Article

Second trimester maternal plasma levels of cytokines IL-1Ra, Il-6 and IL-10 and preterm birth

School of Nursing, The University of Texas at Austin, Austin, TX, USA.
Journal of perinatology: official journal of the California Perinatal Association (Impact Factor: 2.35). 03/2012; 32(7):483-90. DOI: 10.1038/jp.2011.193
Source: PubMed

ABSTRACT To examine the interaction of the cytokines interleukin-1 receptor antagonist (IL)-1Ra, IL-6 and IL-10 to predict preterm birth (PTB) in pregnant Hispanic women (n=470).
In this prospective study, demographic data were obtained prenatally and birth outcome data were obtained from the medical chart. Cytokines were measured from plasma obtained at 22 to 24 weeks gestation. Data analysis utilized logistic regression.
PTB was predicted by level of IL-1Ra (odds ratio (OR)=2.55; 95% confidence interval (CI)=1.24, 5.24). The interaction between IL-1Ra and IL-6 and between IL-1Ra and IL-10 was significant (Wald=4.01, P=0.04 and Wald=8.84, P<0.003, respectively) and was also predictive of PTB. As IL-1Ra levels increased while IL-10 levels were low, the probability of PTB greatly increased.
The interactions of select cytokines and cytokine receptor antagonists were associated with PTB. Future research should focus on the changes in cytokines during pregnancy to identify critical periods of change, and examine predictors of the cytokine response.

Download full-text

Full-text

Available from: Rita Pickler, Aug 12, 2015
0 Followers
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Preterm birth (PTB) is a complex trait, but little is known regarding its major genetic determinants. The objective of this study is to localize genes that influence susceptibility to PTB in Mexican Americans (MAs), a minority population in the United States (US), using predominantly microfilmed birth certificate-based data obtained from the San Antonio Family Birth Weight Study. Only 1,302 singleton births from 288 families with information on PTB and significant covariates were considered for genetic analysis. PTB is defined as a childbirth that occurs at <37 completed weeks of gestation, and the prevalence of PTB in this sample was 6.4%. An approximately 10 cM genetic map was used to conduct a genome-wide linkage analysis using the program SOLAR. The heritability of PTB was high (h(2)±SE: 0.75±0.20) and significant (P=4.5 x 10(-5)), after adjusting for the significant effects of birth weight and birth order. We found significant evidence for linkage of PTB (LOD=3.6; nominal P=2.3 x 10(-5); empirical P=1.0 x 10(-5)) on chromosome 18q between markers D18S1364 and D18S541. Several other chromosomal regions (2q, 9p, 16q, and 20q) were also potentially linked with PTB. A strong positional candidate gene in the 18q linked region is SERPINB2 or PAI-2, a member of the plasminogen activator system that is associated with various reproductive processes. In conclusion, to our knowledge, perhaps for the first time in MAs or US populations, we have localized a major susceptibility locus for PTB on chromosome 18q21.33-q23.
    Molecular Human Reproduction 05/2013; DOI:10.1093/molehr/gat036 · 3.48 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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.
    PLoS ONE 06/2013; 8(6):e65657. DOI:10.1371/journal.pone.0065657 · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: ProblemPrevious studies have investigated the utility of inflammation markers as predictors of preterm birth, but none have compared trends in levels between uncomplicated and preterm pregnancy.Method of studyWe explored longitudinal changes in plasma cytokines, including IL-1β, IL-6, IL-10, and TNF-α, as well as C-reactive protein in pregnant women from a nested case–control study.ResultsIL-6 was associated with increased odds of spontaneous preterm birth, defined by presentation of spontaneous preterm labor and/or preterm premature rupture of the membranes. Associations were strongest later in pregnancy. IL-10 was associated with increased odds of placentally mediated preterm birth, defined by presentation with preeclampsia or intrauterine growth restriction, and odds ratios were also highest near the end of pregnancy.Conclusion Maternal inflammation markers were associated with increased risk of preterm birth, and relationships differed by etiology of preterm delivery and gestational age at sample collection.
    American Journal Of Reproductive Immunology 05/2014; 72(3). DOI:10.1111/aji.12265 · 3.32 Impact Factor
Show more