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1. The inflammasomes
by Couillin, Isabelle and Pétrilli, Virginie and Martinon, Fabio
2011, Progress in inflammation research, ISBN 3034801475, xiii, 224
Including a range of contributions from numerous leading international experts in the field, this book provides an extensive overview of the current knowledge... 
Immunological aspects | Inflammasomes | Mediators | microbiology | Inflammation | analysis | immunology | Clinical & internal medicine
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2. Full Text IL-1R1/MyD88 signaling and the inflammasome are essential in pulmonary inflammation and fibrosis in mice
by Gasse, Pamela and Mary, Caroline and Guenon, Isabelle and Noulin, Nicolas and Charron, Sabine and Schnyder-Candrian, Silvia and Schnyder, Bruno and Akira, Shizuo and Quesniaux, Valérie F.J and Lagente, Vincent and Ryffel, Bernhard and Couillin, Isabelle
Journal of Clinical Investigation, ISSN 0021-9738, 12/2007, Volume 117, Issue 12, pp. 3786 - 3799
The molecular mechanisms of acute lung injury resulting in inflammation and fibrosis are not well established. Here we investigate the roles of the IL-1... 
MONOSODIUM URATE CRYSTALS | MEDICINE, RESEARCH & EXPERIMENTAL | INTERLEUKIN-1 RECEPTOR ANTAGONIST | INDUCED CYTOKINE | INDUCED LUNG INJURY | AIRWAY INFLAMMATION | BLEOMYCIN-INDUCED PNEUMONOPATHY | DEFICIENT MICE | ONSET STILLS-DISEASE | NF-KAPPA-B | CUTTING EDGE | Respiratory Distress Syndrome, Adult - pathology | Interleukin-8 - genetics | Sialoglycoproteins - genetics | Interleukin-1beta - pharmacology | Antibiotics, Antineoplastic - toxicity | Humans | Sialoglycoproteins - metabolism | Pneumonia - pathology | Respiratory Distress Syndrome, Adult - metabolism | Receptors, Interleukin-1 Type I - metabolism | Receptors, Interleukin-1 Type I - antagonists & inhibitors | Respiratory Distress Syndrome, Adult - genetics | Lymphokines - genetics | Pneumonia - chemically induced | Bone Marrow Transplantation | Lymphokines - metabolism | Pulmonary Fibrosis - metabolism | Interleukin 1 Receptor Antagonist Protein - pharmacology | Interleukin-8 - metabolism | Bleomycin - toxicity | Disease Models, Animal | Pneumonia - genetics | Receptors, Interleukin-1 Type I - agonists | Respiratory Distress Syndrome, Adult - chemically induced | Myeloid Differentiation Factor 88 - genetics | Pulmonary Fibrosis - pathology | Signal Transduction - genetics | Recombinant Proteins - pharmacology | Mice, Knockout | Transplantation Chimera - genetics | Transplantation Chimera - metabolism | Animals | Signal Transduction - drug effects | Receptors, Interleukin-1 Type I - genetics | Pulmonary Fibrosis - chemically induced | Mice | Pneumonia - metabolism | Chronic Disease | Myeloid Differentiation Factor 88 - metabolism | Complications and side effects | Bleomycin | Pulmonary fibrosis | Dosage and administration | Research | Health aspects | Risk factors | Apoptosis | Pneumonia | Respiratory Distress Syndrome, Adult | Signal Transduction | Interleukin-1beta | Antibiotics, Antineoplastic | Myeloid Differentiation Factor 88 | Recombinant Proteins | Transplantation Chimera | Interleukin-8 | Lymphokines | Life Sciences | Sialoglycoproteins | Immunology | Pulmonary Fibrosis | Interleukin 1 Receptor Antagonist Protein | Receptors, Interleukin-1 Type I
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3. Full Text Cigarette Smoke-Induced Pulmonary Inflammation Is TLR4/MyD88 and IL-1R1/MyD88 Signaling Dependent
by Doz, Emilie and Noulin, Nicolas and Boichot, Elisabeth and Guenon, Isabelle and Fick, Lizette and Le Bert, Marc and Lagente, Vincent and Ryffel, Bernhard and Schnyder, Bruno and Quesniaux, Valerie F. J and Couillin, Isabelle
The Journal of Immunology, ISSN 0022-1767, 01/2008, Volume 180, Issue 2, pp. 1169 - 1178
Acute cigarette smoke exposure of the airways (two cigarettes twice daily for three days) induces acute inflammation in mice. In this study, we show that... 
