Winram S B, Jonas M, Chi E, Rubens C E
Department of Pediatrics, Division of Infectious Diseases, Children's Hospital and Regional Medical Center, University of Washington, Seattle, Washington 98105, USA.
Infect Immun. 1998 Oct;66(10):4932-41. doi: 10.1128/IAI.66.10.4932-4941.1998.
Group B streptococci (GBS) have been cultured from the chorioamnionic membrane of pregnant women, usually in association with chorioamnionitis and premature labor (K. A. Boggess, D. H. Watts, S. L. Hillier, M. A. Krohn, T. J. Benedetti, and D. A. Eschenbach, Obstet. Gynecol. 87:779-784, 1996). Colonization and infection of placental membranes can be a prelude to neonatal GBS infections even in the presence of intact membranes (R. L. Naeye and E. C. Peters, Pediatrics 61:171-177, 1978), suggesting that GBS cause chorioamnionitis or establish amniotic fluid infections by partial or complete penetration of the placental membranes. We have isolated and grown cultures of primary chorion and amnion cells from human cesarean-section placentas. This has provided a biologically relevant model for investigating GBS adherence to and invasion of the two epithelial barriers of the placental membrane. GBS adhered to chorion cell monolayers to a high degree. Pretreatment of GBS with trypsin reduced adherence up to 10-fold, which suggested that the bacterial ligand(s) was a protein. GBS invaded chorion cells at a high rate in vitro, and invasion was dependent on cellular actin polymerization. GBS could be seen within intracellular vacuoles of chorion cells by transmission electron microscopy. We also demonstrated that GBS were capable of transcytosing through intact chorion cell monolayers without disruption of intracellular junctions. GBS also adhered to amnion cells; in contrast, however, these bacteria failed to invade amnion cells under a variety of assay conditions. GBS interactions with the chorion epithelial cell layer shown here correlate well with epidemiological and pathological studies of GBS chorioamnionitis. Our data also suggest that the amnion cell layer may provide an effective barrier against infection of the amniotic fluid.
B组链球菌(GBS)已从孕妇的绒毛羊膜中培养出来,通常与绒毛膜羊膜炎和早产有关(K. A. 博格斯、D. H. 瓦茨、S. L. 希利尔、M. A. 克罗恩、T. J. 贝内代蒂和D. A. 埃申巴赫,《妇产科学》87:779 - 784,1996年)。即使胎膜完整,胎盘膜的定植和感染也可能是新生儿GBS感染的前奏(R. L. 奈伊和E. C. 彼得斯,《儿科学》61:171 - 177,1978年),这表明GBS通过部分或完全穿透胎盘膜引起绒毛膜羊膜炎或引发羊水感染。我们从人类剖宫产胎盘分离并培养了原代绒毛膜和羊膜细胞。这为研究GBS对胎盘膜两个上皮屏障的黏附和侵袭提供了一个生物学相关模型。GBS高度黏附于绒毛膜细胞单层。用胰蛋白酶预处理GBS可使黏附减少多达10倍,这表明细菌配体是一种蛋白质。GBS在体外以高比率侵袭绒毛膜细胞,且侵袭依赖于细胞肌动蛋白聚合。通过透射电子显微镜可在绒毛膜细胞的细胞内液泡中看到GBS。我们还证明GBS能够通过完整的绒毛膜细胞单层进行跨细胞转运而不破坏细胞内连接。GBS也黏附于羊膜细胞;然而,相比之下,在各种检测条件下这些细菌都未能侵袭羊膜细胞。此处显示的GBS与绒毛膜上皮细胞层的相互作用与GBS绒毛膜羊膜炎的流行病学和病理学研究密切相关。我们的数据还表明羊膜细胞层可能为羊水感染提供有效的屏障。