Progesterone reduces lipopolysaccharide induced interleukin-6 secretion in fetoplacental chorionic arteries, fractionated cord blood, and maternal mononuclear cells

Am J Obstet Gynecol. 2006 Oct;195(4):1015-9. doi: 10.1016/j.ajog.2006.07.002.

Abstract

Objective: The purpose of this study was to characterize effect of progesterone (P4) on interleukin-6 (IL-6) production by fetoplacental artery explants, fetal granulocytes, and fetal and maternal mononuclear cells.

Study design: Arteries and cord blood were obtained from 5 term pregnancies undergoing repeat cesarean section. Maternal blood was obtained from another 6 women at 16 to 20 weeks' gestation. Tissues were fractionated by dissection or Histopaque gradient. Specimens were incubated in physiologic media then exposed to lipopolysaccharide (LPS) or P4 alone, or pretreated with P4 and then exposed to LPS. Samples were evaluated for IL-6 by enzyme-linked immunosorbent assay (ELISA).

Results: Arteries and fetal and maternal mononuclear cells exposed to LPS increased IL-6 secretion by 9-, 27-, and 29-fold, respectively. P4 pretreatment blocked LPS induction of IL-6. Fetal granulocytes did not increase IL-6 production in response to LPS exposure.

Conclusion: LPS induces IL-6 in arteries and fetal and maternal mononuclear cells. P4 pretreatment significantly blocks this effect in these cell populations, suggesting possible targets for anti-inflammatory actions of P4 in prevention of preterm birth.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Arteries / drug effects
  • Arteries / metabolism
  • Chorion / blood supply*
  • Female
  • Fetal Blood / drug effects*
  • Fetal Blood / metabolism
  • Humans
  • Interleukin-6 / biosynthesis*
  • Leukocytes, Mononuclear / drug effects*
  • Leukocytes, Mononuclear / metabolism
  • Lipopolysaccharides / pharmacology*
  • Pregnancy
  • Progesterone / pharmacology*
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Interleukin-6
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Progesterone