Polybrominated diphenyl ethers enhance the production of proinflammatory cytokines by the placenta.

Polybrominated diphenyl ethers enhance the production of proinflammatory cytokines by the placenta.
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DOI:
10.1016/j.placenta.2012.06.005
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发表时间:
2012-09
期刊:
影响因子:
3.8
通讯作者:
Hanna, N.
Hanna, N.
中科院分区:
医学3区
文献类型:
--
作者:
Peltier, M. R.;Kimova, N. G.;Arita, Y.;Gurzenda, E. M.;Murthy, A.;Chawala, K.;Lerner, V.;Richardson, J.;Hanna, N.

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多溴二苯醚 (PBDE) 是普遍存在的环境污染物,可结合并穿过胎盘,但其对妊娠结局的影响尚不清楚。环境污染物可能会通过促进母胎界面的促炎症环境来增加炎症介导的妊娠并发症(例如早产)的风险。我们假设 PBDE 会减少 IL-10 的产生并增强与胎盘外植体早产/分娩相关的促炎细胞因子的产生。将妊娠中期胎盘外植体在载体(对照)或海鳗 47、99 和 100 的 2 μM PBDE 混合物中培养 72 小时。然后用 106 CFU/ml 热灭活的大肠杆菌刺激培养物最后 24 小时孵育,并收获条件培养基用于细胞因子和 PGE2 的定量。然后分别通过组织 ELISA 和 MTT 还原活性对处理组织的 COX-2 含量和活力进行定量。 PBDE 预处理减少了大肠杆菌刺激的 IL-10 产生,并显着增加了大肠杆菌刺激的 IL-1β 分泌。 PBDE 暴露还会增加基础和细菌刺激的 COX-2 表达。 PBDE 暴露也增强了基础 PGE2,但细菌刺激的 PGE2 没有增强。未检测到 PBDE 对外植体培养物活力的影响。总之,胎盘外植体预先暴露于海鳗 47、99 和 100 增强了胎盘对感染的促炎反应。这可能会降低细菌刺激促炎反应的阈值,从而增加感染介导的早产风险。
Polybrominated diphenyl ether(s) (PBDE) are ubiquitous environmental contaminants that bind and cross the placenta but their effects on pregnancy outcome are unclear. It is possible that environmental contaminants increase the risk of inflammation-mediated pregnancy complications such as preterm birth by promoting a proinflammatory environment at the maternal-fetal interface. We hypothesized that PBDE would reduce IL-10 production and enhance the production of proinflammatory cytokines associated with preterm labor/birth by placental explants. Second trimester placental explants were cultured in either vehicle (control) or 2 μM PBDE mixture of congers 47, 99 and 100 for 72 h. Cultures were then stimulated with 106 CFU/ml heat-killed Escherichia coli for a final 24 h incubation and conditioned medium was harvested for quantification of cytokines and PGE2. COX-2 content and viability of the treated tissues were then quantified by tissue ELISA and MTT reduction activity, respectively. PBDE pre-treatment reduced E. coli-stimulated IL-10 production and significantly increased E. coli-stimulated IL-1β secretion. PBDE exposure also increased basal and bacteria-stimulated COX-2 expression. Basal, but not bacteria-stimulated PGE2, was also enhanced by PBDE exposure. No effect of PBDE on viability of the explants cultures was detected. In summary, pre-exposure of placental explants to congers 47, 99, and 100 enhanced the placental proinflammatory response to infection. This may increase the risk of infection-mediated preterm birth by lowering the threshold for bacteria to stimulate a proinflammatory response(s).
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