Modulation of Amniotic Fluid Activin-A and Inhibin-A in Women With Preterm Premature Rupture of the Membranes and Infection-Induced Preterm Birth.
Summary of "Modulation of Amniotic Fluid Activin-A and Inhibin-A in Women With Preterm Premature Rupture of the Membranes and Infection-Induced Preterm Birth."
Citation Rosenberg VA, Buhimschi IA, Dulay AT, Abdel-Razeq SS, Oliver EA, Duzyj CM, Lipkind H, Pettker CM, Buhimschi CS. Modulation of amniotic fluid activin-A and inhibin-A in women with preterm premature rupture of the membranes and infection-induced preterm birth. Am J Reprod Immunol 2011 Problem Activins and inhibins are important modulators of inflammatory processes. We explored activation of amniotic fluid (AF) activin-A and inhibin-A system in women with intra-amniotic infection and preterm premature rupture of the membranes (PPROM). Method of study We analyzed 78 AF samples: '2nd trimester-control' (n = 12), '3rd trimester-control' (n = 14), preterm labor with intact membranes [positive-AF-cultures (n = 13), negative-AF-cultures (n = 13)], and PPROM [positive-AF-cultures (n = 13), negative-AF-cultures (n = 13)]. Activin-A levels were evaluated ex-vivo following incubation of amniochorion and placental villous explants with Gram-negative lipopolysaccharide (LPS) or Gram-positive (Pam3Cys) bacterial mimics. Ability of recombinant activin-A and inhibin-A to modulate inflammatory reactions in fetal membranes was explored through explants' IL-8 release. Results Activin-A and inhibin-A were present in human AF and were gestational age-regulated. Activin-A was significantly upregulated by infection. Lower inhibin-A levels were seen in PPROM. LPS elicited release of activin-A from amniochorion, but not from villous explants. Recombinant activin-A stimulated IL-8 release from amniochorion, an effect that was not reversed by inhibin-A. Conclusion Human AF activin-A and inhibin-A are involved in biological processes linked to intra-amniotic infection/inflammation-induced preterm birth.
Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.
This article was published in the following journal.
Name: American journal of reproductive immunology (New York, N.Y. : 1989)
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21992678
- DOI: http://dx.doi.org/10.1111/j.1600-0897.2011.01074.x
Medical and Biotech [MESH] Definitions
A clear, yellowish liquid that envelopes the FETUS inside the sac of AMNION. In the first trimester, it is likely a transudate of maternal or fetal plasma. In the second trimester, amniotic fluid derives primarily from fetal lung and kidney. Cells or substances in this fluid can be removed for prenatal diagnostic tests (AMNIOCENTESIS).
A condition of abnormally high AMNIOTIC FLUID volume, such as greater than 2,000 ml in the LAST TRIMESTER and usually diagnosed by ultrasonographic criteria (AMNIOTIC FLUID INDEX). It is associated with maternal DIABETES MELLITUS; MULTIPLE PREGNANCY; CHROMOSOMAL DISORDERS; and congenital abnormalities.
The innermost membranous sac that surrounds and protects the developing embryo which is bathed in the AMNIOTIC FLUID. Amnion cells are secretory EPITHELIAL CELLS and contribute to the amniotic fluid.
Embolism, Amniotic Fluid
Blocking of maternal circulation by AMNIOTIC FLUID that is forced into uterine VEINS by strong UTERINE CONTRACTION near the end of pregnancy. It is characterized by the sudden onset of severe respiratory distress and HYPOTENSION that can lead to maternal DEATH.
Activin Receptors, Type I
One of the two types of ACTIVIN RECEPTORS or activin receptor-like kinases (ALK'S). There are several type I activin receptors. The major active ones are ALK-2 (ActR-IA) and ALK-4 (ActR-IB).
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