Gut Microbes (Dec 2024)

DSS treatment does not affect murine colonic microbiota in absence of the host

  • Jannike Lea Krause,
  • Beatrice Engelmann,
  • Stephanie Serena Schaepe,
  • Ulrike Rolle-Kampczyk,
  • Nico Jehmlich,
  • Hyun-Dong Chang,
  • Ulla Slanina,
  • Maximillian Hoffman,
  • Jörg Lehmann,
  • Ana Claudia Zenclussen,
  • Gunda Herberth,
  • Martin von Bergen,
  • Sven-Bastiaan Haange

DOI
https://doi.org/10.1080/19490976.2023.2297831
Journal volume & issue
Vol. 16, no. 1

Abstract

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ABSTRACTThe prevalence of inflammatory bowel disease (IBD) is rising globally; however, its etiology is still not fully understood. Patient genetics, immune system, and intestinal microbiota are considered critical factors contributing to IBD. Preclinical animal models are crucial to better understand the importance of individual contributing factors. Among these, the dextran sodium sulfate (DSS) colitis model is the most widely used. DSS treatment induces gut inflammation and dysbiosis. However, its exact mode of action remains unclear. To determine whether DSS treatment induces pathogenic changes in the microbiota, we investigated the microbiota-modulating effects of DSS on murine microbiota in vitro. For this purpose, we cultured murine microbiota from the colon in six replicate continuous bioreactors. Three bioreactors were supplemented with 1% DSS and compared with the remaining PBS-treated control bioreactors by means of microbiota taxonomy and functionality. Using metaproteomics, we did not identify significant changes in microbial taxonomy, either at the phylum or genus levels. No differences in the metabolic pathways were observed. Furthermore, the global metabolome and targeted short-chain fatty acid (SCFA) quantification did not reveal any DSS-related changes. DSS had negligible effects on microbial functionality and taxonomy in vitro in the absence of the host environment. Our results underline that the DSS colitis mouse model is a suitable model to study host–microbiota interactions, which may help to understand how intestinal inflammation modulates the microbiota at the taxonomic and functional levels.

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