Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice

Huang, Yen-Lin and Chassard, Christophe and Hausmann, Martin and von Itzstein, Mark and Hennet, Thierry. (2015) Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice. Nature Communications, 6. p. 8141.

Full text not available from this repository.

Official URL: http://edoc.unibas.ch/52820/

Downloads: Statistics Overview


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.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Gynecological Research (Heinzelmann)
UniBasel Contributors:Huang, Yen-Lin Eddie
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Nature Publishing Group
Note:Publication type according to Uni Basel Research Database: Journal article
Identification Number:
Last Modified:09 Oct 2017 07:20
Deposited On:09 Oct 2017 07:20

Repository Staff Only: item control page