Epithelial cell-derived neutrophil-activating peptide-78 is present in fetal membranes and amniotic fluid at increased concentrations with intra-amniotic infection and preterm delivery

Biol Reprod. 2004 Jan;70(1):253-9. doi: 10.1095/biolreprod.103.016204. Epub 2003 Sep 17.

Abstract

Intra-amniotic secretion and abundance of epithelial cell-derived neutrophil-activating peptide (ENA)-78, a potent chemoattractant and activator of neutrophils, was studied in the context of term and preterm parturition. Staining of ENA-78 immunoperoxidase was localized predominantly to chorionic trophoblasts and amniotic epithelium in term and preterm gestational membranes, with weaker and less consistent staining in decidual cells. The abundance of ENA-78 in membrane tissue homogenates was significantly increased ( approximately 4-fold) with term labor in amnion (n = 15), and with preterm labor ( approximately 30-fold) in amnion and choriodecidua (n = 31). In amnion tissue homogenate extracts, ENA-78 levels were positively correlated with the degree of leukocyte infiltration (r2 = 0.481). In amniotic fluids, median ENA-78 levels from pregnancies with preterm labor without intra-amniotic infection were significantly lower (P < 0.01 by ANOVA) than those from pregnancies with preterm deliveries with infection; levels in samples derived from term pregnancies were similar before and after labor. Production of ENA-78 by amnion monolayers was stimulated in a concentration-dependent fashion by both interleukin-1beta and tumor necrosis factor alpha. Production of ENA-78 by choriodecidual explants was increased modestly after 2-4 h of exposure to lipopolysaccharide (5 microg/ml). An immunoreactive doublet ( approximately 8 kDa) was detected in choriodecidual explant-conditioned media by immunoblotting. We conclude that ENA-78, derived from the gestational membranes, is present in increased abundance in the amniotic cavity in response to intrauterine infection and, hence, may play a role in the mechanism of infection-driven preterm birth and rupture of membranes secondary to leukocyte recruitment and activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amniotic Fluid / metabolism*
  • Cells, Cultured
  • Chemokine CXCL5
  • Chemokines, CXC*
  • Chorioamnionitis / metabolism*
  • Epithelial Cells / cytology
  • Epithelial Cells / metabolism*
  • Extraembryonic Membranes / cytology
  • Extraembryonic Membranes / metabolism*
  • Female
  • Humans
  • Infant, Newborn
  • Infant, Premature
  • Interleukin-8 / analogs & derivatives
  • Interleukin-8 / metabolism*
  • Pregnancy
  • Pregnancy Complications, Infectious / metabolism
  • Uterus / cytology
  • Uterus / metabolism

Substances

  • CXCL5 protein, human
  • Chemokine CXCL5
  • Chemokines, CXC
  • Interleukin-8