APOPTOSIS | HEAT-SHOCK-PROTEIN-70 | HSP70 | CELLS IN-VITRO | PATHWAY | ENDOTOXIN | DISEASE | TOLL-LIKE RECEPTORS | MICE | IMMUNOLOGY | TLR4 | Immunity, Innate - drug effects | Neutrophils - drug effects | Immunity, Innate - genetics | Myeloid Differentiation Factor 88 - genetics | Neutrophils - immunology | Toll-Like Receptor 4 - genetics | Interleukin-1alpha - metabolism | Signal Transduction - genetics | Smoke | Tobacco - toxicity | HSP70 Heat-Shock Proteins - metabolism | Matrix Metalloproteinase 9 - metabolism | Animals | Interleukin-1beta - metabolism | Mice, Mutant Strains | Pneumonia - chemically induced | Receptors, Interleukin-1 Type I - genetics | Pneumonia - immunology | Macrophages - drug effects | Mice | Macrophages - immunology | Pneumonia - genetics | Interleukin-1alpha | Pneumonia | Toll-Like Receptor 4 | Signal Transduction | Neutrophils | Interleukin-1beta | Myeloid Differentiation Factor 88 | Macrophages | Immunity, Natural | Life Sciences | Tobacco | Immunology | Receptors, Interleukin-1 Type I | HSP70 Heat-Shock Proteins | Matrix Metalloproteinase 9
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4. Full Text ATP release and purinergic signaling in NLRP3 inflammasome activation
by Gombault, Aurélie and Baron, Ludivine and Couillin, Isabelle
Frontiers in Immunology, ISSN 1664-3224, 2012, Volume 3, p. 414
The NLRP3 inflammasome is a protein complex involved in IL-1 beta and IL-18 processing that senses pathogen- and danger-associated molecular patterns (PAMPs... 
Autophagic cell death | P2R | Danger signal | NLRP3 | Inflammasome | ATP | Purinergic signaling | purinergic signaling | autophagic cell death | inflammasome | danger signal | IMMUNOLOGY
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5. Full Text Nanoparticles activate the NLR pyrin domain containing 3 (Nlrp3) inflammasome and cause pulmonary inflammation through release of IL-1α and IL-1β
by Amir S. Yazdi and Greta Guarda and Nicolas Riteau and Stefan K. Drexler and Aubry Tardivel and Isabelle Couillin and Jürg Tschopp and Marc Feldmann
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 11/2010, Volume 107, Issue 45, pp. 19449 - 19454
Nanoparticles are increasingly used in various fields, including biomedicine and electronics. One application utilizes the opacifying effect of nano-TiO₂,... 
Nanoparticles | Asbestos | Lungs | Secretion | Neutrophils | Keratinocytes | Mice | Inflammation | Neutrophil infiltration | Macrophages | Titanium dioxide | Silica dioxide | Caspase-1 | silica dioxide | PARTICLES | MICE DEFICIENT | INTERLEUKIN-1-BETA | MULTIDISCIPLINARY SCIENCES | NALP3 INFLAMMASOME | RESPONSES | PATHWAY | CRYSTALS | titanium dioxide | SECRETION | TITANIUM-DIOXIDE | PROTEINS | caspase-1 | Inflammasomes - metabolism | Pneumonia - etiology | NLR Family, Pyrin Domain-Containing 3 Protein | Interleukin-1alpha - metabolism | Carrier Proteins - drug effects | Nanoparticles - toxicity | Inhalation | Receptors, Interleukin-1 - metabolism | Titanium - toxicity | Signal Transduction - immunology | Animals | Carrier Proteins - metabolism | Silicon Dioxide - toxicity | Inflammasomes - drug effects | Keratinocytes - drug effects | Interleukin-1beta - metabolism | Keratinocytes - metabolism | Zinc Oxide | Biological Sciences
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6. Full Text The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response
by Baroja-Mazo, Alberto and Martín-Sánchez, Fatima and Gomez, Ana I and Martínez, Carlos M and Amores-Iniesta, Joaquín and Compan, Vincent and Barberà-Cremades, Maria and Yagüe, Jordi and Ruiz-Ortiz, Estibaliz and Antón, Jordi and Buján, Segundo and Couillin, Isabelle and Brough, David and Arostegui, Juan I and Pelegrín, Pablo
Nature Immunology, ISSN 1529-2908, 2014, Volume 15, Issue 8, pp. 738 - 748
Assembly of the NLRP3 inflammasome activates caspase-1 and mediates the processing and release of the leaderless cytokine IL-1 beta and thereby serves a... 
