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

作　　者：李莉平[1] 康佳丽[1] 雷蔚华[1] 祝琳[1] 吕军[1] 郭颖[1] 冯淑瑜[1] 

机构地区：[1]广州市第一人民医院妇产科,广州510180

出　　处：《华中科技大学学报（医学版）》2010年第5期672-674,687,共4页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

基　　金：广东省自然科学基金博士启动项目(No.7301628);广东省医学科研基金资助项目(No.A2008512);广州市医药卫生科技项目(No.2007-YB-025)

摘　　要：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.

关 键 词：早产 脂多糖 TOLL样受体4 母胎界面 

分 类 号：R714.21[医药卫生—妇产科学]