Differential modulation of various inflammatory mediators in mesial temporal lobe epilepsy and focal cortical dysplasia patients

Introduction: Neuroinflammation and innate immunity play important role in the pathogenesis of epilepsy. Cytokines and chemokines induced inflammation may lead to a disturbance of the glutamatergic system, and subsequently to the persistence of seizures by chronic neuronal over excitation. Numerous candidate gene specific studies have postulated the role of inflammatory and immune modulators in neuronal death and/or development of pharmacoresistance in MTLEHS however there are not many reports in FCD. Therefore, in this study we have used a multiplex immunoassay approach to measure multiple inflammatory mediators (cytokines, chemokines and growth factors) which includes IL1[H9252], IL1Ra, IL6, IL10, MIP1A (CCL3), MIP1B (CCL4) and TNF[H9251] in brain tissues resected from MTLE and FCD patients.

Methods: Tissue samples collected from MTLE, FCD and tumor periphery of glioma patients (non-epileptic controls) were assessed by quantitative cytokine assays using a customized Bioplex^TM Pro-human cytokine 8-plex panel kit. Scattered plots were generated using SigmaPlot version 13.

Results and conclusion: Analysis of FCD tissue highlighted differences with MTLE. Upregulation of IL-1[H9252], IL-1Ra, IL-6, MIP-1[H9251] and MIP-1[H9252] were observed in both MTLE and FCD patients as compared to controls. Except IL-1[H9252], upregulation was relatively higher in FCD. IL-10 showed down regulation in both, MTLE and FCD as compared to controls. TNF-[H9251] did not show any significant change between groups. Our results are in line with data from mRNA profiling studies on human epileptic tissues. The mechanism and clinical implications of these epilepsy-related immune alterations need to be clarified in a larger cohort of patients with a goal of developing potential anti-epileptic treatment strategies.