Possible involvement of prostaglandin E in development of ACTH response in rats induced by human recombinant interleukin‐1.

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Abstract
1. Intravenous (I.V.) injection of human recombinant interleukin-1.alpha. (IL-1.alpha.) produced dose-dependent monophasic fevers in rats. Moreover, the I.V. injection of IL-1.alpha. produced dose-dependent rises in the plasma concentrations of adrenocorticotrophic hormone (ACTH) 30 min after injections with dosages of 5 .mu.g/kg and 15 .mu.g/kg of IL-1.alpha.. 2. The febrile responses induced by the I.V. injection of IL-1.alpha. (15 .mu.g/kg) were completely abolished, and conversely hypothermia occurred, when the animals were pre-treated with a cyclo-oxygenase inhibitor, indomethacin (INDO). Pre-treatment with INDO also inhibited the increase in the plasma concentrations of ACTH induced by I.V. injection of IL-1.alpha. (15 .mu.g/kg), indicating that enhancement of plasma concentrations of ACTH induced by I.V. injection of IL-1.alpha. is processed through the action of prostaglandins. 3. Intrapreoptic injection of prostaglandin E2 produced a dose-dependent fever with a rapid onset at doses of 25 and 100 ng. Moreover, the intrapreoptic injection of prostaglandin E2 increased the plasma concentrations of ACTH in a dose-dependent manner 30 min after injections. 4. The intrapreoptic injection of IL-1.alpha. (20 ng) caused slow monophasic fever. However, no significant elevation of plasma concentrations of ACTH was observed 30, 90 and 180 min after the intrapreoptic injection of IL-1.alpha., as compared with the ACTH levels at each time in the control group which received an intrapreoptic injection of saline. 5. These results suggest that intrapreoptic prostaglandin E plays an important role in the ACTH response by inducing the release of corticotrophin-releasing factor (CRF).