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Involvement of nuclear factor-kappa B in induction of the interleukin-6
gene by leukemia inhibitory factor
HJ Gruss, MA Brach and F Herrmann
Department of Internal Medicine I, University of Freiburg Medical Center,
Germany.
Recent studies have indicated that the leukemia inhibitory factor (LIF)
induces secretion of interleukin-6 (IL-6) in myeloid cells. We here show
that synthesis of IL-6 by human mononuclear phagocytes exposed to
recombinant human (rh) LIF is preceded by an increase of IL-6 transcript
levels as a result of transcriptional activation of the IL-6 gene. Analysis
of deleted fragments of the IL-6 promoter indicated that transcriptional
activation of the IL-6 promoter was associated with enhanced binding
activity of the transcription factor nuclear factor (NF)-kappa B. Binding
of activation protein (AP)-1 and NF-IL-6, also known to transcriptionally
activate the IL-6 promoter, was not inducible by LIF. Furthermore,
introduction of the NF-kappa B sequence into a heterologous promoter
construct, but not of AP-1- and NF-IL-6- binding sequences, conferred
inducibility by LIF to this promoter. Deletion of the NF-kappa B binding
site in the IL-6 promoter was associated with loss of inducibility by LIF,
lending further support for the notion that the NF-kappa B binding site is
crucial for LIF- mediated induction of the IL-6 promoter. Taken together,
our results show that rhLIF induces IL-6 gene expression in mononuclear
phagocytes through transcriptional gene activation involving NF-kappa B.
Volume 80,
Issue 10,
pp. 2563-2570,
11/15/1992
Copyright © 1992 by The American Society of Hematology
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