Cathelicidins and the Onset of Labour.
Cathelicidins and the Onset of Labour.
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Cathelicidins 和分娩的开始。
DOI：
10.1038/s41598-019-43766-7
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发表时间：
2019
影响因子：
4.6
通讯作者：
Boeckel SRV
中科院分区：
文献类型：
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作者：
Boeckel SRV
早产是指在怀孕37周前分娩，是新生儿死亡和发病的主要原因。感染和炎症是自发性早产的常见先兆。放线菌素是一种抗菌宿主防御肽，由感染和炎症诱导，虽然在生殖道和胎儿组织中表达，但其在自发早产发病机制中的作用尚不清楚。在这里，我们证明了在炎症引产的小鼠子宫中，放线菌素在RNA和蛋白质水平上的表达增加，其中超声引导下在E17的宫内注射脂多糖刺激早产在24 小时内。在宫内注射1 μg内毒素后，缺乏中草药的(CAMP)小鼠比野生型小鼠更不容易早产，同时伴随着循环中IL-6的减少，IL-6是一种与分娩有关的炎症介质。我们还发现，在足月分娩妇女的子宫肌层标本中，放线菌素表达细胞的比例高于临产前。综上所述，这些数据表明，在炎症诱导分娩的小鼠模型中，以及在人类足月分娩中，长春花碱在调节促炎反应方面发挥了作用。
Preterm birth, defined as delivery before 37 weeks of gestation, is the leading cause of neonatal mortality and morbidity. Infection and inflammation are frequent antecedents of spontaneous preterm birth. Cathelicidin, an antimicrobial host defence peptide, is induced by infection and inflammation and although expressed in the reproductive tract and fetal tissues, its role in the pathogenesis of spontaneous preterm birth is unknown. Here we demonstrate that cathelicidin expression is increased at RNA and protein level in the mouse uterus in a model of inflammation-induced labour, where ultrasound guided intrauterine injection of lipopolysaccharide (LPS) at E17 stimulates preterm delivery within 24 hours. Cathelicidin-deficient (Camp−/−)mice are less susceptible to preterm delivery than wild type mice following intrauterine injection of 1 μg of LPS, and this is accompanied by a decrease in circulating IL-6, an inflammatory mediator implicated in the onset of labour. We also show that the proportion of cathelicidin expressing cells in the myometrium is higher in samples obtained from women in labour at term than pre-labour. Together, these data suggest that cathelicidin has roles in mediating pro-inflammatory responses in a murine model of inflammation-induced labour, and in human term labour.