Molecular cascades that mediate the influence of inflammation on epilepsy

Epilepsia. 2011 May;52 Suppl 3(0 3):33-9. doi: 10.1111/j.1528-1167.2011.03034.x.


Experimental evidence strongly indicates a significant role for inflammatory and immune mediators in initiation of seizures and epileptogenesis. Here we will summarize data supporting the involvement of IL-1β, TNF-α and toll-like receptor 4 in seizure generation and the process of epileptogenesis. The physiological homeostasis and control over brain immune response depends on the integrity of the blood-brain barrier, transforming growth factor (TGF)-β signaling and leukocyte migration. To what extent targeting the immune system is successful in preventing epileptogenesis, and which signaling pathway should be beleaguered is still under intensive research.

Publication types

  • Review

MeSH terms

  • Animals
  • Blood-Brain Barrier / immunology
  • Blood-Brain Barrier / pathology
  • Blood-Brain Barrier / physiopathology
  • Encephalitis / immunology*
  • Encephalitis / pathology
  • Epilepsy / immunology
  • Epilepsy / metabolism
  • Epilepsy / pathology*
  • Humans
  • Interleukin-1beta / physiology
  • Signal Transduction / immunology
  • Signal Transduction / physiology*
  • Tumor Necrosis Factor-alpha / physiology


  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha