D A Schwartz

Summary

Affiliation: Duke University Medical Center
Country: USA

Publications

  1. ncbi request reprint The pathophysiology of asthma
    Lee Maddox
    Pulmonary and Critical Care Division, Duke University Medical Center, Research Drive, Durham, North Carolina 27710 e mail
    Annu Rev Med 53:477-98. 2002
  2. ncbi request reprint Environmental genomics: a key to understanding biology, pathophysiology and disease
    David A Schwartz
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Hum Mol Genet 13:R217-24. 2004
  3. ncbi request reprint TLR4 and LPS hyporesponsiveness in humans
    David A Schwartz
    Pulmonary and Critical Care Division, Department of Internal Medicine, Department of Genetics, Department of Veterans Affairs Medical Center, Duke University Medical Center, Durham, NC, USA
    Int J Hyg Environ Health 205:221-7. 2002
  4. ncbi request reprint Relevance of mutations in the TLR4 receptor in patients with gram-negative septic shock
    Eva Lorenz
    Pulmonary and Critical Care Medicine, Duke University Medical Center, Research Drive, Room 275 MSRB, DUMC Box 2629, Durham, NC 27710, USA
    Arch Intern Med 162:1028-32. 2002
  5. ncbi request reprint The genetics of innate immunity
    David A Schwartz
    Pulmonary and Critical Care Division, Department of Medicine, Department of Veterans Affairs Medical Center and Duke University Medical Center, Durham, NC 27710, USA
    Chest 121:62S-68S. 2002
  6. ncbi request reprint The role of TLR4 in endotoxin responsiveness in humans
    D A Schwartz
    Pulmonary and Critical Care Division, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Endotoxin Res 7:389-93. 2001
  7. ncbi request reprint Inhaled endotoxin, a risk for airway disease in some people
    D A Schwartz
    Pulmonary and Critical Care Division, Department of Medicine, Duke University Medical Center, Research Drive, Room 275 MSRB, DUMC Box 2629, Durham, NC 27710, USA
    Respir Physiol 128:47-55. 2001
  8. ncbi request reprint Inhibition of LPS-induced airway hyperresponsiveness and airway inflammation by LPS antagonists
    D A Schwartz
    Pulmonary, Critical Care, and Occupational Medicine Division, Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242, USA
    Am J Physiol Lung Cell Mol Physiol 280:L771-8. 2001
  9. ncbi request reprint Genes other than TLR4 are involved in the response to inhaled LPS
    E Lorenz
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    Am J Physiol Lung Cell Mol Physiol 281:L1106-14. 2001
  10. ncbi request reprint IL-10 reduces grain dust-induced airway inflammation and airway hyperreactivity
    T J Quinn
    Pulmonary, Critical Care, and Occupational Medicine Division, Department of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA
    J Appl Physiol 88:173-9. 2000

Detail Information

Publications94

  1. ncbi request reprint The pathophysiology of asthma
    Lee Maddox
    Pulmonary and Critical Care Division, Duke University Medical Center, Research Drive, Durham, North Carolina 27710 e mail
    Annu Rev Med 53:477-98. 2002
    ..The significance of Th-1 and Th-2 lymphocyte-mediated immunity are discussed, and the inflammatory processes leading to chronic airway inflammation are detailed...
  2. ncbi request reprint Environmental genomics: a key to understanding biology, pathophysiology and disease
    David A Schwartz
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Hum Mol Genet 13:R217-24. 2004
    ..Moreover, exploiting eukaryotic model systems (yeast, Caenorhabditis elegans, zebrafish, Drosophila and rodents) will accelerate our understanding of environmental exposures on human health...
  3. ncbi request reprint TLR4 and LPS hyporesponsiveness in humans
    David A Schwartz
    Pulmonary and Critical Care Division, Department of Internal Medicine, Department of Genetics, Department of Veterans Affairs Medical Center, Duke University Medical Center, Durham, NC, USA
    Int J Hyg Environ Health 205:221-7. 2002
    ....
