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6 results on '"Gras, Delphine"'

1. Lung development, regeneration and plasticity: From disease physiopathology to drug design using induced pluripotent stem cells.

Author

Ahmed E, Sansac C, Assou S, Gras D, Petit A, Vachier I, Chanez P, De Vos J, and Bourdin A

Subjects
Animals, Cell Plasticity, Cell- and Tissue-Based Therapy, Drug Design, Epithelial Cells physiology, Humans, Induced Pluripotent Stem Cells transplantation, Lung Diseases therapy, Regeneration, Lung physiology
Abstract

Lungs have a complex structure composed of different cell types that form approximately 17 million airway branches of gas-delivering bronchioles connected to 500 million gas-exchanging alveoli. Airways and alveoli are lined by epithelial cells that display a low rate of turnover at steady-state, but can regenerate the epithelium in response to injuries. Here, we review the key points of lung development, homeostasis and epithelial cell plasticity in response to injury and disease, because this knowledge is required to develop new lung disease treatments. Of note, canonical signaling pathways that are essential for proper lung development during embryogenesis are also involved in the pathophysiology of most chronic airway diseases. Moreover, the perfect control of these interconnected pathways is needed for the successful differentiation of induced pluripotent stem cells (iPSC) into lung cells. Indeed, differentiation of iPSC into airway epithelium and alveoli is based on the use of biomimetics of normal embryonic and fetal lung development. In vitro iPSC-based models of lung diseases can help us to better understand the impaired lung repair capacity and to identify new therapeutic targets and new approaches, such as lung cell therapy., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Published
2018
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2. Farm dust and endotoxin protect against allergy through A20 induction in lung epithelial cells.

Author

Schuijs MJ, Willart MA, Vergote K, Gras D, Deswarte K, Ege MJ, Madeira FB, Beyaert R, van Loo G, Bracher F, von Mutius E, Chanez P, Lambrecht BN, and Hammad H

Subjects
Animals, Asthma immunology, Asthma prevention & control, Cells, Cultured, Child, Dairying, Dendritic Cells immunology, Female, Humans, Hygiene Hypothesis, Hypersensitivity enzymology, Hypersensitivity immunology, Inhalation Exposure, Lung immunology, Mice, Mice, Inbred C57BL, Respiratory Mucosa immunology, Tumor Necrosis Factor alpha-Induced Protein 3, DNA-Binding Proteins biosynthesis, Dust immunology, Hypersensitivity prevention & control, Intracellular Signaling Peptides and Proteins biosynthesis, Lipopolysaccharides immunology, Lung enzymology, Nuclear Proteins biosynthesis, Pyroglyphidae immunology, Respiratory Mucosa enzymology
Abstract

Growing up on a dairy farm protects children from allergy, hay fever, and asthma. A mechanism linking exposure to this endotoxin (bacterial lipopolysaccharide)-rich environment with protection has remained elusive. Here we show that chronic exposure to low-dose endotoxin or farm dust protects mice from developing house dust mite (HDM)-induced asthma. Endotoxin reduced epithelial cell cytokines that activate dendritic cells (DCs), thus suppressing type 2 immunity to HDMs. Loss of the ubiquitin-modifying enzyme A20 in lung epithelium abolished the protective effect. A single-nucleotide polymorphism in the gene encoding A20 was associated with allergy and asthma risk in children growing up on farms. Thus, the farming environment protects from allergy by modifying the communication between barrier epithelial cells and DCs through A20 induction., (Copyright © 2015, American Association for the Advancement of Science.)

Published
2015
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3. Regulation of CXCR/IL-8 in human airway epithelial cells.

Author

Gras D, Tiers L, Vachier I, de Senneville LD, Bourdin A, Godard P, Lehman S, and Chanez P

Subjects
Antibodies immunology, Antibodies pharmacology, Bronchi cytology, Bronchi metabolism, Epithelial Cells cytology, Epithelial Cells drug effects, Gene Expression genetics, Humans, Intercellular Adhesion Molecule-1 metabolism, Interleukin-6 metabolism, Interleukin-8 pharmacology, Peptides analysis, Peptides metabolism, Proteins analysis, Proteins metabolism, Receptors, CXCR genetics, Receptors, CXCR immunology, Receptors, Interleukin-8A genetics, Receptors, Interleukin-8A immunology, Receptors, Interleukin-8A metabolism, Receptors, Interleukin-8B genetics, Receptors, Interleukin-8B immunology, Receptors, Interleukin-8B metabolism, Respiratory Mucosa cytology, Respiratory Mucosa metabolism, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, Epithelial Cells metabolism, Interleukin-8 metabolism, Lung cytology, Receptors, CXCR metabolism
Abstract

