Research Topics
Genomes and Genes
| Paul W NobleSummaryAffiliation: Yale University Country: USA Publications
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Detail Information
Publications
Back to the future: historical perspective on the pathogenesis of idiopathic pulmonary fibrosisPaul W Noble
Department of Medicine, Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, TAC-441C, New Haven, CT 06520-8057, USA
Am J Respir Cell Mol Biol 33:113-20. 2005
Idiopathic pulmonary fibrosisEric B Meltzer
Department of Medicine, Division of Pulmonary, Allergy and Critical Care, Duke University Medical Center, Durham, North Carolina 27710, USA
Orphanet J Rare Dis 3:8. 2008..Meanwhile, pulmonary transplantation remains a viable option for patients with IPF. It is expected that, during the next decade, considerable progress will be made toward the understanding and treatment of this devastating illness...- Idiopathic pulmonary fibrosis: new insights into pathogenesisPaul W Noble
Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, 441 C CAB, 333 Cedar Street, New Haven, CT 06520 8057, USA
Clin Chest Med 25:749-58, vii. 2004..This article highlights aspects of current thoughts on pathogenesis of IFP and expands on recent reviews... - Matrix regulation of lung injury, inflammation, and repair: the role of innate immunityPaul W Noble
Pulmonary and Critical Care Medicine, Yale University School of Medicine, TAC S441C, PO Box 208057, 333 Cedar Street, New Haven, CT 06520, USA
Proc Am Thorac Soc 3:401-4. 2006..Although TLR2 and TLR4 initiate the innate immune response in noninfectious inflammation, they have a protective role against lung injury on alveolar epithelial cells... - Idiopathic pulmonary fibrosis: natural history and prognosisPaul W Noble
Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, 441 C CAB, 333 Cedar Street, New Haven, CT 06520 8057, USA
Clin Chest Med 27:S11-6, v. 2006..Thus, ongoing epithelial damage and repair processes associated with persistent fibroblastic proliferation seem important in IPF natural history... - Case study reviewPaul W Noble
Pulmonary and Critical Care Section, Yale University School of Medicine, Yale University School of Medicine, 333 Cedar St, PO Box 208057, New Haven, CT 06520 8057, USA
Chest 128:540S-546S. 2005..Each case highlights components of the differential diagnosis, as well as reviews the treatments and prognoses of these patients. The cases provide clinical pearls that are designed to enhance the reader's understanding of ILDs... - Hyaluronan and its catabolic products in tissue injury and repairPaul W Noble
Yale University School of Medicine, Section of Pulmonary and Critical Care Medicine, Department of Medicine, VA Connecticut Healthcare System, LCI 105, 333 Cedar Street, New Haven, CT 06520, USA
Matrix Biol 21:25-9. 2002..The biological properties of these hyaluronan fragments appear to be distinct from the larger precursor molecules. This review examines the biological role of hyaluronan fragments in tissue injury and repair... - Regulation of lung injury and repair by Toll-like receptors and hyaluronanDianhua Jiang
Department of Medicine, Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520, USA
Nat Med 11:1173-9. 2005..Hyaluronan-TLR2 and hyaluronan-TLR4 interactions provide signals that initiate inflammatory responses, maintain epithelial cell integrity and promote recovery from acute lung injury... - A macrophage subpopulation recruited by CC chemokine ligand-2 clears apoptotic cells in noninfectious lung injuryJiurong Liang
Division of Pulmonary, Department of Medicine, Duke Univ School of Medicine, Durham, NC 27710, USA
Am J Physiol Lung Cell Mol Physiol 302:L933-40. 2012..Our data suggested a previously undiscovered role for MHCII IA/IE(int)CD11c(int) cells in apoptotic cell clearance and inflammation resolution... - Inhibition of pulmonary fibrosis in mice by CXCL10 requires glycosaminoglycan binding and syndecan-4Dianhua Jiang
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University School of Medicine, Durham, North Carolina 27710, USA
J Clin Invest 120:2049-57. 2010..Thus, administration of CXCL10 protein defective in CXCR3 binding may represent a novel therapy for pulmonary fibrosis... - Severe lung fibrosis requires an invasive fibroblast phenotype regulated by hyaluronan and CD44Yuejuan Li
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA
J Exp Med 208:1459-71. 2011..Understanding the mechanisms leading to an invasive fibroblast phenotype could lead to novel approaches to the treatment of disorders characterized by severe tissue fibrosis... - Recruited exudative macrophages selectively produce CXCL10 after noninfectious lung injuryRobert M Tighe
Department of Medicine, Duke University Medical Center, Durham, NC, USA
Am J Respir Cell Mol Biol 45:781-8. 2011..Understanding the contribution of ExMacs to the pathobiology of lung injury and repair could lead to new treatment options for fibrosing lung diseases... - MicroRNA-127 inhibits lung inflammation by targeting IgG Fcγ receptor ITing Xie
