Acute intrauterine infection results in an imbalance between pro- and anti-inflammatory cytokines in the pregnant rabbit

Am J Reprod Immunol. 2000 May;43(5):305-11. doi: 10.1111/j.8755-8920.2000.430510.x.

Abstract

Problem: Intrauterine infection results in an increase in cytokines. This study compared the time courses for the pro- and anti-inflammatory cytokine responses in 33 pregnant rabbits at 70% gestation. Pro-inflammatory markers were activated nuclear factor-kappa B (NF-kappaB) in placenta and tumor necrosis factor-alpha (TNF-alpha) in amniotic fluid. These were compared to the anti-inflammatory cytokine, interleukin-1 receptor antagonist (IL-1ra), in placenta and uterus.

Method of study: Does were endoscopically inoculated with Escherichia coli through their cervices and sacrificed at six intervals between 0 and 30 hr post-inoculation.

Results: Activated NF-kappaB, determined by electromobility gel shift assay, increased significantly 16 hr after bacterial inoculation (P < or = 0.05). This was directly mirrored by TNF-alpha concentrations, determined by bioassay, in the amniotic fluid. However, IL-1ra levels, determined by enzyme-linked immunosorbent assay, did not increase in response to infection.

Conclusions: Intrauterine infection results in an imbalance between pro- and anti-inflammatory cytokines that may potentiate infection-induced preterm delivery.

Publication types

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

MeSH terms

  • Amniotic Fluid / metabolism
  • Animals
  • Cytokines / metabolism*
  • Escherichia coli Infections / immunology*
  • Female
  • Interleukin 1 Receptor Antagonist Protein
  • NF-kappa B / metabolism
  • Placenta / metabolism
  • Pregnancy
  • Pregnancy Complications, Infectious / immunology*
  • Rabbits
  • Sialoglycoproteins / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Uterine Diseases / immunology*
  • Uterus / metabolism

Substances

  • Cytokines
  • Interleukin 1 Receptor Antagonist Protein
  • NF-kappa B
  • Sialoglycoproteins
  • Tumor Necrosis Factor-alpha