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首页> 外文期刊>Journal of Reproductive Immunology >2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) enhances placental inflammation
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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) enhances placental inflammation

机译：2,3,7,8-四氯二苯并-对-二恶英（TCDD）增强胎盘炎症

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摘要

Preterm birth is a leading cause of perinatal morbidity and mortality that is often associated with ascending infections from the lower genital tract. Recent studies with animal models have suggested that developmental exposure to the environmental toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can increase the risk of preterm birth in the offspring. How TCDD may modify placental immunity to ascending infections is unclear. Therefore, we studied the effects of TCDD treatment on basal and Escherichia coli-stimulated cytokine production by placental explants. Cultures of second-trimester placentas were treated with up to 40nM TCDD for 72h and then stimulated with 107CFU/ml E. coli for an additional 24h. Concentrations of cytokines and PGE2 were measured in conditioned medium by immunoassay. TCDD exposure increased mRNA levels of IL-1β by unstimulated cultures, but no effects on protein levels of this cytokine were detected. TNF-α production was unaffected by TCDD for unstimulated cultures, but pre-treatment with 40nM TCDD significantly increased E. coli-stimulated TNF-α production. Both basal and bacteria-stimulated PGE2 and COX-2 gene expression were enhanced by TCDD pretreatment. In contrast, production of the anti-inflammatory cytokine, IL-10, was reduced by TCDD pretreatment for both unstimulated and E. coli-stimulated cultures. No effect of TCDD on the viability of the cultures was detected. These results suggest that TCDD exposure may shift immunity to enhance a proinflammatory phenotype at the maternal-fetal interface that could increase the risk of infection-mediated preterm birth.
机译：早产是围产期发病率和死亡率的主要原因，通常与下生殖道感染的上升有关。有关动物模型的最新研究表明，发育暴露于环境毒素2,3,7,8-四氯二苯并-对-二恶英（TCDD）会增加后代早产的风险。尚不清楚TCDD如何改变胎盘对上升感染的免疫力。因此，我们研究了TCDD处理对胎盘外植体对基础和大肠埃希菌刺激的细胞因子产生的影响。用至多40nM TCDD处理孕中期胎盘的培养物72小时，然后再用107CFU / ml大肠杆菌刺激24小时。通过免疫测定在条件培养基中测量细胞因子和PGE 2的浓度。 TCDD暴露通过未经刺激的培养提高了IL-1β的mRNA水平，但未检测到对该细胞因子蛋白质水平的影响。 TNF-α的产生不受未刺激培养物的TCDD的影响，但是用40nM TCDD预处理显着增加了大肠杆菌刺激的TNF-α的产生。 TCDD预处理可增强基础和细菌刺激的PGE2和COX-2基因表达。相反，对于未刺激和大肠杆菌刺激的培养物，通过TCDD预处理降低了抗炎细胞因子IL-10的产生。没有检测到TCDD对培养物活力的影响。这些结果表明，TCDD暴露可能会改变免疫力，以增强母胎界面的促炎表型，从而增加感染介导的早产的风险。

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