Ann Child Neurol.
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
- KMID: 2453789
- DOI: http://doi.org/10.26815/acn.2019.00038
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+.
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