2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) enhances placental inflammation.
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) enhances placental inflammation.
复制标题
DOI：
10.1016/j.jri.2013.02.005
复制
发表时间：
2013-06
影响因子：
3.4
通讯作者：
Hanna N
中科院分区：
文献类型：
--
作者：
Peltier MR;Arita Y;Klimova NG;Gurzenda EM;Koo HC;Murthy A;Lerner V;Hanna N
早产是围产期发病率和死亡率的主要原因，通常与下生殖道的上升感染有关。最近的动物模型研究表明，发育过程中暴露于环境毒素2，3，7，8-四氯二苯并-对二恶英(TCDD)会增加子代早产的风险。TCDD如何改变胎盘对上升感染的免疫力尚不清楚。因此，我们研究了TCDD处理对胎盘外植体基础和大肠杆菌刺激的细胞因子产生的影响。用40 nM的TCDD处理中期胎盘培养72小时，再用107 CFU/ml的大肠杆菌刺激24小时，用免疫分析法检测条件培养液中细胞因子和前列腺素E_2的浓度。在未经刺激的培养条件下，TCDD可增加IL-1β的表达水平，但对该细胞因子的蛋白水平无影响。TCDD对未刺激的培养细胞产生的肿瘤坏死因子-α无明显影响，但40 nM的TCDD可显著增加大肠杆菌刺激的肿瘤坏死因子-α的产生。TCDD可增强基础和细菌刺激的PGE2和COX-2基因的表达。相反，在未经刺激和经大肠杆菌刺激的培养物中，TCDD预处理都减少了抗炎细胞因子IL-10的产生。TCDD对培养物活力无明显影响。这些结果表明，接触TCDD可能会改变免疫力，增强母胎界面的促炎表型，这可能会增加感染介导的早产的风险。
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 40 nM TCDD for 72 h and then stimulated with 107 CFU/ml E. coli for an additional 24 h. 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 40 nM 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.
登录
查看更多内容
DOI：
10.1016/s0002-9378(87)80315-0
发表时间：
1987-11-01
影响因子：
9.8
作者：
GARFIELD, RE;GASC, JM;BAULIEU, EE
通讯作者：
BAULIEU, EE
影响因子：
9.8
作者：
Andrews, WW;Goldenberg, RL;Goepfert, AR
通讯作者：
Goepfert, AR
DOI：
10.1111/j.1471-0528.2008.02008.x
发表时间：
2009-01-01
影响因子：
5.8
作者：
Berghella, V.
通讯作者：
Berghella, V.
影响因子：
3.8
作者：
GRAY, LE;KELCE, WR;BIRNBAUM, LS
通讯作者：
BIRNBAUM, LS
影响因子：
7.1
作者：
Hassan, S. S.;Romero, R.;Creasy, G. W.
通讯作者：
Creasy, G. W.