Header

UZH-Logo

Maintenance Infos

Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice


Huang, Yen-Lin; Chassard, Christophe; Hausmann, Martin; von Itzstein, Mark; Hennet, Thierry (2015). Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice. Nature Communications, 6:9141.

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.

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.

Statistics

Citations

19 citations in Web of Science®
25 citations in Scopus®
Google Scholar™

Altmetrics

Downloads

34 downloads since deposited on 06 Nov 2015
11 downloads since 12 months
Detailed statistics

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Integrative Human Physiology
04 Faculty of Medicine > University Hospital Zurich > Clinic for Gastroenterology and Hepatology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2015
Deposited On:06 Nov 2015 14:43
Last Modified:08 Dec 2017 14:37
Publisher:Nature Publishing Group
ISSN:2041-1723
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1038/ncomms9141
PubMed ID:26303108

Download

Download PDF  'Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice'.
Preview
Content: Accepted Version
Filetype: PDF
Size: 1MB
View at publisher
Download PDF  'Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice'.
Preview
Content: Published Version
Filetype: PDF
Size: 2MB
Licence: Creative Commons: Attribution 4.0 International (CC BY 4.0)