Transplacental Transfer of Interleukin-1 Receptor Agonist and Antagonist Following Maternal Immune Activation

Am J Reprod Immunol. 2016 Jan;75(1):8-12. doi: 10.1111/aji.12444. Epub 2015 Oct 31.


Problem: Prenatal exposure to inflammation increases the incidence of neonatal brain injury. This raise the question whether maternally produced cytokines, especially interleukin (IL)-1 elevated in pathological pregnancies and known to alter fetal development, can cross the placental barrier and affect the fetus directly.

Method of study: We addressed if IL-1 agonist/antagonist could cross the placenta.

Results: Radiolabelled-IL-1 injected maternally reached the fetus in minimal amount. 3% of the amount detected within the placenta was transferred into the fetal liver and less than 1% recovered in the fetal brain 30 min after the injection Importantly, transfer of IL-1 was not affected by maternal exposure to LPS. Maternal administration of IL-1 receptor antagonist also reached the fetus in low concentration.

Conclusions: This suggests that minimal amount of maternally produced IL-1 family members cross the placental barrier. Their negative effects are likely indirect, through their deleterious placental actions.

Keywords: Cytokines; inflammation; placenta; transplacental transfer.

MeSH terms

  • Animals
  • Female
  • Fetus / metabolism*
  • Humans
  • Inflammation / chemically induced
  • Inflammation / immunology*
  • Interleukin 1 Receptor Antagonist Protein / administration & dosage*
  • Interleukin 1 Receptor Antagonist Protein / pharmacology
  • Interleukin-1beta / administration & dosage*
  • Interleukin-1beta / pharmacology
  • Lipopolysaccharides / immunology
  • Maternal-Fetal Exchange
  • Placenta / metabolism*
  • Placental Circulation
  • Pregnancy / immunology
  • Rats
  • Rats, Inbred Lew
  • Receptors, Interleukin-1 / agonists
  • Receptors, Interleukin-1 / antagonists & inhibitors


  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1beta
  • Lipopolysaccharides
  • Receptors, Interleukin-1