引言
作为妊娠期子宫蜕膜的主要功能细胞,基质细胞与免疫细胞频繁互作,共同维持母胎界面的免疫平衡,有利于妊娠的建立和维持。研究表明,蜕膜组织富含大量糖原、脂滴等成分,显示出活跃的糖脂代谢【1,2】。与未孕子宫的内膜基质细胞相比,蜕膜基质细胞中的脂滴数量显著增多【3】。同时,近期多项临床研究表明,母体血清脂质成分的变化与自然流产的发生密切相关【4,5】,提示脂代谢异常可能是不良妊娠结局的潜在致病因素之一。巨噬细胞的表型和功能受微环境中代谢信号的影响和调控,然而目前尚不清楚自然流产时蜕膜组织是否存在脂代谢异常,以及基质细胞与巨噬细胞之间的脂质交流如何影响其免疫功能转化并介导早期妊娠失败的具体机制。
2024年10月24日,复旦大学附属妇产科医院杜美蓉团队在Cell Reports杂志上在线发表了题为CD36-mediated arachidonic acid influx from decidual stromal cells increases inflammatory macrophages in miscarriage的研究论文。研究发现,自然流产蜕膜组织中脂滴蓄积,基质细胞与巨噬细胞脂代谢异常活跃。巨噬细胞高表达CD36,介导花生四烯酸(AA)从基质细胞向巨噬细胞的转运,促进巨噬细胞生成IL-1β,从而诱发免疫炎症反应。同时揭示了催乳素(PRL)能够抑制上述脂质转运过程,在正常妊娠时作为保护因子防止脂质过度累积的调控机制。

参考文献
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排版|探索君
来源|BioArt
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