ASC | MECHANISM | PURIFICATION | CRYSTALS | IL-1-BETA | SECRETION | PYROPTOSOME | IMMUNOLOGY | CASPASE-1 ACTIVATION | NALP3 INFLAMMASOME | CELL-DEATH | Caspases - immunology | Cytoskeletal Proteins - genetics | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Caspase 1 - immunology | Interleukin-1beta - blood | Signal Transduction - immunology | Cryopyrin-Associated Periodic Syndromes - blood | Cytoskeletal Proteins - blood | HEK293 Cells | Carrier Proteins - immunology | Macrophages - immunology | Carrier Proteins - blood | Caspases - genetics | Mice, Inbred C57BL | Cells, Cultured | Phagocytosis - immunology | Interleukin-1beta - immunology | Inflammation - immunology | Mice, Knockout | Carrier Proteins - genetics | Animals | Apoptosis Regulatory Proteins | Cytoskeletal Proteins - immunology | Inflammasomes - blood | Caspase 1 - genetics | CARD Signaling Adaptor Proteins | Inflammasomes - immunology | Mice | Genetic aspects | Inflammation | Immune response | Macrophages | Properties
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7. Full Text Blockade of IL-33R/ST2 Signaling Attenuates Toxoplasma gondii Ileitis Depending on IL-22 Expression
by Ryffel, B and Huang, F and Robinet, P and Panek, C and Couillin, I and Erard, F and Piotet, J and Le Bert, M and Mackowiak, C and Arias, MT and Dimier-Poisson, I and Zheng, SG
FRONTIERS IN IMMUNOLOGY, ISSN 1664-3224, 04/2019, Volume 10, p. 702
Oral T. gondii infection (30 cysts of 76K strain) induces acute lethal ileitis in sensitive C57BL/6 (B6) mice with increased expression of IL-33 and its... 
CELLS | IMMUNITY | IL-33/ST2 receptor | neutralizing antibody | IMMUNOLOGY | PREVENT | IL-22 | Toxoplasma gondii | innate immunity | COLITIS | PATHWAY | parasite-induced ileitis | T1/ST2 | Complications and side effects | Interleukins | Toxoplasmosis | Gastrointestinal diseases | Colorectal diseases | Cellular signal transduction | Genetic aspects | Research | Gene expression | Risk factors | Life Sciences
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8. Full Text The IL-33 receptor ST2 regulates pulmonary inflammation and fibrosis to bleomycin
by Fanny, Manoussa and Nascimento, Mégane and Baron, Ludivine and Schricke, Corinne and Maillet, Isabelle and Akbal, Myriam and Riteau, Nicolas and Bert, Marc Le and Quesniaux, Valérie and Ryffel, Bernhard and Gombault, Aurélie and Même, Sandra and Même, William and Couillin, Isabelle
Frontiers in Immunology, ISSN 1664-3224, 06/2018, Volume 9, p. 1476
Idiopathic pulmonary fibrosis is a progressive, devastating, and yet untreatable fibrotic disease of unknown origin. Interleukin-33 (IL-33), an IL-1 family... 
