Macrophage inhibitory cytokine 1 in fetal membranes and amniotic fluid from pregnancies with and without preterm labour and premature rupture of membranes

Keelan, J.A., Wang, K., Chaiworapongsa, T., Romero, R., Mitchell, M.D., Sato, T.A., Brown, D.A., Fairlie, W.D. and Breit, S.N. (2003) Macrophage inhibitory cytokine 1 in fetal membranes and amniotic fluid from pregnancies with and without preterm labour and premature rupture of membranes. Molecular Human Reproduction, 9 9: 535-540. doi:10.1093/molehr/gag068


Author Keelan, J.A.
Wang, K.
Chaiworapongsa, T.
Romero, R.
Mitchell, M.D.
Sato, T.A.
Brown, D.A.
Fairlie, W.D.
Breit, S.N.
Title Macrophage inhibitory cytokine 1 in fetal membranes and amniotic fluid from pregnancies with and without preterm labour and premature rupture of membranes
Journal name Molecular Human Reproduction   Check publisher's open access policy
ISSN 1360-9947
1360-9947
Publication date 2003-09-01
Sub-type Article (original research)
DOI 10.1093/molehr/gag068
Volume 9
Issue 9
Start page 535
End page 540
Total pages 6
Place of publication Oxford, England
Publisher Published for the European Society for Human Reproduction and Embryology by Oxford University Press
Language eng
Subject 1103 Clinical Sciences
1114 Paediatrics and Reproductive Medicine
1115 Pharmacology and Pharmaceutical Sciences
Abstract The placenta and fetal membranes are the site of expression of macrophage inhibitory cytokine (MIC-1), a member of the transforming growth factor (TGF)-β superfamily. We hypothesized that MIC-1 may act as an immune regulator in pregnancy complications associated with intrauterine inflammation. Decidual cells, chorionic trophoblasts and amnion epithelial cells were identified by immunohistochemistry as the predominant MIC-1-containing cell type in term membranes. Amnion and choriodecidual explants all produced MIC-1 in culture, the latter having the greatest production rate (206 ± 74.5 pg/mg tissue/24 h, n = 6; mean ± SEM). Production was not responsive to stimulation by pro-inflammatory cytokines. MIC-1 was detectable in 217 transabdominal amniotic fluid (AF) samples taken from 15 to 41 weeks gestation, concentrations ranging from 0.9-51.1 ng/ml. AF MIC-1 concentrations in pregnancies with premature rupture of membranes (PROM) or preterm labour, either with or without microbial invasion of the amniotic cavity, were not significantly different from those delivered at term either with or without labour. Treatment with MIC-1 (0.25-25 ng/ml) did not alter production of interleukin-6 or -8 by amnion or choriodecidual cells in vitro. We conclude that AF MIC-1 is derived from the fetal membranes and decidua, but that MIC-1 is unlikely to be involved in the pathophysiology of preterm birth or PROM.
Keyword Amniotic fluid
MIC-1
Pregnancy
Premature rupture of membranes
Preterm Birth
Growth-factor-beta
Pro-Inflammatory Cytokines
Necrosis-factor-alpha
Bacterial Lipopolysaccharide
Gestational Tissues
In-vitro
Superfamily
Cells
MIC-1
Immunomodulators
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
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 14 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 15 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Thu, 26 Aug 2010, 22:56:55 EST