PAUL WESLEY NOBLE

Summary

Affiliation: Duke University Medical Center
Country: USA

Publications

  1. pmc Severe lung fibrosis requires an invasive fibroblast phenotype regulated by hyaluronan and CD44
    Yuejuan 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
  2. pmc Take a deep breath: pulmonary research inspires
    Paul 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
  3. pmc Pulmonary fibrosis: patterns and perpetrators
    Paul 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
  4. pmc Long-term exposure of chemokine CXCL10 causes bronchiolitis-like inflammation
    Dianhua Jiang
    Division of Pulmonary, Duke University School of Medicine, 106 Research Drive, Durham, NC 27710, USA
    Am J Respir Cell Mol Biol 46:592-8. 2012
  5. pmc A macrophage subpopulation recruited by CC chemokine ligand-2 clears apoptotic cells in noninfectious lung injury
    Jiurong 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
  6. pmc Idiopathic pulmonary fibrosis
    Eric 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
  7. doi request reprint Pirfenidone in patients with idiopathic pulmonary fibrosis (CAPACITY): two randomised trials
    Paul W Noble
    Duke University School of Medicine, Durham, NC 27710, USA
    Lancet 377:1760-9. 2011
  8. pmc Bayesian probit regression model for the diagnosis of pulmonary fibrosis: proof-of-principle
    Eric 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
  9. pmc Recruited exudative macrophages selectively produce CXCL10 after noninfectious lung injury
    Robert M Tighe
    Department of Medicine, Duke University Medical Center, Durham, NC, USA
    Am J Respir Cell Mol Biol 45:781-8. 2011

Collaborators

Detail Information

Publications9

  1. pmc Severe lung fibrosis requires an invasive fibroblast phenotype regulated by hyaluronan and CD44
    Yuejuan 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...
  2. pmc Take a deep breath: pulmonary research inspires
    Paul 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...
  3. pmc Pulmonary fibrosis: patterns and perpetrators
    Paul 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...
  4. pmc Long-term exposure of chemokine CXCL10 causes bronchiolitis-like inflammation
    Dianhua Jiang
    Division of Pulmonary, Duke University School of Medicine, 106 Research Drive, Durham, NC 27710, USA
    Am J Respir Cell Mol Biol 46:592-8. 2012
    ..The airway hyperplasia and T-cell inflammation were dependent on the presence of CXCR3. Therefore, long-term exposure of the chemokine CXCL10 in the lung causes bronchiolitis-like inflammation in mice...
  5. pmc A macrophage subpopulation recruited by CC chemokine ligand-2 clears apoptotic cells in noninfectious lung injury
    Jiurong 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...
  6. pmc Idiopathic pulmonary fibrosis
    Eric 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...
  7. doi request reprint Pirfenidone in patients with idiopathic pulmonary fibrosis (CAPACITY): two randomised trials
    Paul W Noble
    Duke University School of Medicine, Durham, NC 27710, USA
    Lancet 377:1760-9. 2011
    ....
  8. pmc Bayesian probit regression model for the diagnosis of pulmonary fibrosis: proof-of-principle
    Eric 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...
  9. pmc Recruited exudative macrophages selectively produce CXCL10 after noninfectious lung injury
    Robert 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...

