Stavros Garantziotis

Summary

Affiliation: Duke University Medical Center
Country: USA

Publications

  1. 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
  2. ncbi request reprint Critical care of the head and neck patient
    Stavros Garantziotis
    Department of Medicine, Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, 275 Medical Sciences Research Building, Box 2629, Durham, NC 27710, USA
    Crit Care Clin 19:73-90. 2003
  3. 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
  4. 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
  5. 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
  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. 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
  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 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

Collaborators

Detail Information

Publications23

  1. 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...
  2. ncbi request reprint Critical care of the head and neck patient
    Stavros Garantziotis
    Department of Medicine, Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, 275 Medical Sciences Research Building, Box 2629, Durham, NC 27710, USA
    Crit Care Clin 19:73-90. 2003
    ..A team approach involving the surgeon, the intensivist, and other caretaking personnel is essential to achieve high-quality care and ensure the best results possible...
  3. 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...
  4. 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...
  5. 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...
  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. 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...
  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 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...
  11. 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...
  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. 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
    ....
  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. 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...
  16. 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...
  17. 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...
  18. 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...
  19. 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
    ....
  20. 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...
  21. 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
    ....
  22. 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...
  23. pmc A novel, non-functional, COL1A1 polymorphism is not associated with lumbar disk disease in young male Greek subjects unlike that of the Sp1 site
    Thalia Bei
    Democritus University of Thrace, Alexandroupolis, Greece
    Hormones (Athens) 7:251-4. 2008
    ..In the present study we searched for a different polymorphism of the COL1A1 gene (which is usually not in linkage disequilibrium with the Sp1 site) in subjects with LDD...