The gut commensal Blautia maintains colonic mucus function under low-fiber consumption through secretion of short-chain fatty acids

Sandra M. Holmberg, Rachel H. Feeney, Vishnu Prasoodanan P.K., Fabiola Puértolas-Balint, Dhirendra K. Singh, Supapit Wongkuna, Lotte Zandbergen, Hans Hauner, Beate Brandl, Anni I. Nieminen, Thomas Skurk and Bjoern O. Schroeder ()
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Sandra M. Holmberg: Umeå University
Rachel H. Feeney: Umeå University
Vishnu Prasoodanan P.K.: Umeå University
Fabiola Puértolas-Balint: Umeå University
Dhirendra K. Singh: Umeå University
Supapit Wongkuna: Umeå University
Lotte Zandbergen: Umeå University
Hans Hauner: TU Munich
Beate Brandl: TU Munich
Anni I. Nieminen: University of Helsinki
Thomas Skurk: TU Munich
Bjoern O. Schroeder: Umeå University

Nature Communications, 2024, vol. 15, issue 1, 1-19

Abstract: Abstract Beneficial gut bacteria are indispensable for developing colonic mucus and fully establishing its protective function against intestinal microorganisms. Low-fiber diet consumption alters the gut bacterial configuration and disturbs this microbe-mucus interaction, but the specific bacteria and microbial metabolites responsible for maintaining mucus function remain poorly understood. By using human-to-mouse microbiota transplantation and ex vivo analysis of colonic mucus function, we here show as a proof-of-concept that individuals who increase their daily dietary fiber intake can improve the capacity of their gut microbiota to prevent diet-mediated mucus defects. Mucus growth, a critical feature of intact colonic mucus, correlated with the abundance of the gut commensal Blautia, and supplementation of Blautia coccoides to mice confirmed its mucus-stimulating capacity. Mechanistically, B. coccoides stimulated mucus growth through the production of the short-chain fatty acids propionate and acetate via activation of the short-chain fatty acid receptor Ffar2, which could serve as a new target to restore mucus growth during mucus-associated lifestyle diseases.

Date: 2024
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DOI: 10.1038/s41467-024-47594-w

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