Richard A Johnston

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure
    Richard A Johnston
    Physiology Program, Dept of Environmental Health, Harvard School of Public Health, Boston, MA 02115 6021, USA
    Am J Physiol Lung Cell Mol Physiol 288:L61-7. 2005
  2. ncbi request reprint Role of interleukin-6 in murine airway responses to ozone
    Richard A Johnston
    Bldg 1, Rm 1304A, Physiology Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115 6021, USA
    Am J Physiol Lung Cell Mol Physiol 288:L390-7. 2005
  3. ncbi request reprint Augmented responses to ozone in obese carboxypeptidase E-deficient mice
    Richard A Johnston
    Physiology Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115 6021, USA
    Am J Physiol Regul Integr Comp Physiol 290:R126-33. 2006
  4. doi request reprint Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation
    Richard A Johnston
    Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
    J Appl Physiol 104:1727-35. 2008
  5. pmc Allergic airway responses in obese mice
    Richard A Johnston
    Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
    Am J Respir Crit Care Med 176:650-8. 2007
  6. pmc Pulmonary responses to subacute ozone exposure in obese vs. lean mice
    Stephanie A Shore
    Molecular and Integrative Physiological Sciences Program, Dept of Environmental Health, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115 6021, USA
    J Appl Physiol 107:1445-52. 2009
  7. pmc Impact of adiponectin deficiency on pulmonary responses to acute ozone exposure in mice
    Ming Zhu
    Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA
    Am J Respir Cell Mol Biol 43:487-97. 2010
  8. pmc Type I interleukin-1 receptor is required for pulmonary responses to subacute ozone exposure in mice
    Richard A Johnston
    Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA
    Am J Respir Cell Mol Biol 37:477-84. 2007
  9. ncbi request reprint Increased pulmonary responses to acute ozone exposure in obese db/db mice
    Frank L Lu
    Physiology Program, Dept of Environmental Health, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115 6021, USA
    Am J Physiol Lung Cell Mol Physiol 290:L856-65. 2006
  10. pmc Onset of obesity in carboxypeptidase E-deficient mice and effect on airway responsiveness and pulmonary responses to ozone
    Richard A Johnston
    Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave, Bldg 1, Rm 311, Boston, MA 02115 6021, USA
    J Appl Physiol 108:1812-9. 2010

