia-inducible transcription factor (HIF) subunits are destabilized via the O 2 -dependent prolyl hydroxylase domain proteins (PHD1, PHD2, and PHD3). We investigated whether inhibition of PHDs via upregulating HIF might promote postischemic neovascularization. Methods and Results— Mice with right femoral artery ligation were treated, by in vivo electrotransfer, with plasmids encoding for an irrelevant short hairpin RNA (shRNA) (shCON [control]) or specific shRNAs directed against HIF-1α (shHIF-1α), PHD1 (shPHD1), PHD2 (shPHD2), and PHD3 (shPHD3). The silencing of PHDs induced a specific and transient downregulation of their respective mRNA and protein levels at day 2 after ischemia and, as expected, upregulated HIF-1α. As a consequence, 2 key hypoxia-inducible proangiogenic actors, vascular endothelial growth factor-A and endothelial nitric oxide synthase, were upregulated at the mRNA and protein levels. In addition, monocyte chemotactic protein-1 mRNA levels and infiltration of Mac-3-positive macrophages were enhanced in ischemic leg of mice treated with shPHD2 and shPHD3. Furthermore, activation of HIF-1α-related pathways was associated with changes in postischemic neovascularization. At day 14, silencing of PHD2 and PHD3 increased vessel density by 2.2- and 2.6-fold, capillary density by 1.8- and 2.1-fold, and foot perfusion by 1.2- and 1.4-fold, respectively, compared with shCON ( P Conclusions— We demonstrated that a direct inhibition of PHDs, and more particularly PHD3, promoted therapeutic revascularization. Furthermore, we showed that activation of the HIF-1 signaling pathway is required to promote this revascularization.

Published
2009
Full Text
View/download PDF

7. Interleukin-10 inhibits elevated chemokine interleukin-8 and regulated on activation normal T cell expressed and secreted production in cystic fibrosis bronchial epithelial cells by targeting the I(k)B kinase alpha/beta complex

Author

Céline Muselet, Jacky Jacquot, Dominique Hubert, Frank Antonicelli, Daniel Dusser, Sandie Escotte, Olivier Tabary, Dynamique cellulaire et moléculaire de la muqueuse respiratoire, Université de Reims Champagne-Ardenne (URCA)-IFR53-Institut National de la Santé et de la Recherche Médicale (INSERM), Croissance et réparation du poumon, Institut National de la Santé et de la Recherche Médicale (INSERM), Matrice extracellulaire et dynamique cellulaire - UMR 7369 (MEDyC), SFR CAP Santé (Champagne-Ardenne Picardie Santé), Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Centre National de la Recherche Scientifique (CNRS), Service de pneumologie [CHU Cochin], Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université de Reims Champagne-Ardenne (URCA) - IFR53 - Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de la Recherche Scientifique (CNRS) - Université de Reims Champagne-Ardenne (URCA) - SFR CAP Santé (Champagne-Ardenne Picardie Santé), Université de Reims Champagne-Ardenne (URCA) - Université de Picardie Jules Verne (UPJV) - Université de Reims Champagne-Ardenne (URCA) - Université de Picardie Jules Verne (UPJV), Assistance publique - Hôpitaux de Paris (AP-HP) - CHU Cochin [AP-HP], Université de Reims Champagne-Ardenne (URCA)-SFR CAP Santé (Champagne-Ardenne Picardie Santé), Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Centre National de la Recherche Scientifique (CNRS), and Birembaut, Philippe

Subjects
Chemokine, MESH: Interleukin-10, Cystic Fibrosis, MESH: I-kappa B Proteins, medicine.medical_treatment, Gene Expression, MESH: NF-kappa B, Sodium Chloride, [SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract, Chemokine CCL5, Cells, Cultured, biology, NF-kappa B, Interleukin, MESH: Bronchi, MESH: Chemokines, MESH : Bronchi, I-kappa B Kinase, Interleukin-10, MESH : Epithelial Cells, Interleukin 10, Cytokine, medicine.anatomical_structure, MESH: Epithelial Cells, MESH : NF-kappa B, Tumor necrosis factor alpha, I-kappa B Proteins, Chemokines, MESH: Cells, Cultured, MESH : Protein-Serine-Threonine Kinases, medicine.medical_specialty, MESH : Interleukin-8, MESH: Gene Expression, MESH: Cystic Fibrosis, Macromolecular Substances, T cell, MESH : Macromolecular Substances, Bronchi, Respiratory Mucosa, Protein Serine-Threonine Kinases, MESH : Interleukin-1, MESH: Protein-Serine-Threonine Kinases, Pathology and Forensic Medicine, Internal medicine, MESH : Interleukin-10, MESH : Cystic Fibrosis, MESH : Cells, Cultured, medicine, Humans, MESH : Chemokines, Interleukin 8, MESH: I-kappa B Kinase, MESH: Humans, Tumor Necrosis Factor-alpha, Interleukin-8, MESH : Humans, MESH: Interleukin-1, Epithelial Cells, MESH : I-kappa B Kinase, MESH: Macromolecular Substances, Molecular biology, MESH: Interleukin-8, MESH : Gene Expression, Endocrinology, Cell culture, biology.protein, [SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract, MESH : I-kappa B Proteins, Interleukin-1, Regular Articles
Abstract

Free FULL TEXT http://ajp.amjpathol.org/cgi/reprint/162/1/293; Accumulating evidence suggests that in cystic fibrosis (CF) patients, airway fluids are characterized by decreased antibacterial activity, elevated NaCl concentration, and high levels of chemokines, resulting in exaggerated activation of the transcriptional nuclear factor (NF)-kappaB in airway epithelial cells. The present study was undertaken to evaluate the effects of anti-inflammatory cytokine interleukin-10 (IL-10) on NaCl-induced chemokine IL-8 and regulated on activation normal T cell expressed and secreted (RANTES) expression through the NF-kappaB signaling in primary deltaF508 CF and non-CF (control) human bronchial epithelial cells. Exposure of CF and non-CF bronchial epithelial cells to hypertonic (170 mmol/L NaCl) milieu compared to isotonic (115 mmol/L NaCl) and hypotonic (85 mmol/L NaCl) milieu caused a significant, NaCl-dependent increase in IL-8 and RANTES gene expression and protein production. Compared to non-CF cells, CF bronchial epithelial cells were characterized by a higher susceptibility to produce elevated IL-8 and RANTES production in an hypertonic NaCl milieu in response to IL-1beta activation. Treatment with IL-10 suppressed IL-8 and RANTES gene expression in both non-CF and CF bronchial epithelial cells was associated with a reduced expression of I(k)B (IKK) alpha/beta kinases, particularly for IKKalpha which is greater expressed in CF bronchial epithelial cells, and resulting in reduced NF-kappaB activation. These findings suggest that IL-10 might have anti-inflammatory benefits in airways of CF patients.

Published
2003

Catalog

Books, media, physical & digital resources
See catalog results