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

ABSTRACT

The 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.

KEYWORDS:

• DSS colitis
• microbiota
• metaproteomics
• metabolomics
• in vitro model
• bioreactor
• IBD

Acknowledgments

We thank Jeremy Knespel, Olivia Pleßow, and Nicole Bock for their technical assistance.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Author contributions

JLK, SSS, NJ, and SH conceptualized the study. JLK, BE, and SH wrote the first draft of this manuscript. MH, US, and JL provided the murine microbiota. JLK performed microbiological experiments. BE and URK were responsible for the untargeted metabolomics, SCFA measurements, and data analysis. SSS, NJ, and SH were responsible for the metaproteome measurements and data analysis. ACZ, HDC, NJ, JL, GH, JL, SR, and MvB provided helpful discussions and revised the manuscript accordingly.

Availability of data and materials

The metaproteome and metabolome datasets supporting the conclusions of this article are available at ProteomeXchange with identifier P×D038429 and Metabolomics workbench with Study IDs ST002394 (SCFA) and ST002393 (untargeted metabolomics).

Supplementary material

Supplemental data for this article can be accessed online at https://doi.org/10.1080/19490976.2023.2297831

Correction Statement

This article has been corrected with minor changes. These changes do not impact the academic content of the article.

Additional information

Funding

Furthermore, we thank the German Federal Environmental Foundation for the financial support from Jannike Lea Krause. Stephanie Schäpe is grateful for the support from a DFG grant within Priority Program 1656. Beatrice Engelmann is grateful for funding from the Novo Nordisk Foundation (grant number NNF21OC0066551). Hyun-Dong Chang was supported by Dr Rolf Schwiete Foundation and DFG Project-ID 375876048 – TRR 241. Lehmann acknowledges partial funding from the Fraunhofer Cluster of Excellence Immune-Mediated Diseases (CIMD). Martin von Bergen acknowledges partial funding from the DFG Priority Program of 2002.