Inflammatory aspects of epileptogenesis: contribution of molecular inflammatory mechanisms.
OBJECTIVE
Epilepsy is a chronic neurological disease characterised with seizures. The aetiology of the most generalised epilepsies cannot be explicitly determined and the seizures are pronounced to be genetically determined by disturbances of receptors in central nervous system. Besides, neurotransmitter distributions or other metabolic problems are supposed to involve in epileptogenesis. Lack of adequate data about pharmacological agents that have antiepileptogenic effects point to need of research on this field. Thus, in this review, inflammatory aspects of epileptogenesis has been focussed via considering several concepts like role of immune system, blood-brain barrier and antibody involvement in epileptogenesis.


METHODS
We conducted an evidence-based review of the literatures in order to evaluate the possible participation of inflammatory processes to epileptogenesis and also, promising agents which are effective to these processes. We searched PubMed database up to November 2015 with no date restrictions.


RESULTS
In the present review, 163 appropriate articles were included. Obtained data suggests that inflammatory processes participate to epileptogenesis in several ways like affecting fibroblast growth factor-2 and tropomyosin receptor kinase B signalling pathways, detrimental proinflammatory pathways [such as the interleukin-1 beta (IL-1β)-interleukin-1 receptor type 1 (IL-1R1) system], mammalian target of rapamycin pathway, microglial activities, release of glial inflammatory proteins (such as macrophage inflammatory protein, interleukin 6, C-C motif ligand 2 and IL-1β), adhesion molecules that are suggested to function in signalling pathways between neurons and microglia and also linkage between these molecules and proinflammatory cytokines.


CONCLUSIONS
The literature research indicated that inflammation is a part of epileptogenesis. For this reason, further studies are necessary for assessing agents that will be effective in clinical use for therapeutic treatment of epileptogenesis.
1Department of Pharmacology,Faculty of Pharmacy,Anadolu University,Eskisehir,Turkey.
Feyza
F
Alyu
1Department of Pharmacology,Faculty of Pharmacy,Anadolu University,Eskisehir,Turkey.
Miriş
M
Dikmen
D000818:Animals; D000906:Antibodies / Q000378:metabolism; D001812:Blood-Brain Barrier / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism; D004660:Encephalitis / Q000378:metabolism*; D004827:Epilepsy / Q000378:metabolism*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D017628:Microglia / Q000378:metabolism; D009414:Nerve Growth Factors / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D015398:Signal Transduction; D013602:T-Lymphocytes, Cytotoxic / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism
D000906:Antibodies; D016207:Cytokines; D018836:Inflammation Mediators; D009414:Nerve Growth Factors; D051193:Toll-Like Receptors
epilepsy; epileptogenesis; inflammation