Cited by 859Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersNeurogenesis and neuroplasticity mechanisms

Interleukin 1 of the central nervous system is produced by ameboid microglia.

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Giulian, D, Baker, T J, Shih, L C, Lachman, L B·1986·The Journal of experimental medicine

Abstract

By screening specific populations of rat brain cells, we found that ameboid microglia secrete an 18 kD peptide with IL-1 biological activity. The IL-1 activity released by microglia was found to be identical to rat macrophage IL-1 on fractionation by gel filtration and high pressure liquid anion-exchange chromatography, and it was neutralized by an antiserum specific for murine IL-1. When added to astroglia grown in culture, microglial IL-1 increased the cell number of five- to sevenfold, and increased astroglial incorporation of [3H]thymidine by three- to fivefold. We propose that the proliferation of astroglia in specific brain regions may be regulated by the signaled release of IL-1 from activated microglial cells.

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Crossref · 10.1084/jem.164.2.594

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  • IL-1β is produced primarily by activated microglia and macrophages.

    “IL-1β is another prominent pro-inflammatory cytokine that is produced primarily by activated microglia and macrophages (Giulian et al., 1986; Sairanen et al., 1997).”

    From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Giulian et al., 1986

    The Results (p. 597) show that stimulated rat microglia release IL-1, and the Discussion (p. 602) identifies ameboid microglia as the major producers of brain IL-1 in vitro. The paper also discusses macrophage IL-1, but it does not identify the measured cytokine specifically as IL-1β or establish that microglia and macrophages are its primary producers generally. (LLM, conf=0.88)

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  • Intraventricular administration of IL-1β was sufficient to induce lipid peroxidation in adult rats, highlighting the causal relationship between inflammatory signaling and metabolic stress.

    “Furthermore, intraventricular administration of IL-1β was sufficient to induce lipid peroxidation in adult rats, highlighting the causal relationship between inflammatory signaling and metabolic stress, the two major characteristics of aging (Giulian et al, 1986).”

    From Microglia Priming with Aging and Stress (2017) · cites this paper as Giulian et al, 1986

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Authors
Giulian, D., Baker, T. J., Shih, L. C., & Lachman, L. B.
Venue
The Journal of experimental medicine
Published
1986-08-01
Volume
164
Issue
2
Pages
594-604
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2159746265
Cited by
859
References
33
Citations by year
2026: 3 · 2025: 8 · 2024: 2 · 2023: 2 · 2022: 7 · 2021: 2 · 2020: 5 · 2019: 4 · 2018: 4 · 2017: 6 · 2016: 8 · 2015: 10 · 2014: 12 · 2013: 10 · 2012: 14
FWCI
21.91
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
  • National Eye Institute (EY04915)
  • National Cancer Institute (CA 38043)
  • National Institute of Neurological Disorders and Stroke (NS2311301)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
interleukin-1, ameboid microglia, microglial activation, astrocyte proliferation, neuroinflammation, rat brain
MeSH terms
Animals, Astrocytes, Brain, Cell Division, Cell Separation, Interleukin-1, Lymphocyte Activation, Nerve Growth Factors, Phagocytes, T-Lymphocytes, Rats

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