激活S100A8/A9 Alarmin可以扩大马上升胎盘炎的炎症路径
Kirsten E Scoggin1, Shimaa I Rakha2, Ahmed M Abdellatif3
1Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546, USA.
International journal of molecular sciences
|February 13, 2026
概括
S100A8 / S100A9 (S100A8 / A9) 警报素在急性和慢性马胎盘炎中都受到上调,导致炎症和组织损伤. 准这种S100A8/A9通路为治疗妊娠损失提供了潜在的潜力.
科学领域:
- 兽医免疫学 兽医免疫学
- 生殖免疫学 生殖免疫学
- 马类病理学 马类病理学
背景情况:
- 上升性胎盘炎是马类妊娠流产的主要原因之一.
- 马胎盘炎的上游炎症触发因素仍然不太清楚.
- S100A8/S100A9 (S100A8/A9) 警示素以前被确定为慢性模型中的潜在上游调节剂.
研究的目的:
- 为了确定S100A8/A9上调是否在急性马胎盘炎和临床病例中持续存在.
- 研究S100A8/A9通路中下游炎症媒介体的表达.
- 阐明S100A8/A9信号轴在马胎盘炎中的作用.
主要方法:
- 在实验性急性和慢性胎盘炎模型中对S100A8/A9mRNA表达的量化.
- 免疫组织化学检测S100A8/A9蛋白在胎盘组织中的定位.
- 对临床胎盘炎病例的RNA测序分析,以确定下游炎症媒介和受体.
主要成果:
- 在急性和慢性马胎盘炎中,S100A8和S100A9的mRNA表达显著上调.
- 在胎盘炎组织中,中性粒细胞和巨细胞密集透S100A8/A9蛋白.
- 临床病例显示,S100A8/A9受体 (TLR4,RAGE) 和NF-κB驱动的炎症调解体 (IL1β,IL6,TNF,CXCL8,CCL2,CXCL10,CASP3) 的同时升高调节.
结论:
- S100A8/A9上调是马胎盘炎的持续特征,不仅限于慢性病理.
- 一个连贯的S100A8/A9-TLR4/RAGE-NF-κB信号轴在临床马胎盘炎中驱动炎症和组织损伤.
- S100A8/A9警示素具有诊断潜力,并代表了一种有前途的治疗标,用于减轻感染引起的马胎儿流产.
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