Lipopolysaccharide and soluble CD14 in cord blood plasma are associated with prematurity and chorioamnionitis.

BACKGROUND: Lipopolysaccharide (LPS), an endotoxin of Gram-negative bacteria, causes preterm birth in animals and has been implicated as a factor triggering preterm labor and systemic complications in humans. Little is known regarding LPS in the cord blood (CB) of term and preterm infants and its association with maternal and fetal characteristics. METHODS: CB was obtained from term (n = 15) and preterm infants (n = 76) after delivery. Plasma levels of LPS, C-reactive protein (CRP), and soluble CD14 (sCD14) were measured using commercially available kits (limulus amebocyte lysate and enzyme-linked immunosorbent assay). Four linear regression models were created in order to identify independent variables that predict plasma LPS levels. RESULTS: The analyte levels were significantly higher in preterm vs. term infant CB: LPS (24.48 vs. 1 pg/ml; P = 0.0009), CRP (87.9 vs. 47 ng/ml; P = 0.01), and sCD14 (0.32 vs.0.35 µg/ml; P = 0.013). There was a (significant) positive correlation between CB LPS levels and gestational age, birth weight, CRP levels, sCD14 levels, and association with both clinical and histological chorioamnionitis. CONCLUSION: Our data suggest that LPS is associated with preterm labor and inflammation (CRP elevation and chorioamnionitis). These findings may be relevant to the understanding of the role of LPS in prematurity and its role in preterm morbidities.

Neonatal T-cell maturation and homing receptor responses to Toll-like receptor ligands differ from those of adult naive T cells: relationship to prematurity.

INTRODUCTION: Inflammation and infection are associated with premature birth and with activation of the fetal immune system. We hypothesized that exposure to microbial Toll-like receptor (TLR) ligands plays an important role in neonatal T-cell maturation and that early exposure to microbial products may result in early T-cell maturation and a tendency for these matured effector cells to change their homing receptor patterns. RESULTS: Expression of the CD45RO marker was induced in term neonatal T cells after in vitro exposure to TLR ligands for 7 days. Interestingly, naive T cells from adult blood were unaffected by TLR ligand exposure. In addition, neonatal T cells had more cells with decreased expression of the α4ß7 integrins and increased expression of CCR4 after in vitro exposure of TLR ligands-similar to the expression of these molecules in adult naive T cells. DISCUSSION: These findings are relevant for the understanding of neonatal T-cell maturation and may contribute to our understanding of multiorgan inflammatory complications of prematurity. METHODS: Cord blood was obtained from term and preterm infants. Using flow cytometry, we identified a mature (CD45RO(+)) phenotype in preterm infant cord blood (CB) T cells that had decreased expression of the α4ß7 integrins and increased expression of the C-C chemokine receptor 4 (CCR4) as compared with term infant CB.