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Symbiotic polyamine metabolism regulates epithelial proliferation and macrophage differentiation in the colon

Authors :
Shin Kurihara
Atsuo Nakamura
Yutaka Nakamura
Koji Hase
Daisuke Takahashi
Shunsuke Kimura
Wakana Ohashi
Masayoshi Onuki
Yukiko Sasazawa
Aiko Kume
Yukihiro Furusawa
Shinji Fukuda
Shinji Saiki
Mitsuharu Matsumoto
Yuuki Obata
Source :
Nature Communications, Vol 12, Iss 1, Pp 1-14 (2021), Nature Communications
Publication Year :
2021
Publisher :
Nature Portfolio, 2021.

Abstract

Intestinal microbiota-derived metabolites have biological importance for the host. Polyamines, such as putrescine and spermidine, are produced by the intestinal microbiota and regulate multiple biological processes. Increased colonic luminal polyamines promote longevity in mice. However, no direct evidence has shown that microbial polyamines are incorporated into host cells to regulate cellular responses. Here, we show that microbial polyamines reinforce colonic epithelial proliferation and regulate macrophage differentiation. Colonisation by wild-type, but not polyamine biosynthesis-deficient, Escherichia coli in germ-free mice raises intracellular polyamine levels in colonocytes, accelerating epithelial renewal. Commensal bacterium-derived putrescine increases the abundance of anti-inflammatory macrophages in the colon. The bacterial polyamines ameliorate symptoms of dextran sulfate sodium-induced colitis in mice. These effects mainly result from enhanced hypusination of eukaryotic initiation translation factor. We conclude that bacterial putrescine functions as a substrate for symbiotic metabolism and is further absorbed and metabolised by the host, thus helping maintain mucosal homoeostasis in the intestine.<br />Polyamines produced by intestinal bacteria are thought to have beneficial effects on the host. Here the authors show that these polyamines increase regulatory macrophage abundance and are taken up by colonic epithelial cells to enhance colonic barrier function and immunity in mice.

Details

Language :
English
ISSN :
20411723
Volume :
12
Issue :
1
Database :
OpenAIRE
Journal :
Nature Communications
Accession number :
edsair.doi.dedup.....79e77ede725cbc3b5e79582c55386c44