Rui Rangel (Portugal)

Centro Hospitalar Universitário do Porto (CHUP/HSA) Neurosurgery Department

Author Of 1 Presentation

Free Communication

IL-6 ROLE IN MESIAL TEMPORAL LOBE EPILEPSY DEVELOPMENT

Session Type
Free Communication
Date
04.10.2021, Monday
Session Time
11:30 - 12:50
Room
Free Communication A
Lecture Time
11:50 - 12:00
Presenter
  • Bárbara Guerra Leal (Portugal)

Abstract

Background and Aims:

Inflammation is an epilepsy hallmark with a prominent role assigned to Interleukin-6 (IL-6). This cytokine is claimed to partake in synaptic modulation and neuronal development. IL-6 overexpression has been documented in Mesial Temporal Lobe Epilepsy (MTLE) patients suggesting the influence of IL6 polymorphisms, namely rs1800795 (-174 G>C) in genetic susceptibility to MTLE. We sought to quantify IL-6 brain expression in MTLE patients and analyse the role of rs1800875 polymorphism in epilepsy susceptibility.

Methods:

A cohort of 212 MTLE patients (116 F; 111 with Febrile Seizure Antecendent; 165 refractory to treatment) and 143 healthy individuals were studied. All patients were diagnosed with Hippocampal Sclerosis (MTLE-HS). Twelve out of these patients have been submitted to resective surgery with hippocampal and adjacent neocortex tissue available for gene expression studies. As tissue control the same brain regions were obtained from 9 normal autopsied controls. Molecular biology techniques were applied in genotyping and gene expression analysis.

Results:

Rs1800795 genotypic and allelic frequencies were similar in MTLE-HS patients and controls (G: 68.4% vs 63.6%; C: 31.6% vs 36.4%. p = n.s). Noteworthy, MTLE-HS patients had a 3-fold higher IL-6 expression in hippocampus and neocortical tissue comparing to controls.

Conclusions:

Our results suggest that IL-6 overexpression is not genetically determined but may be seizure-induced. It is widely accepted that a vicious cycle seizure-damage-inflammation is associated with MTLE-HS progression. This hypothesis is supported by our observations in neocortical tissue, suggesting that IL-6 plays a role in MTLE-HS progression.

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