PDF(Pubmed)
Abstract：
Exposure to environmental toxicants (such as dioxins) has been epidemiologically linked to adverse reproductive health outcomes, including placental inflammation and preterm birth. However, the molecular underpinnings that govern these outcomes in gravid reproductive tissues remain largely unclear. Placental macrophages (also known as Hofbauer cells) are crucial innate immune cells that defend the gravid reproductive tract and help promote maternal-fetal tolerance. We hypothesized that exposure to environmental toxicants such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) could alter placental macrophage responses to inflammatory insults such as infection. To test this, placental macrophages were cultured in the presence or absence of TCDD and then infected with the perinatal pathogen Group B Streptococcus (GBS). Our results indicate that TCDD is lethal to placental macrophages at and above a 5 nM concentration and that sublethal dioxin exposure inhibits phagocytosis and cytokine production. Taken together, these results indicate that TCDD paralyzes placental macrophage responses to bacterial infection.
摘要：
在流行病学上，暴露于环境毒物（如二恶英）与不良生殖健康结果有关，包括胎盘炎症和早产。然而,在妊娠生殖组织中控制这些结果的分子基础仍不清楚.胎盘巨噬细胞（也称为Hofbauer细胞）是至关重要的先天免疫细胞，可保护妊娠生殖道并有助于促进母胎耐受性。我们假设暴露于环境毒物如2,3,7,8-四氯二苯并-p-二恶英（TCDD）可以改变胎盘巨噬细胞对炎症损伤如感染的反应。为了测试这个，在存在或不存在TCDD的情况下培养胎盘巨噬细胞，然后用围产期病原体B组链球菌（GBS）感染。我们的结果表明，TCDD在5nM浓度及以上对胎盘巨噬细胞具有致死性，并且亚致死二恶英暴露会抑制吞噬作用和细胞因子的产生。一起来看,这些结果表明，TCDD麻痹胎盘巨噬细胞对细菌感染的反应。
