J W Hollingsworth

Summary

Affiliation: Duke University Medical Center
Country: USA

Publications

  1. 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
  2. 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
  3. 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
  4. 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
  5. pmc Ozone and pulmonary innate immunity
    John W Hollingsworth
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Box 3136, Durham, NC 27710, USA
    Proc Am Thorac Soc 4:240-6. 2007
  6. ncbi request reprint Successful treatment of Ochroconis gallopavum infection in an immunocompetent host
    J W Hollingsworth
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Box 3136, Durham, NC 27710, USA
    Infection 35:367-9. 2007
  7. 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
  8. 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
  9. 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
  10. 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

Detail Information

Publications26

  1. 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...
  2. 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...
  3. 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...
  4. 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...
  5. pmc Ozone and pulmonary innate immunity
    John W Hollingsworth
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Box 3136, Durham, NC 27710, USA
    Proc Am Thorac Soc 4:240-6. 2007
    ..The functional response to ambient O(3) seems to be dependent on many components of the innate immune signaling. In this article, we review the complex interaction between inhalation of O(3) and pulmonary innate immunity...
  6. ncbi request reprint Successful treatment of Ochroconis gallopavum infection in an immunocompetent host
    J W Hollingsworth
    Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Box 3136, Durham, NC 27710, USA
    Infection 35:367-9. 2007
    ..We report the first case of active O. gallopavum pulmonary infection in an immunocompetent host with rapid and complete response to oral antifungal therapy...
  7. 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...
  8. 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...
  9. 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...
  10. 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...
  11. 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...
  12. 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...
  13. pmc The extracellular matrix protein mindin regulates trafficking of murine eosinophils into the airspace
    Zhuowei Li
    Department of Immunology, Duke University Medical Center, Box 103004, Durham, NC 27710, USA
    J Leukoc Biol 85:124-31. 2009
    ..In conclusion, these data suggest that mindin participates in integrin-dependent trafficking of eosinophils and can contribute to the severity of allergic airways disease...
  14. ncbi request reprint Contraindications and safety of transbronchial lung biopsy via flexible bronchoscopy. A survey of pulmonologists and review of the literature
    Momen M Wahidi
    Departments of Internal Medicine, Division of Pulmonary Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Respiration 72:285-95. 2005
    ..Limited scientific data exist concerning the risk of this procedure in patients with conditions that may adversely affect the rate of procedural complications...
  15. 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...
  16. 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...
  17. pmc Differential regulation of the PGC family of genes in a mouse model of Staphylococcus aureus sepsis
    Timothy E Sweeney
    Department of Pathology, Duke University Medical Center, Durham, North Carolina, United States of America
    PLoS ONE 5:e11606. 2010
    ..Moreover, the identification of mir-202-3p as a potential factor for Ppargc1a and Ppargc1b repression in acute inflammation may open new avenues for mitochondrial research and, potentially, therapy...
  18. 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
    ....
  19. 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...
  20. pmc Nitric oxide synthase-2 induction optimizes cardiac mitochondrial biogenesis after endotoxemia
    Crystal M Reynolds
    Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA
    Free Radic Biol Med 46:564-72. 2009
    ..These findings demonstrate the decisive participation of NOS2 induction by TLR4 in optimization of mitochondrial biogenesis and MHC expression after gram-negative challenge...
  21. 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...
  22. 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...
  23. pmc c-Kit is essential for alveolar maintenance and protection from emphysema-like disease in mice
    James Y Lindsey
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA
    Am J Respir Crit Care Med 183:1644-52. 2011
    ..Increases in the percentage of cells expressing c-Kit have previously been associated with protection against injury-induced emphysema...
  24. 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...
  25. 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
    ....
  26. 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...