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA
J Immunol 188:2437-44. 2012..Understanding how miRNAs regulate lung inflammation may represent an attractive way to control inflammation induced by infectious or noninfectious lung injury... - Comprehensive microRNA analysis in bleomycin-induced pulmonary fibrosis identifies multiple sites of molecular regulationTing Xie
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University School of Medicine, Durham, North Carolina 27710, USA
Physiol Genomics 43:479-87. 2011..The miRNAs and their potential target genes identified may contribute to the understanding of the complex transcriptional program of lung fibrosis... - CD44 is a negative regulator of acute pulmonary inflammation and lipopolysaccharide-TLR signaling in mouse macrophagesJiurong Liang
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA
J Immunol 178:2469-75. 2007..Collectively, these data suggest CD44 plays a previously unrecognized role in preventing exaggerated inflammatory responses to LPS by promoting the expression of negative regulators of TLR-4 signaling... - β-arrestin deficiency protects against pulmonary fibrosis in mice and prevents fibroblast invasion of extracellular matrixAlysia Kern Lovgren
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
Sci Transl Med 3:74ra23. 2011..These data implicate β-arrestins as mediators of fibroblast invasion and the development of pulmonary fibrosis, and as a potential target for therapeutic intervention in patients with idiopathic pulmonary fibrosis... - Ozone inhalation promotes CX3CR1-dependent maturation of resident lung macrophages that limit oxidative stress and inflammationRobert M Tighe
Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
J Immunol 187:4800-8. 2011..Our results identify a novel subset of lung macrophages, which are derived from a resident intermediate, are dependent upon CX3CR1, and appear to protect the host from the biological response to ozone... - The role of Toll-like receptors in non-infectious lung injuryDianhua Jiang
Department of Medicine, Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
Cell Res 16:693-701. 2006..These studies identify that host matrix component HA and TLR interactions provide signals that initiate inflammatory responses, maintain epithelial cell integrity, and promote recovery from acute lung injury... - Regulation of non-infectious lung injury, inflammation, and repair by the extracellular matrix glycosaminoglycan hyaluronanDianhua Jiang
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University School of Medicine, Durham, North Carolina, USA
Anat Rec (Hoboken) 293:982-5. 2010..Elucidating the protean roles of HA in tissue injury, inflammation, and repair will generate new insights into mechanisms of diseases characterized by chronic inflammation and tissue remodeling... - Cutting edge: TLR4 deficiency confers susceptibility to lethal oxidant lung injuryXuchen Zhang
Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
J Immunol 175:4834-8. 2005..Taken together, our results suggest a protective role of TLR4 in oxidant-mediated injury, providing novel mechanistic links among innate immunity, oxidant stress, and apoptosis... - Pulmonary fibrosis: patterns and perpetratorsPaul W Noble
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University School of Medicine, Durham, NC, USA
J Clin Invest 122:2756-62. 2012..Understanding the heterogeneity of these diseases and elucidating the final common pathways of fibrogenesis are critical for the development of efficacious therapies for severe fibrosing lung diseases... - Regulation of pulmonary fibrosis by chemokine receptor CXCR3Dianhua Jiang
Department of Medicine, Section of Pulmonary and Critical Care, Yale University School of Medicine, New Haven, Connecticut 06520 8057, USA
J Clin Invest 114:291-9. 2004..These data demonstrate a nonredundant role for CXCR3 in limiting tissue fibroproliferation and suggest that this effect may be mediated, in part, by the innate production of IFN-gamma following lung injury... - Bayesian probit regression model for the diagnosis of pulmonary fibrosis: proof-of-principleEric B Meltzer
Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina, USA
BMC Med Genomics 4:70. 2011..The accurate diagnosis of idiopathic pulmonary fibrosis (IPF) is a major clinical challenge. We developed a model to diagnose IPF by applying Bayesian probit regression (BPR) modelling to gene expression profiles of whole lung tissue... - Hyaluronan in tissue injury and repairDianhua Jiang
Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University School of Medicine, Durham, NC 27710, USA
Annu Rev Cell Dev Biol 23:435-61. 2007..Thus, the interactions between the endogenous matrix component hyaluronan and its signaling receptors initiate inflammatory responses, maintain structural cell integrity, and promote recovery from tissue injury... 
