Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT 06520, USA.
Am J Reprod Immunol. 2012 Feb;67(2):122-31. doi: 10.1111/j.1600-0897.2011.01074.x. Epub 2011 Oct 13.
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).
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.
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.
Human AF activin-A and inhibin-A are involved in biological processes linked to intra-amniotic infection/inflammation-induced preterm birth.
激活素和抑制素是炎症过程的重要调节剂。我们探讨了羊水中激活素-A 和抑制素-A 系统在羊膜内感染和早产胎膜早破(PPROM)妇女中的激活情况。
我们分析了 78 份羊水样本:“中期对照”(n=12)、“晚期对照”(n=14)、胎膜完整的早产临产[阳性-AF 培养物(n=13)、阴性-AF 培养物(n=13)]和 PPROM[阳性-AF 培养物(n=13)、阴性-AF 培养物(n=13)]。通过将羊膜绒毛和胎盘绒毛外植体与革兰氏阴性脂多糖(LPS)或革兰氏阳性(Pam3Cys)细菌模拟物孵育,评估激活素-A 水平。通过外植体 IL-8 释放,探讨重组激活素-A 和抑制素-A 对胎儿膜炎症反应的调节能力。
激活素-A 和抑制素-A 存在于人羊水,并受胎龄调节。感染使激活素-A 显著上调。PPROM 中抑制素-A 水平较低。LPS 从羊膜绒毛中释放激活素-A,但不从绒毛外植体中释放。重组激活素-A 刺激羊膜绒毛释放 IL-8,抑制素-A 不能逆转这一作用。
人羊水激活素-A 和抑制素-A 参与与羊膜内感染/炎症引起的早产相关的生物学过程。