Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice

Yen-Lin Huang, Christophe Chassard, Martin Hausmann, Mark von Itzstein and Thierry Hennet ()
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Yen-Lin Huang: Institute of Physiology and Zurich Center of Integrative Human Physiology, University of Zurich
Christophe Chassard: Laboratory of Food Biotechnology, Institute of Food, Nutrition and Health, ETH Zurich
Martin Hausmann: University Hospital of Zurich
Mark von Itzstein: Institute for Glycomics, Griffith University
Thierry Hennet: Institute of Physiology and Zurich Center of Integrative Human Physiology, University of Zurich

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: Abstract 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.

Date: 2015
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DOI: 10.1038/ncomms9141

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