Prevention of preterm labour via the modulation of inflammatory pathways
Prevention of preterm labour via the modulation of inflammatory pathways
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DOI：
10.3109/14767058.2012.666114
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发表时间：
2012-04-01
影响因子：
1.8
通讯作者：
Bennett, Phillip R.
中科院分区：
文献类型：
--
作者：
MacIntyre, David A.;Sykes, Lynne;Bennett, Phillip R.
妊娠的特点是先天性和获得性免疫系统调节的炎症事件的复杂相互作用。类似地，分娩可以被视为“促分娩”炎症通路的激活，其驱动宫颈成熟和子宫肌层激活。这些途径的过早激活，例如，通过感染，可导致早产和分娩。核因子κ β是这些途径和功能的关键调节剂，通过调节与足月分娩和早产相关的肾上腺素、趋化因子和促炎细胞因子的表达。因此，针对炎症和免疫激活的关键介质的未来治疗设计将是预防早产和免疫介导的新生儿脑损伤的合理方法。
Pregnancy is characterized by a complex interplay of inflammatory events regulated by both the innate and acquired immune systems. Similarly, parturition can be viewed as the activation of "pro-labour" inflammatory pathways, which drive cervical ripening and myometrial activation. Premature activation of these pathways, for example, by infection, can lead to preterm labour and birth. Nuclear factor kappa beta is a key modulator of these pathways and functions by regulating the expression of prostaglandins, chemokines and pro-inflammatory cytokines involved in both term and preterm labour. Future design of therapeutics that target key mediators of inflammation and immune activation would therefore be a rational approach for preventing preterm labour and immune-mediated neonatal brain damage.