Release of Multiple Hormones by a Direct Action of Interleukin-1 on Pituitary Cells

TLDR

Bacterial endotoxins are known to trigger anterior pituitary hormone release and induce IL‑1 production by macrophages and monocytes. The study examined whether IL‑1 directly modulates hormone secretion in cultured rat pituitary monolayers. IL‑1β at 10⁻⁹–10⁻¹² M stimulated ACTH, LH, GH, and TSH while suppressing prolactin, effects that were neutralized by anti‑IL‑1 antibody, indicating IL‑1 can directly regulate pituitary hormones during infection.

Abstract

Exposure to bacterial endotoxins has long been known to stimulate the release of anterior pituitary hormones; administration of endotoxin was at one time a common clinical test of anterior pituitary function. Endotoxin is a potent stimulus for production of the endogenous pyrogenic protein, interleukin-1 (IL-1), by macrophages and monocytes. The possibility that IL-1 has a direct effect on the secretion of hormones by rat pituitary cells in a monolayer culture was investigated. Recombinant human IL-1β stimulated the secretion of adrenocorticotropic hormone, luteinizing hormone, growth hormone, and thyroid-stimulating hormone. Increased hormone secretion into culture supernatants was found with IL-1 concentrations ranging from 10 -9 M to 10 -12 M . Prolactin secretion by the monolayers was inhibited by similar doses. These concentrations of IL-1 are within the range reported for IL-1 in serum, suggesting that IL-1 generated peripherally by mononuclear immune cells may act directly on anterior pituitary cells to modulate hormone secretion in vivo. Incubation of IL-1 solutions with antibody to IL-1 neutralized these actions. These pituitary effects of IL-1 suggest that this monokine may be an important regulator of the metabolic adaptations to infectious stressors.