| Literature DB >> 31006637 |
Simone Herp1, Sandrine Brugiroux1, Debora Garzetti2, Diana Ring2, Lara M Jochum1, Markus Beutler1, Claudia Eberl1, Saib Hussain1, Steffi Walter3, Roman G Gerlach3, Hans J Ruscheweyh4, Daniel Huson4, Mikael E Sellin5, Emma Slack6, Buck Hanson7, Alexander Loy7, John F Baines8, Philipp Rausch9, Marijana Basic10, André Bleich10, David Berry7, Bärbel Stecher11.
Abstract
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.Entities:
Keywords: ASF; Agr2; OMM; Oligo-MM; SPI-1; Salmonella pathogenicity island; T3SS; altered Schaedler flora; anterior gradient protein 2 homolog; colonization resistance; microbiome; nitrate respiration
Mesh:
Year: 2019 PMID: 31006637 DOI: 10.1016/j.chom.2019.03.004
Source DB: PubMed Journal: Cell Host Microbe ISSN: 1931-3128 Impact factor: 21.023