Oct 1, 1987

Interleukin-1 stimulates ACTH release by an indirect action which requires endogenous corticotropin releasing factor

Endocrinology
A UeharaA Arimura

Abstract

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.

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Mentioned in this Paper

Corticotropin Releasing Hormone Measurement
Crh
Biological Adaptation to Stress
Response to interleukin-1
Intravenous Injections
Interleukin-1
POMC wt Allele
August Rats
Pituitary Diseases
Brain

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