Effect of interferon gamma-1b on survival in patients with idiopathic pulmonary fibrosis (INSPIRE): a multicentre, randomised, placebo-controlled trialTalmadge E King
Department of Medicine, University of California San Francisco, San Francisco, CA 94143 0120, USA
Lancet 374:222-8. 2009..We assessed whether treatment with interferon gamma-1b improved survival compared with placebo in patients with idiopathic pulmonary fibrosis and mild-to-moderate impairment of pulmonary function...- Hyaluronan as an immune regulator in human diseasesDianhua Jiang
Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University School of Medicine, Durham, North Carolina 27710, USA
Physiol Rev 91:221-64. 2011..This review focuses on the role of hyaluronan as an immune regulator in human diseases... - Innate immune activation potentiates alloimmune lung disease independent of chemokine (C-X-C motif) receptor 3Tereza Martinu
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
J Heart Lung Transplant 30:717-25. 2011..We hypothesized that the chemokine (C-X-C motif) receptor 3 (CXCR3) receptor is necessary for the development of LPS-induced pulmonary GVHD... - Early growth response gene 1-mediated apoptosis is essential for transforming growth factor beta1-induced pulmonary fibrosisChun Geun Lee
Section of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar St, 441c TAC, New Haven, CT 06520, USA
J Exp Med 200:377-89. 2004..They also demonstrate that Egr-1-mediated apoptosis is a prerequisite for TGF-beta(1)-induced fibrosis and remodeling... - Idiopathic pulmonary fibrosis. New insights into classification and pathogenesis usher in a new era therapeutic approachesPaul W Noble
Yale University School of Medicine, Section of Pulmonary and Critical Care Medicine, New Haven, Connecticut, USA
Am J Respir Cell Mol Biol 29:S27-31. 2003 - Resolution of lung inflammation by CD44Priit Teder
Department of Medicine, Pulmonary and Critical Care Section, Yale University School of Medicine, New Haven, CT 06520, USA
Science 296:155-8. 2002..This phenotype was partially reversed by reconstitution with CD44+ cells, thus demonstrating a critical role for this receptor in resolving lung inflammation... - Small interfering RNA targeting heme oxygenase-1 enhances ischemia-reperfusion-induced lung apoptosisXuchen Zhang
Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8057, USA
J Biol Chem 279:10677-84. 2004.... - Take a deep breath: pulmonary research inspiresPaul W Noble
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA
J Clin Invest 122:2722-3. 2012..The articles of this Review Series highlight recent progress in understanding the pathophysiology of several pulmonary diseases and suggest how these insights are leading to the development of new therapeutic strategies... - Airway epithelial progenitors are region specific and show differential responses to bleomycin-induced lung injuryHuaiyong Chen
Division of Pulmonary, Allergy and Critical Care, Department of Medicine, Durham, North Carolina, USA
Stem Cells 30:1948-60. 2012..These data reveal intrinsic differences in the properties of regional progenitors and suggest that their unique responses to tissue damage drive local tissue remodeling... - Airway fibroblasts in asthma manifest an invasive phenotypeJennifer L Ingram
Department of Medicine, Duke University Medical Center, 201 MSRB 1, Research Drive, Box 2641, Durham, NC 27710, USA
Am J Respir Crit Care Med 183:1625-32. 2011..Cellular invasiveness is thought to be mediated by transforming growth factor (TGF)-β1 and matrix metalloproteinases (MMPs). IL-13 is a key T(H)2 cytokine that directs many features of airway remodeling through TGF-β1 and MMPs... - Multiple stromal populations contribute to pulmonary fibrosis without evidence for epithelial to mesenchymal transitionJason R Rock
Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA
Proc Natl Acad Sci U S A 108:E1475-83. 2011..Taken together, our results show a previously unappreciated heterogeneity of cell types proliferating in fibrotic lesions and exclude pericytes and two epithelial cell populations as the origin of myofibroblasts... - Analyses of efficacy end points in a controlled trial of interferon-gamma1b for idiopathic pulmonary fibrosisTalmadge E King
Department of Medicine, San Francisco General Hospital, University of California at San Francisco, San Francisco, CA 94110, USA
Chest 127:171-7. 2005..Idiopathic pulmonary fibrosis (IPF) is a devastating disease, yet validated, reliable criteria for evaluating patient response to therapies in clinical trials are lacking... - Patient experiences with pulmonary fibrosisHarold R Collard
Department of Medicine, San Francisco General Hospital, University of California San Francisco, 1001 Potrero Avenue, San Francisco, CA 94110, USA
Respir Med 101:1350-4. 2007..These results suggest there is a substantial need for improved patient education regarding the diagnosis and management of pulmonary fibrosis... - CD44 deficiency leads to enhanced neutrophil migration and lung injury in Escherichia coli pneumonia in miceQin Wang
Department of Pediatrics, Division of Integrative Biology, Rainbow Babies and Children s Hospital, 11100 Euclid Avenue, Cleveland, OH 44106, USA
Am J Pathol 161:2219-28. 2002..These data demonstrate that CD44 deficiency results in enhanced inflammation in E. coli but not S. pneumoniae-induced pneumonia, suggesting a previously unrecognized role for CD44 in limiting the inflammatory response to E. coli... - Extracellular superoxide dismutase inhibits inflammation by preventing oxidative fragmentation of hyaluronanFei Gao
Department of Pathology, University of Pittsburgh, Pittsburgh, PA 15260, USA
J Biol Chem 283:6058-66. 2008..These data indicate that inhibition of oxidative hyaluronan fragmentation probably represents one mechanism by which EC-SOD inhibits inflammation in response to lung injury... - Signaling properties of hyaluronan receptorsEva A Turley
London Regional Cancer Center, University of Western Ontario, London N6A 4L6, Canada
J Biol Chem 277:4589-92. 2002 - A placebo-controlled trial of interferon gamma-1b in patients with idiopathic pulmonary fibrosisGanesh Raghu
Division of Pulmonary Medicine, University of Washington, Seattle 98195, USA
N Engl J Med 350:125-33. 2004..Idiopathic pulmonary fibrosis is a progressive, fatal disease with no known efficacious therapy... - Time will tell: predicting survival in idiopathic interstitial pneumoniaPaul W Noble
Am J Respir Crit Care Med 168:510-1. 2003 - The clinical course of patients with idiopathic pulmonary fibrosisFernando J Martinez
University of Michigan, Ann Arbor, Michigan 48109, USA
Ann Intern Med 142:963-7. 2005..Prospective data defining the clinical course in idiopathic pulmonary fibrosis (IPF) are sparse... - Idiopathic pulmonary fibrosis and pulmonary hypertension: connecting the dotsSteven D Nathan
Medical Director, Advanced Lung Disease and Transplant Program, Inova Heart and Vascular Institute, Inova Fairfax Hospital, Falls Church, VA 22042, USA
Am J Respir Crit Care Med 175:875-80. 2007..Which agent(s) might be useful and when they should be implemented mandate the appropriate studies being performed. Some of the data presented in this article have previously been reported in abstract form only...