Contribution of IL6 ?74 G>C and IL1B +3954 C>T polymorphisms to congenital infection with Toxoplasma gondii
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  • 作者:W. Wujcicka ; Z. Gaj ; J. Wilczyński…
  • 刊名:European Journal of Clinical Microbiology & Infectious Diseases
  • 出版年:2015
  • 出版时间:November 2015
  • 年:2015
  • 卷:34
  • 期:11
  • 页码:2287-2294
  • 全文大小:882 KB
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  • 作者单位:W. Wujcicka (1) (2)
    Z. Gaj (1) (2)
    J. Wilczyński (2)
    D. Nowakowska (2)

    1. Scientific Laboratory of the Center of Medical Laboratory Diagnostics, Polish Mother’s Memorial Hospital—Research Institute, 281/289 Rzgowska Street, Lodz, 93-338, Poland
    2. Department of Perinatology and Gynecology, Polish Mother’s Memorial Hospital—Research Institute, Lodz, Poland
  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Biomedicine
    Medical Microbiology
    Internal Medicine
  • 出版者:Springer Berlin / Heidelberg
  • ISSN:1435-4373
文摘
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 ?74 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) 1.24-4.50 in the codominant model, p?≤-.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?≤-.050). It is concluded that IL6 ?74 G>C and IL1B +3954 C>T SNPs might be involved in the development of congenital T. gondii infection.
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