Max von Pettenkofer Institute of Hygiene and Medical Microbiology, Faculty of Medicine, LMU Munich, 80336 Munich, Germany.
Max von Pettenkofer Institute of Hygiene and Medical Microbiology, Faculty of Medicine, LMU Munich, 80336 Munich, Germany; German Center for Infection Research (DZIF), partner site LMU Munich, 80336 Munich, Germany.
Cell Host Microbe. 2021 Nov 10;29(11):1680-1692.e7. doi: 10.1016/j.chom.2021.09.004. Epub 2021 Oct 4.
The composition of intrinsic microbial communities determines if invading pathogens will find a suitable niche for colonization and cause infection or be eliminated. Here, we investigate how commensal E. coli mediate colonization resistance (CR) against Salmonella Typhimurium (S. Tm). Using synthetic bacterial communities, we show that the capacity of E. coli Mt1B1 to block S. Tm colonization depends on the microbial context. In an infection-permissive context, E. coli utilized a high diversity of carbon sources and was unable to block S. Tm invasion. In mice that were stably colonized by twelve phylogenetically diverse murine gut bacteria (OMM), establishing a protective context, E. coli depleted galactitol, a substrate otherwise fueling S. Tm colonization. Here, Lachnospiraceae, capable of consuming C5 and C6 sugars, critically contributed to CR. We propose that E. coli provides CR by depleting a limited carbon source when in a microbial community adept at removing simple sugars from the intestine.
内在微生物群落的组成决定了入侵病原体是否会找到适合定殖和引起感染的小生境，还是会被清除。在这里，我们研究了共生大肠杆菌如何介导对鼠伤寒沙门氏菌（S. Tm）的定植抗性（CR）。使用合成细菌群落，我们表明大肠杆菌 Mt1B1 阻止 S. Tm 定植的能力取决于微生物环境。在感染允许的环境中，大肠杆菌利用了多种碳源，并且无法阻止 S. Tm 的入侵。在由 12 种具有不同系统发育的肠道细菌（OMM）稳定定植的小鼠中，建立了一个保护性环境，大肠杆菌耗尽了半乳糖醇，否则这是 S. Tm 定植的燃料。在这里，能够消耗 C5 和 C6 糖的拉克诺普希拉菌科对 CR 做出了重要贡献。我们提出，当大肠杆菌处于能够从肠道中去除简单糖的微生物群落中时，它通过耗尽有限的碳源来提供 CR。
