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

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 remain...

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Bibliographic Details
Published in:Allergology international 2016-09, Vol.65 (S), p.S38-S44
Main Authors: Miyasaka, Tomomitsu, Okuyama-Dobashi, Kaori, Masuda, Chiaki, Iwami, Shunya, Sato, Miki, Mizoguchi, Hirokazu, Kawano, Tasuku, Ohkawara, Yuichi, Sakurada, Shinobu, Takayanagi, Motoaki, Ohno, Isao
Format: Article
Language:English
Subjects:
Animals
Antigens - immunology
Bronchial asthma
Bronchial Hyperreactivity - etiology
Bronchial Hyperreactivity - metabolism
Bronchial Hyperreactivity - pathology
Bronchoalveolar Lavage Fluid - immunology
Central Nervous System - drug effects
Central Nervous System - metabolism
Cytokines - biosynthesis
Disease Models, Animal
Disease Progression
Epinastine
Female
Histamine Antagonists - pharmacology
Histamine receptors
Immunoglobulin E - blood
Immunoglobulin E - immunology
Mice
Mucus - secretion
Psychological stress
Receptors, Histamine - metabolism
Stress, Psychological
Thioperamide
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Summary: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. 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. 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. These results suggest that H1R, but not H3/4R, may be involved in stress-induced asthma exacerbations in the central nervous system.
ISSN:1323-8930
1440-1592
DOI:10.1016/j.alit.2016.05.015