Stavros Garantziotis

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. 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
  2. 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
  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 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
  5. pmc Sulfite-mediated oxidation of myeloperoxidase to a free radical: immuno-spin trapping detection in human neutrophils
    Kalina Ranguelova
    Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Free Radic Biol Med 60:98-106. 2013
  6. pmc The role of the extracellular matrix protein mindin in airway response to environmental airways injury
    Sarah Frush
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University, Durham, North Carolina, USA
    Environ Health Perspect 119:1403-8. 2011
  7. 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
  8. 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
  9. 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
  10. pmc Serum inter-alpha-trypsin inhibitor and matrix hyaluronan promote angiogenesis in fibrotic lung injury
    Stavros Garantziotis
    Clinical Research Unit, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Am J Respir Crit Care Med 178:939-47. 2008

Detail Information

Publications27

  1. 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...
  2. 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...
  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 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
    ....
  5. pmc Sulfite-mediated oxidation of myeloperoxidase to a free radical: immuno-spin trapping detection in human neutrophils
    Kalina Ranguelova
    Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Free Radic Biol Med 60:98-106. 2013
    ..Our present study demonstrates that myeloperoxidase initiates (bi)sulfite oxidation leading to MPO radical damage, possibly leading to (bi)sulfite-exacerbated allergic reactions...
  6. pmc The role of the extracellular matrix protein mindin in airway response to environmental airways injury
    Sarah Frush
    Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University, Durham, North Carolina, USA
    Environ Health Perspect 119:1403-8. 2011
    ..Our previous work demonstrated that the extracellular matrix protein mindin contributes to allergic airways disease. However, the role of mindin in nonallergic airways disease has not previously been explored...
  7. 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...
  8. 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...
  9. 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...
  10. pmc Serum inter-alpha-trypsin inhibitor and matrix hyaluronan promote angiogenesis in fibrotic lung injury
    Stavros Garantziotis
    Clinical Research Unit, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Am J Respir Crit Care Med 178:939-47. 2008
    ..Inter-alpha-trypsin inhibitor (IaI) is a serum protein that can bind to hyaluronan (HA) and may contribute to the angiogenic response to tissue injury...
  11. 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...
  12. pmc Hyaluronan signaling during ozone-induced lung injury requires TLR4, MyD88, and TIRAP
    Zhuowei Li
    Department of Medicine, Duke University, Durham, North Carolina, United States of America
    PLoS ONE 6:e27137. 2011
    ..In conclusion, our findings support that ozone-induced airway hyperresponsiveness is dependent on the HA-TLR4-MyD88-TIRAP signaling pathway...
  13. 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...
  14. pmc Innate immune activation potentiates alloimmune lung disease independent of chemokine (C-X-C motif) receptor 3
    Tereza 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...
  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. pmc Allogeneic splenocyte transfer and lipopolysaccharide inhalations induce differential T cell expansion and lung injury: a novel model of pulmonary graft-versus-host disease
    Tereza Martinu
    Department of Medicine, Duke University Medical Center, Durham, North Carolina, United States of America
    PLoS ONE 9:e97951. 2014
    ....
  17. pmc Cerium dioxide nanoparticles do not modulate the lipopolysaccharide-induced inflammatory response in human monocytes
    Salik Hussain
    Clinical Research Unit, National Institute of Environmental Health Sciences National Institute of Health, Research Triangle Park, Durham, NC 27709, USA
    Int J Nanomedicine 7:1387-97. 2012
    ..We investigated the inflammation-modulating effects of CeO(2) nanoparticles at noncytotoxic concentrations in human peripheral blood monocytes...
  18. pmc Ecogenomics of respiratory diseases of public health significance
    Stavros Garantziotis
    Clinical Research Program and Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Annu Rev Public Health 31:37-51 1 p following 51. 2010
    ....
  19. pmc Cyclooxygenase-2 inhibits T helper cell type 9 differentiation during allergic lung inflammation via down-regulation of IL-17RB
    Hong Li
    Laboratory of Respiratory Biology, Division of Intramural Research, National Institutes of Health National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Am J Respir Crit Care Med 187:812-22. 2013
    ..Cyclooxygenase (COX)-1 and COX-2 play important roles in allergic lung inflammation and asthma. It is unknown whether COX-derived eicosanoids regulate Th9 cells during allergic lung inflammation...
  20. 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...
  21. pmc Inflammasome activation in airway epithelial cells after multi-walled carbon nanotube exposure mediates a profibrotic response in lung fibroblasts
    Salik Hussain
    Clinical Research Unit, National Institute of Environmental Health Sciences NIEHS National Institute of Health NIH, Research Triangle Park, Durham, NC, USA
    Part Fibre Toxicol 11:28. 2014
    ..However, the mechanism leading to remodeling is poorly understood. Particularly, there is limited insight about the role of airway epithelial injury in these changes...
  22. ncbi request reprint Host-environment interactions in pulmonary fibrosis
    Stavros Garantziotis
    Division of Allergy, Pulmonary, and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina, USA
    Semin Respir Crit Care Med 27:574-80. 2006
    ..We discuss the theoretical framework of this hypothesis and we present data in support of the concept that genetic and nongenetic host susceptibility may interact with repetitive environmental injury to lead to IPF...
  23. pmc Formation of reactive sulfite-derived free radicals by the activation of human neutrophils: an ESR study
    Kalina Ranguelova
    Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Free Radic Biol Med 52:1264-71. 2012
    ..Therefore, we propose that the potential toxicity of (bi)sulfite during pulmonary inflammation or lung-associated diseases such as asthma may be related to free radical formation...
  24. ncbi request reprint Genetics and genomics in human lung transplantation
    Stavros Garantziotis
    Duke University Medical Center, Duke Lung and Heart Lung Transplant Center, Division of Pulmonary, Allergy and Critical Care Medicine, Durham, NC 27710, USA
    Expert Rev Respir Med 1:271-8. 2007
    ....
  25. 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...
  26. ncbi request reprint Fatal re-expansion pulmonary edema associated with increased lung IL-8 levels following high-dose chemotherapy and autologous stem cell transplant
    Stavros Garantziotis
    Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Respiration 69:351-4. 2002
    ..This suggests that patients who have recently undergone HDC/ASCT may be at increased risk for the development of REPE following thoracentesis...
  27. pmc A mechanistic role for cardiac myocyte apoptosis in heart failure
    Detlef Wencker
    Department of Medicine Molecular Cardiology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Clin Invest 111:1497-504. 2003
    ..To our knowledge, these data provide the first direct evidence that myocyte apoptosis may be a causal mechanism of heart failure, and they suggest that inhibition of this cell death process may constitute the basis for novel therapies...