  4. ncbi request reprint Relevance of mutations in the TLR4 receptor in patients with gram-negative septic shock
    Eva Lorenz
    Pulmonary and Critical Care Medicine, Duke University Medical Center, Research Drive, Room 275 MSRB, DUMC Box 2629, Durham, NC 27710, USA
    Arch Intern Med 162:1028-32. 2002
    ..We recently identified a common polymorphism in toll-like receptor 4 (TLR4) that is associated with hyporesponsiveness to inhaled endotoxin or lipopolysaccharide in humans...
  5. ncbi request reprint The genetics of innate immunity
    David A Schwartz
    Pulmonary and Critical Care Division, Department of Medicine, Department of Veterans Affairs Medical Center and Duke University Medical Center, Durham, NC 27710, USA
    Chest 121:62S-68S. 2002
    ....
  6. ncbi request reprint The role of TLR4 in endotoxin responsiveness in humans
    D A Schwartz
    Pulmonary and Critical Care Division, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Endotoxin Res 7:389-93. 2001
    ....
  7. ncbi request reprint Inhaled endotoxin, a risk for airway disease in some people
    D A Schwartz
    Pulmonary and Critical Care Division, Department of Medicine, Duke University Medical Center, Research Drive, Room 275 MSRB, DUMC Box 2629, Durham, NC 27710, USA
    Respir Physiol 128:47-55. 2001
    ....
  8. ncbi request reprint Inhibition of LPS-induced airway hyperresponsiveness and airway inflammation by LPS antagonists
    D A Schwartz
    Pulmonary, Critical Care, and Occupational Medicine Division, Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242, USA
    Am J Physiol Lung Cell Mol Physiol 280:L771-8. 2001
    ..These results suggest that LPS antagonists may be an effective and potentially safe treatment for endotoxin-induced airway disease...
  9. ncbi request reprint Genes other than TLR4 are involved in the response to inhaled LPS
    E Lorenz
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    Am J Physiol Lung Cell Mol Physiol 281:L1106-14. 2001
    ....
  10. ncbi request reprint IL-10 reduces grain dust-induced airway inflammation and airway hyperreactivity
    T J Quinn
    Pulmonary, Critical Care, and Occupational Medicine Division, Department of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA
    J Appl Physiol 88:173-9. 2000
    ..05). These findings indicate that exogenous IL-10 is effective in reducing airway inflammation and airway hyperreactivity due to the inhalation of CDE...
  11. ncbi request reprint TLR4 mutations are associated with endotoxin hyporesponsiveness in humans
    N C Arbour
    1 Department of Medicine, Department of Veterans Affairs Medical Center, The University of Iowa, Iowa City, Iowa, USA
    Nat Genet 25:187-91. 2000
    ....
  12. ncbi request reprint Alloimmune lung injury induced by local innate immune activation through inhaled lipopolysaccharide
    Stavros Garantziotis
    Department of Medicine, Duke University Medical Center, Durham, NC 27709, USA
    Transplantation 84:1012-9. 2007
    ..We have developed and pursued the hypothesis that local activation of pulmonary innate immunity through toll-like receptor (TLR)-4 is critical to the development of posttransplant alloimmune lung injury...
  13. ncbi request reprint Variable airway responsiveness to inhaled lipopolysaccharide
    J N Kline
    Departments of Medicine, Pediatrics, and Preventive Medicine, University of Iowa College of Medicine, Department of Veterans Affairs Medical Center, Iowa City, Iowa, USA
    Am J Respir Crit Care Med 160:297-303. 1999
    ..These findings demonstrate that an LPS phenotype can be reproducibly elicited in humans, which creates an opportunity to identify genes involved in this response to inhaled LPS...
  14. pmc Beta-arrestin-2 regulates the development of allergic asthma
    Julia K L Walker
    Department of Medicine, Duke University Medical Center, Box 3821, Durham, North Carolina 27710, USA
    J Clin Invest 112:566-74. 2003
    ..Because beta-arrestin-2 regulates the development of allergic inflammation at a proximal step in the inflammatory cascade, novel therapies focused on this protein may prove useful in the treatment of asthma...
