J Korean Child Neurol Soc.  2019 Jun;27(2):38-45. 10.26815/acn.2019.00038.

Association of Tumor Necrosis Factor-α Gene Promotor Variant, Not Interleukin-10, with Febrile Seizures and Genetic Epilepsy with Febrile Seizure Plus

Affiliations
  • 1Department of Pediatrics, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul National University College of Medicine, Seoul, Korea. jechoi66@snu.ac.kr
  • 2Department of Pediatrics, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea.
  • 3Department of Pediatrics, Pediatric Clinical Neuroscience Center, Seoul National University Children's Hospital, Seoul National University College of Medicine, Seoul, Korea.
  • 4Department of Biostatistics, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul National University College of Medicine, Seoul, Korea.
  • 5Department of Microbiology, Brain Korea 21 Plus Project for Medical Science, Severance Biomedical Science Institute and Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, Korea. jsshin6203@yuhs.ac

Abstract

PURPOSE
Cytokines demonstrate active roles in the occurrence of febrile seizures (FS). However, whether a genetic predisposition to inflammation is implicated in FS, febrile seizure plus (FS+) or genetic epilepsy with febrile seizure plus (GEFS+) are still unclear. Therefore we perform this study to find the association of promotor variants in pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) genes and anti-inflammatory cytokine interleukin 10 (IL-10) genes either with FS, FS+, and GEFS+ in Korean children.
METHODS
Fifty-seven children with FS, 32 FS+, and 12 GEFS+ patients were compared with 108 controls. The allelic and genotypic distributions were compared for TNF-α-238 (rs361525), −308 (rs1800629), −857 (rs1799724), −863 (rs1800630), and IL-10-592 (rs1800872), −819 (rs1800871), −1082 (rs1800896), and −1352 (rs1800893).
RESULTS
Allelic and genotypic frequencies of TNF-α and IL-10 promotor variants showed no significant differences between FS, FS+, and GEFS+ versus controls. However, AA genotypes at TNF-α-863 were present only in controls. TNF-α-863 (rs1800630) promoter variants showed an association with FS, FS+, and GEFS+ in a recessive mode of inheritance pattern (P<0.05).
CONCLUSION
Our results suggest that AA genotypes at TNF-α-863 may be associated with FS, FS+, and GEFS+, implicating protective roles against to development of FS, FS+, and GEFS+.

Keyword

Tumor necrosis factor-alpha; Interleukin-10; Epilepsy; Seizures, febrile; Variants

MeSH Terms

Child
Cytokines
Epilepsy*
Genetic Predisposition to Disease
Genotype
Humans
Inflammation
Inheritance Patterns
Interleukin-10*
Necrosis*
Seizures, Febrile*
Tumor Necrosis Factor-alpha
Cytokines
Interleukin-10
Tumor Necrosis Factor-alpha
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