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• W2016039678 abstract "ObjectiveIntra-amniotic infection and/or pro-inflammatory cytokine production reduces the rate of respiratory distress syndrome (RDS) in preterm neonates. We previously demonstrated that the first born neonate of multifetal pregnancies was most susceptible to pro-inflammatory immune activation. Cytokine binding to its receptor initiates pro-inflammatory activity. TNFR2 is the receptor for tumor necrosis factor-α on immune and endothelial cells. We examined whether a T > G polymorphism in the TNFR2 gene influenced the rate of RDS in multifetal pregnancies. Possession of TNFR2∗G is associated with increased pro-inflammatory activity.Study designBuccal swabs were obtained from 112 twin and five triplet sets. Cellular DNA was analyzed by polymerase chain reaction and restriction endonuclease digestion for a single nucleotide T > G polymorphism at codon 196 in exon 6 of the TNFR2 gene. Pregnancy and neonatal outcome data were obtained.ResultsRDS occurred in 17 first born neonates and 20 second born neonates. In first borns, TNFR2∗T homozygosity was present in 15 (88.2%) neonates with RDS as opposed to 47/98 (48.0%) neonates with no RDS (P = .002). Conversely, the carriage rate of the TNFR2∗G allele was 31.1% in those with no RDS and only 10.9% in neonates with RDS (P = .006). In contrast, there was no relation between TNFR2 genotype or allele and RDS in the second born neonates. TNFR2 genotype was also unrelated to occurrence of preterm premature rupture of fetal membranes or spontaneous preterm birth with intact membranes, patients´ ethnicity or neonatal birthweight.ConclusionIncreased pro-inflammatory immune activity (TNFR2∗G carriage) is strongly associated with a reduced rate of RDS in the first born neonate of multifetal pregnancies. This suggests that the observations by others in singleton gestations that pro-inflammatory immune activation protects against development of RDS may only be relevant to the first born neonate in multifetal pregnancies, owing, perhaps, to an enhanced exposure to immune activating substances. ObjectiveIntra-amniotic infection and/or pro-inflammatory cytokine production reduces the rate of respiratory distress syndrome (RDS) in preterm neonates. We previously demonstrated that the first born neonate of multifetal pregnancies was most susceptible to pro-inflammatory immune activation. Cytokine binding to its receptor initiates pro-inflammatory activity. TNFR2 is the receptor for tumor necrosis factor-α on immune and endothelial cells. We examined whether a T > G polymorphism in the TNFR2 gene influenced the rate of RDS in multifetal pregnancies. Possession of TNFR2∗G is associated with increased pro-inflammatory activity. Intra-amniotic infection and/or pro-inflammatory cytokine production reduces the rate of respiratory distress syndrome (RDS) in preterm neonates. We previously demonstrated that the first born neonate of multifetal pregnancies was most susceptible to pro-inflammatory immune activation. Cytokine binding to its receptor initiates pro-inflammatory activity. TNFR2 is the receptor for tumor necrosis factor-α on immune and endothelial cells. We examined whether a T > G polymorphism in the TNFR2 gene influenced the rate of RDS in multifetal pregnancies. Possession of TNFR2∗G is associated with increased pro-inflammatory activity. Study designBuccal swabs were obtained from 112 twin and five triplet sets. Cellular DNA was analyzed by polymerase chain reaction and restriction endonuclease digestion for a single nucleotide T > G polymorphism at codon 196 in exon 6 of the TNFR2 gene. Pregnancy and neonatal outcome data were obtained. Buccal swabs were obtained from 112 twin and five triplet sets. Cellular DNA was analyzed by polymerase chain reaction and restriction endonuclease digestion for a single nucleotide T > G polymorphism at codon 196 in exon 6 of the TNFR2 gene. Pregnancy and neonatal outcome data were obtained. ResultsRDS occurred in 17 first born neonates and 20 second born neonates. In first borns, TNFR2∗T homozygosity was present in 15 (88.2%) neonates with RDS as opposed to 47/98 (48.0%) neonates with no RDS (P = .002). Conversely, the carriage rate of the TNFR2∗G allele was 31.1% in those with no RDS and only 10.9% in neonates with RDS (P = .006). In contrast, there was no relation between TNFR2 genotype or allele and RDS in the second born neonates. TNFR2 genotype was also unrelated to occurrence of preterm premature rupture of fetal membranes or spontaneous preterm birth with intact membranes, patients´ ethnicity or neonatal birthweight. RDS occurred in 17 first born neonates and 20 second born neonates. In first borns, TNFR2∗T homozygosity was present in 15 (88.2%) neonates with RDS as opposed to 47/98 (48.0%) neonates with no RDS (P = .002). Conversely, the carriage rate of the TNFR2∗G allele was 31.1% in those with no RDS and only 10.9% in neonates with RDS (P = .006). In contrast, there was no relation between TNFR2 genotype or allele and RDS in the second born neonates. TNFR2 genotype was also unrelated to occurrence of preterm premature rupture of fetal membranes or spontaneous preterm birth with intact membranes, patients´ ethnicity or neonatal birthweight. ConclusionIncreased pro-inflammatory immune activity (TNFR2∗G carriage) is strongly associated with a reduced rate of RDS in the first born neonate of multifetal pregnancies. This suggests that the observations by others in singleton gestations that pro-inflammatory immune activation protects against development of RDS may only be relevant to the first born neonate in multifetal pregnancies, owing, perhaps, to an enhanced exposure to immune activating substances. Increased pro-inflammatory immune activity (TNFR2∗G carriage) is strongly associated with a reduced rate of RDS in the first born neonate of multifetal pregnancies. This suggests that the observations by others in singleton gestations that pro-inflammatory immune activation protects against development of RDS may only be relevant to the first born neonate in multifetal pregnancies, owing, perhaps, to an enhanced exposure to immune activating substances." @default.
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• W2016039678 title "Association of neonatal tumor necrosis factor receptor 2 (TNFR2) gene polymorphism with respiratory distress syndrome (RDS) in the first born neonate of multifetal pregnancies" @default.
• W2016039678 doi "https://doi.org/10.1016/j.ajog.2004.09.064" @default.
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