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  Std fimbriae-fucose interaction increases Salmonella-induced intestinal inflammation and prolongs colonization

Suwandi, A., Galeev, A., Riedel, R., Sharma, S., Seeger, K., Sterzenbach, T., et al. (2019). Std fimbriae-fucose interaction increases Salmonella-induced intestinal inflammation and prolongs colonization. PLoS Pathogens, 15(7): e1007915. doi:10.1371/journal.ppat.1007915.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0004-5BE7-2 Version Permalink: http://hdl.handle.net/21.11116/0000-0004-5BE8-1
Genre: Journal Article

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 Creators:
Suwandi, Abdulhadi, Author
Galeev, Alibek, Author
Riedel, René1, Author              
Sharma, Samriti, Author
Seeger, Katrin, Author
Sterzenbach, Torsten, Author
García Pastor, Lucía, Author
Boyle, Erin C., Author
Gal-Mor, Ohad, Author
Hensel, Michael, Author
Casadesús, Josep, Author
Baines, John F.1, Author              
Grassl, Guntram A., Author
Affiliations:
1Guest Group Evolutionary Genomics, Max Planck Institute for Evolutionary Biology, Max Planck Society, ou_1445638              

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 Abstract: Author summary The intestinal epithelium is a crucial biological interface, interacting with both commensal and pathogenic microorganisms. It’s lined with heavily glycosylated proteins and glycolipids which can act as both attachment sites and energy sources for intestinal bacteria. Fut2, the enzyme governing epithelial α1,2-fucosylation, has been implicated in the interaction between microbes and intestinal epithelial cells. Salmonella is one of the most important bacterial gastrointestinal pathogens affecting millions of people worldwide. Salmonella possesses fimbrial and non-fimbrial adhesins which can be used to adhere to host cells. Here we show that Salmonella expresses Std fimbriae in the gastrointestinal tract in vivo and exploit Std fimbriae to bind fucosylated structures in the mucus and on the intestinal epithelium. Furthermore, we demonstrate that the Std fimbriae-fucose interaction is necessary for bacterial colonization of the intestine and for triggering intestinal inflammation. These data lend new insights into bacterial adhesion-epithelial interactions which are essential for bacterial pathogenesis and key factors in determining tissue tropism and host susceptibility to infectious disease.

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Language(s): eng - English
 Dates: 2019-02-212019-06-132019-07-222019-07
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: -
 Identifiers: DOI: 10.1371/journal.ppat.1007915
 Degree: -

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Project name : BMBF Infect-ERA consortium Grant
Grant ID : 031L0093B
Funding program : DFG (SPP1656/1)
Funding organization : -
Project name : DFG collaborative research center SFB 900 TP8
Grant ID : 158989968
Funding program : DFG (SPP1656/2 )
Funding organization : -
Project name : BMBF Infect-ERA consortium grant DFG SFB 944 project P4
Grant ID : 031L0093A
Funding program : DFG under Germany`s Excellence Strategy (EXC 22167-390884018)
Funding organization : -
Project name : DFG
Grant ID : TS 1921/3-1
Funding program : -
Funding organization : -

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Title: PLoS Pathogens
  Other : PLoS Pathog.
Source Genre: Journal
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Publ. Info: San Francisco, CA : Public Library of Science
Pages: - Volume / Issue: 15 (7) Sequence Number: e1007915 Start / End Page: - Identifier: ISSN: 1553-7366
CoNE: https://pure.mpg.de/cone/journals/resource/1000000000018830