Suppression of tumorigenicity 2 | Bleomycin | Magnetic resonance imaging | Interleukin-33 | Lung | Fibrosis | Inflammation | bleomycin | magnetic resonance imaging | ACTIVATION | CHROMATIN | MACROPHAGES | INDUCED LUNG INJURY | CYTOKINE | INNATE LYMPHOID-CELLS | IMMUNOLOGY | interleukin-33 | PROTEIN ST2 | lung | inflammation | IN-VIVO | fibrosis | suppression of tumorigenicity 2 | MICE | Complications and side effects | Pulmonary fibrosis | Interleukins | Dosage and administration | Research | Risk factors | Life Sciences
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9. Full Text Interleukin-17 is a negative regulator of established allergic asthma
by Schnyder-Candrian, Silvia and Togbe, Dieudonnée and Couillin, Isabelle and Mercier, Isabelle and Brombacher, Frank and Quesniaux, Valérie and Fossiez, Francois and Ryffel, Bernhard and Schnyder, Bruno
Journal of Experimental Medicine, ISSN 0022-1007, 11/2006, Volume 203, Issue 12, pp. 2715 - 2725
T helper (Th) 17 cells producing interleukin (IL)-17 play a role in autoimmune and allergic inflammation. Here, we show that IL-23 induces IL-17 in the lung... 
MEDICINE, RESEARCH & EXPERIMENTAL | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | COLONY-STIMULATING FACTOR | DENDRITIC CELLS | INDUCED RANTES | IL-17 | AIRWAY INFLAMMATION | TNF-ALPHA | IL-17-DEFICIENT MICE | IMMUNOLOGY | T-CELLS | NEUTROPHIL RECRUITMENT | Chemokine CCL17 | Asthma - prevention & control | Dendritic Cells - immunology | Mice, Inbred C57BL | Cells, Cultured | Interleukin-17 - physiology | Chemokine CCL11 | Chemokine CCL5 - antagonists & inhibitors | Mice, Knockout | Allergens - administration & dosage | Chemokines, CC - antagonists & inhibitors | Animals | Chemokine CCL5 - biosynthesis | Ovalbumin - administration & dosage | Asthma - immunology | Chemokines, CC - biosynthesis | Mice | Mice, Inbred BALB C | Asthma - pathology | Dendritic Cells - metabolism
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10. Full Text Uric Acid Is a Danger Signal Activating NALP3 Inflammasome in Lung Injury Inflammation and Fibrosis
by Gasse, Pamela and Riteau, Nicolas and Charron, Sabine and Girre, Sandra and Fick, Lizette and Petrilli, Virginie and Tschopp, Jurg and Lagente, Vincent and Quesniaux, Valerie F. J and Ryffel, Bernhard and Couillin, Isabelle
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 05/2009, Volume 179, Issue 10, pp. 903 - 913
Rationale Lung injury leads to pulmonary inflammation and fibrosis through myeloid differentiation primary response gene 88 (MyD88) and the IL-1 receptor 1... 
