Evidence of Participation of the Soluble Tumor Necrosis Factor Receptor I in the Host Response to Intrauterine Infection in Preterm Labor

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Abstract
PROBLEM: This study was conducted to determine whether: (1) the soluble tumor necrosis factor receptor I (sTNF‐r I) is present in human amniotic fluid, neonatal urine, and the feto‐maternal plasma; (2) there are changes in the concentration of the sTNF‐r I in amniotic fluid with gestational age; and (3) microbial invasion of the amniotic cavity (in term and preterm parturition) is associated with changes in amniotic fluid sTNF‐r I concentrations. METHOD: Amniotic fluid was retrieved by amniocentesis from 185 women classified into 11 groups according to gestational age (midtrimester, preterm gestation, and term), the presence or absence of labor, spontaneous rupture of membranes and microbial invasion of the amniotic cavity. sTNF‐r I was assayed with a sensitive and enzyme‐linked immunosorbent assay (ELISA) validated for amniotic fluid. In addition, sTNF‐r I concentrations were determined in fetal blood obtained by cordocentesis in preterm gestations (N = 24) or at the time of delivery after spontaneous labor at term (N = 10). sTNF‐r I concentrations were also measured in maternal venous and cord blood and neonatal urine (n = 13). RESULTS: sTNF‐r I was found to be present in all amniotic fluid samples, maternal blood and fetal blood and neonatal urine samples; sTNF‐r I concentrations were higher in the midtrimester than at term (mean ± SD:36.2 ± 12.2 ng/ml versus mean ± SD:5.56 ± 5.72ng/ml [P < .05]); patients with preterm labor and microbial invasion of the amniotic cavity (with intact or with ruptured membranes) had significantly higher amniotic fluid concentrations of sTNF‐r I than patients without microbial invasion; in the absence of microbial invasion, parturition (both term and preterm) was not associated with changes in amniotic fluid concentrations of sTNF‐r I; neonatal urine contained the highest concentrations of sTNF‐r I of all biological fluids assayed including maternal and neonatal/fetal blood and amniotic fluid. CONCLUSIONS: It was concluded that sTNF‐r I is a physiologic constitutent of amniotic fluid, as well as of the fetal and maternal plasma; that amniotic fluid sTNF‐r I concentrations decrease as a function of gestional age and increases in the concentration of the sTNF‐r I are part of the host response to intrauterine infection in preterm parturition.