炎症诱导性早产小鼠胎盘淋巴细胞表型分析

Analysis of Placenta Lymphocytes Phenotype in Inflammation-induced Preterm Delivery of Mice

目的探讨Toll样受体4(TLR4)在炎症诱导性早产中的作用。方法预先阻断TLR4或不阻断TLR4的条件下,腹腔注射脂多糖(LPS)建立小鼠炎症诱导性早产模型,计算早产率和死胎率。采用流式细胞术检测胎盘CD45+CD86+、CD45+CD49b+和CD49b+CD69+细胞的百分率。结果 LPS组的早产率和死胎率均明显高于对照组,抗TLR4组的早产率和死胎率均显著低于LPS组。预先阻断TLR4明显抑制LPS所致的胎盘CD45+CD86+、CD45+CD49b+和CD49b+CD69+细胞水平的升高。结论 TLR4在炎症诱导性早产中具有重要作用。

Objective To investigate the potential role of Toll-like receptor 4（TLR4）in inflammation-induced preterm delivery.Methods Intraperitoneal injection of lipopolysaccharide（LPS）in the presence or absence of previous TLR4 blockade was performed to establish a murine model of preterm delivery.The incidences of preterm delivery and fetal death were calculated.Flow cytometry was used to examine the percentages of placenta CD45^＋CD86^＋,CD45^＋CD49b^＋ and CD49b^＋CD69^＋ cell subsets.Results Blocking TLR4 significantly decreased LPS-induced preterm delivery and fetal death.LPS treatment markedly up-regulated percentage of placenta CD45^＋CD86^＋,CD45^＋CD49b^＋ and CD49b^＋CD69^＋ cells.Previous TLR4 blockade significantly decreased LPS-induced elevated cell proportions.Conclusion TLR4 plays a critical role in inflammation-induced preterm delivery.