促肾上腺皮质激素释放激素缺乏揭示了肾上腺素的促炎作用。
Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine.
作者信息
Karalis K P, Kontopoulos E, Muglia L J, Majzoub J A
机构信息
Division of Endocrinology, Children's Hospital, Boston, MA 02115, USA.
出版信息
Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):7093-7. doi: 10.1073/pnas.96.12.7093.
Abstract
Traditionally, the adrenal gland has been considered an important endocrine component of the pathway to inhibit acute inflammation via hypothalamic corticotropin-releasing hormone (CRH)-mediated secretion of glucocorticoid. Immunoreactive CRH found in inflamed tissues is a potent proinflammatory factor. Using genetic and pharmacological models of CRH deficiency, we now show that CRH deficiency unmasks a major proinflammatory effect of epinephrine secreted from the adrenal medulla. Together, epinephrine and peripheral CRH stimulate inflammation, and glucocorticoid acts as a counterbalancing force in this regard. Our findings suggest that stimulation of the acute inflammatory response should be included with the other "fight-or-flight" actions of epinephrine.
摘要
传统上，肾上腺被认为是通过下丘脑促肾上腺皮质激素释放激素（CRH）介导的糖皮质激素分泌来抑制急性炎症途径中的一个重要内分泌组成部分。在炎症组织中发现的免疫反应性CRH是一种强大的促炎因子。利用CRH缺乏的遗传和药理学模型，我们现在表明，CRH缺乏揭示了肾上腺髓质分泌的肾上腺素的主要促炎作用。总之，肾上腺素和外周CRH刺激炎症，而糖皮质激素在这方面起到平衡作用。我们的研究结果表明，急性炎症反应的刺激应与肾上腺素的其他“战斗或逃跑”作用一起考虑。
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