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The role of interleukin-1beta in febrile seizures Heida JG; Moshe SL; Pittman QJBrain Dev 2009[May]; 31 (5): 388-93Febrile 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.|Animals[MESH]|Brain/drug effects/*immunology/*physiopathology[MESH]|Disease Models, Animal[MESH]|Hippocampus/drug effects/immunology/physiopathology[MESH]|Humans[MESH]|Hypothalamus/drug effects/immunology/physiopathology[MESH]|Infant[MESH]|Interleukin 1 Receptor Antagonist Protein/pharmacology/*physiology[MESH]|Interleukin-1beta/pharmacology/*physiology[MESH]|Neuroimmunomodulation/drug effects/physiology[MESH]|Rats[MESH]|Seizures, Febrile/*immunology/metabolism/*physiopathology[MESH]|Synaptic Transmission/drug effects/immunology[MESH] |
