来自微生物群的酸通过LuxS定数感应抑制沙门氏菌毒性基因表达
Qianyun Zhang1, Qidong Zhu1, Yunqi Xiao1
1Jiangsu lnstitute of Poultry Science, Yangzhou, 225125, China.
Microbiome
|February 19, 2026
概括
肠道微生物可以抑制病原体的毒性. 来自西藏的代谢物propionate通过准LuxS/AI-2定数感应系统来抑制沙门氏菌毒性基因表达,为传染病控制提供了新的策略.
科学领域:
- 微生物学 微生物学
- 肠道微生物组研究研究
- 传染性疾病 传染性疾病
背景情况:
- 众所周知,共生微生物可以增强宿主防御能力,但它们在抑制病原体毒性方面的直接作用尚未完全理解.
- 研究抗感染的西藏提供了一个独特的模型来探索可以减少病原体毒性的微生物代谢物.
研究的目的:
- 为了识别来自西藏的肠道微生物群代谢物,抑制沙门氏菌的毒性.
- 阐明这些代谢物抑制LuxS/AI-2定数感应系统的分子机制.
主要方法:
- 在西藏和肉感染沙门氏菌后对病毒性基因表达的比较分析.
- 从西藏到肉的便微生物群移植 (FMT).
- 16S rRNA基因测序用于微生物组成分析.
- 在体外和体内实验,以评估代谢物对沙门氏菌毒性和定数感应的影响.
- 分子对接和突变发生,以验证LuxS/AI-2通路的抑制.
主要成果:
- 与肉相比,西藏的沙门氏菌毒性基因表达显著降低.
- 从西藏到肉的FMT减少了毒性基因表达,与增加的微生物多样性和有益细菌相关.
- 短链脂肪酸 (SCFA) propionate 的含量显著增加,与毒性因子表达有负相关.
- 氨酸通过向LuxS/AI-2通路来抑制沙门氏菌生物膜的形成,降低AI-2活动,并降低病毒性基因的调节.
- 一个luxS淘汰突变证实了LuxS/AI-2在酸盐的作用机制中的重要作用.
结论:
- 来自肠道的酸直接通过抑制LuxS/AI-2定数感应系统来抑制沙门氏菌毒性基因表达.
- 这些发现凸显了酸作为微生物群驱动的病原体控制的关键媒介.
- 提供了基于微生物群的策略在管理传染病的潜力.
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