Michael T Borchers

Summary

Affiliation: University of Cincinnati
Country: USA

Publications

  1. pmc The NKG2D-activating receptor mediates pulmonary clearance of Pseudomonas aeruginosa
    Michael T Borchers
    Department of Environmental Health, Division of Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, OH 45267 0056, USA
    Infect Immun 74:2578-86. 2006
  2. pmc Nonredundant functions of alphabeta and gammadelta T cells in acrolein-induced pulmonary pathology
    Michael T Borchers
    Division of Environmental Genetics and Molecular Toxicology, Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH 45267 0056, USA
    Toxicol Sci 105:188-99. 2008
  3. pmc CD8+ T cells contribute to macrophage accumulation and airspace enlargement following repeated irritant exposure
    Michael T Borchers
    Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology, University of Cincinnati, College of Medicine, Cincinnati, OH 45267, USA
    Exp Mol Pathol 83:301-10. 2007
  4. ncbi request reprint NKG2D ligands are expressed on stressed human airway epithelial cells
    Michael T Borchers
    Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology, University of Cincinnati College of Medicine, OH 45267, USA
    Am J Physiol Lung Cell Mol Physiol 291:L222-31. 2006
  5. pmc Sustained CTL activation by murine pulmonary epithelial cells promotes the development of COPD-like disease
    Michael T Borchers
    Department of Environmental Health, Division of Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, OH 45267 0056, USA
    J Clin Invest 119:636-49. 2009
  6. pmc Chronic cigarette smoke exposure generates pathogenic T cells capable of driving COPD-like disease in Rag2-/- mice
    Gregory T Motz
    Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology, University of Cincinnati, College of Medicine, Cincinnati, OH 45267 0056, USA
    Am J Respir Crit Care Med 181:1223-33. 2010
  7. pmc NKG2D is critical for NK cell activation in host defense against Pseudomonas aeruginosa respiratory infection
    Scott C Wesselkamper
    Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    J Immunol 181:5481-9. 2008
  8. pmc Matrix metalloproteinase-14 mediates a phenotypic shift in the airways to increase mucin production
    Hitesh S Deshmukh
    Department of Environmental Health, University of Cincinnati, Cincinnati, Ohio, USA
    Am J Respir Crit Care Med 180:834-45. 2009
  9. pmc The role of metallothionein in the pathogenesis of acute lung injury
    Scott C Wesselkamper
    Department of Environmental Health, University of Cincinnati Medical Center, Cincinnati, OH 45267 0056, USA
    Am J Respir Cell Mol Biol 34:73-82. 2006
  10. doi request reprint Chronic cigarette smoke exposure primes NK cell activation in a mouse model of chronic obstructive pulmonary disease
    Gregory T Motz
    Division of Environmental Genetics and Molecular Toxicology, Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    J Immunol 184:4460-9. 2010

