Modulation of amniotic fluid activin-a and inhibin-a in women with preterm premature rupture of the membranes and infection-induced preterm birth.

Modulation of amniotic fluid activin-a and inhibin-a in women with preterm premature rupture of the membranes and infection-induced preterm birth.
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DOI:
10.1111/j.1600-0897.2011.01074.x
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发表时间:
2012-02
期刊:
American journal of reproductive immunology (New York, N.Y. : 1989)
影响因子:
--
通讯作者:
Buhimschi CS
Buhimschi CS
中科院分区:
其他
文献类型:
--
作者:
Rosenberg VA;Buhimschi IA;Dulay AT;Abdel-Razeq SS;Oliver EA;Duzyj CM;Lipkind H;Pettker CM;Buhimschi CS

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激活素和抑制素是炎症过程的重要调节剂。我们探讨了羊膜内感染和胎膜早破 (PPROM) 女性羊水 (AF) 激活素 A 和抑制素 A 系统的激活情况。我们分析了 78 个 AF 样本:“第二个三个月对照”(n=12)、“第三个三个月对照”(n=14)、胎膜完整的早产 [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)]。将羊膜绒毛膜和胎盘绒毛外植体与革兰氏阴性 (LPS) 或革兰氏阳性 (Pam3Cys) 细菌模拟物一起孵育后,体外评估激活素 A 水平。通过外植体 IL-8 的释放,探索了重组激活素 A 和抑制素 A 调节胎膜炎症反应的能力。激活素-A 和抑制素-A 存在于人类 AF 中,并且受孕龄调节。感染后激活素 A 显着上调。 Lower inhibin-A levels were seen in PPROM. LPS 引起羊膜绒毛膜释放激活素 A,但绒毛外植体不释放激活素 A。重组激活素 A 刺激羊膜绒毛膜释放 IL-8,但抑制素 A 无法逆转这一作用。人 AF 激活素 A 和抑制素 A 参与与羊膜内感染/炎症诱发的早产相关的生物过程。
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 (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.
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