The study on the regulation of allergic responses by opioid network in bronchial asthma

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1.The effects of acute stress on allergic responses in asthma(1)Allergen-induced airway inflammation, in terms of the numbers of inflammatory cells in lung lavage fluids, in both restrain stressed-C57BL/6 and Balb/C female mice during allergen inhalation (acute stress) was significantly weaker than that in non restrain stressed-mice.(2)This effect of acute stress on the airway inflammation was observed also in μ opioid receptor-defficient C57BL/6 female mice.2.The effects of chronic stress on allergic responses in asthma(1)Following restrain stress during allergen inhalation, mice were further loaded with the stress once a day for 6 consecutive days (chronic stress). After the last stress, mice were inhaled with allergen, and lung lavage fluids were collected.(2)The numbers of inflammatory cells and the contents of Th2 cytokine including IL-4, IL-5 and IL-13 in lung lavage fluids in chronic stressed- C57BL/6 female mice were significantly higher than those in non chronic stressed-mice.(3)The increase of inflammatory cell numbers in chronic stressed-mice was abolished by the simultaneous administration of a μ opiois receptor antagonist β-FNA, with the stress.(4)In μ opioid receptor-defficient C57BL/6 female mice, the numbers of inflammatory cells and the contents of Th2 cytokine in lung lavage fluids were not significantly different between with and without chronic stress.These results suggest,that acute and chronic stress have opposite effects, the improvement and exacerbation, respectively, on allergen-induced airway inflammation.that the effect of chronic stress, but not acute stress, was mediated, at least in part, by μ opioid receptors,and that one of the mechanisms underlying the exacerbation by chronic stress is the shift of immune responses to Th2 through the activation of μ opioid receptors.We are attempting to investigate the role of μ opioid receptors on hypothalamus-pituitary-adrenal axis and on T lymphocytes in the immune deviation.