David M Brass

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Using mouse genomics to understand idiopathic interstitial fibrosis
    David M Brass
    Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Proc Am Thorac Soc 4:92-100. 2007
  2. ncbi request reprint The IL-1 type 1 receptor is required for the development of LPS-induced airways disease
    David M Brass
    National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    J Allergy Clin Immunol 120:121-7. 2007
  3. ncbi request reprint CD14 is an essential mediator of LPS-induced airway disease
    David M Brass
    National Institute of Environmental Health Sciences, Rall Bldg, Rm C224, PO Box 12233 MD C2 15, 111 Alexander Dr, Research Triangle Park, NC 27709, USA
    Am J Physiol Lung Cell Mol Physiol 293:L77-83. 2007
  4. pmc Evaluating genome-wide DNA methylation changes in mice by Methylation Specific Digital Karyotyping
    Kathy Boon
    National Heart Lung and Blood Institute National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    BMC Genomics 9:598. 2008
  5. pmc Chronic LPS inhalation causes emphysema-like changes in mouse lung that are associated with apoptosis
    David M Brass
    Environmental Lung Diseases Research Group, Laboratory of Respiratory Biology, National Heart Lung and Blood Institute at the National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA
    Am J Respir Cell Mol Biol 39:584-90. 2008
  6. doi request reprint Host-environment interactions in exposure-related diffuse lung diseases
    David M Brass
    National Heart Lung and Blood Institute at the National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
    Semin Respir Crit Care Med 29:603-9. 2008
  7. ncbi request reprint LPS binding protein is important in the airway response to inhaled endotoxin
    David M Brass
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Durham, NC 27710 0001, USA
    J Allergy Clin Immunol 114:586-92. 2004
  8. pmc In utero supplementation with methyl donors enhances allergic airway disease in mice
    John W Hollingsworth
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Clin Invest 118:3462-9. 2008
  9. doi request reprint Fibroproliferation in LPS-induced airway remodeling and bleomycin-induced fibrosis share common patterns of gene expression
    David M Brass
    Department of Pediatrics Neonatology, Duke University Medical Center, 403 Alex R Sands Laboratory Building, DUMC 3373, Durham, NC 27710, USA
    Immunogenetics 60:353-69. 2008
  10. ncbi request reprint Neutrophils play a critical role in development of LPS-induced airway disease
    Jordan D Savov
    Pulmonary and Critical Care Division, Department of Medicine, Duke University Medical Center and Veterans Affairs Medical Center, Durham, North Carolina 27710, USA
    Am J Physiol Lung Cell Mol Physiol 283:L952-62. 2002

