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Salmonella re-engineers the intestinal environment to break colonization resistance in the presence of a compositionally intact microbiota
Cell Host & Microbe ( IF 20.6 ) Pub Date : 2024-08-23 , DOI: 10.1016/j.chom.2024.07.025
Andrew W L Rogers 1 , Lauren C Radlinski 1 , Henry Nguyen 1 , Connor R Tiffany 1 , Thaynara Parente Carvalho 1 , Hugo L P Masson 1 , Michael L Goodson 2 , Lalita Bechtold 1 , Kohei Yamazaki 3 , Megan J Liou 1 , Brittany M Miller 1 , Scott P Mahan 1 , Briana M Young 1 , Aurore M Demars 1 , Sophie R Gretler 1 , Anaïs B Larabi 1 , Jee-Yon Lee 1 , Derek J Bays 4 , Renee M Tsolis 1 , Andreas J Bäumler 1
Affiliation  

The gut microbiota prevents harmful microbes from entering the body, a function known as colonization resistance. The enteric pathogen Salmonella enterica serovar (S.) Typhimurium uses its virulence factors to break colonization resistance through unknown mechanisms. Using metabolite profiling and genetic analysis, we show that the initial rise in luminal pathogen abundance was powered by a combination of aerobic respiration and mixed acid fermentation of simple sugars, such as glucose, which resulted in their depletion from the metabolome. The initial rise in the abundance of the pathogen in the feces coincided with a reduction in the cecal concentrations of acetate and butyrate and an increase in epithelial oxygenation. Notably, these changes in the host environment preceded changes in the microbiota composition. We conclude that changes in the host environment can weaken colonization resistance even in the absence of overt compositional changes in the gut microbiota.

中文翻译:


沙门氏菌重新设计肠道环境,以在成分完整的微生物群存在下打破定植抵抗



肠道微生物群阻止有害微生物进入体内,这一功能称为定植抵抗。肠道病原体肠道沙门氏菌血清型 (S.)鼠伤寒利用其毒力因子通过未知机制打破定植抗性。使用代谢物分析和遗传分析,我们表明管腔病原体丰度的最初增加是由有氧呼吸和单糖(如葡萄糖)的混合酸发酵共同驱动的,这导致它们从代谢组中耗尽。粪便中病原体丰度的最初增加与乙酸盐和丁酸盐盲肠浓度的降低以及上皮氧合的增加相吻合。值得注意的是,宿主环境的这些变化先于微生物群组成的变化。我们得出结论,即使在肠道微生物群没有明显的组成变化的情况下,宿主环境的变化也会削弱定植抗性。
更新日期:2024-08-23
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