微生物群释放的宿主糖促进了肠道病原体在抗生素后的扩张
Katharine M Ng1, Jessica A Ferreyra, Steven K Higginbottom
1Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, USA.
Nature
|September 3, 2013
概括
抗生素的使用破坏了肠道微生物群,允许像沙门氏菌和困难杆菌这样的病原体通过消耗释放的糖来繁荣. 针对这种糖代谢提供了针对肠道感染的新治疗策略.
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:
- 人的肠道微生物群保护人免受细菌病原体的侵害.
- 抗生素对微生物群的破坏可能导致肠道病原体的出现.
- 病原体利用微生物群破坏的机制尚不清楚.
研究的目的:
- 研究肠道病原体沙门氏菌 (Salmonella enterica serovar Typhimurium (S. typhimurium)) 和困难菌如何利用抗生素诱导的微生物群衰竭.
- 确定这些病原体在肠道内扩散的常见策略.
主要方法:
- 在 gnotobiotic 和常规小鼠中研究了 S. typhimurium 和 C. difficile.
- 利用缺少碳水化合物催化路径的遗传突变.
- 给药抗生素和外源性酸以评估病原体扩张.
- 测量了粘膜中的碳水化合物可用性和病原体基因表达.
主要成果:
- 无论是S. typhimurium还是C. difficile都利用微生物群释放的粘膜碳水化合物 (糖,酸) 来进行肠道扩张.
- 这些代谢途径的遗传破坏损害了病原体的竞争力.
- 抗生素治疗增加了自由酸,有利于C. difficile和S. typhimurium.
- 缺酸酶的细菌减少了自由酸,阻碍了C. difficile的扩散.
结论:
- 肠道病原体利用抗生素诱导的肠道碳水化合物可用性的变化.
- 粘膜碳水化合物的催化是病原体扩散的共同策略.
- 针对病原体的碳水化合物代谢,为抗生素相关的肠道感染提供了潜在的治疗途径.
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