Article

Inflammatory cytokine gene polymorphisms and spontaneous preterm birth

Department of Obstetrics and Gynecology, Alagoas State University, Alagoas, Brazil.
Journal of Reproductive Immunology (Impact Factor: 2.82). 04/2009; 80(1-2):115-21. DOI: 10.1016/j.jri.2008.11.007
Source: PubMed

ABSTRACT

The objective was to search for an association between spontaneous preterm birth (sPTB) and single and/or combined polymorphisms in genes TNFA -308 G>A, IL10 -1082 G>A, IL10 -819 C>T, IL10 -592 C>A, IL6 -174 G>C, and IFNG +874 A>T. Genotyping was performed on 410 Brazilian ethnically matched women managed at two hospitals (two independent case-control sets). One set consisted of 122 cases and 101 controls, and the other set comprised 82 cases and 105 controls. We compared genotype and genotype-combination frequencies between cases and controls using Fisher's exact or the chi(2) tests and confirmed results using logistic regression. Among the six SNPs studied, we found no independent association between any single SNP and sPTB risk. The multi-locus analysis revealed a significant association between sPTB and the TNFA(GG)/IL6(GG)/IFNG(AA) genotype combination (p=0.002), confirmed by logistic regression. Our data suggest that the combination of TNF-alpha, IFN-gamma, and IL-6 maternal gene polymorphisms might contribute to susceptibility to sPTB. This finding could be investigated as a possible genetic marker for the risk of spontaneous preterm birth.

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    • "Moreover, there are significant racial/ ethnic disparities in the incidence of SPTB, with African Americans running more than twice as great a risk of SPTB as European-American women. In addition, association studies have identified a number of genetic polymorphisms related to infection, inflammation and innate immune systems that are risk factors for SPTB[4,5,6,7,8,9]. Despite these advances, the alleles accounting for the bulk of genetic susceptibility to SPTB remain undiscovered, particularly in Chinese populations. "
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    ABSTRACT: Inflammation plays an important role in the etiology and pathophysiology of spontaneous preterm birth (SPTB), and selenoprotein S (SEPS1) is involved in regulating the inflammatory response. Recently the G-105A promoter polymorphism in SEPS1 was shown to increase pro-inflammatory cytokine expression. We examined whether this functional polymorphism was related to the risk of SPTB in a Chinese population. We also examined the impact of premature rupture of membranes (PROM) on susceptibility to SPTB. The SEPS1 G-105A polymorphism was genotyped in 569 preterm singleton neonates and 673 term neonates by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. χ (2) tests and logistic regression analyses were used to calculate the odds ratios (ORs) and 95% confidence intervals (95% CIs). We observed that, compared with the GG genotype, -105A positive genotypes (GA + AA genotypes) were associated with significantly increased susceptibility to SPTB (adjusted OR, 1.87; 95% CI, 1.36-2.57; P<0.001). The -105A positive genotypes were also significantly associated with increased susceptibility to SPTB, both in the patients with PROM (adjusted OR, 2.65; 95% CI, 1.73-4.03; P<0.001) and in those without PROM (adjusted OR, 1.56; 95% CI, 1.09-2.24; P = 0.015). The -105A positive genotypes were also significantly associated with increased susceptibility to SPTB between extremely preterm neonates and controls (adjusted OR, 4.46; 95% CI, 1.86-10.73; P = 0.002) and between moderately preterm neonates and controls (adjusted OR, 1.76; 95% CI, 1.25-2.47; P = 0.001). Our findings suggest that the SEPS1 G-105A polymorphism contributes to the risk of developing SPTB in a Chinese population.
    Full-text · Article · Jun 2013 · PLoS ONE
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    • "They did find a significant association between PTB and a combination of variants by a multilocus analysis. TLR SNPs were not included (Moura et al., 2009). Uruguayan population has been described fundamentally as of European origin. "

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