IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v6y2015i1d10.1038_ncomms9141.html
   My bibliography  Save this article

Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice

Author

Listed:
  • 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
    Present address: Institut National de la Recherche Agronomique, UR 545 URF, 15000 Aurillac, France)

  • 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)

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.

Suggested Citation

  • Yen-Lin Huang & Christophe Chassard & Martin Hausmann & Mark von Itzstein & Thierry Hennet, 2015. "Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice," Nature Communications, Nature, vol. 6(1), pages 1-11, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9141
    DOI: 10.1038/ncomms9141
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms9141
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms9141?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Elvin Koh & In Young Hwang & Hui Ling Lee & Ryan De Sotto & Jonathan Wei Jie Lee & Yung Seng Lee & John C. March & Matthew Wook Chang, 2022. "Engineering probiotics to inhibit Clostridioides difficile infection by dynamic regulation of intestinal metabolism," Nature Communications, Nature, vol. 13(1), pages 1-13, December.
    2. K. E. Huus & T. T. Hoang & A. Creus-Cuadros & M. Cirstea & S. L. Vogt & K. Knuff-Janzen & P. J. Sansonetti & P. Vonaesch & B. B. Finlay, 2021. "Cross-feeding between intestinal pathobionts promotes their overgrowth during undernutrition," Nature Communications, Nature, vol. 12(1), pages 1-14, December.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9141. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.