欧巴克 (Eubacterium coprostanoligenes) 通过增强肠道粘液屏障来缓解化疗诱导的肠道粘膜炎
Dongsheng Bai1, Jiawei Zhao1, Runde Wang1
1State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, Department of Physiology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, China.
欧细菌coprostanoligenes通过增加粘素的生产来增强肠道粘液屏障. 这一发现为缓解化疗诱导的粘膜炎提供了一种新的策略,而不会影响抗瘤效果.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
背景情况:
- 化疗诱导的粘膜炎是癌症治疗的严重副作用,导致肠道上皮细胞受损.
- 目前对化疗诱导的粘膜炎的治疗方法有限,这凸显了对新型治疗策略的需求.
- 肠道粘液屏障在保护肠道免受微生物入侵和炎症方面发挥着至关重要的作用.
研究的目的:
- 研究Eubacterium coprostanoligenes在缓解化疗诱导的粘膜炎中的潜力.
- 阐明E. coprostanoligenes对肠道屏障施加保护作用的基本机制.
- 为了确定E. coprostanoligenes是否影响化疗的抗瘤疗效.
主要方法:
- 将Eubacterium coprostanoligenes 给一个模型系统.
- 评估了杯状细胞粘素分泌和肠粘液屏障完整性的变化.
- 研究了AUF1和Muc2mRNA的表达.
- 检查了阿里尔碳化合物受体 (AhR) 途径的激活.
主要成果:
- 欧细菌 (Eubacterium coprostanoligenes) 显著促进了杯细胞的粘素分泌,增强了肠道粘液屏障的完整性.
- 这种增强的屏障功能减少了微生物入侵和炎症反应.
- E. coprostanoligenes上调了AUF1的表达,导致Muc2mRNA的稳定,并增加了粘素的合成.
- 保护作用是通过激活AhR/AUF1通路来实现的.
- 重要的是,E. coprostanoligenes没有干扰化疗药物的抗瘤疗效.
结论:
- 欧细菌coprostanoligenes通过加强肠道粘液屏障,有效地缓解化疗诱导的肠炎.
- 该机制涉及AhR/AUF1通路的激活,促进Muc2mRNA的稳定性和粘素的产生.
- 这种益生菌干预代表了一种有希望的治疗方法,用于管理癌症治疗的关键副作用.
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