Interleukin-1 alpha and tumor necrosis factor alpha cause placental injury in the rat

Am J Pathol. 1989 Aug;135(2):239-44.

Abstract

Bacterial endotoxins (LPS) causes placental injury and fetal demise in pregnant animals. Because several biological effects of LPS are mediated by interleukin-1 (IL-1) and tumor necrosis factor (TNF), the hypothesis that these cytokines could cause placental injury similar to that seen in LPS-treated pregnant rats was tested. On day 12 of gestation, rats were injected intraperitoneally with saline, LPS, native or heat-inactivated (HI) rHIL 1 alpha, or rH-TNF alpha. Seven days later, grossly abnormal implantation sites and fetal demise were observed in rats injected with rHIL-1, rHTNF, or LPS but not in those injected with saline or HI-cytokines. Necrosis of placental, decidual, and fetal tissues was observed in cytokine-treated animals. The necrosis was more severe in LPS-treated rats, in which no fetal remains were identifiable. These data suggest that IL-1 and TNF may play a role in the fetoplacental injury observed in LPS-treated pregnant rats.

Publication types

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

MeSH terms

  • Animals
  • Endotoxins / pharmacology
  • Female
  • Fetus / drug effects
  • Fetus / pathology
  • Interleukin-1 / metabolism
  • Interleukin-1 / pharmacology*
  • Placenta / drug effects*
  • Placenta / pathology
  • Pregnancy
  • Rats
  • Rats, Inbred Strains
  • Salmonella enteritidis
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Endotoxins
  • Interleukin-1
  • Tumor Necrosis Factor-alpha