Progesterone reduces lipopolysaccharide induced interleukin-6 secretion in fetoplacental chorionic arteries, fractionated cord blood, and maternal mononuclear cells

被引:25
作者
Gotkin, Jennifer L.
Celver, Jeremy
McNutt, Patrick
Shields, Andrea D.
Howard, Bobby C.
Paonessa, Damian J.
Napolitano, Peter G.
机构
[1] Madigan Army Med Ctr, Antenatal Diagnost Ctr, OBGYN, Div Maternal Fetal Med, Tacoma, WA 98431 USA
[2] Madigan Army Med Ctr, Dept Clin Invest, Tacoma, WA 98431 USA
关键词
progesterone; cytokines; inflammation; fetal artery; interleukin-6;
D O I
10.1016/j.ajog.2006.07.002
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective: The purpose of this study was to characterize effect of progesterone (P4) on interleukin-6 (IL-6) production by fetoplacental artery explants, fetal granulocytes, and fetal and maternal mononuclear cells. Study design: Arteries and cord blood were obtained from 5 term pregnancies undergoing repeat cesarean section. Maternal blood was obtained from another 6 women at 16 to 20 weeks' gestation. Tissues were fractionated by dissection or Histopaque gradient. Specimens were incubated in physiologic media then exposed to lipopolysaccharide (LPS) or P4 alone, or pretreated with P4 and then exposed to LPS. Samples were evaluated for IL-6 by enzyme-linked immunosorbent assay (ELISA). Results: Arteries and fetal and maternal mononuclear cells exposed to LPS increased IL-6 secretion by 9-, 27-, and 29-fold, respectively. P4 pretreatment blocked LPS induction of IL-6. Fetal granulocytes did not increase IL-6 production in response to LPS exposure. Conclusion: LPS induces IL-6 in arteries and fetal and maternal mononuclear cells. P4 pretreatment significantly blocks this effect in these cell populations, suggesting possible targets for anti-inflammatory actions of P4 in prevention of preterm birth. (c) 2006 Mosby, Inc. All rights reserved.
引用
收藏
页码:1015 / 1019
页数:5
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