碳水化合物消费驱动着大肠杆菌的适应性突变,与系统性感染风险增加有关
bioRxiv : the preprint server for biology
|April 8, 2025
概括
乳糖,用于肝脏脑病变,通过促进有益的突变,意外地增强了大肠杆菌的肠道殖民. 这种适应性增加了肝硬化患者的感染风险,建议新的饮食策略来控制肠道细菌和预防疾病.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 传染性疾病 传染性疾病
背景情况:
- 肠道微生物群的传播有助于败血症和严重疾病.
- 肝硬化患者容易感染,并且经常用乳糖治疗肝脏脑病变 (HE).
- 乳糖对肠道病原体的直接影响及其在细菌适应中的作用仍然不清楚.
研究的目的:
- 研究乳糖对肠道病原体,特别是大肠杆菌的直接影响.
- 阐明乳糖影响细菌适应和殖民的机制.
- 探索乳糖诱导的微生物变化对肝硬化患者感染风险的临床影响.
主要方法:
- 使用实验室系统,小鼠模型和临床样本来研究大肠杆菌.
- 分析了大肠杆菌乳糖 (lac) *操作调节中的突变.
- 对肝硬化和感染住院风险的患者进行了大型流行病学研究.
主要成果:
- 乳糖的消费选择了大肠杆菌的lac操作子中的突变,增强了其代谢适应性和殖民.
- 突变使大肠杆菌能够使用乳糖作为碳来源,增加肠道殖民.
- 乳糖糖与肝硬化患者感染住院的风险增加有矛盾的关联.
结论:
- 矛盾的是,施用乳糖可以促进潜在有害的大肠杆菌菌株的生长.
- 食基质对肠道微生物群施加选择性压力,影响微生物进化和感染风险.
- 饮食中的寡糖可以抑制适应乳糖的大肠杆菌的出现,并减轻感染风险.
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