Lipopolysaccharide differently affects prostaglandin E2 levels in fetal and maternal compartments of perfused human term placenta

Alaa Amash, Gershon Holcberg, Eyal Sheiner, Sigal Fleisher-Berkovich, Leslie Myatt, Mahmoud Huleihel

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

The aim of the present study was to examine the effect of lipopolysaccharide (LPS) on the levels of prostaglandin E2 (PGE2) in the perfusates of the fetal and the maternal compartments of perfused human term placental tissue. Term placentas were perfused for 10 h in the absence [control, (n = 4)] and presence of LPS [LPS = 1 μg/kg perfused placental tissue, (n = 4)] in the maternal reservoir. Perfusate samples from the fetal and the maternal circulations were collected every 30 min and examined for PGE2 levels by radio-immunoassay. PGE2 levels in the fetal circulation were gradually increased reaching significant peak value of 479 ± 159 pg/ml, as compared to PGE2 levels in the maternal circulation (140 ± 146 pg/ml) (p <0.05). After 10 hours of perfusion with control medium, PGE2 levels in the maternal circulation (347 ± 144 pg/ml) were significantly higher as compared to the fetal circulation (150 ± 57 pg/ml) (p <0.05). In presence of LPS, PGE2 levels in the fetal circulation increased reaching a peak value of 1028 ± 663 pg/ml after 240 min of perfusion. The levels of PGE2 in the control group after 240 min of perfusion were significantly lower (156 ± 77 pg/ml) (p <0.05). No significant differences were detected in the levels of PGE2 in the perfusate of the maternal compartment in presence of LPS, as compared to control. Our results suggest that the placenta may play an important role in maintaining high levels of PGE2 in the fetal circulation and low PGE2 levels in the maternal circulation during normal pregnancy. Moreover, placental PGE2 release into the fetal and the maternal circulations may be differently affected in presence of intra-uterine infection/inflammation.

Original languageEnglish (US)
Pages (from-to)18-22
Number of pages5
JournalProstaglandins and Other Lipid Mediators
Volume88
Issue number1-2
DOIs
StatePublished - Jan 2009
Externally publishedYes

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Dinoprostone
Placenta
Lipopolysaccharides
Mothers
Perfusion
Tissue
Radio
Immunoassay
Inflammation
Pregnancy
Control Groups

Keywords

  • Lipopolysaccharide
  • Perfusion
  • Placenta
  • Prostaglandin E

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Pharmacology
  • Cell Biology

Cite this

Lipopolysaccharide differently affects prostaglandin E2 levels in fetal and maternal compartments of perfused human term placenta. / Amash, Alaa; Holcberg, Gershon; Sheiner, Eyal; Fleisher-Berkovich, Sigal; Myatt, Leslie; Huleihel, Mahmoud.

In: Prostaglandins and Other Lipid Mediators, Vol. 88, No. 1-2, 01.2009, p. 18-22.

Research output: Contribution to journalArticle

Amash, Alaa ; Holcberg, Gershon ; Sheiner, Eyal ; Fleisher-Berkovich, Sigal ; Myatt, Leslie ; Huleihel, Mahmoud. / Lipopolysaccharide differently affects prostaglandin E2 levels in fetal and maternal compartments of perfused human term placenta. In: Prostaglandins and Other Lipid Mediators. 2009 ; Vol. 88, No. 1-2. pp. 18-22.
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AB - The aim of the present study was to examine the effect of lipopolysaccharide (LPS) on the levels of prostaglandin E2 (PGE2) in the perfusates of the fetal and the maternal compartments of perfused human term placental tissue. Term placentas were perfused for 10 h in the absence [control, (n = 4)] and presence of LPS [LPS = 1 μg/kg perfused placental tissue, (n = 4)] in the maternal reservoir. Perfusate samples from the fetal and the maternal circulations were collected every 30 min and examined for PGE2 levels by radio-immunoassay. PGE2 levels in the fetal circulation were gradually increased reaching significant peak value of 479 ± 159 pg/ml, as compared to PGE2 levels in the maternal circulation (140 ± 146 pg/ml) (p <0.05). After 10 hours of perfusion with control medium, PGE2 levels in the maternal circulation (347 ± 144 pg/ml) were significantly higher as compared to the fetal circulation (150 ± 57 pg/ml) (p <0.05). In presence of LPS, PGE2 levels in the fetal circulation increased reaching a peak value of 1028 ± 663 pg/ml after 240 min of perfusion. The levels of PGE2 in the control group after 240 min of perfusion were significantly lower (156 ± 77 pg/ml) (p <0.05). No significant differences were detected in the levels of PGE2 in the perfusate of the maternal compartment in presence of LPS, as compared to control. Our results suggest that the placenta may play an important role in maintaining high levels of PGE2 in the fetal circulation and low PGE2 levels in the maternal circulation during normal pregnancy. Moreover, placental PGE2 release into the fetal and the maternal circulations may be differently affected in presence of intra-uterine infection/inflammation.

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