Serum levels of inflammasome complex factors are suppressed in focal epilepsy patients

Küçükali C. İ., Tüzün E., Ulusoy C. A., Bebek N., Baykal B.

AAN 71st Annual Meeting, Pennsylvania, United States Of America, 4 - 10 May 2019, pp.92-15

  • Publication Type: Conference Paper / Summary Text
  • City: Pennsylvania
  • Country: United States Of America
  • Page Numbers: pp.92-15
  • Istanbul University Affiliated: Yes


Objective: To investigate the role of inflammasomes in focal epilepsy syndromes with and without neuronal autoantibodies (NOA).

Background: Although there is increasing evidence on the importance of inflammation in the pathophysiology of epilepsy, the role of inflammasome complex in focal epilepsy has not been studied in detail.

Design/Methods: Consecutive patients diagnosed with focal epilepsy of unknown cause (FEoUC) (n=47) or mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) (n=35) as per International League against Epilepsy classification criteria and healthy controls (n=47) were enrolled. Serum levels of inflammasome complex components (NLRP1, NLRP3, ASC, caspase-1), pro-inflammatory and anti-inflammatory cytokines (IL-1β, IL-6, TNF-α, IL-4, IL-10, IL-18), nuclear factor kappaB (NF-KB), HMGB1 and nitric oxide synthase (NOS) isoforms were measured with ELISA. NOA were investigated with cell-based assays.

Results: The onset age of epilepsy was 16.30 ± 11.45, the duration of the disease was 21.28 ± 12.00 years. In 10 epilepsy patients various NOA (NMDAR, CASPR2, GAD, VGKC-complex and glycine receptor antibodies) were identified. In the epilepsy group all investigated parameters of inflammation were found to be reduced as compared to the healthy controls. Moreover, levels of major inflammasome complex components were significantly lower in patients receiving polytherapy (NLRP1, p=0.017; NLRP3 p=0.020). Although patients with NOA showed trends towards higher inflammasome factor levels, these differences did not attain statistical significance. No significant association could be found with treatment resistance.

Conclusions: Our findings suggest that levels of inflammasome components are suppressed by antiepileptic medications. Alternatively, serum levels of inflammation factors might have been reduced due to overconsumption of these molecules in the epileptic brain. Prospective studies with newly diagnosed patients without treatment and measurement of inflammasome factor levels in the surgically resected brain tissues of epilepsy patients are required to understand the precise role of inflammasome molecules in chronic epilepsy.