Collaborators

Detail Information

Publications30

  1. pmc The NKG2D-activating receptor mediates pulmonary clearance of Pseudomonas aeruginosa
    Michael T Borchers
    Department of Environmental Health, Division of Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, OH 45267 0056, USA
    Infect Immun 74:2578-86. 2006
    ....
  2. pmc Nonredundant functions of alphabeta and gammadelta T cells in acrolein-induced pulmonary pathology
    Michael T Borchers
    Division of Environmental Genetics and Molecular Toxicology, Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH 45267 0056, USA
    Toxicol Sci 105:188-99. 2008
    ..These data provide strong evidence that T-cell subpopulations in the lung are major determinants of pulmonary pathology and highlight the advantages of dissecting their effector functions in response to toxicant exposures...
  3. pmc CD8+ T cells contribute to macrophage accumulation and airspace enlargement following repeated irritant exposure
    Michael T Borchers
    Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology, University of Cincinnati, College of Medicine, Cincinnati, OH 45267, USA
    Exp Mol Pathol 83:301-10. 2007
    ..In this study, we utilize a mouse model of COPD to examine the contributions of CD8(+) T cells in the persistent macrophage accumulation and airspace enlargement resulting from chronic irritant exposure...
  4. ncbi request reprint NKG2D ligands are expressed on stressed human airway epithelial cells
    Michael T Borchers
    Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology, University of Cincinnati College of Medicine, OH 45267, USA
    Am J Physiol Lung Cell Mol Physiol 291:L222-31. 2006
    ..The induction of NKG2D ligands on stressed airway epithelial cells represents a potentially important mechanism of immune cell activation in regulation of pulmonary health and disease...
  5. pmc Sustained CTL activation by murine pulmonary epithelial cells promotes the development of COPD-like disease
    Michael T Borchers
    Department of Environmental Health, Division of Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, OH 45267 0056, USA
    J Clin Invest 119:636-49. 2009
    ..These results demonstrate that aberrant, persistent NKG2D ligand expression in the pulmonary epithelium contributes to the development of COPD pathologies...
  6. pmc Chronic cigarette smoke exposure generates pathogenic T cells capable of driving COPD-like disease in Rag2-/- mice
    Gregory T Motz
    Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology, University of Cincinnati, College of Medicine, Cincinnati, OH 45267 0056, USA
    Am J Respir Crit Care Med 181:1223-33. 2010
    ..We previously demonstrated that chronic cigarette smoke (CS) exposure causes oligoclonal expansion of lung CD4(+) T cells and CD8(+) T cells in a mouse model of COPD, thus implicating these cells in disease pathogenesis...
  7. pmc NKG2D is critical for NK cell activation in host defense against Pseudomonas aeruginosa respiratory infection
    Scott C Wesselkamper
    Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    J Immunol 181:5481-9. 2008
    ..aeruginosa respiratory infection...
  8. pmc Matrix metalloproteinase-14 mediates a phenotypic shift in the airways to increase mucin production
    Hitesh S Deshmukh
    Department of Environmental Health, University of Cincinnati, Cincinnati, Ohio, USA
    Am J Respir Crit Care Med 180:834-45. 2009
    ..Previously, we reported that acrolein levels found in COPD sputum could activate matrix metalloproteinase-9 (MMP9)...
  9. pmc The role of metallothionein in the pathogenesis of acute lung injury
    Scott C Wesselkamper
    Department of Environmental Health, University of Cincinnati Medical Center, Cincinnati, OH 45267 0056, USA
    Am J Respir Cell Mol Biol 34:73-82. 2006
    ....
  10. doi request reprint Chronic cigarette smoke exposure primes NK cell activation in a mouse model of chronic obstructive pulmonary disease
    Gregory T Motz
    Division of Environmental Genetics and Molecular Toxicology, Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    J Immunol 184:4460-9. 2010
    ..Together, these results reveal a novel mechanism of activation of the innate immune system and highlight NK cells as important cellular targets in controlling COPD exacerbations...
  11. pmc Acrolein-activated matrix metalloproteinase 9 contributes to persistent mucin production
    Hitesh S Deshmukh
