The involvement of central nervous system histamine receptors in psychological stress-induced exacerbation of allergic airway inflammation in mice

  • Miyasaka Tomomitsu
    Department of Pathophysiology, Tohoku Pharmaceutical University
  • Okuyama-Dobashi Kaori
    Department of Pathophysiology, Tohoku Pharmaceutical University Department of Microbiology, Division of Medicine, Interdisciplinary Graduate School of Medicine and Engineering (Faculty of Medicine), University of Yamanashi
  • i Masuda Chiaki
    Department of Pathophysiology, Tohoku Pharmaceutical University
  • Iwami Shunya
    Department of Pathophysiology, Tohoku Pharmaceutical University
  • Sato Miki
    Department of Pathophysiology, Tohoku Pharmaceutical University
  • Mizoguchi Hirokazu
    Department of Physiology and Anatomy, Tohoku Pharmaceutical University
  • Kawano Tasuku
    Department of Pathophysiology, Tohoku Pharmaceutical University
  • Ohkawara Yuichi
    Department of Pathophysiology, Tohoku Pharmaceutical University
  • Sakurada Shinobu
    Department of Physiology and Anatomy, Tohoku Pharmaceutical University
  • Takayanagi Motoaki
    Department of Pathophysiology, Tohoku Pharmaceutical University
  • Ohno Isao
    Department of Pathophysiology, Tohoku Pharmaceutical University

Abstract

Background: Psychological stress is one of the major risk factors for asthma exacerbation. Although histamine in the brain acts as an excitatory and inhibitory neurotransmitter associated with psychological stress, the contribution of brain histamine to psychological stress-induced exacerbation of asthma remains unclear. The objective of this study was to investigate the role of histamine receptors in the CNS on stress induced asthma aggravation. Methods: We monitored the numbers of inflammatory cells and interleukin (IL)-13 levels in bronchoalveolar lavage fluid, airway responsiveness to inhaled methacholine, mucus secretion in airway epithelial cells, and antigen-specific IgE contents in sera in a murine model of stress-induced asthma treated with epinastine (an H1R antagonist), thioperamide (an H3/4R antagonist), or solvent. Results: All indicators of stress-induced asthma exacerbation were significantly reduced in stressed mice treated with epinastine compared with those treated with solvent, whereas treatment with thioperamide did not reduce the numbers of inflammatory cells in the stressed mice. Conclusions: These results suggest that H1R, but not H3/4R, may be involved in stress-induced asthma exacerbations in the central nervous system.

Journal

Citations (4)*help

See more

References(34)*help

See more

Related Projects

See more

Details 詳細情報について

Report a problem

Back to top