Interleukin-1β and interleukin-1receptor antagonist polymorphisms in Egyptian children with febrile seizures: A

Salah Al Morshedy1, Hosam F Elsaadany, Hany E Ibrahim

  • 1Department of Pediatrics Department of Pediatrics, Faculty of Medicine, Cairo University Department of Pediatrics, Faculty of Medicine, Aswan University Department of Clinical pathology Department of Microbiology and Immunology Department of Internal Medicine, Faculty of Medicine, Zagazig University, Egypt.

Medicine
|March 16, 2017
PubMed

Insights

Certain genetic variations in interleukin-1 beta (IL-1β) and interleukin-1 receptor antagonist (IL-1RA) genes are associated with an increased risk of febrile seizures in Egyptian children. These findings highlight potential genetic markers for febrile seizure susceptibility.

Area of Science:

  • Genetics
  • Immunology
  • Pediatrics

Background:

  • Febrile seizure (FS) is the most common seizure disorder in childhood.
  • Interleukin-1 (IL-1) is a key pro-inflammatory cytokine and endogenous pyrogen.
  • Genetic predisposition plays a role in the susceptibility to febrile seizures.

Purpose of the Study:

  • To investigate the association between single-nucleotide polymorphisms (SNPs) in the interleukin-1 beta (IL-1β) gene promoter (-31 and -511 positions) and the interleukin-1 receptor antagonist (IL-1RA) gene variable number of tandem repeats (VNTR) in intron 2.
  • To determine if these polymorphisms are risk factors for febrile seizures in Egyptian children.
  • To measure serum IL-1β levels and assess their relationship with the identified polymorphisms.

Main Methods:

  • A case-control study involving 155 Egyptian children with febrile seizures and 155 matched healthy controls.
  • Genotyping of IL-1β promoter SNPs (-31 C/T, -511 C/T) and IL-1RA gene VNTR polymorphisms using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).
  • Serum IL-1β levels were quantified using enzyme-linked immunosorbent assay (ELISA).

Main Results:

  • The IL-1β-511 TT genotype and T allele showed a significantly higher frequency in children with febrile seizures compared to controls (OR: 3.96, P=0.001 for TT; OR: 1.65, P=0.003 for T allele).
  • The IL-1RA II/II genotype and II allele were overrepresented in the febrile seizure group (OR: 4.02, P=0.001 for II/II; OR: 1.73, P=0.001 for II allele).
  • A significant positive association was found between IL-1RA II/II genotype and allele II with susceptibility to sporadic febrile seizures.
  • Carriers of IL-1RA II/II genotype and II allele exhibited higher serum IL-1β levels.

Conclusions:

  • The T allele or TT genotype at position -511 of the IL-1β gene promoter and the IL-1RA II/II genotype are identified as risk factors for developing febrile seizures in Egyptian children.
  • These genetic polymorphisms may serve as potential biomarkers for febrile seizure susceptibility.
  • The study provides novel insights into the genetic underpinnings of febrile seizures in the Egyptian pediatric population.

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