Molecular Human Reproduction, Vol. 9, No. 9, 535-540,
September 2003
© 2003 European Society of Human Reproduction and Embryology
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Macrophage inhibitory cytokine 1 in fetal membranes and amniotic fluid from pregnancies with and without preterm labour and premature rupture of membranes
Submitted on February 25, 2003; accepted on May 13, 2003
1 Liggins Institute, Department of Pharmacology and Clinical Pharmacology, and 2 Department of Obstetrics and Gynecology, University of Auckland Faculty of Medical and Health Sciences, Auckland, New Zealand, 3 Perinatology Research Branch, National Institute of Child Health and Human Development, NIH/DHHS, Detroit, MI and Bethesda, MD, USA and 4 Centre for Immunology, St Vincent’s Hospital and University of New South Wales, Sydney, NSW 2010, Australia
5 To whom correspondence should be addressed at: Liggins Institute, University of Auckland, 2–6 Park Avenue, Grafton, Auckland, New Zealand. e-mail: j.keelan{at}auckland.ac.nz
The placenta and fetal membranes are the site of expression of macrophage inhibitory cytokine (MIC-1), a member of the transforming growth factor (TGF)-ß 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.
Key words: amniotic fluid/MIC-1/pregnancy/premature rupture of membranes/preterm birth
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