  15. ncbi request reprint Finding fibrosis genes: the lung
    Lauranell H Burch
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Durham, NC, USA
    Methods Mol Med 117:293-313. 2005
    ..Testing of candidate genes and standards for formal proof of gene discovery are discussed...
  16. pmc Both hematopoietic-derived and non-hematopoietic-derived {beta}-arrestin-2 regulates murine allergic airway disease
    John W Hollingsworth
    Duke University Medical Center, Durham, NC 27710, USA
    Am J Respir Cell Mol Biol 43:269-75. 2010
    ..Our data demonstrate that the expression of beta-arrestin-2 in at least two divergent cell types contributes to the pathogenesis of allergic airway disease...
  17. ncbi request reprint Endotoxin responsiveness and subchronic grain dust-induced airway disease
    C L George
    Division of Pediatric Critical Care, Department of Pediatrics, College of Public Health, University of Iowa, Iowa City, Iowa 52242, USA
    Am J Physiol Lung Cell Mol Physiol 280:L203-13. 2001
    ....
  18. ncbi request reprint Bronchial hyperreactivity is associated with enhanced grain dust-induced airflow obstruction
    J N Kline
    Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa 52242, USA
    J Appl Physiol 89:1172-8. 2000
    ..These results suggest that, although subjects with BHR develop a more precipitous decline in FEV(1) after exposure to CDE, the inflammatory response to CDE is similar in subjects with and without BHR...
  19. pmc CpG motifs in bacterial DNA cause inflammation in the lower respiratory tract
    D A Schwartz
    Pulmonary, Critical Care, and Occupational Medicine Division, The University of Iowa, Iowa City, Iowa 52242, USA
    J Clin Invest 100:68-73. 1997
    ..These findings suggest that bacterial DNA, and unmethylated CpG motifs in particular, may play an important pathogenic role in inflammatory lung disease...
  20. pmc Protection from experimental asthma by an endogenous bronchodilator
    Loretta G Que
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Science 308:1618-21. 2005
    ..Our results indicate that endogenous SNOs, governed by GSNOR, are critical regulators of airway responsivity and may provide new therapeutic approaches to asthma...
  21. pmc TLR4 is necessary for hyaluronan-mediated airway hyperresponsiveness after ozone inhalation
    Stavros Garantziotis
    National Institute of Environmental Health Sciences, Research Triangle Park, Durham, North Carolina, USA
    Am J Respir Crit Care Med 181:666-75. 2010
    ..However, the relation between TLR4 and hyaluronan in the airway response to ozone remains unexplored...
  22. pmc Spontaneous mutations in recombinant inbred mice: mutant toll-like receptor 4 (Tlr4) in BXD29 mice
    Donald N Cook
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    Genetics 172:1751-5. 2006
    ..Our results also suggest that the frequency of such unidentified, spontaneously occurring mutations is an issue that should be considered when RI strains are used to identify QTL...
  23. pmc A novel polymorphism in the toll-like receptor 2 gene and its potential association with staphylococcal infection
    E Lorenz
    Department of Medicine, The University of Iowa, Iowa City, USA
    Infect Immun 68:6398-401. 2000
    ..More importantly, both of the subjects with the TLR2 Arg753Gln polymorphism had staphylococcal infections. These findings suggest that a mutation in the TLR2 gene may predispose individuals to life-threatening bacterial infections...
  24. pmc Toll-like receptor 4 (TLR4)-deficient murine macrophage cell line as an in vitro assay system to show TLR4-independent signaling of Bacteroides fragilis lipopolysaccharide
    Eva Lorenz
    Department of Internal Medicine, Section of Infectious Diseases, Wake Forest University Medical Center, Winston Salem, NC, USA
    Infect Immun 70:4892-6. 2002
    ..This gives rise to the notion that LPS from some bacterial species will utilize alternative receptors to stimulate the innate immune response...
  25. ncbi request reprint Altered surfactant protein A gene expression and protein metabolism associated with repeat exposure to inhaled endotoxin
    Caroline L S George
    Department of Pediatrics, Division of Pediatric Critical Care, University of Iowa, Iowa City, IA 52242, USA
    Am J Physiol Lung Cell Mol Physiol 285:L1337-44. 2003
    ..Furthermore, these alterations in SP-A gene activity and protein metabolism are dependent on an intact endotoxin signaling system...