Inflammasome | Lung inflammation | Bleomycin | Uric acid | Fibrosis | bleomycin | DENDRITIC CELLS | CASPASE-1 | INNATE IMMUNE-RESPONSE | CUTTING EDGE | MONOSODIUM URATE CRYSTALS | RECEPTOR-DEFICIENT MICE | ADAPTIVE IMMUNITY | DYING CELLS | RESPIRATORY SYSTEM | inflammasome | APOPTOTIC CELLS | fibrosis | uric acid | PULMONARY-FIBROSIS | lung inflammation | CRITICAL CARE MEDICINE | Bleomycin - antagonists & inhibitors | NLR Family, Pyrin Domain-Containing 3 Protein | Bronchoalveolar Lavage Fluid - immunology | Lung Injury - metabolism | Myeloid Differentiation Factor 88 - immunology | Pneumonia - immunology | Uric Acid - administration & dosage | Interleukin-1beta - biosynthesis | Lung - metabolism | Pulmonary Fibrosis - metabolism | Carrier Proteins - immunology | Disease Models, Animal | Biomarkers - metabolism | Lung - pathology | Uric Acid - metabolism | Enzyme-Linked Immunosorbent Assay | Biomarkers - analysis | Pulmonary Fibrosis - immunology | Interleukin-1beta - immunology | Bleomycin - administration & dosage | Uric Acid - immunology | Animals | Carrier Proteins - metabolism | Lung - drug effects | Allopurinol - pharmacology | Mice | Lung Injury - chemically induced | Pneumonia - metabolism | Lung Injury - immunology | Lung - immunology | Index Medicus | Abridged Index Medicus | Bronchoalveolar Lavage Fluid | Pneumonia | Biological Markers | Allopurinol | Lung | Interleukin-1beta | Myeloid Differentiation Factor 88 | Life Sciences | Immunology | Uric Acid | Pulmonary Fibrosis | Lung Injury | Carrier Proteins
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11. Full Text TLR4 gene dosage contributes to endotoxin-induced acute respiratory inflammation
by Dieudonnée Togbe and Silvia Schnyder-Candrian and Bruno Schnyder and Isabelle Couillin and Isabelle Maillet and Franck Bihl and Danielle Malo and Bernhard Ryffel and Valerie F. J. Quesniaux
Journal of Leukocyte Biology, ISSN 0741-5400, 09/2006, Volume 80, Issue 3, pp. 451 - 457
Toll‐like receptor (TLR)4 is critical for endotoxin recognition and cellular responses. Using Tlr4 transgenic mice, we investigated the influence of Tlr4 gene... 
lung | Toll‐like receptor transgenic mice | CXCL1 | lipopolysaccharide | vascular leak | Lipopolysaccharide | Lung | Toll-like receptor transgenic mice | Vascular leak | LUNG INJURY | IMMUNOLOGY | BINDING PROTEIN | HOST RESPONSE | NEUTROPHIL SEQUESTRATION | CELL BIOLOGY | TOLL-LIKE RECEPTOR-4 | INNATE IMMUNE-RESPONSES | BRONCHOCONSTRICTION | MICE | INFECTION | HEMATOLOGY | toll-like receptor transgenic mice | CXCLl-KC | Acute Disease | Dose-Response Relationship, Immunologic | Lipopolysaccharides - toxicity | Gene Expression Regulation - immunology | Lipopolysaccharides - administration & dosage | Mice, Inbred C57BL | Neutrophils - immunology | Pneumonia - pathology | Toll-Like Receptor 4 - genetics | Gene Dosage - immunology | Mice, Transgenic | Toll-Like Receptor 4 - immunology | Administration, Intranasal | Animals | Toll-Like Receptor 4 - deficiency | Pneumonia - immunology | Mice | Cytokines - biosynthesis | Cytokines - immunology | Pneumonia - genetics | Life Sciences | Immunology
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12. Full Text Allergic lung inflammation is mediated by soluble Tumor Necrosis Factor (TNF) and attenuated by dominant-negative TNF biologics
by Maillet, Isabelle and Schnyder-Candrian, Silvia and Couillin, Isabelle and Quesniaux, Valerie F. J and Erard, Francois and Moser, René and Fleury, Sébastien and Kanda, Akira and Dombrowicz, David and Szymkowski, David E and Ryffel, Bernhard
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 10/2011, Volume 45, Issue 4, pp. 731 - 739
Tumor Necrosis Factor (TNF) is a pleiotropic cytokine consisting of soluble and transmembrane forms, with distinct roles in inflammation and immunity. TNF is... 