Background: Severe asthma is characterized by neutrophilic inflammation and high levels of interleukin (IL)-8. Airway epithelial cells play a pivotal role in the pathogenesis and chronicity of asthma. The objective of this work was to determine whether CXC receptors were involved in human small airway epithelial cell (SAEC) activity by incubating them with IL-8; the investigation also included a proteomic approach., Methods: IL-6 and intercellular adhesion molecule-1 (ICAM-1) were assessed by ELISA and flow cytometry, respectively. CXCR-1 and CXCR-2 receptor mRNA and protein expressions were analyzed by RT-PCR, immunocytochemistry and flow cytometry. Cells were incubated with different concentrations (0-100 ng/ml) of IL-8. The involvement of both receptors was assessed using specific antibodies., Results: Only the CXCR-1 receptor was expressed in SAECs. IL-8 (50 ng/ml, 12 h) induced the release of IL-6 and had no effect on ICAM-1. Supernatants analyzed by surface enhanced laser desorption ionization time of flight mass spectrometry (SELDI-TOF MS) showed very weak differences in peptide profiles. Interestingly, 4,820-m/z peptide release was detected in the presence of IL-8 and abolished by CXCR-1 antibody., Discussion: The present study illustrated the fact that IL-8 mediated by CXCR-1 increased IL-6. We also highlight the usefulness of SELDI ProteinChip technology to confirm the potential variation of peptide profile. Moreover, we were able to detect the 4,820-m/z peptide secreted in vitro by human airway epithelial cells induced by IL-8 via CXCR-1 receptor. Determination of the protein secretion profile in response to inflammatory stimuli could be an important therapeutic strategy in severe asthma., (Copyright 2009 S. Karger AG, Basel.)

Published
2010
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4. Safety and Dose Study of Targeted Lung Denervation in Moderate/Severe COPD Patients

Author

Valipour, Arschang, Shah, Pallav L, Pison, Christophe, Ninane, Vincent, Janssens, Wim, Perez, Thierry, Kessler, Romain, Deslee, Gaetan, Garner, Justin, Abele, Christine, Hartman, Jorine E, Slebos, Dirk-Jan, Chen, A, Gorden, J, Issa, Z, McDonald, G, Pulling, C, Aalbers, R, Ferrera, D, Leh, L, Firlinger, Irene, Kothakuzhakal, Kiran, Duller, Marina, Muylle, Inge, Rummens, Peter, De Cock, Frederique, Dooms, Christophe, DeBent, Kristien, Briault, Amandine, Arbib, Francois, Jondot, Marie, Ferretti, Gilbert, Fournier, Clement, Matran, Regis, Catto, Michele, Bautin, Nathalie, De Broucker, Virginie, Willemin, Marie, Prevotat, Anne, Wemeau, Ludivine, Gicquello, Alice, Foulon, Morgane, Camara, Hasna, Vallerand, Herve, Dury, Sandra, Gras, Delphine, Bonnaire-Verdier, Margaux, Hirschi, Sandrine, Porzio, Michele, Degot, Tristan, Canuet, Mathieu, Schuller, Armelle, Stauder, Julien, Azouaou, Sahra Ali, Srikanthan, Karthi, Caneja, Cielito, Thornton, John, Ten Hacken, Nick, Hartman, Jorine, Augustijn, Sonja, Klooster, Karin, Groningen Research Institute for Asthma and COPD (GRIAC), Department of Respiratory and Critical Care Medicine, Ludwig-Boltzmann-Institute for COPD and Respiratory Epidemiology, Otto-Wagner-Spital, Vienna, Royal Brompton and Harefield NHS Trust, Chelsea and Westminster Hospital, and Imperial College, London, Centre Hospitalier Universitaire [Grenoble] (CHU), Laboratory of Fundamental and Applied Bioenergetics = Laboratoire de bioénergétique fondamentale et appliquée (LBFA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019]), CHU Saint-Pierre, Université libre de Bruxelles, Bruxelles, Department of Respiratory Diseases, KU Leuven, University Hospitals Leuven, Leuven, Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 (CIIL), Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université de Lille-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Service de Pneumologie, Nouvel Hôpital Civil, Université de Strasbourg, Strasbourg, Hôpital Maison Blanche, Centre Hospitalier Universitaire de Reims (CHU Reims), University Medical Center Groningen [Groningen] (UMCG), Imperial College London, Université libre de Bruxelles (ULB), Institut Pasteur de Lille, and Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Pulmonary and Respiratory Medicine, Male, [SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract, law.invention, 03 medical and health sciences, Pulmonary Disease, Chronic Obstructive, 0302 clinical medicine, Quality of life, Randomized controlled trial, law, Bronchoscopy, Parasympathectomy, medicine, Clinical endpoint, Humans, Interventional Pulmonology, 030212 general & internal medicine, Dosing, Adverse effect, Lung, Aged, COPD, business.industry, Radiofrequency ablation, Middle Aged, medicine.disease, Acetylcholine, 3. Good health, medicine.anatomical_structure, 030228 respiratory system, Anesthesia, Lung disease obstructive, Female, Pneumologie, Airway, business
Abstract

