Although the role of inflammation in epilepsy pathogenesis has been extensively investigated, the
inflammasome complex, a key component of neuroinflammation, has been understudied in epilepsy patients.
Methods: To better understand the involvement of this system in epilepsy, levels of inflammasome complex
components (NLRP1, NLRP3, CASP1, ASC), end-products of inflammasome complex activity [IL-1β, IL-18, nitric
oxide synthase (NOS) isoforms] and other inflammatory factors (NFκB, IL-6, TNF-α) were measured in peripheral
blood of patients with focal epilepsy of unknown cause (FEoUC) (n = 47), mesial temporal lobe epilepsy
with hippocampal sclerosis (MTLE-HS) (n = 35) and healthy controls using real time qPCR and/or ELISA.
Results: Inflammasome complex associated factors were either downregulated or unchanged in epilepsy patients.
Likewise, flow cytometry studies failed to show an increase in ratios of NLRP3-expressing CD3+ and CD14+
peripheral blood mononuclear cells (PBMC) in epileptic patients. Anti-neuronal antibody positive epilepsy patients
showed increased NLRP1 and neuronal NOS mRNA expression levels, whereas patients under poly-therapy
showed reduced serum inflammasome levels. FEoUC patients demonstrated increased PBMC NFκB mRNA expression
levels and serum IL-1β and IL-6 levels. Both MTLE-HS and FEoUC patients displayed higher ratios of
NFκB-expressing CD14+ PBMC than healthy controls.
Conclusions: Although previous clinical studies have implicated increased inflammasome complex expression
levels in epilepsy, our results indicate suppressed inflammasome complex activity in the peripheral blood of focal
epilepsy patients. Alternatively, the IL-6-NFκB signaling pathway, appears to be activated in focal epilepsy,
suggesting that factors of this pathway might be targeted for future theranostic applications.