Endoglin in Amniotic Fluid as a Risk Factor for the Subsequent Development of Bronchopulmonary Dysplasia
Article first published online: 24 DEC 2012
Published 2012. This article is a U.S. Government work and is in the public domain in the USA.
American Journal of Reproductive Immunology
Volume 69, Issue 2, pages 105–123, February 2013
How to Cite
Endoglin in amniotic fluid as a risk factor for the subsequent development of bronchopulmonary dysplasia.Am J Reprod Immunol 2013; 69: 105–123, , , , , , , , .
- Issue published online: 8 JAN 2013
- Article first published online: 24 DEC 2012
- Manuscript Accepted: 23 OCT 2012
- Manuscript Received: 9 OCT 2012
- National Institute of Child Health and Human Development
- Perinatology Research Branch, Division of Intramural Research
- Eunice Kennedy Shriver
- Adverse neonatal outcome;
- intra-amniotic infection;
- intra-amniotic inflammation;
- preterm labor;
- preterm prelabor rupture of membranes
Cross-talk between inflammation and angiogenesis pathways has been recently reported. The objectives of this study were to: (i) examine whether amniotic fluid (AF) concentrations of soluble endoglin (sEng), a protein with anti-angiogenic properties, change during pregnancy, parturition, or intra-amniotic infection and/or inflammation (IAI); (ii) determine whether an increase in sEng in the AF of patients with preterm labor (PTL) and preterm prelabor rupture of membranes (PROM) is associated with adverse neonatal outcomes; and (iii) investigate potential sources of sEng in AF.
A cross-sectional study was conducted to include patients in the following groups: (i) mid-trimester (n = 20); (ii) PTL with term delivery (n = 95); (iii) PTL leading to preterm delivery with (n = 40) and without IAI (n = 46); (iv) preterm PROM with (n = 37) and without IAI (n = 37); (v) term in labor (n = 48) and not in labor (n = 44). AF concentrations of sEng were determined by enzyme-linked immunosorbent assay. Chorioamniotic membranes, umbilical cord blood, and AF macrophages were examined for the expression of endoglin.
(i) Patients with IAI had a higher median AF concentration of sEng than those without IAI (P = 0.02 for PTL and 0.06 for preterm PROM); (ii) AF concentrations of sEng in the 3rd and 4th quartiles were associated with IAI (OR 2.5 and 7.9, respectively); (iii) an AF sEng concentration ≥779.5 pg/mL was associated with bronchopulmonary dysplasia (BPD) (OR 7.9); (iv) endoglin was co-localized with CD14+ macrophages in AF pellets of patients with IAI by immunofluorescence and flow cytometry; and (v) the concentration of sEng in the supernatant was significantly increased after the treatment of macrophages with endotoxin or TNF-α.
Soluble endoglin participates in the host response against IAI. Activated macrophages may be a source of sEng concentrations in the AF of patients with IAI. An increase of sEng in the AF is associated with BPD and adverse neonatal outcomes.