Rationale: Targeted lung denervation (TLD) is a novel bronchoscopic treatment for the disruption of parasympathetic innervation of the lungs. Objectives: To assess safety, feasibility, and dosing of TLD in patients with moderate to severe COPD using a novel device design. Methods: Thirty patients with COPD (forced expiratory volume in 1 s 30-60%) were 1:1 randomized in a double-blinded fashion to receive TLD with either 29 or 32 W. Primary endpoint was the rate of TLD-associated adverse airway effects that required treatment through 3 months. Assessments of lung function, quality of life, dyspnea, and exercise capacity were performed at baseline and 1-year follow-up. An additional 16 patients were enrolled in an open-label confirmation phase study to confirm safety improvements after procedural enhancements following gastrointestinal adverse events during the randomized part of the trial. Results: Procedural success, defined as device success without an in-hospital serious adverse event, was 96.7% (29/30). The rate of TLD-associated adverse airway effects requiring intervention was 3/15 in the 32 W versus 1/15 in the 29 W group, p = 0.6. Five patients early in the randomized phase experienced serious gastric events. The study was stopped and procedural changes made that reduced both gastrointestinal and airway events in the subsequent phase of the randomized trial and follow-up confirmation study. Improvements in lung function and quality of life were observed compared to baseline values for both doses but were not statistically different. Conclusions: The results demonstrate acceptable safety and feasibility of TLD in patients with COPD, with improvements in adverse event rates after procedural enhancements., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2019
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5. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues

Author

Ziegler, Carly GK, Allon, Samuel J, Nyquist, Sarah K, Mbano, Ian M, Miao, Vincent N, Tzouanas, Constantine N, Cao, Yuming, Yousif, Ashraf S, Bals, Julia, Hauser, Blake M, Feldman, Jared, Muus, Christoph, Wadsworth, Marc H, Kazer, Samuel W, Hughes, Travis K, Doran, Benjamin, Gatter, G James, Vukovic, Marko, Taliaferro, Faith, Mead, Benjamin E, Guo, Zhiru, Wang, Jennifer P, Gras, Delphine, Plaisant, Magali, Ansari, Meshal, Angelidis, Ilias, Adler, Heiko, Sucre, Jennifer MS, Taylor, Chase J, Lin, Brian, Waghray, Avinash, Mitsialis, Vanessa, Dwyer, Daniel F, Buchheit, Kathleen M, Boyce, Joshua A, Barrett, Nora A, Laidlaw, Tanya M, Carroll, Shaina L, Colonna, Lucrezia, Tkachev, Victor, Peterson, Christopher W, Yu, Alison, Zheng, Hengqi Betty, Gideon, Hannah P, Winchell, Caylin G, Lin, Philana Ling, Bingle, Colin D, Snapper, Scott B, Kropski, Jonathan A, Theis, Fabian J, Schiller, Herbert B, Zaragosi, Laure-Emmanuelle, Barbry, Pascal, Leslie, Alasdair, Kiem, Hans-Peter, Flynn, JoAnne L, Fortune, Sarah M, Berger, Bonnie, Finberg, Robert W, Kean, Leslie S, Garber, Manuel, Schmidt, Aaron G, Lingwood, Daniel, Shalek, Alex K, Ordovas-Montanes, Jose, HCA Lung Biological Network. Electronic Address: Lung-Network@Humancellatlas.Org, HCA Lung Biological Network, Yousif, Ashraf S [0000-0001-9215-3853], Hauser, Blake M [0000-0002-0100-1684], Kazer, Samuel W [0000-0002-7380-9594], Sucre, Jennifer MS [0000-0002-6613-1439], Tkachev, Victor [0000-0001-6011-0576], Zheng, Hengqi Betty [0000-0003-0575-6475], Bingle, Colin D [0000-0002-5405-6988], and Apollo - University of Cambridge Repository

Subjects
Adolescent, Pneumonia, Viral, ACE2, non-human primate, HIV Infections, Peptidyl-Dipeptidase A, Cell Line, ISG, Betacoronavirus, Mice, scRNA-seq, Influenza, Human, Animals, Humans, Tuberculosis, human, Child, Lung, Pandemics, mouse, Cells, Cultured, SARS-CoV-2, Serine Endopeptidases, COVID-19, interferon, Mycobacterium tuberculosis, respiratory system, Macaca mulatta, Up-Regulation, Nasal Mucosa, Enterocytes, Alveolar Epithelial Cells, Interferon Type I, Receptors, Virus, Angiotensin-Converting Enzyme 2, Goblet Cells, Single-Cell Analysis, influenza, Coronavirus Infections
Abstract

There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.

