Evelien E de Vries1, Bart van den Munckhof2, Kees P J Braun3, Annet van Royen-Kerkhof4, Wilco de Jager5, Floor E Jansen6. 1. Brain Center Rudolf Magnus, Department of Pediatric Neurology, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: eveliendevriez@gmail.com. 2. Brain Center Rudolf Magnus, Department of Pediatric Neurology, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: B.vandenMunckhof@umcutrecht.nl. 3. Brain Center Rudolf Magnus, Department of Pediatric Neurology, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: K.Braun@umcutrecht.nl. 4. Department of Pediatric Immunology, Laboratory of Translational Immunology, University Medical Centre Utrecht, Utrecht, The Netherlands. Electronic address: A.vanRoyen@umcutrecht.nl. 5. Department of Pediatric Immunology, Laboratory of Translational Immunology, University Medical Centre Utrecht, Utrecht, The Netherlands. Electronic address: wjager@umcutrecht.nl. 6. Brain Center Rudolf Magnus, Department of Pediatric Neurology, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: F.E.Jansen@umcutrecht.nl.
Abstract
BACKGROUND: Accumulating evidence suggests a role for inflammation in the pathophysiology of epilepsy. METHODS: We performed a systematic review and meta-analysis of studies that investigated inflammatory mediators in human epilepsy. Studies reporting on inflammatory mediators in serum, cerebrospinal fluid or brain tissue of epilepsy patients were included. Studies comparing patients to controls were included in a meta-analysis. RESULTS: 66 articles reporting on 1934 patients were included. IL-1ra, IL-1β, IL-6, IL-10, IFN-γ and TNF-α were the most extensively investigated proteins. Elevated levels for IL-1ra, IL-1β, IL-6 and CXCL8/IL-8 were reported in several different epilepsy etiologies and media, while other proteins were specifically increased for one etiology. IL-1α, IL-7 and IL-13, as well as the chemokines CCL2-5, -19 and -22, were increased exclusively in brain tissue. In an aggregate meta-analysis, we found significantly different protein levels for serum IL-6, IL-17 and CSF IL-1β and IL-10. CONCLUSION: Inflammatory pathways are involved in epilepsy. Future studies may further clarify their role, and prove potential of targeted anti-inflammatory treatment.
BACKGROUND: Accumulating evidence suggests a role for inflammation in the pathophysiology of epilepsy. METHODS: We performed a systematic review and meta-analysis of studies that investigated inflammatory mediators in humanepilepsy. Studies reporting on inflammatory mediators in serum, cerebrospinal fluid or brain tissue of epilepsypatients were included. Studies comparing patients to controls were included in a meta-analysis. RESULTS: 66 articles reporting on 1934 patients were included. IL-1ra, IL-1β, IL-6, IL-10, IFN-γ and TNF-α were the most extensively investigated proteins. Elevated levels for IL-1ra, IL-1β, IL-6 and CXCL8/IL-8 were reported in several different epilepsy etiologies and media, while other proteins were specifically increased for one etiology. IL-1α, IL-7 and IL-13, as well as the chemokines CCL2-5, -19 and -22, were increased exclusively in brain tissue. In an aggregate meta-analysis, we found significantly different protein levels for serum IL-6, IL-17 and CSF IL-1β and IL-10. CONCLUSION: Inflammatory pathways are involved in epilepsy. Future studies may further clarify their role, and prove potential of targeted anti-inflammatory treatment.
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