  26. ncbi request reprint Subchronic endotoxin inhalation causes persistent airway disease
    D M Brass
    Pulmonary and Critical Care Medicine, Duke Univ Medical Center, Research Dr, Rm 277 MSRB, DUMC Box 2629, Durham, NC 27710 0001, USA
    Am J Physiol Lung Cell Mol Physiol 285:L755-61. 2003
    ..Our findings demonstrate that subchronic inhalation of LPS results in the development of persistent airway disease in endotoxin-responsive mice...
  27. ncbi request reprint TNF-alpha and IL-1 beta are not essential to the inflammatory response in LPS-induced airway disease
    J G Moreland
    Department of Pediatrics, The University of Iowa, Iowa City, Iowa 52242, USA
    Am J Physiol Lung Cell Mol Physiol 280:L173-80. 2001
    ..These results indicate that TNF-alpha and IL-1 beta do not appear to have an essential role in mediating the physiological or inflammatory response to inhaled LPS...
  28. ncbi request reprint Association of TLR4 mutations and the risk for acute GVHD after HLA-matched-sibling hematopoietic stem cell transplantation
    E Lorenz
    Department of Medicine, Duke University, Durham, North Carolina, USA
    Biol Blood Marrow Transplant 7:384-7. 2001
    ..A much larger study population would be needed to confirm the role of LPS in the pathogenesis of GVHD in humans...
  29. ncbi request reprint Toll-like receptor 4 mediates mitochondrial DNA damage and biogenic responses after heat-inactivated E. coli
    Hagir B Suliman
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    FASEB J 19:1531-3. 2005
    ..These data disclose the dual role of TLR4 in mtDNA damage and compensatory mitochondrial biogenic responses after innate immune activation...
  30. 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
    ....
  31. ncbi request reprint Association between the Asp299Gly polymorphisms in the Toll-like receptor 4 and premature births in the Finnish population
    Eva Lorenz
    Department of Internal Medicine, Section of Infectious Diseases, Wake Forest University School of Medicine, Winston Salem, North Carolina 27157, USA
    Pediatr Res 52:373-6. 2002
    ..024, p = 0.028, respectively) or in premature multiples (p = 0.036, p = 0.044, respectively). According to the present results an allelic variation in the TLR4 receptor was associated with increased risk of premature birth...
  32. pmc Etiology and pathogenesis of airway disease in children and adults from rural communities
    D A Schwartz
    Veterans Administration Medical Center, Iowa City, IA 52242, USA
    Environ Health Perspect 107:393-401. 1999
    ..These unique problems must be considered in developing interventions that effectively reduce the morbidity and mortality of asthma in children from rural communities...
  33. ncbi request reprint Genetic regulation of rejection and survival following human lung transplantation by the innate immune receptor CD14
    S M Palmer
    Departments of Medicine, University of Arizona, Tucson, AZ, USA
    Am J Transplant 7:693-9. 2007
    ..Inhibition of innate immune activation through CD14 represents a novel and potentially important therapeutic target to prevent post-transplant rejection and improve outcomes after human lung transplantation...
  34. ncbi request reprint The role of innate immunity in acute allograft rejection after lung transplantation
    Scott M Palmer
    Department of Medicine, Duke University Medical Center, Durham, NC, USA
    Am J Respir Crit Care Med 168:628-32. 2003
    ..Therapies directed at inhibition of innate immune responses mediated by TLR4 may represent a novel and effective means to prevent acute rejection after lung transplantation...
  35. pmc Multistrain genetic comparisons reveal CCR5 as a receptor involved in airway hyperresponsiveness
    Julia K L Walker
    Department of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    Am J Respir Cell Mol Biol 34:711-8. 2006
    ..In addition, gene expression profiling data have revealed other potential novel targets for therapeutics-based research and has enhanced the understanding of the molecular mechanisms underlying the etiology of "asthma."..
