Abstract
We have investigated the effects of interleukin-1 beta (IL-1 beta) on the induction of substance P (SP) in cultured sympathetic ganglia. Northern blot analysis reveals that SP increases are secondary to an increase in mRNA coding for the preprotachykinin (PPT) precursor of SP. Nuclear transcription assays detect an early increase in PPT-specific nascent transcripts, suggesting that the ultimate effect of IL-1 is on transcription itself. Depolarizing agents, interferon-gamma, glucocorticoid hormones, and prostaglandin synthesis inhibitors all diminish the induction of SP and PPT mRNA by IL-1. Since SP has stimulatory effects on the immune system, the IL-1-induced increase in ganglionic SP may be one means by which the nervous and immune systems interact during an acute response to ganglionic injury.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Animals, Newborn
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Blotting, Northern
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Cell Nucleus / physiology
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DNA Probes
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Ganglia, Sympathetic / drug effects
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Ganglia, Sympathetic / physiology*
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Gene Expression Regulation / drug effects
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Indomethacin / pharmacology
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Interferon-gamma / pharmacology
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Interleukin-1 / pharmacology*
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Neurons / drug effects
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Neurons / physiology*
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Organ Culture Techniques
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Protein Precursors / genetics
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RNA, Messenger / genetics
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Rats
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Recombinant Proteins / pharmacology
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Substance P / genetics*
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Tachykinins / genetics
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Transcription, Genetic / drug effects
Substances
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DNA Probes
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Interleukin-1
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Protein Precursors
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RNA, Messenger
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Recombinant Proteins
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Tachykinins
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preprotachykinin
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Substance P
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Interferon-gamma
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Indomethacin