Cultured sympathetic neurons synthesize and release the cytokine interleukin 1 beta.
Open accessAbstract
Autonomic neurons help to regulate immune responses, and there are reciprocal interactions between the nervous and immune systems. This study seeks to define some of the molecular mechanisms that may underlie such interactions. Immunoblot analysis indicated that cultured sympathetic neurons synthesize and release the cytokine interleukin 1 beta (IL-1 beta). In addition, RNA blot analysis of cultured sympathetic neurons demonstrated that the neurons contain mRNA encoding IL-1 beta. It was previously shown that explant cultures of sympathetic ganglia and dissociated cocultures of neurons with ganglionic nonneuronal cells synthesize substance P, whereas in situ levels of substance P and its mRNA are low. An antagonist at the interleukin 1 receptor markedly depressed this increase in substance P in cultures, suggesting that endogenous IL-1 beta mediates the synthetic response, at least in part. Because pure neuronal cultures do not contain substance P and neurons synthesize and release IL-1 beta, the actions of the cytokine require the presence of ganglion nonneuronal cells. These observations suggest a role for autonomic neurons in influencing immune responses by synthesizing and secreting at least two known immunoregulators, the cytokine IL-1 beta and the neuropeptide substance P.
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Central cytokines are usually secreted from astrocytes or microglia, but neurons can secrete them in certain conditions.
“Central cytokines are usually secreted from astrocytes or microglia, but neurons can secrete them in certain conditions[12].”
From Neuroinflammation and cytokine abnormality in major depression: cause or consequence in that illness? (2016) · cites this paper as [12]
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- Authors
- Freidin, M., Bennett, M. V., & Kessler, J. A.
- Affiliations
- Albert Einstein College of Medicine (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1992-11
- Volume
- 89
- Issue
- 21
- Pages
- 10440-10443
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC50354
- OpenAlex
- W1989518830
- Cited by
- 113
- References
- 17
- Citations by year
- 2025: 3 · 2023: 5 · 2022: 4 · 2021: 5 · 2020: 2 · 2019: 2 · 2018: 4 · 2017: 4 · 2016: 3 · 2015: 3 · 2014: 6 · 2013: 2 · 2012: 2
- FWCI
- 2.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (NS-20778, R01NS020778, NS20013, R01NS020013)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Keywords
- IL-1β, sympathetic neurons, cytokine production, substance P, neuroimmune interactions, sympathetic ganglia, non-neuronal cells, interleukin-1 receptor antagonist, neuropeptides, immune regulation
- MeSH terms
- Animals, Animals, Newborn, Cells, Cultured, Cloning, Molecular, Ganglia, Sympathetic, Interleukin-1, Neurons, Recombinant Proteins, RNA, RNA, Messenger, Sialoglycoproteins, Immunoblotting, Restriction Mapping, Macromolecular Substances, Rats, Interleukin 1 Receptor Antagonist Protein
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