Association of tumor necrosis factor-α gene promotor variant, not interleukin-10, with febrile seizures and genetic epilepsy with febrile seizure plus

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 sig-nificant 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+.