产前尿液等离子体引起感染 结肠粘液屏障缺陷:对肠道病理的影响
Charlotte van Gorp1, Ilse H de Lange2, Matthias C Hütten1,3
1Department of Pediatrics, School for Oncology and Reproduction (GROW), Maastricht University, 6229 ER Maastricht, The Netherlands.
International journal of molecular sciences
|April 13, 2024
概括
在胆膜炎期间产前接触Ureaplasma parvum (UP) 会使结肠粘液层变厚,但会损害其功能. 这种UP诱导的肠道屏障缺陷可能会导致新生儿死性肠球炎 (NEC) 的发展.
科学领域:
- 产科和妇科 产科和妇科
- 新生儿科学 新生儿科学
- 微生物学 微生物学
背景情况:
- 胎儿膜感染的冠状腺炎是已知的死角性肠球炎 (NEC) 的风险因素,这是早产婴儿严重的肠道疾病.
- 尿液等离子体 (Ureaplasma parvum) (UP) 经常被检测到胆膜炎病例中,但其在疾病发展中的作用尚未完全理解.
- 虽然在胆 ?? 膜炎中记录了叶屏障变化,但结肠粘液屏障的完整性及其与NEC的联系仍未得到充分研究.
研究的目的:
- 调查假设产前Ureaplasma parvum (UP) 暴露会破坏结肠粘液屏障的完整性,可能有助于死性肠球炎 (NEC) 的发病.
- 探索UP诱导的结肠屏障功能障碍的潜在机制,包括内质网膜 (ER) 应激和线粒体完整性.
- 通过将实验结果与人类NEC患者结肠样本进行比较来验证实验结果的临床相关性.
主要方法:
- 建立了一种羊类胆 ?? 膜炎模型,将羊羔暴露在UP或盐水中.
- 使用组织学和超结构技术分析了结肠粘液层厚度,MUC2表达,ER压力标志物和线粒体形态.
- 从患有NEC的人类新生儿和对照人群的结肠样本进行了比较分析.
主要成果:
- 暴露于UP的羊羔表现出更厚的,但功能障碍的结肠粘液层,允许细菌转移到上皮.
- 在暴露于UP的羊羔的结肠表皮中观察到扰乱的杯状细胞MUC2折叠,亲细胞亡ER压力和线粒体功能障碍.
- 人类NEC患者的结肠表现出类似的线粒体异常,这表明肠道屏障损伤始于产前胆子膜炎.
结论:
- 产前Ureaplasma parvum (UP) 感染导致结肠粘液屏障的显著缺陷,从而建立了胆膜炎和死性肠球炎 (NEC) 之间的机制联系.
- 在怀孕期间,UP表现出致病的潜力,损害了胎儿的肠道屏障.
- 这项研究强调了研究微生物在胆膜炎中的作用及其对新生儿结局的影响的重要性,如NEC.
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