肠道微生物群和细菌转移在肝纤维化病原体中的作用
Roman Maslennikov1,2, Elena Poluektova1,2, Oxana Zolnikova1
1Department of Internal Medicine, Gastroenterology and Hepatology, Sechenov University, 119048 Moscow, Russia.
International journal of molecular sciences
|November 25, 2023
概括
肠肝轴的干扰,特别是肠道失调,有助于肝硬化发展. 针对细菌转移的干预措施可能会减缓肝纤维化进展.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 肝硬化,肝纤维化的末期阶段,是一个重要的医疗挑战.
- 肠肝轴在慢性肝病和肝硬化病的发病过程中起着至关重要的作用.
- 肠道失调,以特定的微生物转移为特征,在肝脏损伤之前,并促进细菌转移.
研究的目的:
- 阐明将肠道失调与肝纤维化进展联系起来的机制.
- 探索针对肠肝轴的治疗策略,以预防或逆转肝纤维化.
主要方法:
- 分析肠道微生物群的组成及其与肝病阶段的相关性.
- 研究细菌转位通路及其对肝炎的影响.
- 评估库普弗细胞和肝星细胞在纤维化发展中的作用.
主要成果:
- 肠道失生症,与增加的细菌/蛋白质细菌和减少的闭膜细菌,促进细菌转移,即使在前肝硬化阶段.
- 转位的细菌通过Toll-like受体4激活库普费尔细胞,从而释放益生菌性细胞因子.
- 激活的库普费尔细胞刺激肝脏的恒星细胞,推动原蛋白的产生和细胞外基质的积累.
结论:
- 肠道功能失调是肝纤维化的关键驱动因素,通过细菌转位和随后的炎症激活.
- 使用抗生素,益生菌或共生菌阻止细菌转移在动物模型中显示出减缓纤维化的前景.
- 为了验证这些发现和治疗方法,需要对人类进行进一步的长期随机对照试验.
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