Research Topics
Genomes and Genes
| Michael T BorchersSummaryAffiliation: University of Cincinnati Country: USA Publications
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Detail Information
Publications
The NKG2D-activating receptor mediates pulmonary clearance of Pseudomonas aeruginosaMichael 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....- Nonredundant functions of alphabeta and gammadelta T cells in acrolein-induced pulmonary pathologyMichael 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... 
NKG2D ligands are expressed on stressed human airway epithelial cellsMichael 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...- Sustained CTL activation by murine pulmonary epithelial cells promotes the development of COPD-like diseaseMichael 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... - CD8+ T cells contribute to macrophage accumulation and airspace enlargement following repeated irritant exposureMichael 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... - Chronic cigarette smoke exposure generates pathogenic T cells capable of driving COPD-like disease in Rag2-/- miceGregory 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... - The role of metallothionein in the pathogenesis of acute lung injuryScott 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.... - Matrix metalloproteinase-14 mediates a phenotypic shift in the airways to increase mucin productionHitesh 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)... - NKG2D is critical for NK cell activation in host defense against Pseudomonas aeruginosa respiratory infectionScott 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... 
Chronic cigarette smoke exposure primes NK cell activation in a mouse model of chronic obstructive pulmonary diseaseGregory 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...- Acrolein-activated matrix metalloproteinase 9 contributes to persistent mucin productionHitesh 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... - Gene expression changes during the development of acute lung injury: role of transforming growth factor betaScott 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... - Pseudomonas aeruginosa exotoxin pyocyanin causes cystic fibrosis airway pathogenesisCharles 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... - CCR7 deficiency leads to leukocyte activation and increased clearance in response to pulmonary Pseudomonas aeruginosa infectionBryan 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... - Functional characterization of T cell populations in a mouse model of chronic obstructive pulmonary diseaseBryan 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... - Persistence of lung CD8 T cell oligoclonal expansions upon smoking cessation in a mouse model of cigarette smoke-induced emphysemaGregory 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... - NKG2D mediates NK cell hyperresponsiveness and influenza-induced pathologies in a mouse model of chronic obstructive pulmonary diseaseBrian 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... - Metalloproteinases mediate mucin 5AC expression by epidermal growth factor receptor activationHitesh 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... - Lung-restricted macrophage activation in the pearl mouse model of Hermansky-Pudlak syndromeLisa 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... - Mucin apoprotein expression in COPDGeorge 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... - 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 speciesMarie-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... - Galphai2-mediated signaling events in the endothelium are involved in controlling leukocyte extravasationRalph 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... - A causative relationship exists between eosinophils and the development of allergic pulmonary pathologies in the mouseHuaHao 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... - Methacholine-induced airway hyperresponsiveness is dependent on Galphaq signalingMichael 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... - Ablation of eosinophils leads to a reduction of allergen-induced pulmonary pathologyJ 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... - Gq signaling is required for allergen-induced pulmonary eosinophiliaMichael T Borchers
Division of Pulmonary Medicine, Mayo Clinic, Scottsdale AZ 85259, USA
J Immunol 168:3543-9. 2002.... - In vitro assessment of chemokine receptor-ligand interactions mediating mouse eosinophil migrationMichael 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... - Identification of an alternative G{alpha}q-dependent chemokine receptor signal transduction pathway in dendritic cells and granulocytesGuixiu Shi
Trudeau Institute, Saranac Lake, NY 12983, USA
J Exp Med 204:2705-18. 2007....