中枢性μ-オピオイド受容体とグルココルチコイド受容体を介した慢性ストレスによる喘息悪化

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  • The involvement of central μ-opioid receptors and glucocorticoid receptors in psychological stress-induced asthma exacerbation
  • チュウスウセイ ミュー オピオイド ジュヨウタイ ト グルココルチコイド ジュヨウタイ オ カイシタ マンセイ ストレス ニ ヨル ゼンソク アッカ

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Stress and other psychological factors have long been etiologically demonstrated to be associated with asthma symptoms. We recently reported that μ-opioid receptors (MORs) were involved in asthma exacerbations caused by psychological stress in a murine asthma model. On the other hand, MOR activation in central nervous system (CNS) by psychological stress can stimulate hypothalamus-pituitary-adrenal (HPA) axis, resulting in the release of glucocorticoid. Glucocorticoid has been reported to shift the immune response from helper T (Th) 1 to Th2. These findings led us to hypothesize that psychological stress-induced exacerbations of asthma was attributable to cortisol release due to HPA axis stimulation via the activation of MOR in CNS. Female C57BL/6 mice sensitized with ovalbumin were exposed to chronic restraint stress as psychological stress. Either intracereberoventricular administration of an MOR antagonist or systemic administration of a glucocorticoid receptor antagonist during stress exposure abolished stress-induced exacerbation of airway inflammation. On the other hand, the elevation of stress-induced plasma corticosterone level was not affected by the administration of the MOR antagonist to CNS, and observed also in MOR knockout mice. These results suggest that both MOR in CNS and glucocorticoid are involved in the psychological stress-induced exacerbation of allergic airway inflammation, but the sress-induced HPA axis stimulation did not depend on MOR activation in this model.

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