The adaptation of the uterine environment into a favorable immunological and inflammatory milieu is a physiological process needed in normal pregnancy. A uterine hyperinflammatory state, whether idiopathic or secondary to hormonal or organic uterine disorders (polycystic ovary syndromes, endometriosis/adenomyosis and fibroids), negatively influences the interactions between decidua and trophoblast, early in gestation, and between chorion and decidua later in pregnancy. Abnormal activation of uterine inflammatory pathways not only contributes to the pathogenesis of the obstetric syndromes, i.e. recurrent pregnancy loss (RPL), pre-term delivery (PTD) and pre-eclampsia (PE), but also to correlates with severity. In this review, we summarize recent advances in the knowledge of uterine molecular mechanisms of inflammatory modulation in normal pregnancy and obstetric syndromes (RPL, PTD and PE). In particular, we focus on two regulators of uterine/placental inflammation: the NLRP3 inflammasome and the chemokines decoy receptor D6. We performed comprehensive review of the literature in PubMed and Google Scholar databases from 1994 to 2018. The available evidence suggests that: (i) the expression of inflammasome NLRP3 is increased in the endometrium of women with unexplained RPL, in the chorioamniotic membranes of women with PTL and in the placenta of women with PE; (ii) there is a role for abnormal expression and function of D6 decoy receptor at the feto-maternal interface in cases of RPL and PTD and (iii) the function of placental D6 decoy receptor is impaired in PE. A wider comprehension of the inflammatory molecular mechanisms involved in the pathogenesis of the obstetric syndromes might lead to the identification of new potential therapeutic targets.

中文翻译：

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产科综合征子宫异常炎症：趋化因子诱饵受体D6和炎症小分子NLRP3的分子生物学见解。

子宫环境适应良好的免疫和炎症环境是正常妊娠所需要的生理过程。无论是特发性还是继发于激素性或器质性子宫疾病（多囊卵巢综合征，子宫内膜异位/子宫腺肌病和肌瘤）的子宫高发炎状态，都会对蜕膜和滋养细胞之间，孕早期以及绒毛和蜕膜之间的相互作用产生不利影响。子宫炎性途径的异常激活不仅会导致产科综合征的发病机理，即反复妊娠流失（RPL），早产（PTD）和先兆子痫（PE），而且还与严重程度相关。在这篇评论中 我们总结了在正常妊娠和产科综合症（RPL，PTD和PE）中炎症调节的子宫分子机制知识的最新进展。特别是，我们专注于子宫/胎盘炎症的两种调节剂：NLRP3炎性小体和趋化因子诱饵受体D6。我们从1994年至2018年对PubMed和Google Scholar数据库中的文献进行了全面回顾。现有证据表明：（i）具有无法解释的RPL的女性子宫内膜中，炎性小分子NLRP3的表达增加。 PTL和患有PE的妇女的胎盘中；（ii）在RPL和PTD的情况下，D6诱饵在胎儿-母体界面的异常表达和功能中起作用，并且（iii）PE中胎盘D6诱饵的功能受损。