THE ENHANCED PRODUCTION OF PLACENTAL INTERLEUKIN-1 DURING LABOR AND INTRAUTERINE INFECTION

被引：104

作者：

TANIGUCHI, T ^{[1
]}

MATSUZAKI, N ^{[1
]}

KAMEDA, T ^{[1
]}

SHIMOYA, K ^{[1
]}

JO, T ^{[1
]}

SAJI, F ^{[1
]}

TANIZAWA, O ^{[1
]}

机构：

[1] OSAKA UNIV,SCH MED,DEPT OBSTET & GYNECOL,1-1-50 FUKUSHIMA,FUKUSHIMA KU,OSAKA 553,JAPAN

来源：

AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY | 1991年 / 165卷 / 01期

关键词：

PLACENTAL INTERLEUKIN-1; TROPHOBLAST; LABOR; INTRAUTERINE INFECTION;

D O I：

10.1016/0002-9378(91)90241-I

中图分类号：

R71 [妇产科学];

学科分类号：

100211 ;

摘要：

The purpose of this study was to determine the effect of labor and chorioamnionitis in interleukin-1 production by human placenta. We studied the activity of the placenta to produce interleukin-1 with an enzyme immunoassay by culturing tissue blocks. The placental tissue obtained after labor produced a larger amount of interleukin-1 than placental tissue obtained before labor. All the placental tissues produced more interleukin-1-beta than interleukin-1-alpha. The placentas with labor and chorioamnionitis produced about seventeenfold more interleukin-1 than placentas with labor only. We immunohistochemically identified interleukin-1-producing cells in the placenta and found that syncytiotrophoblasts produced both interleukin-1-alpha and interleukin-1-beta, while Hofbauer cells produced only interleukin-1-beta. In vitro analysis of the trophoblast activities to produce interleukin-1 revealed that microbial byproducts enhanced interleukin-1 production, possibly inducing accumulation of interleukin-1 receptor-positive cells at the sites of inflammation. In addition to stimulation of prostaglandin biosynthesis and labor, the placental interleukin-1 may act as an inflammatory mediator, leading to systemic and local changes at fetomaternal interface and activating fetomaternal immune systems against intrauterine infection.

引用

页码：131 / 137

页数：7

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