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新生儿败血症和死性肠球炎的临床关联和潜在的分子机制
Xue Liu1,2, Wenqiang Sun1,2, Jingtao Bian1,2
1Department of Neonatology, Children's Hospital of Soochow University, Suzhou, China.
Frontiers in molecular biosciences
|October 20, 2025
概括
新生儿败血症 (NS) 通过共享的炎症途径增加了死角 enterokolitis (NEC) 的风险. 关键生物标志物FPR1,S100A12和CSF3R显示出在早产婴儿中早期识别的诊断潜力.
科学领域:
- 新生儿免疫学 新生儿免疫学
- 胃肠病学 胃肠病学
- 发现生物标志物的发现.
背景情况:
- 结核性肠球炎 (NEC) 是早产婴儿的严重肠道疾病,死亡率高.
- 新生儿败血症 (NS) 是NEC的独立风险因素,但共同的分子机制尚不清楚.
研究的目的:
- 调查NS和NEC之间共享的分子机制.
- 为了确定两种情况的潜在诊断生物标志物.
主要方法:
- 结合了NS和NEC数据集的临床队列分析和转录组分析.
- 确定了重叠的差异表达基因 (DEGs),并构建了一个蛋白质-蛋白质相互作用 (PPI) 网络.
- 使用独立队列验证了核心基因的诊断疗效,并构建了一个转录因子-mRNA调节网络.
主要成果:
- NS显著增加了NEC的风险 (OR = 3.02,P = 0.002).
- 确定了70个重叠的DEG,富含中性粒细胞化学反应和IL-17信号通路.
- FPR1,S100A12和CSF3R的诊断性能中等 (AUC为0.723-0.813),并且参与炎症过程.
结论:
- 新生儿败血症是NEC通过共享炎症途径发展的危险因素.
- FPR1,S100A12和CSF3R是潜在的生物标志物,可用于高风险婴儿的早期鉴定.
- 需要进一步的临床验证来确认治疗影响.
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