Association between maternal-fetal proinflammatory cytokine genotype and preterm birth was studied. Isolated genomic DNA from maternal and cord blood samples of 100 preterm and 101 term labors were used for TNF alpha (-238G/A, -308G/A), IL-1 alpha (4845G/T), and IL-1 beta (-511C/T) genotyping. TNF alpha -238 GA genotype in term neonates was significantly higher than the premature neonates (p < 0.05). Maternal-fetal TNFa -238 heterozygosity was associated with term labor (p < 0.05). TNF alpha -308 GA and AA genotypes were associated with term labor (mothers and neonates, respectively; p < 0.05 and p < 0.001). The incidence of term labor was significantly increased in TNF alpha -308 GA genotype. If a -308GA carrier has a fetus with GG genotype, the incidence of preterm labor increases (p < 0.01). The 4845 T allele was significantly higher in preterm mothers and neonates (p < 0.001 and p < 0.001). The effect of maternal-fetal genotype for the pregnancy outcome reveals that maternal 4845GG and GT genotypes increase term labor incidence, whereas fetal 4845 TT genotype was a significant independent risk factor for preterm birth (p < 0.01). IL-1 beta -511 TT genotype was significantly higher in preterm neonates. The preterm labor risk was significantly increased in maternal -511 TT genotype and fetal CT genotypes, whereas with maternal -511 CT or TT genotypes or a -511 TT fetus, the incidence of term pregnancy increases (p < 0.01).
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