Abstract
The purpose of this investigation was the determination of the distribution of genotypes and alleles, residing within interleukin 6 (IL6) and interleukin 1 (IL1) polymorphisms, among fetuses and neonates, congenitally infected with Toxoplasma gondii, and among uninfected control cases. The study included 22 fetuses and newborns infected with T. gondii and 49 control cases. Screening for IgG and IgM antibodies against the parasite and IgG avidity was performed by enzyme-linked fluorescent assay (ELFA) tests. Quantitation of T. gondii DNA in amniotic fluids was assayed by the real-time Q PCR technique for the parasitic B1 gene. Genotypes at IL6 and IL1 single nucleotide polymorphisms (SNPs) were determined by a self-designed, nested polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. Representative genotypes at the studied loci were confirmed by sequencing. All the genotypes were estimated for Hardy–Weinberg equilibrium and IL1 genotypes were tested for linkage disequilibrium. Genotypes and haplotypes at the studied SNPs were investigated for their possible association with the occurrence of congenital T. gondii infection, using a logistic regression model. GC heterozygotes at the IL6 −174 G>C SNP were significantly associated with toxoplasmosis and increased the risk of T. gondii infection [odds ratio (OR) 4.24, 95 % confidence interval (CI) 1.24–14.50 in the codominant model, p ≤ 0.050]. In case of IL1 SNPs, similar prevalence rates were observed between T. gondii-infected and -uninfected offspring. Regarding allelic variability, the C alleles at both IL6 and IL1B SNPs were significantly more frequent in the infected than in the uninfected cases (p ≤ 0.050). It is concluded that IL6 −174 G>C and IL1B +3954 C>T SNPs might be involved in the development of congenital T. gondii infection.
Highlights
Toxoplasma gondii is one of the most common intrauterine infections worldwide and the major cause of perinatal morbidity and mortality [1,2,3,4]
The genotypes at all the analyzed polymorphic sites preserved the Hardy– Weinberg (H-W) equilibrium in the fetuses and neonates infected with T. gondii (p=0.081, p=0.430, and p=0.680, for IL1A −889 C>T, IL1B +3954 C>T, and interleukin 6 (IL6) −174 G>C single nucleotide polymorphisms (SNPs), respectively)
We found that infants and neonates with GC genotypes at the IL6 −174 G>C SNP were at an approximately four times higher risk of congenital infection with T. gondii as compared to GG and CC homozygotes
Summary
Toxoplasma gondii is one of the most common intrauterine infections worldwide and the major cause of perinatal morbidity and mortality [1,2,3,4]. Considering the immune response against T. gondii, several studies have shown the role of proinflammatory cytokines, including interleukin (IL) 6 and IL1 [7,8,9]. Among women infected with T. gondii, IL6 expression was estimated to be twice as high compared to the control cases [10]. The development of toxoplasmosis-related ocular lesions among T. gondii-infected patients was reported to be associated with high IL1 and TNF-α levels [11]. The mice with more severe inflammation in the retina and vitreous humor, related to ocular toxoplasmosis, had a reduced expression of ocular IL1A and an increased production of TNFA mRNA as compared to WT mice [12]. In an in vitro study, the human monocytic wild-type MonoMac cells, infected with T. gondii, showed significantly higher levels of IL-1β as compared to non-infected cells [13]. Considering a possible participation of the genetic alterations, located at IL1 and IL6 molecule encoding genes, the −174 G>C single nucleotide polymorphism (SNP) from the IL6 gene was reported to be
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