Interleukin-1 stimulates ACTH release by an indirect action which requires endogenous corticotropin releasing factor.
The present study was performed in order to clarify the mechanism by which interleukin-1 (IL-1) activates the hypothalamic-pituitary-adrenal (H-P-A) axis. The iv administration of IL-1 into freely moving, conscious rats significantly elevated the plasma levels of ACTH. This ACTH response to IL-1 was, however, completely abolished by preinjection of 0.5 ml rabbit antiserum generated against rat CRF, but not by normal rabbit serum (NRS). The IL-1-induced ACTH release did not seem to be caused by a general stress effect of IL-1 because plasma PRL levels, another indicator of a stress response, were not altered by the injection of IL-1. These results suggest that IL-1 acts centrally in the brain to stimulate the secretion of CRF, thereby eliciting ACTH release, and that a direct action of IL-1 on the pituitary gland is unlikely.
Uehara
A
A
US-Japan Biomedical Research Laboratories, Tulane University Hebert Center, Belle Chasse, LA 70037.
Gottschall
P E
PE
Dahl
R R
RR
Arimura
A
A
D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism*; D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000502:physiology*; D007158:Immunologic Techniques; D007275:Injections, Intravenous; D007375:Interleukin-1 / Q000494:pharmacology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013268:Stimulation, Chemical
D007375:Interleukin-1; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone