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. 2021 Apr 8;12:2105. doi: 10.1038/s41467-021-22212-1

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Low-molecular metabolites produced by the intestinal microbiota remain in the lumen (Metabolite A) or are absorbed from the intestinal lumen to systemic circulation (Metabolite B and C). Metabolite B, which are represented by short-chain fatty acids, directory act on host cells to exert physiological activities. Meanwhile, a part of inactive metabolites may be further converted to bioactive substances via host metabolic pathways after absorption (Metabolite C). The entities of such symbiotic metabolism, however, remain obscure. Our study using gnotobiotic mice demonstrated that microbial putrescine is uptaken by the colonic epithelial cells to produce bioactive spermidine that accelerates epithelial renewal and increases the abundance of anti-inflammatory macrophages in the colon. Thus, microbial putrescine serves as a source (precursor) of bioactive substances in the host animals. This observation provides evidence for symbiotic metabolism contributing to the maintenance of intestinal homoeostasis.