Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine.
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.
Karalis
K P
KP
Division of Endocrinology, Children's Hospital, Boston, MA 02115, USA. karalis@a1.tch.harvard.edu
Kontopoulos
E
E
Muglia
L J
LJ
Majzoub
J A
JA
D000311:Adrenal Glands / Q000502:physiology*; D000818:Animals; D002395:Catecholamines / Q000502:physiology; D003346:Corticotropin-Releasing Hormone / Q000502:physiology*; D004837:Epinephrine / Q000502:physiology*; D007249:Inflammation / Q000503:physiopathology*; D008297:Male; D051379:Mice; D018345:Mice, Knockout
D002395:Catecholamines; D003346:Corticotropin-Releasing Hormone; D004837:Epinephrine