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Interleukin-1 system in CNS stress: seizures, fever, and neurotrauma

Academic Article
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Overview

authors

  • Bartfai, Tamas
  • Sanchez-Alavez, Manuel
  • Andell-Jonsson, S.
  • Schultzberg, M.
  • Vezzani, A.
  • Danielsson, E.
  • Conti, Bruno

publication date

  • 2007

journal

  • Annals of the New York Academy of Sciences  Journal

abstract

  • Proteins of the interleukin-1 (IL-1) system include the secreted agonist IL-1beta, and the receptor antagonist IL-1ra, both competing for binding to the IL-1 receptor (IL-1R). IL-1beta and IL-1ra are highly inducible under different forms of stress, such as excitatory neurotransmitter excess occurring during seizures, in infection and inflammation, and during neurotrauma. In each of these conditions induction of IL-1beta precedes that of IL-1ra, resulting in up to 10-20-fold elevation of IL-1beta concentrations. Consequently, IL-1beta induces the elevation of other proinflammatory molecules, including IL-6, IL-1R1, COX2, and iNOS, as well as of IL-1ra. Elevation of IL-1ra is of key importance for quenching the inflammatory response at the IL-1R1 as part of an autoregulatory loop. In seizures, IL-1ra is a strong anticonvulsant and in IL-1beta-dependent fever, a powerful antipyretic. In traumatic brain injury (TBI), the ability of patients to mount an IL-1ra response, as measured in the CSF, strongly correlated with the neurological outcome. Selective induction or pharmacological application of IL-1ra may be sparing neurons in seizures and neurotrauma.

subject areas

  • Animals
  • Brain Injuries
  • Central Nervous System
  • Disease Models, Animal
  • Fever
  • Humans
  • Infection
  • Inflammation
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1beta
  • Mice
  • Mice, Transgenic
  • Neurons
  • Neurotransmitter Agents
  • Seizures
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Research

keywords

  • anticonvulsant
  • fever
  • interleukin-1 beta; interleukin-1 receptor antagonist
  • neurotrauma
  • seizure
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Identity

International Standard Serial Number (ISSN)

  • 0077-8923 978-1-57331-675-0

Digital Object Identifier (DOI)

  • 10.1196/annals.1391.022

PubMed ID

  • 17656565
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Additional Document Info

start page

  • 173

end page

  • 177

volume

  • 1113

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