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Review
. 2009 May;31(5):388-93.
doi: 10.1016/j.braindev.2008.11.013. Epub 2009 Feb 13.

The role of interleukin-1beta in febrile seizures

James G Heida  1 , Solomon L Moshé, Quentin J Pittman
Affiliations
Review

The role of interleukin-1beta in febrile seizures

James G Heida et al. Brain Dev. 2009 May.

Abstract

Febrile seizures (FS) occur in children as a result of fever. Despite their prevalence, the pathophysiology of FS has remained unclear. Recent evidence from clinical and experimental studies has highlighted a potential role of immune generated products in the genesis of FS. Of particular interest are the pro-inflammatory cytokine, interleukin-1beta (IL-1beta) and its naturally occurring antagonist, interleukin 1 receptor antagonist (IL-1ra). Using a novel animal model of FS, involving the generation of physiological fever, we investigated the role of the IL-1beta/IL-1ra system in the genesis of FS. We found that animals with FS had increased hippocampal and hypothalamic IL-1beta compared to equally treated animals without FS, which was first evident at onset of FS in the hippocampus. There were no differences in IL-1ra levels. ICV IL-1beta increased the number of animals with FS while IL-1ra had an opposite anti-convulsant effect. The data from these studies, in combination with recent results from other laboratories, have established a putative role for the IL-1beta/IL-1ra system in the genesis of FS.

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Figures

FIGURE 1
FIGURE 1
The peripheral and central response to LPS. Peripherially LPS stimulates macrophages to secrete pro- and anti-inflammatory cytokines. These can then act through perivascular endothelial cells circumventricular organs (CVOs) or vagal afferents to stimulate COX-2. COX-2 activation increases the production of prostaglandin E2 which then causes fever (path 1). At the same time pro- (TNFα, IL-1β, and IL-6) and anti-flammatory (IL-1ra) cytokines are generated in the brain (path 2). These cytokines have been shown to modulate neurotransmission and ultimately could contribute to the generation of seizures during fever.
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