  36. pmc Identification of novel genes that mediate innate immunity using inbred mice
    Ivana V Yang
    Department of Medicine, National Jewish Health, Denver, Colorado 80206, USA
    Genetics 183:1535-44. 2009
    ..These genes could represent potential sepsis biomarkers or therapeutic targets that should be further investigated in human populations...
  37. ncbi request reprint Polymorphisms of the Toll-like receptors and human disease
    David A Schwartz
    Department of Medicine, Duke University Medical Center, The Durham Veterans Affairs Medical Center, Durham, North Carolina, USA
    Clin Infect Dis 41:S403-7. 2005
    ..These findings have resulted in new opportunities to study the pathogenesis of disease, identify subpopulations at greater risk of disease, and, potentially, identify novel therapeutic approaches...
  38. ncbi request reprint Innate immunity and the lung: defense at the interface between host and environment
    Aimee K Zaas
    Division of Infectious Diseases and International Health, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA
    Trends Cardiovasc Med 15:195-202. 2005
    ..This article will discuss the key cellular and secreted components of the pulmonary innate immune system...
  39. 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...
  40. pmc Clinical and pathologic features of familial interstitial pneumonia
    Mark P Steele
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
    Am J Respir Crit Care Med 172:1146-52. 2005
    ..Several lines of evidence suggest that genetic factors and environmental exposures play a role in the development of pulmonary fibrosis...
  41. ncbi request reprint The effect of toll-like receptors and toll-like receptor genetics in human disease
    Stavros Garantziotis
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    Annu Rev Med 59:343-59. 2008
    ..The genetics of TLRs provides important insights in gene-environment interactions in health and disease, and it may enable scientists to assess patients' susceptibility to diseases or predict their response to treatments...
  42. pmc Fine ambient particles induce oxidative stress and metal binding genes in human alveolar macrophages
    Yuh Chin T Huang
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27705, USA
    Am J Respir Cell Mol Biol 41:544-52. 2009
    ..5) induced a gene expression profile prevalent with genes related to metal binding and oxidative stress in human AMs, independent of oxidative stress. Metals associated with PM may play an important role in particle-induced gene changes...
  43. ncbi request reprint Donor polymorphisms in Toll-like receptor-4 influence the development of rejection after renal transplantation
    Scott M Palmer
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Clin Transplant 20:30-6. 2006
    ..In the present investigation, we sought to evaluate the role of innate immune activation through TLR4, in either donor or recipient, upon the development of renal allograft rejection...
  44. 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...
  45. pmc Nitric oxide mediates relative airway hyporesponsiveness to lipopolysaccharide in surfactant protein A-deficient mice
    Amy M Pastva
    Duke University Medical Center, Durham, NC 27710, USA
    Am J Respir Cell Mol Biol 44:175-84. 2011
    ..These findings may have clinical significance, because recent studies reported associations between surfactant protein polymorphisms and a variety of lung diseases...
  46. ncbi request reprint Cytokine gene polymorphisms are not associated with bronchiolitis obliterans syndrome or survival after lung transplant
    Laurie D Snyder
    Division of Pulmonary, Allergy and Critical Care, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Heart Lung Transplant 25:1330-5. 2006
    ..Cytokine polymorphisms are inconsistently associated with transplant rejection and other adverse outcomes. To address this controversy, we evaluated cytokine single nucleotide polymorphisms (SNPs) in a lung transplant cohort...
  47. 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...
  48. pmc A micro-computed tomography-based method for the measurement of pulmonary compliance in healthy and bleomycin-exposed mice
    Scott Shofer
    Pulmonary, Allergy, and Critical Care, Duke University Medical Center, Durham, North Carolina 27710, USA
    Exp Lung Res 33:169-83. 2007
    ..MicroCT pulmonary compliance measurements are suitable for longitudinal measurements, and correlate with physiologic measurements of pulmonary compliance...
  49. ncbi request reprint Genetic basis of murine antibacterial defense to streptococcal lung infection
    John W Hollingsworth
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, P O Box 3136, Durham, NC 27710, USA
    Immunogenetics 59:713-24. 2007
    ..These results demonstrate that innate differences in pulmonary host defense to S. zooepidemicus are dependent on host genetic factors...
  50. 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...
