Evidence map›Paper›PMID 26385345›Full record

ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2015

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

W Wujcicka, Z Gaj, J Wilczyński, D Nowakowska

Open access · hybridAbstract read
In one paragraph

Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

W WujcickaScientific Laboratory of the Center of Medical Laboratory Diagnostics, Polish Mother's Memorial Hospital-Research Institute, 281/289 Rzgowska Street, Lodz, 93-338, Poland. wwujcicka@yahoo.com.
Z GajScientific Laboratory of the Center of Medical Laboratory Diagnostics, Polish Mother's Memorial Hospital-Research Institute, 281/289 Rzgowska Street, Lodz, 93-338, Poland.
J WilczyńskiDepartment of Perinatology and Gynecology, Polish Mother's Memorial Hospital-Research Institute, Lodz, Poland.
D NowakowskaDepartment of Perinatology and Gynecology, Polish Mother's Memorial Hospital-Research Institute, Lodz, Poland.
Polish Mother’s Memorial Hospital Research Institute · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAmniotic FluidAntibody AffinityCase-Control StudiesDNA, ProtozoanEnzyme-Linked Immunosorbent AssayFemaleGene FrequencyGenotypeGenotyping TechniquesHumansImmunoglobulin GImmunoglobulin MInfant, NewbornInterleukin-1betaDNA, ProtozoanIL6 protein, humanImmunoglobulin GImmunoglobulin MInterleukin-1betaInterleukin-6

Identifiers

PMID26385345
PMCPMC4607712
OpenAlexW1953755177

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.