Airway hyperreactivity | XENP1595 | Etanercept | Asthma | RHEUMATOID-ARTHRITIS | COLLAGEN-INDUCED ARTHRITIS | airway hyperreactivity | MEMBRANE TNF | etanercept | ASTHMA MODEL | TUBERCULOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | asthma | FACTOR-ALPHA BLOCKADE | CELL BIOLOGY | TRANSMEMBRANE TNF | RESPIRATORY SYSTEM | AIRWAY HYPERRESPONSIVENESS | MICE | MYCOBACTERIAL INFECTION | Tumor Necrosis Factor-alpha - metabolism | Pneumonia - physiopathology | Bronchial Hyperreactivity - immunology | Humans | Hyperplasia | Pulmonary Eosinophilia - genetics | Tumor Necrosis Factor-alpha - genetics | Pneumonia - pathology | Pneumonia - prevention & control | Goblet Cells - drug effects | Biological Products - pharmacology | Tumor Necrosis Factor-alpha - deficiency | Bronchial Hyperreactivity - genetics | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | Goblet Cells - immunology | Bronchial Hyperreactivity - physiopathology | Inflammation Mediators - metabolism | Immunoglobulin G - pharmacology | Pneumonia - immunology | Disease Models, Animal | Pneumonia - genetics | Pulmonary Eosinophilia - immunology | Ovalbumin | Lung - pathology | Pulmonary Eosinophilia - prevention & control | Cytokines - metabolism | Immunoglobulin E - metabolism | Mice, Inbred C57BL | Mice, Transgenic | Lung - physiopathology | Bronchial Hyperreactivity - prevention & control | Mice, Knockout | Tumor Necrosis Factor-alpha - pharmacology | Bronchial Hyperreactivity - pathology | Animals | Receptors, Tumor Necrosis Factor | Lung - drug effects | Mice | Mice, Inbred BALB C | Goblet Cells - pathology | Mutation | Lung - immunology | Tumor Necrosis Factor-alpha - antagonists & inhibitors
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13. Full Text IL-1 and IL-23 mediate early IL-17A production in pulmonary inflammation leading to late fibrosis
by Gasse, Paméla and Riteau, Nicolas and Vacher, Rachel and Michel, Marie-Laure and Fautrel, Alain and di Padova, Franco and Fick, Lizette and Charron, Sabine and Lagente, Vincent and Eberl, Gérard and Le Bert, Marc and Quesniaux, Valérie F. J and Huaux, François and Leite-de-Moraes, Maria and Ryffel, Bernhard and Couillin, Isabelle
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 8, pp. e23185 - e23197
Background: Idiopathic pulmonary fibrosis is a devastating as yet untreatable disease. We demonstrated recently the predominant role of the NLRP3 inflammasome... 
COLLAGEN-INDUCED ARTHRITIS | TGF-BETA | ROR-GAMMA-T | HELPER-CELLS | BIOLOGY | LUNG INJURY | DELTA-T-CELLS | NEUTROPHIL RECRUITMENT | RECEPTOR ANTAGONIST | AIRWAY NEUTROPHILIA | TH17 CELLS | Transforming Growth Factor beta1 - metabolism | Pneumonia - pathology | Male | Pulmonary Fibrosis - genetics | Interleukin-1beta - genetics | Lung Injury - etiology | Interleukin-23 - genetics | Interleukin-23 Subunit p19 - metabolism | Flow Cytometry | Interleukin-23 - metabolism | Interleukin-1beta - metabolism | T-Lymphocyte Subsets - drug effects | Interleukin-23 Subunit p19 - genetics | Lung Injury - metabolism | Female | Lung - metabolism | Pulmonary Fibrosis - metabolism | Pneumonia - genetics | Lung - pathology | Enzyme-Linked Immunosorbent Assay | Mice, Inbred C57BL | Interleukin-17 - genetics | Mice, Transgenic | Pulmonary Fibrosis - pathology | Bleomycin - administration & dosage | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Interleukin-17 - metabolism | Animals | Interleukin-1beta - administration & dosage | T-Lymphocyte Subsets - metabolism | Lung - drug effects | Mice | Pneumonia - metabolism | Collagen | Analysis | Lung diseases | Fibrosis | Bone morphogenetic proteins | Inflammation | T cells | Transforming growth factors | Flow cytometry | Traumatic brain injury | Laboratories | Antibodies | Homeostasis | Inflammatory response | Interleukin 23 | Infections | Lymphocytes T | Bleomycin | E coli | Lymphocytes | Rodents | Interleukin 1 | Chronic obstructive pulmonary disease | Drug dosages | Medical research | Wound healing | Bacterial infections | Cytokines | Neutrophils | Interleukin 17 | Signaling | Infectious diseases | Pulmonary fibrosis | Rheumatoid arthritis
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14. Full Text Extracellular ATP is a danger signal activating P2X 7 receptor in lung inflammation and fibrosis
by Riteau, Nicolas and Gasse, Pamela and Fauconnier, Louis and Gombault, Aurélie and Couegnat, Marion and Fick, Lizette and Kanellopoulos, Jean and Quesniaux, Valérie F. J and Marchand-Adam, Sylvain and Crestani, Bruno and Ryffel, Bernhard and Couillin, Isabelle
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 09/2010, Volume 182, Issue 6, pp. 774 - 783
receptor | P2X | Pannexin-1 | Inflammation | ATP | Lung fibrosis
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15. Full Text Early endosome autoantigen 1 regulates IL-1 beta release upon caspase-1 activation independently of gasdermin D membrane permeabilization
by Baroja-Mazo, A and Compan, V and Martin-Sanchez, F and Tapia-Abellan, A and Couillin, I and Pelegrin, P
SCIENTIFIC REPORTS, ISSN 2045-2322, 04/2019, Volume 9, Issue 1, pp. 5788 - 10
Unconventional protein secretion represents an important process of the inflammatory response. The release of the pro-inflammatory cytokine interleukin (IL)-1... 