    Center for Environmental Genetics, University of Cincinnati, Cincinnati, USA
    Am J Respir Cell Mol Biol 38:446-54. 2008
    ..Augmentation of hMMP9 activity, in turn, could contribute to persistent excessive mucin production...
  12. pmc Gene expression changes during the development of acute lung injury: role of transforming growth factor beta
    Scott C Wesselkamper
    Department of Environmental Health, P O Box 670056, University of Cincinnati, Cincinnati, OH 45267 0056, USA
    Am J Respir Crit Care Med 172:1399-411. 2005
    ..Acute lung injury can occur from multiple causes, resulting in high mortality. The pathophysiology of nickel-induced acute lung injury in mice is remarkably complex, and the molecular mechanisms are uncertain...
  13. pmc CCR7 deficiency leads to leukocyte activation and increased clearance in response to pulmonary Pseudomonas aeruginosa infection
    Bryan L Eppert
    Department of Environmental Health, University of Cincinnati College of Medicine, 3223 Eden Avenue, Cincinnati, OH 45267 0056, USA
    Infect Immun 78:2099-107. 2010
    ..aeruginosa infection. In conclusion, our results suggest that CCR7 deficiency results in a heightened proinflammatory environment in response to acute pulmonary P. aeruginosa infection and contributes to more efficient clearance...
  14. pmc Pseudomonas aeruginosa exotoxin pyocyanin causes cystic fibrosis airway pathogenesis
    Charles C Caldwell
    Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
    Am J Pathol 175:2473-88. 2009
    ..In summary, this study establishes that PCN is an important P. aeruginosa virulence factor capable of directly inducing pulmonary pathophysiology in mice, consistent with changes observed in CF and other bronchiectasis lungs...
  15. pmc Functional characterization of T cell populations in a mouse model of chronic obstructive pulmonary disease
    Bryan L Eppert
    Division of Environmental Genetics and Molecular Toxicology, Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    J Immunol 190:1331-40. 2013
    ..These results are direct evidence for an autoimmune response initiated by CS exposure...
  16. ncbi request reprint Persistence of lung CD8 T cell oligoclonal expansions upon smoking cessation in a mouse model of cigarette smoke-induced emphysema
    Gregory T Motz
    Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology, University of Cincinnati, College of Medicine, Cincinnati, OH 45267 0056, USA
    J Immunol 181:8036-43. 2008
    ..These findings have important implications for therapeutic approaches in the treatment of COPD, and provide insight into potential mechanisms involved in disease pathogenesis...
  17. pmc NKG2D mediates NK cell hyperresponsiveness and influenza-induced pathologies in a mouse model of chronic obstructive pulmonary disease
    Brian W Wortham
    Division of Environmental Genetics and Molecular Toxicology, Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    J Immunol 188:4468-75. 2012
    ..Our findings indicate that NKG2D stimulation during long-term CS exposure is a central pathway in the development of NK cell hyperresponsiveness and influenza-mediated exacerbations of COPD...
  18. ncbi request reprint Metalloproteinases mediate mucin 5AC expression by epidermal growth factor receptor activation
    Hitesh S Deshmukh
    University of Cincinnati, P O Box 670056, Cincinnati, OH 45267 0056, USA
    Am J Respir Crit Care Med 171:305-14. 2005
    ..In addition, a prolonged effect of acrolein may be mediated by altering MMP9 and TIMP3 transcription...
  19. pmc Lung-restricted macrophage activation in the pearl mouse model of Hermansky-Pudlak syndrome
    Lisa R Young
    Department of Medicine, Division of Pulmonary and Critical Care, University of Cincinnati, OH 45267, USA
    J Immunol 176:4361-8. 2006
    ..Similar abnormalities were identified in AMs and BAL from another HPS model, pale ear HPS1 mice. We conclude that the lungs of HPS mice exhibit hyperresponsiveness to LPS and constitutive and organ-specific macrophage activation...
  20. ncbi request reprint Mucin apoprotein expression in COPD
    George D Leikauf
    Molecular Toxicology Division, Department of Environmental Health, University of Cincinnati, Cincinnati, OH 45267 0056, USA
    Chest 121:166S-182S. 2002
    ..As our understanding of the functional genomics of mucin biology increases, further clinical targets and therapeutic strategies are likely to emerge...