  51. ncbi request reprint Inter-alpha-trypsin inhibitor attenuates complement activation and complement-induced lung injury
    Stavros Garantziotis
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    J Immunol 179:4187-92. 2007
    ..This novel function of IaI provides a mechanistic explanation for its observed salutary effects in sepsis and opens new possibilities for its use as a treatment agent in inflammatory diseases...
  52. ncbi request reprint Safety of incremental inhaled lipopolysaccharide challenge in humans
    John S Sundy
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Endotoxin Res 12:113-9. 2006
    ..Inhaled airway challenge using lipopolysaccharide in humans has been performed for over 20 years to assess the airway response to endotoxin. However, there are no published data on the short-term safety of endotoxin inhalation protocols...
  53. 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
  54. 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
    ....
  55. ncbi request reprint Pitch is determined by naturally occurring periodic sounds
    David A Schwartz
    Center for Cognitive Neuroscience and Department of Neurobiology, Duke University, Box 90999, Durham, NC 27708 0999, USA
    Hear Res 194:31-46. 2004
    ..We conclude from these findings that pitch entails an auditory process that relates inevitably ambiguous sound stimuli to their probable natural sources...
  56. ncbi request reprint Genetic regulation of endotoxin-induced airway disease
    Donald N Cook
    Department of Medicine, Duke University Medical Center, P O Box 2629, and the Durham VAMC, Durham, NC 27710, USA
    Genomics 83:961-9. 2004
    ..Functional studies of these genes are expected to reveal important molecular mechanisms regulating the magnitude of biologic responses to LPS...
  57. 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...
  58. ncbi request reprint Ozone-induced acute pulmonary injury in inbred mouse strains
    Jordan D Savov
    Department of Medicine, Duke University Medical Center and VA Medical Center, Durham, NC 27710, USA
    Am J Respir Cell Mol Biol 31:69-77. 2004
    ..In aggregate, our approach has identified O3-resistant (C3H/HeJ and A/J) and -vulnerable (C57BL/6J and 129/SvIm) strains of mice, and determined novel genomic loci, suggesting a clear genetic basis for the lung response to inhaled O3...
  59. 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...
  60. ncbi request reprint Allergen-induced airway disease is mouse strain dependent
    Gregory S Whitehead
    Pulmonary and Critical Care Medicine, Duke University Medical Center, Research Drive, Rm 275 MSRB, DUMC Box 2629, Durham, NC 27710 0001, USA
    Am J Physiol Lung Cell Mol Physiol 285:L32-42. 2003
    ....
  61. ncbi request reprint The genetics of innate immunity in the lung
    Donald N Cook
    Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Chest 123:369S. 2003
  62. 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...
  63. pmc Pulmonary fibrosis: thinking outside of the lung
    Stavros Garantziotis
    Department of Medicine at Duke University Medical Center, Durham, North Carolina 27710, USA
    J Clin Invest 114:319-21. 2004
    ..Previous mechanistic research has focused on the local fibroproliferative process in the lung. However, emerging evidence suggests that circulating cells of hematopoietic origin play a crucial role in the pathogenesis of this disease...
  64. 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
    ....
  65. 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...
  66. ncbi request reprint Endotoxin and the lung: Insight into the host-environment interaction
    Jaspal Singh
    Duke University Medical Center, Durham, NC 27710, USA
    J Allergy Clin Immunol 115:330-3. 2005
    ..In this review, we provide a brief overview on the role of endotoxin in asthma and COPD, highlighting a few of the major discoveries, but also discussing future directions...
  67. ncbi request reprint Innate immunity influences long-term outcomes after human lung transplant
    Scott M Palmer
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Am J Respir Crit Care Med 171:780-5. 2005
    ....
  68. 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...
  69. 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
    ....
  70. ncbi request reprint Toll-like receptors in the pathogenesis of human disease
    Donald N Cook
    Department of Medicine, Duke University Medical Center, and the Durham Veterans Administration Medical Center, Durham, North Carolina 27710, USA
    Nat Immunol 5:975-9. 2004
    ..As this body of data grows, it will provide new insights into disease pathogenesis as well as valuable information on the merits of various therapeutic options...
