Contribution of IL6 −174 G>C and IL1B +3954 C>T polymorphisms to congenital infection with Toxoplasma gondii

• DOI: 10.1007/s10096-015-2481-z
• Publication Date: 2015-09-18T10:33:39Z
• Authors: W. Wujcicka; Z. Gaj; J. Wilczyński; D. Nowakowska
• Keywords: Linkage Disequilibrium; Toxoplasmosis

The purpose of this investigation was the determination distribution genotypes and alleles, residing within interleukin 6 (IL6) 1 (IL1) polymorphisms, among fetuses neonates, congenitally infected with Toxoplasma gondii, uninfected control cases. study included 22 newborns T. gondii 49 Screening for IgG IgM antibodies against parasite avidity performed by enzyme-linked fluorescent assay (ELFA) tests. Quantitation DNA in amniotic fluids assayed real-time Q PCR technique parasitic B1 gene. Genotypes at IL6 IL1 single nucleotide polymorphisms (SNPs) were determined a self-designed, nested polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. Representative studied loci confirmed sequencing. All estimated Hardy–Weinberg equilibrium tested linkage disequilibrium. haplotypes SNPs investigated their possible association occurrence congenital infection, using logistic regression model. GC heterozygotes −174 G>C SNP significantly associated toxoplasmosis increased risk infection [odds ratio (OR) 4.24, 95 % confidence interval (CI) 1.24–14.50 codominant model, p ≤ 0.050]. In case SNPs, similar prevalence rates observed between gondii-infected -uninfected offspring. Regarding allelic variability, C alleles both IL1B more frequent than cases (p 0.050). It is concluded that +3954 C>T might be involved development infection.