  21. pmc TLR and NKG2D signaling pathways mediate CS-induced pulmonary pathologies
    Brian W Wortham
    Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America
    PLoS ONE 8:e78735. 2013
    ..Activation of these pathways plays a major role in the altered NK cell function, pulmonary inflammation and remodeling related to long-term CS exposure. ..
  22. doi request reprint Chronic obstructive pulmonary disease (COPD): evaluation from clinical, immunological and bacterial pathogenesis perspectives
    Daniel J Hassett
    Departments of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA
    J Microbiol 52:211-26. 2014
    ..We offer a non-conventional, biocidal treatment that may be effective for COPD airway infections as well as with combinations of current antibiotic regimens for more effective treatment outcomes and relief for patients with COPD. ..
  23. pmc Galphai2-mediated signaling events in the endothelium are involved in controlling leukocyte extravasation
    Ralph S Pero
    Division of Hematology Oncology, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ 85259, USA
    Proc Natl Acad Sci U S A 104:4371-6. 2007
    ..Collectively, these data suggest that specific Galpha(i2)-mediated signaling between endothelial cells and leukocytes is required for the extravasation of leukocytes and for tissue-specific accumulation...
  24. ncbi request reprint A causative relationship exists between eosinophils and the development of allergic pulmonary pathologies in the mouse
    HuaHao H Shen
    Division of Hematology Oncology, Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, S C Johnson Medical Research Center, Scottsdale, AZ 85259, USA
    J Immunol 170:3296-305. 2003
    ..These data support an expanded view of T cell and eosinophil activities and suggest that eosinophil effector functions impinge directly on lung function...
  25. ncbi request reprint Methacholine-induced airway hyperresponsiveness is dependent on Galphaq signaling
    Michael T Borchers
    Department of Biochemistry and Molecular Biology, SCJMRB RESEARCH, Mayo Clinic Scottsdale, 13400 E Shea Blvd, Scottsdale, AZ 85259, USA
    Am J Physiol Lung Cell Mol Physiol 285:L114-20. 2003
    ..These findings indicate that cholinergic receptor-mediated responses are dependent on Galphaq-mediated signaling events and identify Galphaq as a potential target of preventative/intervening therapies for lung dysfunction...
  26. ncbi request reprint Ablation of eosinophils leads to a reduction of allergen-induced pulmonary pathology
    J Paul Justice
    Division of Hematology Oncology and Pulmonary Medicine, Department of Biochemistry and Molecular Biology, S C Johnson Medical Research Building, Mayo Clinic Scottsdale, 13400 E Shea Boulevard, Scottsdale, AZ 85259, USA
    Am J Physiol Lung Cell Mol Physiol 284:L169-78. 2003
    ..These data demonstrate a direct causative relationship between allergen-mediated pulmonary pathologies and eosinophils...
  27. ncbi request reprint Gq signaling is required for allergen-induced pulmonary eosinophilia
    Michael T Borchers
    Division of Pulmonary Medicine, Mayo Clinic, Scottsdale AZ 85259, USA
    J Immunol 168:3543-9. 2002
    ....
  28. ncbi request reprint A tale of two controversies: defining both the role of peroxidases in nitrotyrosine formation in vivo using eosinophil peroxidase and myeloperoxidase-deficient mice, and the nature of peroxidase-generated reactive nitrogen species
    Marie Luise Brennan
    Department of Cell Biology, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    J Biol Chem 277:17415-27. 2002
    ..We speculate that the latter reaction generates a labile Fe-ONOO complex, which may be released following protonation under acidic conditions such as might exist at sites of inflammation...
  29. pmc Identification of an alternative G{alpha}q-dependent chemokine receptor signal transduction pathway in dendritic cells and granulocytes
    Guixiu Shi
    Trudeau Institute, Saranac Lake, NY 12983, USA
    J Exp Med 204:2705-18. 2007
    ....
  30. ncbi request reprint In vitro assessment of chemokine receptor-ligand interactions mediating mouse eosinophil migration
    Michael T Borchers
    Mayo Clinic Scottsdale, Scottsdale, Arizona 85259, USA
    J Leukoc Biol 71:1033-41. 2002
    ..Collectively, these observations reveal physiologically relevant distinctions in mechanisms mediating human and mouse eosinophil migration that potentially reflect evolutionary disparities between these species...