John F Alcorn

Summary

Affiliation: University of Vermont
Country: USA

Publications

  1. pmc Transforming growth factor-beta1 suppresses airway hyperresponsiveness in allergic airway disease
    John F Alcorn
    Department of Pathology, University of Vermont, Burlington, Vermont 05405, USA
    Am J Respir Crit Care Med 176:974-82. 2007
  2. pmc Strain-dependent activation of NF-kappaB in the airway epithelium and its role in allergic airway inflammation
    John F Alcorn
    Department of Pathology, Univ of Vermont, HSRF Bldg, Rm 216A, Burlington, VT 05405, USA
    Am J Physiol Lung Cell Mol Physiol 298:L57-66. 2010
  3. pmc Distinct functions of airway epithelial nuclear factor-kappaB activity regulate nitrogen dioxide-induced acute lung injury
    Jennifer L Ather
    Department of Pathology, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 43:443-51. 2010
  4. pmc c-Jun N-terminal kinase 1 is required for the development of pulmonary fibrosis
    John F Alcorn
    Department of Pathology, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 40:422-32. 2009
  5. pmc The endogenous Th17 response in NO2-promoted allergic airway disease is dispensable for airway hyperresponsiveness and distinct from Th17 adoptive transfer
    Rebecca A Martin
    Vermont Lung Center, Division of Pulmonary Disease and Critical Care, University of Vermont, Burlington, Vermont, United States of America
    PLoS ONE 8:e74730. 2013
  6. pmc Interleukin-1 receptor and caspase-1 are required for the Th17 response in nitrogen dioxide-promoted allergic airway disease
    Rebecca A Martin
    Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 48:655-64. 2013
  7. pmc c-Jun N-terminal kinase 1 promotes transforming growth factor-β1-induced epithelial-to-mesenchymal transition via control of linker phosphorylation and transcriptional activity of Smad3
    Jos L J van der Velden
    Department of Pathology, Health Sciences Research Facility, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 44:571-81. 2011
  8. pmc Influenza induces endoplasmic reticulum stress, caspase-12-dependent apoptosis, and c-Jun N-terminal kinase-mediated transforming growth factor-β release in lung epithelial cells
    Elle C Roberson
    Department of Pathology, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 46:573-81. 2012
  9. pmc Differential requirement for c-Jun N-terminal kinase 1 in lung inflammation and host defense
    Jos van der Velden
    Department of Pathology, University of Vermont, Burlington, Vermont, United States of America
    PLoS ONE 7:e34638. 2012
  10. pmc The receptor for advanced glycation end products is a central mediator of asthma pathogenesis
    Pavle S Milutinovic
    Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
    Am J Pathol 181:1215-25. 2012

