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Am J Physiol Regul Integr Comp Physiol 265: R739-R742, 1993;
0363-6119/93 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 265, Issue 4 739-R742, Copyright © 1993 by American Physiological Society

ARTICLES

Modulation of systemic interleukin-6 induction by central interleukin-1

M. G. De Simoni, A. De Luigi, L. Gemma, M. Sironi, A. Manfridi and P. Ghezzi
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.

Centrally administered interleukin (IL)-1 [both alpha and beta forms, 200 ng/rat intracerebroventricularly (icv)] results in a larger increase in serum IL-6 than after systemic injection, indicating the brain's role in the acute phase response. This action was prevented by the IL-1-receptor antagonist IL-1Ra (20 micrograms/rat icv). Neither antiserum against corticotropin-releasing factor (CRF) nor the alpha-helical-CRF antagonist (25 micrograms/rat icv) affected IL-6 induction by central IL-1 beta, which, however, was significantly prevented by the synthetic glucocorticoid dexamethasone [3 mg/kg intraperitoneally (ip)]. Naloxone, the opiate antagonist, but not naloxone methiodide, its quaternary salt that does not penetrate the blood-brain barrier (both administered at 10 mg/kg ip), antagonized this action of IL-1 beta. After intracerebroventricular IL-1 beta, IL-6 levels in brain areas (striatum, hippocampus, hypothalamus) were extremely low, suggesting that the brain does not significantly contribute to IL-6 synthesis in this condition. The results show that induction of high serum IL-6 levels by central IL-1 beta is mediated by brain IL-1 receptors and is sensitive to inhibition by corticosteroids. The inhibitory effect of naloxone suggests that central opiates are required for this action of IL-1 beta.


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