Cited by 139Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersTraumatic Brain Injury and Neurovascular Disturbances

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Interleukin‐1 in the Brain: Mechanisms of Action in Acute Neurodegeneration

PATEL, H. C., BOUTIN, H., ALLAN, S. M.·2003·Annals of the New York Academy of Sciences

DOI 10.1111/j.1749-6632.2003.tb03136.x

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Abstract

A bstract: Interleukin‐1 (IL‐1) exerts a number of diverse actions in the brain, and it is currently well accepted that it contributes to experimentally induced neurodegeneration. Much of this is based on studies using the IL‐1 receptor antagonist, which inhibits cell death caused by ischemia, brain injury, or excitotoxins. Our aim is to determine how and where in the brain IL‐1 acts to produce these effects. Most of the neurodegenerative effects of IL‐1 are thought to be through IL‐1β. However, we have data implicating IL‐1α in excitotoxic cell death. Furthermore mice lacking both IL‐1α and IL‐1β show dramatically reduced ischemic cell death, whereas deletion of IL‐1α or IL‐1β alone fails to modify damage. It has also been demonstrated that IL‐1 exacerbates ischemic injury in mice in the absence of the type I IL‐1 receptor, suggesting the existence of novel IL‐1 receptors in the brain. IL‐1 also dramatically exacerbates neuronal loss in response to intrastriatal administration of the excitotoxin AMPA in the rat brain, an effect accompanied by marked increases in cytokine expression in the frontoparietal cortex, which precedes subsequent cell death in this region. Intrastriatal AMPA also results in limbic seizures that are exacerbated by IL‐1, and we hypothesize, therefore, that IL‐1 exacerbates cell death through increased seizure activity. Therefore, IL‐1 appears to induce acute neurodegeneration through a number of mechanisms.

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Authors: PATEL, H. C., BOUTIN, H., & ALLAN, S. M.
Affiliations: University of Manchester (GB)
Corresponding author: ALLAN, S. M.
ORCID: PATEL, H. C.
BOUTIN, H.
ALLAN, S. M.
Venue: Annals of the New York Academy of Sciences
Publisher: Wiley
Published: 2003-05
Volume: 992
Issue: 1
Pages: 39-47
ISSN: 0077-8923 (ISSN-L)
1749-6632
DOI: 10.1111/j.1749-6632.2003.tb03136.x
OpenAlex: W2021461507
Cited by: 139
References: 34
Citations by year: 2026: 1 · 2025: 4 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 4 · 2020: 4 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 5 · 2015: 2 · 2014: 4 · 2013: 7 · 2012: 11
FWCI: 1.73
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 999 d)
Locations: Annals of the New York Academy of Sciences (publishedVersion)
PubMed (publishedVersion)
HAL (submittedVersion)
Research Explorer (The University of Manchester) (submittedVersion)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords: interleukin-1, interleukin-1 alpha, IL-1β, neurodegeneration, excitotoxic cell death, ischemic cell death, interleukin-1 receptor antagonist, IL-1 receptor type I, limbic seizures, cytokine expression, brain injury
MeSH terms: Acute Disease, Animals, Brain, Brain Injuries, Brain Ischemia, Disease Models, Animal, Humans, Interleukin-1, Nerve Degeneration, Recombinant Proteins, Seizures, Mice

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Interleukin‐1 in the Brain: Mechanisms of Action in Acute Neurodegeneration

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