HIV-1感染女性胎盘滋养层细胞产生干扰素和β趋化因子。
Production of interferons and beta-chemokines by placental trophoblasts of HIV-1-infected women.
作者信息
Lee B N, Hammill H, Popek E J, Cron S, Kozinetz C, Paul M, Shearer W T, Reuben J M
机构信息
Department of Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
出版信息
Infect Dis Obstet Gynecol. 2001;9(2):95-104. doi: 10.1155/S1064744901000175.
OBJECTIVE
The mechanism whereby the placental cells of a human immunodeficiency virus (HIV)-1-infected mother protect the fetus from HIV-1 infection is unclear. Interferons (IFNs) inhibit the replication of viruses by acting at various stages of the life cycle and may play a role in protecting against vertical transmission of HIV-1. In addition the beta-chemokines RANTES (regulated on activation T cell expressed and secreted), macrophage inflammatory protein-1-alpha (MIP-1alpha), and MIP-1beta can block HIV-1 entry into cells by preventing the binding of the macrophage-trophic HIV-1 strains to the coreceptor CCR5. In this study the production of IFNs and beta-chemokines by placental trophoblasts of HIV-1-infected women who were HIV-1 non-transmitters was examined.
METHODS
Placental trophoblastic cells were isolated from 29 HIV-1-infected and 10 control subjects. Supernatants of trophoblast cultures were tested for the production of IFNs and beta-chemokines by enzyme linked immunosorbent assay (ELISA). Additionally, HIV-1-gag and IFN-beta transcripts were determined by a semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) assay.
RESULTS
All placental trophoblasts of HIV-1-infected women contained HIV-1-gag transcripts. There were no statistical differences in the median constitutive levels of IFN-alpha and IFN-gamma produced by trophoblasts of HIV-1 infected and control subjects. In contrast, trophoblasts of HIV-1-infected women constitutively produced significantly higher levels of IFN-beta protein than trophoblasts of control subjects. Furthermore, the median levels of beta-chemokines produced by trophoblasts of HIV-infected and control women were similar.
CONCLUSIONS
Since there was no correlation between the placental HIV load and the production of interferons or beta-chemokines, the role of trophoblast-derived IFNs and beta-chemokines in protecting the fetus from infection with HIV-1 is not clear.
目的
人类免疫缺陷病毒1型（HIV-1）感染母亲的胎盘细胞保护胎儿免受HIV-1感染的机制尚不清楚。干扰素（IFN）通过在病毒生命周期的各个阶段发挥作用来抑制病毒复制，可能在预防HIV-1垂直传播中发挥作用。此外，β趋化因子调节激活正常T细胞表达和分泌的因子（RANTES）、巨噬细胞炎性蛋白-1α（MIP-1α）和MIP-1β可通过阻止嗜巨噬细胞性HIV-1毒株与共受体CCR5结合来阻断HIV-1进入细胞。在本研究中，检测了HIV-1非传播者的HIV-1感染女性胎盘滋养层细胞产生干扰素和β趋化因子的情况。
方法
从29名HIV-1感染女性和10名对照者中分离胎盘滋养层细胞。通过酶联免疫吸附测定（ELISA）检测滋养层细胞培养上清液中干扰素和β趋化因子的产生情况。此外，通过半定量逆转录聚合酶链反应（RT-PCR）检测HIV-1- gag和IFN-β转录本。
结果
所有HIV-1感染女性的胎盘滋养层细胞均含有HIV-1- gag转录本。HIV-1感染组和对照组滋养层细胞产生的IFN-α和IFN-γ的中位组成水平无统计学差异。相比之下，HIV-1感染女性的滋养层细胞组成性产生的IFN-β蛋白水平显著高于对照组滋养层细胞。此外，HIV感染组和对照组女性滋养层细胞产生的β趋化因子的中位水平相似。
结论
由于胎盘HIV载量与干扰素或β趋化因子的产生之间没有相关性，滋养层来源的干扰素和β趋化因子在保护胎儿免受HIV-1感染中的作用尚不清楚。
Zotero 插件