Research Grants33

  1. Immune Mechanisms in Non-Infectious Lung Inflammation
    Paul Noble; Fiscal Year: 2004
    ..3. Define the mechanisms by which CD44 and the TLR signaling pathway mediate HA fragment-induced gene expression in vitro using CD44, MyD88, and TLR (1-5, 9)-deficient mice. ..
  2. Immune Mechanisms in Non-Infectious Lung Inflammation
    Paul Noble; Fiscal Year: 2003
    ..3. Define the mechanisms by which CD44 and the TLR signaling pathway mediate HA fragment-induced gene expression in vitro using CD44, MyD88, and TLR (1-5, 9)-deficient mice. ..
  3. INTERDISCIPLINARY TRAINING PROGRAM IN LUNG DISEASE
    Paul Noble; Fiscal Year: 2007
    ..The program is intended to optimally prepare trainees for academic research careers wherein they will be able to acquire and maintain independent funding in a highly competitive research environment. ..
  4. MECHANISMS OF MACROPHAGE ACTIVATION IN LUNG INFLAMMATION
    Paul Noble; Fiscal Year: 2005
    ..4) Characterize the role of Toll-like receptor 2 in mediating HA fragment-induced gene expression in vitro using TLR2 and MyD88-deficient mice. ..
  5. Immune Mechanisms in Non-Infectious Lung Inflammation
    Paul Noble; Fiscal Year: 2005
    ..3. Define the mechanisms by which CD44 and the TLR signaling pathway mediate HA fragment-induced gene expression in vitro using CD44, MyD88, and TLR (1-5, 9)-deficient mice. ..
  6. MECHANISMS OF MACROPHAGE ACTIVATION IN LUNG INFLAMMATION
    Paul Noble; Fiscal Year: 2006
    ..3. Determine the mechanisms by which CD44 negatively regulates macrophage activation and TLR signaling in vivo and in vitro. ..
  7. Survivin Regulation of Pulmonary Fibrosis
    Paul Noble; Fiscal Year: 2006
    ..2. Determine the role of survivin in vivo in the initiation and progression of experimental pulmonary fibrosis. 3. Determine the role of survivin in regulating the IPF fibroblast phenotype in vitro. ..
  8. Regulation of Pulmonary Fibrosis by CXCR3
    Paul Noble; Fiscal Year: 2007
    ..Identifying mechanisms of progressive fibrosis and failures in host defense could lead to new therapeutic options in patients with IPF. ..
  9. Regulation of Pulmonary Fibrosis by CXCR3
    Paul Noble; Fiscal Year: 2006
    ..Identifying mechanisms of progressive fibrosis and failures in host defense could lead to new therapeutic options in patients with IPF. ..
  10. Innate Immune Mechanisms in Non-infectious Lung Inflammation
    Paul Noble; Fiscal Year: 2009
    ..This grant proposal is to find to treatments for lung inflammation by understanding how injured lung tissue causes chronic lung inflammation. ..
  11. MECHANISMS OF MACROPHAGE ACTIVATION IN LUNG INFLAMMATION
    Paul Noble; Fiscal Year: 2009
    ..3. Determine the mechanisms by which CD44 negatively regulates macrophage activation and TLR signaling in vivo and in vitro. ..
  12. Innate Immune Mechanisms in Non-infectious Lung Inflammation
    PAUL WESLEY NOBLE; Fiscal Year: 2010
    ..This grant proposal is to find to treatments for lung inflammation by understanding how injured lung tissue causes chronic lung inflammation. ..
  13. MECHANISMS OF MACROPHAGE ACTIVATION IN LUNG INFLAMMATION
    PAUL WESLEY NOBLE; Fiscal Year: 2010
    ..3. Determine the mechanisms by which CD44 negatively regulates macrophage activation and TLR signaling in vivo and in vitro. ..
  14. Immune Mechanisms in Non-Infectious Lung Inflammation
    Paul Noble; Fiscal Year: 2006
    ..3. Define the mechanisms by which CD44 and the TLR signaling pathway mediate HA fragment-induced gene expression in vitro using CD44, MyD88, and TLR (1-5, 9)-deficient mice. ..
  15. Regulation of Pulmonary Fibrosis by CXCR3
    Paul Noble; Fiscal Year: 2006
    ..Identifying mechanisms of progressive fibrosis and failures in host defense could lead to new therapeutic options in patients with IPF. ..
  16. MECHANISMS OF MACROPHAGE ACTIVATION IN LUNG INFLAMMATION
    Paul Noble; Fiscal Year: 2002
    ..4) Characterize the role of Toll-like receptor 2 in mediating HA fragment-induced gene expression in vitro using TLR2 and MyD88-deficient mice. ..
  17. MECHANISMS OF MACROPHAGE ACTIVATION IN LUNG INFLAMMATION
    Paul Noble; Fiscal Year: 2003
    ..4) Characterize the role of Toll-like receptor 2 in mediating HA fragment-induced gene expression in vitro using TLR2 and MyD88-deficient mice. ..
  18. Survivin Regulation of Pulmonary Fibrosis
    Paul Noble; Fiscal Year: 2003
    ..2. Determine the role of survivin in vivo in the initiation and progression of experimental pulmonary fibrosis. 3. Determine the role of survivin in regulating the IPF fibroblast phenotype in vitro. ..
  19. MECHANISMS OF MACROPHAGE ACTIVATION IN LUNG INFLAMMATION
    Paul Noble; Fiscal Year: 2004
    ..4) Characterize the role of Toll-like receptor 2 in mediating HA fragment-induced gene expression in vitro using TLR2 and MyD88-deficient mice. ..
  20. Regulation of Pulmonary Fibrosis by CXCR3
    Paul Noble; Fiscal Year: 2005
    ..Identifying mechanisms of progressive fibrosis and failures in host defense could lead to new therapeutic options in patients with IPF. ..
  21. Survivin Regulation of Pulmonary Fibrosis
    Paul Noble; Fiscal Year: 2005
    ..2. Determine the role of survivin in vivo in the initiation and progression of experimental pulmonary fibrosis. 3. Determine the role of survivin in regulating the IPF fibroblast phenotype in vitro. ..
  22. Immune Mechanisms in Non-Infectious Lung Inflammation
    Paul Noble; Fiscal Year: 2002
    ..3. Define the mechanisms by which CD44 and the TLR signaling pathway mediate HA fragment-induced gene expression in vitro using CD44, MyD88, and TLR (1-5, 9)-deficient mice. ..
  23. MECHANISMS OF MACROPHAGE ACTIVATION IN LUNG INFLAMMATION
    Paul Noble; Fiscal Year: 2007
    ..3. Determine the mechanisms by which CD44 negatively regulates macrophage activation and TLR signaling in vivo and in vitro. ..
  24. Survivin Regulation of Pulmonary Fibrosis
    Paul Noble; Fiscal Year: 2004
    ..2. Determine the role of survivin in vivo in the initiation and progression of experimental pulmonary fibrosis. 3. Determine the role of survivin in regulating the IPF fibroblast phenotype in vitro. ..
  25. Regulation of Pulmonary Fibrosis by CXCR3
    PAUL WESLEY NOBLE; Fiscal Year: 2010
    ..Understanding the roles of the CXCL10/CXCR3 axis in the pathobiology of lung injury and repair could lead to new therapies for progressive pulmonary fibrosis. ..