Collaborators

Detail Information

Publications16

  1. ncbi request reprint CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure
    Richard A Johnston
    Physiology Program, Dept of Environmental Health, Harvard School of Public Health, Boston, MA 02115 6021, USA
    Am J Physiol Lung Cell Mol Physiol 288:L61-7. 2005
    ..These results indicate CXCR2 is essential for maximal neutrophil recruitment, epithelial cell sloughing, and persistent increases in MCh responsiveness after an acute O(3) exposure...
  2. ncbi request reprint Role of interleukin-6 in murine airway responses to ozone
    Richard A Johnston
    Bldg 1, Rm 1304A, Physiology Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115 6021, USA
    Am J Physiol Lung Cell Mol Physiol 288:L390-7. 2005
    ..Our results indicate that IL-6 deficiency reduces airway neutrophilia, as well as the levels of BALF sTNFR1 and sTNFR2 following acute high dose and/or subacute low-dose O(3) exposure, but has no effect on O(3)-induced AHR...
  3. ncbi request reprint Augmented responses to ozone in obese carboxypeptidase E-deficient mice
    Richard A Johnston
    Physiology Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115 6021, USA
    Am J Physiol Regul Integr Comp Physiol 290:R126-33. 2006
    ..These results also suggest that chronic systemic inflammation may enhance airway responses to O3 in obese mice...
  4. doi request reprint Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation
    Richard A Johnston
    Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
    J Appl Physiol 104:1727-35. 2008
    ..However, mice with DIO must remain obese for an extended period of time before this pulmonary phenotype is observed...
  5. pmc Allergic airway responses in obese mice
    Richard A Johnston
    Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
    Am J Respir Crit Care Med 176:650-8. 2007
    ..Epidemiologic data indicate an increased incidence of asthma in the obese...
  6. pmc Pulmonary responses to subacute ozone exposure in obese vs. lean mice
    Stephanie A Shore
    Molecular and Integrative Physiological Sciences Program, Dept of Environmental Health, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115 6021, USA
    J Appl Physiol 107:1445-52. 2009
    ..In summary, the neutrophilic inflammation induced by prolonged low level ozone exposure was attenuated in obese mice and appeared to result from an absence of IL-6-dependent neutrophil recruitment in the obese mice...
  7. pmc Impact of adiponectin deficiency on pulmonary responses to acute ozone exposure in mice
    Ming Zhu
    Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA
    Am J Respir Cell Mol Biol 43:487-97. 2010
    ..Our results indicate that adiponectin deficiency inhibits pulmonary inflammation induced by acute O(3) exposure, and that T-cadherin does not mediate the effects of adiponectin responsible for these events...
  8. pmc Type I interleukin-1 receptor is required for pulmonary responses to subacute ozone exposure in mice
    Richard A Johnston
    Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA
    Am J Respir Cell Mol Biol 37:477-84. 2007
    ..In addition, these results suggest that the induction of IL-6 via IL-1RI may be important in mediating the effects of O(3) during subacute exposure...
  9. ncbi request reprint Increased pulmonary responses to acute ozone exposure in obese db/db mice
    Frank L Lu
    Physiology Program, Dept of Environmental Health, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115 6021, USA
    Am J Physiol Lung Cell Mol Physiol 290:L856-65. 2006
    ..Differences between ob/ob mice, which lack leptin, and db/db mice, which lack Ob-R(b) but not Ob-R(a), suggest leptin, acting through Ob-R(a), can modify some pulmonary responses to O(3)...
  10. pmc Onset of obesity in carboxypeptidase E-deficient mice and effect on airway responsiveness and pulmonary responses to ozone
    Richard A Johnston
    Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave, Bldg 1, Rm 311, Boston, MA 02115 6021, USA
    J Appl Physiol 108:1812-9. 2010
    ..These results suggest that the mechanistic bases for these responses are different and may develop according to the nature and degree of the chronic systemic inflammation that is present...
  11. ncbi request reprint Effect of leptin on allergic airway responses in mice
    Stephanie A Shore
    Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115 6021, USA
    J Allergy Clin Immunol 115:103-9. 2005
    ..Epidemiologic data indicate that the incidence of asthma is increased in obese patients...
  12. pmc Ozone exposure in a mouse model induces airway hyperreactivity that requires the presence of natural killer T cells and IL-17
    Muriel Pichavant
    Children s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA
    J Exp Med 205:385-93. 2008
    ....
  13. ncbi request reprint Pulmonary responses to acute ozone exposure in fasted mice: effect of leptin administration
    Richard A Johnston
    Physiology Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115 6021, USA
    J Appl Physiol 102:149-56. 2007
    ..These effects of fasting are the result of declines in serum leptin. The mechanistic basis for this protective effect of leptin in fasted mice remains to be determined but is not related to effects on ozone-induced inflammation...
  14. ncbi request reprint Macrophage inflammatory protein-2 levels are associated with changes in serum leptin concentrations following ozone-induced airway inflammation
    Richard A Johnston
    Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115 6021, USA
    Chest 123:369S-70S. 2003
  15. ncbi request reprint Obesity and asthma
    Stephanie A Shore
    Physiology Program, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA
    Pharmacol Ther 110:83-102. 2006
    ..Understanding the mechanistic basis for the relationship between obesity and asthma may lead to new therapeutic strategies for treatment of this susceptible population...
  16. ncbi request reprint Hyperosmolar solution effects in guinea pig airways. IV. Lipopolysaccharide-induced alterations in airway reactivity and epithelial bioelectric responses to methacholine and hyperosmolarity
    Richard A Johnston
    Department of Pharmacology and Toxicology, Robert C Byrd Health Sciences Center of West Virginia University, Morgantown, West Virginia, USA
    J Pharmacol Exp Ther 308:37-46. 2004
    ..These changes may involve LPS-induced bioelectric alterations in the epithelium...