Interleukin-1 induces substance P in sympathetic ganglia through the induction of leukemia inhibitory factor (LIF)

It has become increasingly clear that immune cytokines perform growth and differentiation functions in the nervous system similar to those performed in the immune system. In previous studies we have shown that interleukin-1 beta (IL-1 beta) raises substance P (SP) and the mRNA coding for its preprot...

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Bibliographic Details
Published in:The Journal of neuroscience 1993-06, Vol.13 (6), p.2601-2609
Main Authors: Shadiack, AM, Hart, RP, Carlson, CD, Jonakait, GM
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Base Sequence
Biological and medical sciences
Choline O-Acetyltransferase - metabolism
Culture Media, Conditioned
Dexamethasone - pharmacology
Fundamental and applied biological sciences. Psychology
Ganglia, Sympathetic - cytology
Ganglia, Sympathetic - metabolism
Growth Inhibitors - genetics
Growth Inhibitors - metabolism
Interleukin-1 - pharmacology
Interleukin-6
Isolated neuron and nerve. Neuroglia
Leukemia Inhibitory Factor
Lymphokines - genetics
Lymphokines - metabolism
Molecular Probes - genetics
Molecular Sequence Data
Neurons - metabolism
Polymerase Chain Reaction
Precipitin Tests
Rats
RNA, Messenger - metabolism
Substance P - metabolism
Veratrine - pharmacology
Vertebrates: nervous system and sense organs
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Summary:It has become increasingly clear that immune cytokines perform growth and differentiation functions in the nervous system similar to those performed in the immune system. In previous studies we have shown that interleukin-1 beta (IL-1 beta) raises substance P (SP) and the mRNA coding for its preprotachykinin precursor in cultured sympathetic superior cervical ganglia (SCG) (Jonakait and Schotland, 1990; Hart et al., 1991a). The action of IL-1 is blocked both by depolarization of the ganglia and by glucocorticoid hormones (Hart et al., 1991a). In the present report, we have found that IL-1 does not act directly upon neurons to raise SP, but rather induces the production of a soluble intermediate molecule that raises both SP and the cholinergic-specific enzyme ChAT. Its induction by IL-1 is blocked by the synthetic glucocorticoid hormone dexamethasone; its action is compromised under depolarizing conditions. Because medium conditioned by IL-1 (IL-1CM) is functionally similar to leukemia inhibitory factor (LIF), we sought to determine whether this molecule might be an active constituent of IL-1CM. Immunoprecipitation with an antiserum directed against LIF eliminated large proportions of SP-inducing activity from IL-1CM. In addition, steady-state levels of mRNA coding for LIF are increased by IL-1 treatment of SCG. These data suggest that LIF, induced by IL-1, may ultimately be responsible for the IL-1 induction of SP.
ISSN:0270-6474
1529-2401
DOI:10.1523/jneurosci.13-06-02601.1993