Research Grants

Collaborators

Detail Information

Publications15

  1. pmc Transforming growth factor-beta1 suppresses airway hyperresponsiveness in allergic airway disease
    John F Alcorn
    Department of Pathology, University of Vermont, Burlington, Vermont 05405, USA
    Am J Respir Crit Care Med 176:974-82. 2007
    ..The cytokine transforming growth factor (TGF)-beta has been shown to have a central role in asthma pathogenesis and in mouse models of allergic airway disease...
  2. pmc Strain-dependent activation of NF-kappaB in the airway epithelium and its role in allergic airway inflammation
    John F Alcorn
    Department of Pathology, Univ of Vermont, HSRF Bldg, Rm 216A, Burlington, VT 05405, USA
    Am J Physiol Lung Cell Mol Physiol 298:L57-66. 2010
    ....
  3. pmc Distinct functions of airway epithelial nuclear factor-kappaB activity regulate nitrogen dioxide-induced acute lung injury
    Jennifer L Ather
    Department of Pathology, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 43:443-51. 2010
    ....
  4. pmc c-Jun N-terminal kinase 1 is required for the development of pulmonary fibrosis
    John F Alcorn
    Department of Pathology, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 40:422-32. 2009
    ..Collectively, these findings demonstrate an important requirement for JNK1 in promoting collagen deposition in multiple models of fibrosis...
  5. pmc The endogenous Th17 response in NO2-promoted allergic airway disease is dispensable for airway hyperresponsiveness and distinct from Th17 adoptive transfer
    Rebecca A Martin
    Vermont Lung Center, Division of Pulmonary Disease and Critical Care, University of Vermont, Burlington, Vermont, United States of America
    PLoS ONE 8:e74730. 2013
    ....
  6. pmc Interleukin-1 receptor and caspase-1 are required for the Th17 response in nitrogen dioxide-promoted allergic airway disease
    Rebecca A Martin
    Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 48:655-64. 2013
    ..These data implicate a role for caspase-1 and IL-1β in the IL-1 receptor-dependent Th17 response manifest in NO2-promoted allergic airway disease...
  7. pmc c-Jun N-terminal kinase 1 promotes transforming growth factor-β1-induced epithelial-to-mesenchymal transition via control of linker phosphorylation and transcriptional activity of Smad3
    Jos L J van der Velden
    Department of Pathology, Health Sciences Research Facility, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 44:571-81. 2011
    ....
  8. pmc Influenza induces endoplasmic reticulum stress, caspase-12-dependent apoptosis, and c-Jun N-terminal kinase-mediated transforming growth factor-β release in lung epithelial cells
    Elle C Roberson
    Department of Pathology, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 46:573-81. 2012
    ..Proc Am Thorac Soc 2004;1:115-120) and idiopathic pulmonary fibrosis (Umeda Y, et al. Int Med 2010;49:2333-2336)...
  9. pmc Differential requirement for c-Jun N-terminal kinase 1 in lung inflammation and host defense
    Jos van der Velden
    Department of Pathology, University of Vermont, Burlington, Vermont, United States of America
    PLoS ONE 7:e34638. 2012
    ..These data identify JNK1 as an important signaling molecule in host defense and demonstrate a pathogen specific role in disease. Manipulation of the JNK1 pathway may represent a novel therapeutic target in pneumonia...
  10. pmc The receptor for advanced glycation end products is a central mediator of asthma pathogenesis
    Pavle S Milutinovic
    Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
    Am J Pathol 181:1215-25. 2012
    ..Finally, the results in the HDM model are recapitulated in an ovalbumin model of asthma, suggesting that RAGE plays a role in asthma irrespective of the identity of the allergens involved...
  11. pmc Jun N-terminal kinase 1 regulates epithelial-to-mesenchymal transition induced by TGF-beta1
    John F Alcorn
    Department of Pathology, University of Vermont, Burlington, VT 05405, USA
    J Cell Sci 121:1036-45. 2008
    ..In aggregate, these results illuminate the novel role of airway epithelial-dependent JNK1 activation in EMT...
  12. pmc Nuclear factor-kappaB activation in airway epithelium induces inflammation and hyperresponsiveness
    Cristen Pantano
    Department of Pathology, University of Vermont, Burlington, Vermont 05405, USA
    Am J Respir Crit Care Med 177:959-69. 2008
    ..Previous studies demonstrated that inhibition of NF-kappaB in airway epithelium causes attenuation of allergic inflammation...
  13. pmc TH17 cells mediate steroid-resistant airway inflammation and airway hyperresponsiveness in mice
    Laura McKinley
    Department of Pediatrics, Lung Immunology and Host Defense Laboratory, University of Pittsburgh, Pittsburgh, PA 15213, USA
    J Immunol 181:4089-97. 2008
    ..Both T(H)2 and T(H)17 cells are able to induce AHR, whereas T(H)17 cell-mediated airway inflammation and AHR are steroid resistant, indicating a potential role for T(H)17 cells in steroid-resistant asthma...
  14. ncbi request reprint Degradation of pulmonary surfactant protein D by Pseudomonas aeruginosa elastase abrogates innate immune function
    John F Alcorn
    Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 279:30871-9. 2004
    ..These data show that degradation of SP-D occurs in the BAL environment and that degradation eliminates many normal immune functions of SP-D...
  15. ncbi request reprint Pseudomonas aeruginosa elastase degrades surfactant proteins A and D
    William I Mariencheck
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Am J Respir Cell Mol Biol 28:528-37. 2003
    ..We speculate that degradation of SP-A and SP-D is a virulence mechanism in the pathogenesis of chronic P. aeruginosa infection...

Research Grants1

  1. The Role of JNK in Allergen-Induced Airway Remodeling
    JOHN ALCORN; Fiscal Year: 2006
    ..The outcome of this study will better define the role of the JNK signaling pathway in the development of pulmonary fibrosis in a murine asthma model. ..