PROBLEM Vitamin D is well-known for having anti-inflammatory and immunomodulatory properties. Impaired maternal vitamin D status has been known to increase the risk of adverse pregnancy outcomes like pre-term birth. The present study aims to evaluate the impact of fetal cord serum 25-hydroxyvitamin D-mediated signaling in mediating inflammatory responses in placenta during pre-term birth. METHOD OF STUDY For the above purpose, cord serum 25 hydroxyvitamin D 25(OH)D were measured in term (n = 20) and pre-term (n = 20) born babies using ELISA. Vitamin D downstream signaling has also been checked in placenta (VDR, CYP27B1, cathelicidin LL37) along with expression of inflammatory markers (S100A8, HMGB1, TLR2, p-NF-kappaB) using Western blotting and immunohistochemistry. Pearson correlation model was used to do correlation study. RESULTS Compared with term born babies (59.31 ± 3.476), decline in cord serum 25(OH)D levels is observed in pre-term born babies (22.26 ± 1.083, P = <0.0001) that showed strong positive correlation with gestational age (r = .9368***) and birthweight (r = .9559***). On the other hand, vitamin D signaling markers were found to be downregulated and inflammatory markers were upregulated in placental tissue of pre-term born babies. CONCLUSION Thus, our study demonstrated that insufficient cord 25(OH)D levels may disturb the homeostasis of inflammation in placenta. Altered cord serum 25(OH)D mediated anti-inflammatory signaling may be acting as trigger signals in modulating inflammatory responses in placenta and eliciting premature activation of spontaneous labor in pre-term birth.

中文翻译：

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脐带血清25-羟基维生素D信号改变和胎盘炎症与早产有关。

问题维生素D具有抗炎和免疫调节特性，众所周知。已知孕妇维生素D状况受损会增加不良妊娠结局（如早产）的风险。本研究旨在评估早产期间胎儿血清25-羟维生素D介导的信号传导在胎盘中介导炎症反应中的作用。研究方法为了上述目的，使用ELISA对足月儿（n = 20）和早产儿（n = 20）的脐带血清25羟基维生素D 25（OH）D进行了测量。还使用Western印迹和免疫组化方法检查了胎盘中的维生素D下游信号传导（VDR，CYP27B1，Cathelicidin LL37）以及炎症标志物（S100A8，HMGB1，TLR2，p-NF-kappaB）的表达。使用Pearson相关模型进行相关研究。结果与足月婴儿（59.31±3.476）相比，早产婴儿（22.26±1.083，P = <0.0001）脐带血清25（OH）D水平下降，与胎龄呈正相关（r = .9368 ***）和出生体重（r = .9559 ***）。另一方面，早产婴儿的胎盘组织中维生素D信号标记被发现下调，而炎症标记被上调。结论因此，我们的研究表明脐带25（OH）D水平不足可能会干扰胎盘炎症的稳态。改变的脐带血清25（OH）D介导的抗炎信号可能在调节胎盘中的炎性反应并引起早产中自发性分娩的过早活化中充当触发信号。早产儿的脐血25（OH）D水平下降（22.26±1.083，P = <0.0001），与胎龄（r = .9368 ***）和出生体重（r = .9559 ***）。另一方面，早产婴儿的胎盘组织中维生素D信号标记被发现下调，炎症标记被上调。结论因此，我们的研究表明脐带25（OH）D水平不足可能会干扰胎盘炎症的稳态。改变的脐带血清25（OH）D介导的抗炎信号可能在调节胎盘中的炎性反应并引起早产中自发性分娩的过早活化中充当触发信号。早产儿的脐血25（OH）D水平下降（22.26±1.083，P = <0.0001），与胎龄（r = .9368 ***）和出生体重（r = .9559 ***）。另一方面，早产婴儿的胎盘组织中维生素D信号标记被发现下调，而炎症标记被上调。结论因此，我们的研究表明脐带25（OH）D水平不足可能会干扰胎盘炎症的稳态。改变的脐带血清25（OH）D介导的抗炎信号可能在调节胎盘中的炎性反应并引起早产中自发性分娩的过早活化中充当触发信号。0001）与胎龄（r = .9368 ***）和出生体重（r = .9559 ***）呈显着正相关。另一方面，早产婴儿的胎盘组织中维生素D信号标记被发现下调，炎症标记被上调。结论因此，我们的研究表明脐带25（OH）D水平不足可能会干扰胎盘炎症的稳态。改变的脐带血清25（OH）D介导的抗炎信号可能在调节胎盘中的炎性反应并引起早产中自发性分娩的过早活化中充当触发信号。0001）与胎龄（r = .9368 ***）和出生体重（r = .9559 ***）呈显着正相关。另一方面，早产婴儿的胎盘组织中维生素D信号标记被发现下调，而炎症标记被上调。结论因此，我们的研究表明脐带25（OH）D水平不足可能会干扰胎盘炎症的稳态。改变的脐带血清25（OH）D介导的抗炎信号可能在调节胎盘中的炎性反应并引起早产中自发性分娩的过早活化中充当触发信号。结论因此，我们的研究表明脐带25（OH）D水平不足可能会干扰胎盘炎症的稳态。改变的脐带血清25（OH）D介导的抗炎信号可能在调节胎盘中的炎性反应并引起早产中自发性分娩的过早活化中充当触发信号。结论因此，我们的研究表明脐带25（OH）D水平不足可能会干扰胎盘炎症的稳态。改变的脐带血清25（OH）D介导的抗炎信号可能在调节胎盘中的炎性反应并引起早产中自发性分娩的过早活化中充当触发信号。