Induction of pituitary sensitivity to interleukin-1: A new function for corticotropin-releasing hormone

Academic Article


  • 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, α-helical (αh) 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. © 1994 Academic Press, Inc.
  • Authors

    Digital Object Identifier (doi)

    Pubmed Id

  • 5808069
  • Author List

  • Payne LC; Weigent DA; Blalock JE
  • Start Page

  • 480
  • End Page

  • 484
  • Volume

  • 198
  • Issue

  • 2