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首页> 外文期刊>Cytokine >Surfactant protein A modulates the lipopolysaccharide-induced inflammatory response related to preterm birth.
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Surfactant protein A modulates the lipopolysaccharide-induced inflammatory response related to preterm birth.

机译：表面活性蛋白A调节脂多糖诱导的与早产有关的炎症反应。

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Surfactant protein A (SP-A) functions in homeostasis of lung surfactant and in innate immunity. SP-A is secreted by the fetal lung into amniotic fluid. Additionally it has been detected in gestational tissues. We propose that SP-A influences intrauterine inflammation that is commonly associated with preterm birth, the main underlying cause of neonatal mortality and morbidity. We used our previously established mouse model of LPS-induced preterm birth of live-born pups to investigate the role of SP-A in preterm birth. Mice overexpressing rat SP-A (rSP-A) under the control of human SP-C promoter were used. Cytokine concentrations in maternal and fetal serum and in amniotic fluid and mRNA levels of several inflammatory mediators in lungs and in intrauterine tissues were quantified using Cytometric Bead Array and RNase Protection Assay, respectively. Higher levels of SP-A mRNA were observed in fetal lungs and intrauterine tissues of rSP-A mice compared with wild-type. Using Western blot we detected excess of SP-A protein in fetal lung and in amniotic fluid of rSP-A animals. Despite some differences in the basal levels of TNF-alpha and IL-10 between rSP-A and wild-type animals, there were no differences in the duration of pregnancy. However, the levels of TNF-alpha, IL-10 and some other inflammatory mediators in intrauterine tissues and in amniotic fluid differed significantly between the mouse lines after maternal LPS given at 17dpc. We conclude that SP-A modulates the levels of intrauterine inflammatory mediators involved in preterm birth and may contribute to inflammatory processes related to spontaneous preterm labor.
机译：表面活性剂蛋白A（SP-A）在肺表面活性剂的稳态和先天免疫中起作用。 SP-A由胎肺分泌为羊水。另外，已经在妊娠组织中检测到它。我们建议SP-A影响通常与早产相关的子宫内炎症，早产是早产，新生儿死亡和发病的主要原因。我们使用我们先前建立的LPS诱导的活产幼犬早产小鼠模型来研究SP-A在早产中的作用。使用在人SP-C启动子控制下的过表达鼠SP-A（rSP-A）的小鼠。分别使用Cytometric Bead Array和RNase Protection Assay对母体和胎儿血清，羊水中的细胞因子浓度以及肺和子宫内组织中几种炎症介质的mRNA水平进行了定量。与野生型相比，在rSP-A小鼠的胎儿肺和子宫内组织中观察到更高水平的SP-A mRNA。使用蛋白质印迹，我们在胎儿肺和rSP-A动物的羊水中检测到过量的SP-A蛋白。尽管rSP-A和野生型动物之间的TNF-α和IL-10的基础水平存在一些差异，但怀孕时间没有差异。但是，在母体给予17dpc的LPS后，子宫内组织和羊水中的TNF-α，IL-10和一些其他炎症介质的水平在小鼠品系之间存在显着差异。我们得出的结论是，SP-A调节参与早产的子宫内炎症介质的水平，并可能促进与自发早产有关的炎症过程。

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