Interleukin-1-β Modulation of Prolactin Secretion from Rat Anterior Pituitary Cells: Involvement of Adenylate Cyclase Activity and Calcium Mobilization*

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Abstract
Recent findings indicate that interleukin-1β (IL1β), a monokine secreted by stimulated macrophages and monocytes, modulates neuroendocrine functions in a manner similar to classical hormones. In this study we show that IL1 modulates PRL secretion, assessed by reverse hemolytic plaque assay, and describe the effect of the monokine on adenylate cyclase activity and calcium fluxes in rat normal pituitary cells. In basal and vasoactive intestinal peptide (VIP)-stimulated conditions, low doses of ILl reduced the mean plaque area, a direct index of PRL secretion without affecting the percentage of PRLsecreting cells. Similarly, low concentrations of ILl inhibited adenylate cyclase activity in both basal and VIP-stimulated conditions, while higher concentrations restored the enzymatic activity to the control value. ILl also caused a biphasic effect on the free intracellular calcium increase induced by maitotoxin, a calcium channel activator, being inhibitory at low and stimulatory at high concentrations. The effects of ILl on adenylate cyclase activity and calcium fluxes were reversed by preincubation of the monokine with its polyclonal antibody, thus confirming the specificity of the effects. In conclusion, our data show that ILl modulates PRL secretion by acting directly on pituitary cells through interaction with the adenylate cyclase-cAMP system and calcium flux. (Endocrinology126: 1435–1441, 1990)