Bacterial lipopolysaccharide-mediated murine fetal death: The role of interleukin-1

Silver, R.M., Edwin, S.S., Umar, F., Dudley, D.J., Branch, D.W. and Mitchell, M.D. (1997) Bacterial lipopolysaccharide-mediated murine fetal death: The role of interleukin-1. American Journal of Obstetrics and Gynecology, 176 3: 544-549. doi:10.1016/S0002-9378(97)70545-3

Author Silver, R.M.
Edwin, S.S.
Umar, F.
Dudley, D.J.
Branch, D.W.
Mitchell, M.D.
Title Bacterial lipopolysaccharide-mediated murine fetal death: The role of interleukin-1
Journal name American Journal of Obstetrics and Gynecology   Check publisher's open access policy
ISSN 0002-9378
Publication date 1997-03
Sub-type Article (original research)
DOI 10.1016/S0002-9378(97)70545-3
Volume 176
Issue 3
Start page 544
End page 549
Total pages 6
Place of publication St. Louis, Mo. U.S.A.
Publisher Mosby
Language eng
Subject 1103 Clinical Sciences
1114 Paediatrics and Reproductive Medicine
Formatted abstract
Our purpose was to determine whether interleukin-1 is an important mediator of lipopolysaccharide-induced fetal death and, if so, whether interleukin-1 causes fetal death by inducing prostanoid formation in gestational tissues.

Pregnant C3H/HeN mice were administered lipopolysaccharide, interleukin-1α, interleukin-β, or vehicle on days 11 to 13 of pregnancy. Mice were killed 72 hours later and the fetal status was determined. Some mice were pretreated with anti-interleukin-1-receptor antibodies or indomethacin. Decidual explants were established from treated mice, and supernatants were assayed for interleukin-1β and prostaglandin E2.

Decidua taken from lipopolysaccharide-treated mice produced significantly increased amounts of interleukin-1β, and pretreatment with anti-interleukin-1-receptor antibodies reduced the proportion of fetal deaths after lipopolysaccharide administration from 100% to 33%. The administration of interleukin-1α caused fetal death in a dose-dependent fashion, and decidua taken from interleukin-1-treated mice produced significantly increased amounts of prostaglandin E2. However, pretreatment with doses of indomethacin that abrogated decidual prostaglandin E2 production did not reduce the proportion of fetal death after interleukin-1α administration.

Interleukin-1 is an important mediator of lipopolysaccharide- induced fetal death and causes fetal death by prostaglandin-independent effects.
Keyword Lipopolysaccharide
Fetal death
Receptor Antagonist
Preterm Labor
Histologic Chorioamnionitis
Intra-Amniotic Infection
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: UQ Centre for Clinical Research Publications
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Citation counts: TR Web of Science Citation Count  Cited 28 times in Thomson Reuters Web of Science Article | Citations
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Created: Thu, 26 Aug 2010, 13:17:22 EST