چکیده (انگلیسی):

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.