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  • Title: Induction of pituitary sensitivity to interleukin-1: a new function for corticotropin-releasing hormone.
    Author: Payne LC, Weigent DA, Blalock JE.
    Journal: Biochem Biophys Res Commun; 1994 Jan 28; 198(2):480-4. PubMed ID: 8297358.
    Abstract:
    Activation of the hypothalamic-pituitary-adrenal axis to release corticotropin-releasing hormone (CRH), corticotropin (ACTH), and glucocorticoids during inflammatory stress is now considered a key function of interleukin-1 (IL-1). Current dogma suggests that in vivo ACTH release due to IL-1 is indirect and entirely results from IL-1-mediated-CRH release from the hypothalamus. The present findings show that low levels of exogenous or endogenous CRH can sensitize the pituitary gland to the direct ACTH releasing activity of IL-1. Once sensitized, IL-1 induced ACTH release is not inhibitable by the CRH antagonist, alpha-helical (alpha h) CRF [9-41]. Thus, IL-1 effects ACTH release at the level of both the hypothalamus and pituitary gland. Perhaps more importantly, the results suggest pituitary sensitization to cytokines, such as IL-1, as a new function for CRH. This action would represent a novel interactive point between the nervous, endocrine, and immune systems whereby very mild psychological or physical stress could have a profound impact on an inflammatory response by increasing pituitary sensitivity to immunological mediators such as IL-1.
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