Abstract
BackgroundIncreasing evidence supports the role of soluble inflammatory mediators in the pathogenesis of refractory temporal lobe epilepsy (TLE). Hippocampal sclerosis (HS) is a well-described pathohistological abnormality in TLE. The association of proinflammatory cytokines with epileptic disease profiles is well established; however, the potential significance of circulating interleukin 10 (IL-10), particularly in TLE-associated HS, is still poorly understood. Therefore, taking into consideration the neuroprotective and anticonvulsive effects of IL-10, we performed this study to examine the role of the plasma levels of IL-10 in patients with TLE with HS (TLE + HS), TLE without HS (TLE-HS) and with other types of epilepsy.MethodsThis study included 270 patients with refractory epilepsy who were classified into four groups: i) 34 patients with TLE + HS, ii) 105 patients with TLE-HS, iii) 95 patients with extra-TLE (XLE) and iv) 36 patients with idiopathic generalized epilepsy (IGE). The plasma IL-10 levels were quantified using a commercially available enzyme-linked immunosorbent assay (ELISA).ResultsIL-10 levels were significantly lower in TLE + HS than in TLE-HS (p = 0.013). In a subgroup of TLE-HS patients who had seizures 1 month before sampling, patients with seizures had significantly higher IL-10 levels than patients who were seizure-free (p = 0.039). Among a small group (n = 15) of non-refractory TLE-HS patients, IL-10 levels showed a moderate negative correlation with the duration of epilepsy (r = − 0.585, p = 0.023).ConclusionsThis study demonstrated that chronically reduced levels of plasma IL-10 were associated with HS in TLE patients, suggesting that there was an inadequate systemic anti-inflammatory immune response. These results could provide new biological insights into the pathophysiology of HS in TLE. We also found that the production of IL-10 could be affected by the seizure frequency and declined concomitantly with increased disease durations. Therefore, the measurement of plasma IL-10 may have diagnostic value as a biomarker for stratifying TLE + HS from other epilepsy types or as a marker of disease progression towards a progressive form of epilepsy.
Highlights
Increasing evidence supports the role of soluble inflammatory mediators in the pathogenesis of refractory temporal lobe epilepsy (TLE)
We showed that IL-6 is increased in the plasma of TLE patients compared to extra-temporal lobe epilepsy (XLE) patients, suggesting that the epilepsy type is a major factor in the seizure-induced production of IL-6 [7]
Assessment of interleukin 10 (IL-10) levels in different patient cohorts Among the study groups, the plasma levels of IL-10 were significantly lower in the TLE + Hippocampal sclerosis (HS) group than in the TLE without HS (TLE-HS) group (p = 0.035) but were not lower than those in the Extra-temporal lobe epilepsy (XLE) group (p = 0.126)
Summary
Increasing evidence supports the role of soluble inflammatory mediators in the pathogenesis of refractory temporal lobe epilepsy (TLE). Growing evidence suggests that inflammatory mediators play an important role in the underlying pathophysiology of epilepsy, contributing to the onset and perpetuation of seizures [2]. Chronic inflammatory characteristics, such as the infiltration of leukocytes, reactive gliosis, and the overexpression of cytokines, were reported in surgically resected brain tissue from patients with refractory focal epilepsy, supporting a link between inflammation and epilepsy [3]. Among the variety of cytokine classes, interleukins (ILs) are widely studied in epilepsy The level of these molecules are altered during inflammation, are associated with seizure susceptibility and are possibly involved in epileptogenesis [4]. The putative role of other cytokines, such as TNF-α, IL-1β, and IL-1 receptor antagonist (IL-1RA), in the immunological activation of different stages of seizure disorders was studied [8]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