ACTIVE CASPASE-1 | EEA1 | AUTOANTIBODIES | PROTEIN | MECHANISM | INTERLEUKIN-1-BETA | MULTIDISCIPLINARY SCIENCES | NLRP3 INFLAMMASOME | SECRETION | PYROPTOSIS | PLASMA-MEMBRANE | Proteins | Cytokines | Secretion | Caspase | Inflammation | Lactic acid | IL-1β | L-Lactate dehydrogenase | Membrane proteins | Caspase-1
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16. Full Text Uncoupling between inflammatory and fibrotic responses to silica: Evidence from MyD88 knockout mice
by Lo Re, Sandra and Yakoub, Yousof and Devosse, Raynal and Uwambayinema, Francine and Couillin, Isabelle and Ryffel, Bernard and Marbaix, Etienne and Lison, Dominique and Huaux, François
PLoS ONE, ISSN 1932-6203, 07/2014, Volume 9, Issue 7, pp. e99383 - e99383
The exact implication of innate immunity in granuloma formation and irreversible lung fibrosis remains to be determined. In this study, we examined the lung... 
FIBROSIS | TUMOR-NECROSIS-FACTOR | INDUCED PULMONARY INFLAMMATION | NMRI MICE | INDUCED LUNG INFLAMMATION | C57BL/6 MICE | MULTIDISCIPLINARY SCIENCES | RECEPTOR ANTAGONIST | MURINE SILICOSIS | T-LYMPHOCYTES | NALP3 INFLAMMASOME | Immunohistochemistry | Inflammation - chemically induced | T-Lymphocytes, Regulatory - metabolism | Granuloma - metabolism | Interleukin-1alpha - immunology | Receptors, Interleukin-1 - genetics | Immunity, Innate - genetics | Interleukin-1alpha - metabolism | Pulmonary Fibrosis - genetics | Interleukin-1beta - genetics | Silicosis - genetics | T-Lymphocytes, Regulatory - immunology | Signal Transduction - immunology | Flow Cytometry | Th17 Cells - metabolism | Interleukin-1beta - metabolism | Myeloid Differentiation Factor 88 - immunology | Interleukin-1alpha - genetics | Cytokines - genetics | Silicosis - immunology | Cytokines - immunology | Granuloma - genetics | Silicosis - etiology | Cytokines - metabolism | Receptors, Interleukin-1 - immunology | Silicon Dioxide - immunology | Mice, Inbred C57BL | Myeloid Differentiation Factor 88 - genetics | Pulmonary Fibrosis - immunology | Interleukin-1beta - immunology | Inflammation - immunology | Signal Transduction - genetics | Mice, Knockout | Receptors, Interleukin-1 - metabolism | Immunity, Innate - immunology | Animals | Silicon Dioxide - toxicity | Inflammation - genetics | Pulmonary Fibrosis - chemically induced | Th17 Cells - immunology | Granuloma - immunology | Myeloid Differentiation