Published
2020
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6. Spatiotemporal organization of cilia drives multiscale mucus swirls in model human bronchial epithelium

Author

Khelloufi , Mustapha-Kamel, Loiseau , Etienne, Jaeger , Marc, Molinari , Nicolas, Chanez , Pascal, Gras , Delphine, Viallat , Annie, Centre Interdisciplinaire de Nanoscience de Marseille (CINaM), Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), Laboratoire de Mécanique, Modélisation et Procédés Propres (M2P2), Centre National de la Recherche Scientifique (CNRS)-École Centrale de Marseille (ECM)-Aix Marseille Université (AMU), Physiologie & médecine expérimentale du Cœur et des Muscles [U 1046] (PhyMedExp), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Centre recherche en CardioVasculaire et Nutrition = Center for CardioVascular and Nutrition research (C2VN), Institut National de la Recherche Agronomique (INRA)-Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), ANR MUCOCIL project, of the French Agence Nationale de la Recherche [ANR-13-BSV5-0015], MedBioMed, European Project: 609102,EC:FP7:PEOPLE,FP7-PEOPLE-2013-COFUND,PRESTIGE(2014), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Aix Marseille Université (AMU)-École Centrale de Marseille (ECM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Centre recherche en CardioVasculaire et Nutrition (C2VN), Centre Interdisciplinaire de Nanoscience de Marseille ( CINaM ), Aix Marseille Université ( AMU ) -Centre National de la Recherche Scientifique ( CNRS ), Laboratoire de Mécanique, Modélisation et Procédés Propres ( M2P2 ), Aix Marseille Université ( AMU ) -Ecole Centrale de Marseille ( ECM ) -Centre National de la Recherche Scientifique ( CNRS ), Institut Montpelliérain Alexander Grothendieck ( IMAG ), Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ), Centre recherche en CardioVasculaire et Nutrition ( C2VN ), Institut National de la Recherche Agronomique ( INRA ) -Aix Marseille Université ( AMU ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), and ANR-13BSV5-0015-02,Mucocil ,Agence Nationale de Recherche (ANR) Mucocil project

Subjects
Cells, lcsh:Medicine, Bronchi, Respiratory Mucosa, Stress, Models, Biological, [SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract, Article, Tissue Culture Techniques, Pulmonary Disease, Chronic Obstructive, Bronchoscopy, Humans, Disease, Cilia, lcsh:Science, Lung, lcsh:R, [SPI.MECA.BIOM]Engineering Sciences [physics]/Mechanics [physics.med-ph]/Biomechanics [physics.med-ph], respiratory system, Newborn, Asthma, Biomechanical Phenomena, Mucus, Retention, Mucociliary Clearance, Case-Control Studies, Mouse Airway, [ SPI.MECA.MEFL ] Engineering Sciences [physics]/Mechanics [physics.med-ph]/Fluids mechanics [physics.class-ph], Hydrodynamics, Clearance, lcsh:Q, Mucociliary Transport, Severe Asthma, Rheology
Abstract

International audience; Mucociliary clearance is a biomechanical mechanism of airway protection. It consists of the active transport along the bronchial tree of the mucus, a fluid propelled by the coordinated beating of a myriad of cilia on the epithelial surface of the respiratory tract. The physics of mucus transport is poorly understood because it involves complex phenomena such as long-range hydrodynamic interactions, active collective ciliary motion, and the complex rheology of mucus. We propose a quantitative physical analysis of the ciliary activity and mucus transport on a large panel of human bronchial cultures from control subjects, patients with asthma and chronic obstructive pulmonary disease obtained from endobronchial biopsies. Here we report on the existence of multiple ciliary domains with sizes ranging from the tens of a micron to the centimeter, where ciliary beats present a circular orientational order. These domains are associated with circular mucus flow patterns, whose size scales with the average cilia density. In these domains, we find that the radial increase of the ciliated cell density coupled with the increase in the orientational order of ciliary beats result in a net local force proportional to the mucus velocity. We propose a phenomenological physical model that supports our results.

Published
2018
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