Max-von-Pettenkofer Institute, LMU Munich, Pettenkoferstr. 9a, 80336 Munich, Germany.
Max-von-Pettenkofer Institute, LMU Munich, Pettenkoferstr. 9a, 80336 Munich, Germany; German Center for Infection Research (DZIF), partner site LMU Munich, 80336 Munich, Germany.
Cell Host Microbe. 2019 May 8;25(5):681-694.e8. doi: 10.1016/j.chom.2019.03.004. Epub 2019 Apr 18.
The microbiota and the gastrointestinal mucus layer play a pivotal role in protection against non-typhoidal Salmonella enterica serovar Typhimurium (S. Tm) colitis. Here, we analyzed the course of Salmonella colitis in mice lacking a functional mucus layer in the gut. Unexpectedly, in contrast to mucus-proficient littermates, genetically deficient mice were protected against Salmonella-induced gut inflammation in the streptomycin colitis model. This correlated with microbiota alterations and enrichment of the bacterial phylum Deferribacteres. Using gnotobiotic mice associated with defined bacterial consortia, we causally linked Mucispirillum schaedleri, currently the sole known representative of Deferribacteres present in the mammalian microbiota, to host protection against S. Tm colitis. Inhibition by M. schaedleri involves interference with S. Tm invasion gene expression, partly by competing for anaerobic electron acceptors. In conclusion, this study establishes M. schaedleri, a core member of the murine gut microbiota, as a key antagonist of S. Tm virulence in the gut.
肠道微生物群和胃肠道黏液层在预防非伤寒沙门氏菌血清型 Typhimurium（S. Typhimurium）结肠炎方面发挥着关键作用。在这里，我们分析了肠道中缺乏功能性黏液层的小鼠中沙门氏菌结肠炎的病程。出乎意料的是，与黏液丰富的同窝小鼠相比，遗传缺陷小鼠在链霉素结肠炎模型中免受沙门氏菌引起的肠道炎症的影响。这与微生物群的改变和细菌门 Deferribacteres 的富集有关。使用与特定细菌组合相关的无菌小鼠，我们将 Mucispirillum schaedleri （目前是哺乳动物微生物群中唯一已知的 Deferribacteres 代表）与宿主对 S. Typhimurium 结肠炎的保护联系起来。M. schaedleri 的抑制作用涉及干扰 S. Typhimurium 侵袭基因表达，部分原因是竞争厌氧电子受体。总之，这项研究确立了 M. schaedleri 作为肠道微生物群的核心成员，是肠道中 S. Typhimurium 毒力的关键拮抗剂。
