Interleukin-1-beta induces pituitary adrenocorticotropin secretion: evidence for glucocorticoid modulation.

Using an in vitro continuous perifusion system, the effects of interleukin-1 (IL-1) on adrenocorticotropin (ACTH) secretion at the pituitary level were investigated. On one hand, we observed that IL-1 beta increases ACTH secretion from perifused anterior pituitary cells in a dose-dependent manner, between 1.5 and 6 pM. This stimulatory action of IL-1 on ACTH was significantly attenuated by a short in vitro dexamethasone pretreatment. This fact suggests a regulatory glucocorticoid negative feedback analogous to that observed upon the pituitary action of corticotropin-releasing factor (CRF). We also examined the effect of simultaneous treatment with IL-1 and CRF. The results indicated that the effect of IL-1 resulted additive to the CRF-induced ACTH secretion. It is concluded that the anterior pituitary could be an important site of IL-1 action to activate the hypothalamic-pituitary-adrenocortical axis function, and that this action is under an inhibitory glucocorticoid regulation.