Purpose: Brain inflammation occurs during epileptogenesis and may contribute to the development and progression of temporal lobe epilepsy. Recently, several studies have indicated that seizures may also increase specific blood plasma cytokine levels in animal models as well as in human patients with epilepsy, suggesting that peripheral inflammation may serve as a biomarker for epilepsy. Moreover, studies in epilepsy animal models have shown that peripheral inflammation may play either a pathogenic or neuroprotective role.
Methods: We evaluated the inflammatory response in blood plasma after electrically induced status epilepticus (SE) in a rat model for temporal lobe epilepsy. We measured blood plasma levels of the inflammation markers interleukin 1β (IL-1β), interleukin 6 (IL-6), by enzyme-linked immunosorbent assays (ELISAs) and C-reactive protein (CRP) by immunoturbidimetry, at 1 day after SE (acute period), at 1 week (during the latent period), and at 2 months after SE, which is the chronic epileptic phase when spontaneous seizures occur. Plasma levels were also measured during pilocarpine-induced SE. These were compared with plasma levels after lipopolysaccharide injection, which causes sepsis.
Key findings: Although sepsis induced a huge surge in IL-1β and IL-6 levels, we did not detect a change in IL-1β, IL-6, or CRP plasma levels at any time point after electrically induced SE compared to control animals. SE induced by pilocarpine produced a rise in IL-6 and CRP but not IL-1β levels.
Significance: These findings suggest that plasma levels of these inflammatory proteins cannot be used as biomarkers for temporal lobe epileptogenesis.
Wiley Periodicals, Inc. © 2013 International League Against Epilepsy.