Innate and adaptive immunity during epileptogenesis and spontaneous seizures: evidence from experimental models and human temporal lobe epilepsy.
By T. Ravizza, B. Gagliardi, Francesco M. Noe, K. Boer, Eleonora Aronica, A. Vezzani. Neurobiology of Disease, 2008
686 citations recorded by the source corpus.
We investigated the activation of the IL-1 beta system and markers of adaptive immunity in rat brain during epileptogenesis using models of temporal lobe epilepsy (TLE). The same inflammatory markers were studied in rat chronic epileptic tissue and in human TLE with hippocampal sclerosis (HS). IL-1 beta was expressed by both activated microglia and astrocytes within 4 h from the onset of status epilepticus (SE) in forebrain areas recruited in epileptic activity; however, only astrocytes sustained inflammation during epileptogenesis. Activation of the IL-1 beta system during epileptogenesis was associated with neurodegeneration and blood-brain barrier breakdown. In rat and human chronic epileptic tissue, IL-1 beta and IL-1 receptor type 1 were broadly expressed by astrocytes, microglia and neurons. Granulocytes appeared transiently in rat brain during epileptogenesis while monocytes/macrophages were present in the hippocampus from 18 h after SE onset until chronic seizures develop, and they were found also in human TLE hippocampi. In rat and human epileptic tissue, only scarce B- and T-lymphocytes and NK cells were found mainly associated with microvessels. These data show that specific inflammatory pathways are chronically activated during epileptogenesis and they persist in chronic epileptic tissue, suggesting they may contribute to the etiopathogenesis of TLE.
Subfields: Cellular and Molecular Neuroscience, Neurology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/a1ad45c0706e2f61b1df9b3ba7f6f14b910fbec5
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Citations in the corpus
- Toll-like receptor 4 and high-mobility group box-1 are involved in ictogenesis and can be targeted to reduce seizures (2010, background): “Pronounced inflammatory processes have been described in epileptogenic brain tissue from drug-resistant patients with temporal lobe epilepsy (TLE”