Detail Information

Publications20

  1. pmc Using mouse genomics to understand idiopathic interstitial fibrosis
    David M Brass
    Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Proc Am Thorac Soc 4:92-100. 2007
    ....
  2. ncbi request reprint The IL-1 type 1 receptor is required for the development of LPS-induced airways disease
    David M Brass
    National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    J Allergy Clin Immunol 120:121-7. 2007
    ..The contribution of IL-1beta signaling through the IL-1 type 1 receptor (IL-1R1) to the development of persistent LPS-induced airway disease has not been investigated...
  3. ncbi request reprint CD14 is an essential mediator of LPS-induced airway disease
    David M Brass
    National Institute of Environmental Health Sciences, Rall Bldg, Rm C224, PO Box 12233 MD C2 15, 111 Alexander Dr, Research Triangle Park, NC 27709, USA
    Am J Physiol Lung Cell Mol Physiol 293:L77-83. 2007
    ....
  4. pmc Evaluating genome-wide DNA methylation changes in mice by Methylation Specific Digital Karyotyping
    Kathy Boon
    National Heart Lung and Blood Institute National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    BMC Genomics 9:598. 2008
    ..The method generates 21 base pairs long sequence tags derived from specific locations in the genome. The resulting tag frequencies determine in a quantitative manner the methylation level of the corresponding loci...
  5. pmc Chronic LPS inhalation causes emphysema-like changes in mouse lung that are associated with apoptosis
    David M Brass
    Environmental Lung Diseases Research Group, Laboratory of Respiratory Biology, National Heart Lung and Blood Institute at the National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA
    Am J Respir Cell Mol Biol 39:584-90. 2008
    ....
  6. doi request reprint Host-environment interactions in exposure-related diffuse lung diseases
    David M Brass
    National Heart Lung and Blood Institute at the National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
    Semin Respir Crit Care Med 29:603-9. 2008
    ....
  7. ncbi request reprint LPS binding protein is important in the airway response to inhaled endotoxin
    David M Brass
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Durham, NC 27710 0001, USA
    J Allergy Clin Immunol 114:586-92. 2004
    ....
  8. pmc In utero supplementation with methyl donors enhances allergic airway disease in mice
    John W Hollingsworth
    Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Clin Invest 118:3462-9. 2008
    ..Our findings indicate that dietary factors can modify the heritable risk of allergic airway disease through epigenetic mechanisms during a vulnerable period of fetal development in mice...
  9. doi request reprint Fibroproliferation in LPS-induced airway remodeling and bleomycin-induced fibrosis share common patterns of gene expression
    David M Brass
    Department of Pediatrics Neonatology, Duke University Medical Center, 403 Alex R Sands Laboratory Building, DUMC 3373, Durham, NC 27710, USA
    Immunogenetics 60:353-69. 2008
    ..This analysis yielded a list of 212 genes in common suggesting that there is a common subset of genes that regulate fibroproliferation in the lung independent of etiologic agent and site of injury...
  10. ncbi request reprint Neutrophils play a critical role in development of LPS-induced airway disease
    Jordan D Savov
    Pulmonary and Critical Care Division, Department of Medicine, Duke University Medical Center and Veterans Affairs Medical Center, Durham, North Carolina 27710, USA
    Am J Physiol Lung Cell Mol Physiol 283:L952-62. 2002
    ..These studies demonstrate that neutrophils play a critical role in the development of chronic LPS-induced airway disease...
  11. ncbi request reprint Ambient ozone primes pulmonary innate immunity in mice
    John W Hollingsworth
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Box 3136, Durham, NC 27710, USA
    J Immunol 179:4367-75. 2007
    ..These observations indicate that ozone exposure increases both the pulmonary and the systemic biologic response to inhaled LPS by priming the innate immune system...
  12. ncbi request reprint Identifying fibrosis susceptibility genes in two strains of inbred mice
    Arnold R Brody
    Lung Biology Program, Tulane University Health Sciences Center, New Orleans, LA 70112 2699, USA
    Chest 121:31S. 2002
  13. pmc CD44 regulates macrophage recruitment to the lung in lipopolysaccharide-induced airway disease
    John W Hollingsworth
    Division of Pulmonary, Allergy, and Critical Care Medicine, DUMC 3136, Duke University Medical Center, Durham, NC 27710, USA
    Am J Respir Cell Mol Biol 37:248-53. 2007
    ..In addition, CD44-deficient animals had 150% fewer neutrophils at 24 h and 50% greater neutrophils 48 h after LPS exposure. These results support the role of CD44 in modulating the biologic response to inhaled LPS...
  14. ncbi request reprint Fibrinolysis in LPS-induced chronic airway disease
    Jordan D Savov
    Duke Univ Medical Center, P O Box 2629, Durham, NC 27710, USA
    Am J Physiol Lung Cell Mol Physiol 285:L940-8. 2003
    ..We conclude that an active fibrinolytic system can substantially alter the development and resolution of the postinflammatory airway remodeling observed after chronic LPS inhalation...
  15. ncbi request reprint The role of Toll-like receptor 4 in environmental airway injury in mice
    John W Hollingsworth
    Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Am J Respir Crit Care Med 170:126-32. 2004
    ..These data demonstrate in the mouse that the requirement of TLR4 for pulmonary inflammation depends on the nature of the toxin and appears specific to toxin and exposure conditions...
  16. pmc Leukocyte-derived IL-10 reduces subepithelial fibrosis associated with chronically inhaled endotoxin
    Stavros Garantziotis
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Box 3683, Durham, NC 27710, USA
    Am J Respir Cell Mol Biol 35:662-7. 2006
    ..The role of IL-10 on airway hyperreactivity is complex: IL-10 deficiency protects against LPS-induced hyperreactivity, and is associated with higher eNOS, iNOS, and airway nitrate levels...
  17. ncbi request reprint Toll-like receptor 4 antagonist (E5564) prevents the chronic airway response to inhaled lipopolysaccharide
    Jordan D Savov
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA
    Am J Physiol Lung Cell Mol Physiol 289:L329-37. 2005
    ....
  18. ncbi request reprint The critical role of hematopoietic cells in lipopolysaccharide-induced airway inflammation
    John W Hollingsworth
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Box 3221, Durham, NC 27710, USA
    Am J Respir Crit Care Med 171:806-13. 2005
    ..These data demonstrate the critical role of hematopoietic cells and alveolar macrophages in initiating LPS-induced neutrophil recruitment from the vascular space to the airspace...
  19. ncbi request reprint A matrix for new ideas in pulmonary fibrosis
    Donald N Cook
    Pulmonary and Critical Care Division, Department of Medicine, and the Department of Veterans Affairs Medical Center and Duke University Medical Center, Durham, North Carolina, USA
    Am J Respir Cell Mol Biol 27:122-4. 2002
  20. ncbi request reprint Intercellular adhesion molecule-1 plays a pivotal role in endotoxin-induced airway disease
    David M Brass
    Department of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Chest 123:416S. 2003