  71. ncbi request reprint The acute respiratory distress syndrome
    Claude A Piantadosi
    Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    Ann Intern Med 141:460-70. 2004
  72. pmc Plasminogen alleles influence susceptibility to invasive aspergillosis
    Aimee K Zaas
    Duke University Medical Center, Durham, North Carolina, United States of America
    PLoS Genet 4:e1000101. 2008
    ..Furthermore, we demonstrated that plasminogen directly binds to Aspergillus fumigatus. We propose that genetic variation within the plasminogen pathway influences the pathogenesis of this invasive fungal infection...
  73. ncbi request reprint TLR4 signaling attenuates ongoing allergic inflammation
    John W Hollingsworth
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Durham, NC 27710, USA
    J Immunol 176:5856-62. 2006
    ..Together, these findings show that low doses of endotoxin can have regulatory effects on allergic inflammation, particularly in the setting of ongoing allergen exposure...
  74. pmc Identification of innate immunity genes and pathways using a comparative genomics approach
    Scott Alper
    Laboratory of Environmental Lung Disease, National Heart Lung and Blood Institute, National Institutes of Health, 111 TW Alexander Drive, Durham, NC 27709, USA
    Proc Natl Acad Sci U S A 105:7016-21. 2008
    ..These genes may prove critical to understanding host defense and represent potential therapeutic targets for infectious and immunological diseases...
  75. ncbi request reprint Loss-of-function mutation in tryptophan hydroxylase-2 identified in unipolar major depression
    Xiaodong Zhang
    Department of Cell Biology, Center for Models of Human Disease, Institute for Genome Sciences and Policy, Duke University Medical Center, Durham, NC 27710, USA
    Neuron 45:11-6. 2005
    ..Identification of a loss-of-function mutation in hTPH2 suggests that defect in brain serotonin synthesis may represent an important risk factor for unipolar major depression...
  76. pmc Exposures to the Kuwait oil fires and their association with asthma and bronchitis among gulf war veterans
    Jeffrey L Lange
    Department of Occupational and Environmental Health, College of Public Health, College of Medicine, University of Iowa, Iowa City, Iowa, USA
    Environ Health Perspect 110:1141-6. 2002
    ..In contrast, there was no association between the modeled exposure and any of the outcomes. These findings do not support speculation that exposures to oil-fire smoke caused respiratory symptoms among veterans...
  77. ncbi request reprint Toll-like receptors and the genetics of innate immunity
    Donald N Cook
    Department of Medicine, Duke University Medical Center, Durham Veteran s Administration Medical Center VAMC, Durham, North Carolina 27710, USA
    Curr Opin Allergy Clin Immunol 3:523-9. 2003
    ..This review summarizes recent work in which genetic approaches have been used to identify novel and important facets of Toll-like receptor function...
  78. ncbi request reprint Complement levels and activity in the normal and LPS-injured lung
    Molly S Bolger
    Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA
    Am J Physiol Lung Cell Mol Physiol 292:L748-59. 2007
    ....
  79. ncbi request reprint Utility of a lung biopsy for the diagnosis of idiopathic pulmonary fibrosis
    G W Hunninghake
    Department of Medicine, University of Iowa and Veterans Affairs Medical Center, Iowa City, IA 52242, USA
    Am J Respir Crit Care Med 164:193-6. 2001
    ..Lung biopsy is most helpful when clinical and radiologic data result in an uncertain diagnosis or when patients are thought not to have IPF...
  80. ncbi request reprint Cryptosporidium, enterocytozoon, and cyclospora infections in pediatric and adult patients with diarrhea in Tanzania
    J P Cegielski
    Duke University Medical Center, Durham, North Carolina, USA
    Clin Infect Dis 28:314-21. 1999
    ..Cryptosporidium and Enterocytozoon were associated with malnutrition. Asymptomatic fecal shedding of Enterocytozoon in otherwise healthy, HIV children has not been described previously...
