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Six different cytokines that share GP130 as a receptor subunit, induce
serum amyloid A and potentiate the induction of interleukin-6 and the
activation of the hypothalamus-pituitary-adrenal axis by interleukin-1
F Benigni, G Fantuzzi, S Sacco, M Sironi, P Pozzi, CA Dinarello, JD Sipe, V Poli, M Cappelletti, G Paonessa, D Pennica, N Panayotatos and P Ghezzi
Division of Geographic Medicine and Infectious Diseases, New England
Medical Center, Boston, MA, USA.
Ciliary neurotrophic factor (CNTF) and interleukin-6 (IL-6) potentiate the
elevation of serum corticosterone induced by suboptimal doses of
interleukin-1 (IL-1). CNTF also potentiates IL-1-induced serum IL-6. Here,
we report that four other cytokines (leukemia inhibitory factor [LIF],
oncostatin M [OSM], interleukin-11 and cardiotrophin-1) also potentiated
the elevation of serum corticosterone and IL-6 levels induced by IL-1.
Furthermore, all the six cytokines studied induced the acute-phase protein
serum amyloid A when administered alone. Because these cytokines differ
both in structure and in function, but share gp130 as a subunit of their
receptors, these results indicate that signaling through gp130 mediates
potentiation of IL-1 activities. The potentiation of IL-1-induced serum
corticosterone levels is not a consequence of the increased serum IL-6
observed after IL-1 administration. In fact, in IL-6 deficient mice, IL-1
increased serum corticosterone to a level comparable to that observed in
wild-type mice. Thus, either endogenous IL-6 does not mediate IL-1-induced
corticosterone increase, or its role may be fulfilled by other cytokines.
To the extent that gp130-dependent cytokines may serve this role, they may
be important feedback regulators of inflammation through the activation of
the hypothalamus-pituitary-adrenal axis and the potentiation of acute-phase
protein synthesis.
Volume 87,
Issue 5,
pp. 1851-1854,
03/01/1996
Copyright © 1996 by The American Society of Hematology
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