Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice

Rapid shifts in microbial composition frequently occur during intestinal inflammation, but the mechanisms underlying such changes remain elusive. Here we demonstrate that an increased caecal sialidase activity is critical in conferring a growth advantage for some bacteria including Escherichia coli...

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Bibliographic Details
Published in:Nature communications 2015-08, Vol.6 (1), p.8141-8141, Article 8141
Main Authors: Huang, Yen-Lin, Chassard, Christophe, Hausmann, Martin, von Itzstein, Mark, Hennet, Thierry
Format: Article
Language:English
Subjects:
Animals
Anti-Bacterial Agents
Bacteroides - enzymology
Colitis - chemically induced
Colitis - enzymology
Colitis - microbiology
Dendritic Cells - physiology
Dextran Sulfate
Escherichia coli - physiology
Life Sciences
Male
Mice, Inbred C57BL
Mice, Knockout
Microbiota
N-Acetylneuraminic Acid - metabolism
Neuraminidase - metabolism
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Summary:Rapid shifts in microbial composition frequently occur during intestinal inflammation, but the mechanisms underlying such changes remain elusive. Here we demonstrate that an increased caecal sialidase activity is critical in conferring a growth advantage for some bacteria including Escherichia coli (E. coli) during intestinal inflammation in mice. This sialidase activity originates among others from Bacteroides vulgatus, whose intestinal levels expand after dextran sulphate sodium administration. Increased sialidase activity mediates the release of sialic acid from intestinal tissue, which promotes the outgrowth of E. coli during inflammation. The outburst of E. coli likely exacerbates the inflammatory response by stimulating the production of pro-inflammatory cytokines by intestinal dendritic cells. Oral administration of a sialidase inhibitor and low levels of intestinal α2,3-linked sialic acid decrease E. coli outgrowth and the severity of colitis in mice. Regulation of sialic acid catabolism opens new perspectives for the treatment of intestinal inflammation as manifested by E. coli dysbiosis.
ISSN:2041-1723
2041-1723
DOI:10.1038/ncomms9141