  81. ncbi request reprint Relative release of interleukin-1 beta and interleukin-1 receptor antagonist by alveolar macrophages. A study in asbestos-induced lung disease, sarcoidosis, and idiopathic pulmonary fibrosis
    J N Kline
    Department of Internal Medicine, Veteran s Affairs Medical Center, Iowa City
    Chest 104:47-53. 1993
    ..Current smoking was associated with lower IL-1 beta and IL-1ra release in ILD. The IL-1AI is a convenient method for comparison of IL-1 beta activity between patient populations...
  82. ncbi request reprint Exclusion of Ifa and Ifb as the Lps gene and mapping of three markers near the Lps locus
    S Peiffer-Schneider
    Department of Internal Medicine, College of Medicine, University of Iowa, Iowa City 52242, USA
    Mamm Genome 8:785-6. 1997
  83. ncbi request reprint Toll-like receptor 4 polymorphisms and atherogenesis
    Stefan Kiechl
    Department of Neurology, University Clinic, Innsbruck, Austria
    N Engl J Med 347:185-92. 2002
    ..We determined whether recently discovered genetic variants of toll-like receptor 4 (TLR4) that confer differences in the inflammatory response elicited by bacterial lipopolysaccharide are related to the development of atherosclerosis...
  84. doi request reprint Translating the genome
    David A Schwartz
    Am J Respir Crit Care Med 178:662-3. 2008
  85. ncbi request reprint CD11b and intercellular adhesion molecule-1 are involved in pulmonary neutrophil recruitment in lipopolysaccharide-induced airway disease
    Jessica G Moreland
    Division of Critical Care, Department of Pediatrics, University of Iowa, Iowa City 52242, USA
    Am J Respir Cell Mol Biol 27:474-80. 2002
    ..These findings suggest that CD11b and ICAM-1 are important mediators of LPS-induced airway inflammation, but do not appear to be critical to the development of LPS-induced airway hyperreactivity...
  86. ncbi request reprint Susceptibility to asbestos-induced and transforming growth factor-beta1-induced fibroproliferative lung disease in two strains of mice
    G Sakuntala Warshamana
    Lung Biology Program, Department of Pathology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112 2699, USA
    Am J Respir Cell Mol Biol 27:705-13. 2002
    ..These findings suggest that certain sequences in a gene or a cluster of genes in the 129 mouse strain impart a phenotype in which there is a delay in, or protection from, the development of lung fibrogenesis...
  87. 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
    ....
  88. ncbi request reprint From quantitative trait locus to gene: a work in progress
    Steven R Kleeberger
    Am J Respir Crit Care Med 171:804-5. 2005
  89. ncbi request reprint Calcaneal ultrasound bone densitometry is not a useful tool to screen patients with inflammatory bowel disease at high risk for metabolic bone disease
    David A Schwartz
    Inflammatory Bowel Disease Center, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
    Inflamm Bowel Dis 11:749-54. 2005
    ..This would reduce the number of patients undergoing DXA testing unnecessarily. We tried to determine if calcaneal ultrasound bone densitometry is a useful tool in screening high-risk patients with IBD for metabolic bone disease...
  90. ncbi request reprint The transcriptional response to lipopolysaccharide reveals a role for interferon-gamma in lung neutrophil recruitment
    Lauranell H Burch
    National Institute of Environmental Health Sciences, Division of Pulmonary, Allergy, and Critical Care Medicine, Research Triangle Park, NC 27709, USA
    Am J Physiol Lung Cell Mol Physiol 291:L677-82. 2006
    ....
  91. pmc Gene expression profiling of familial and sporadic interstitial pneumonia
    Ivana V Yang
    Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, P O Box 12233, MD B3 08, Research Triangle Park, NC 27909, USA
    Am J Respir Crit Care Med 175:45-54. 2007
    ..Both the genetics and the histologic type of IIP play a role in the etiology and pathogenesis of interstitial lung disease, but transcriptional signatures of these subtypes are unknown...
  92. pmc Genetic basis of murine responses to hyperoxia-induced lung injury
    Gregory S Whitehead
    National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Immunogenetics 58:793-804. 2006
    ..These data suggest that the response to O2 depends, in part, on the genetic background and that some of the strains analyzed can be used to identify specific loci and genes underlying the response to O2...
  93. 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...
  94. 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
    ....