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MUCDIFF

Competition between the enteric pathogen Clostridium difficile and the commensal members of the gut microbiota for mucosal sugars

Total Cost €

0

EC-Contrib. €

0

Partnership

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 MUCDIFF project word cloud

Explore the words cloud of the MUCDIFF project. It provides you a very rough idea of what is the project "MUCDIFF" about.

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Project "MUCDIFF" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITAT WIEN 

Organization address
address: UNIVERSITATSRING 1
city: WIEN
postcode: 1010
website: www.univie.ac.at

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Austria [AT]
 Project website http://www.microbial-ecology.net/research/competition-between-the-enteric-pathogen-clostridium-difficile-and-the-commensal-members-of-the-gut-microbiota-for-mucosal-sugars
 Total cost 166˙156 €
 EC max contribution 166˙156 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2015
 Duration (year-month-day) from 2015-09-01   to  2017-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITAT WIEN AT (WIEN) coordinator 166˙156.00

Map

 Project objective

Clostridium difficile is a Gram-positive, anaerobic bacterium that relies on the disturbance of the normal gut microbiota to colonize the human intestinal tract and cause infection and disease. In the last decade new strains of C. difficile have emerged to cause outbreaks of increased disease severity and higher recurrence and mortality rates. C. difficile infection (CDI) is becoming refractory to the conventional antibiotic treatments and probiotic-based approaches are viewed as promising alternative therapies to effectively treat CDI. The development of such bacterial-based treatments requires the identification of the mechanisms by which the commensal members of the gut microbiota are able to eradicate C. difficile, as well as of the identity of the members of the gut microbiota that orchestrate those mechanisms. Since nutrient competition is an important mechanism by which the colonic microbiota suppresses the growth of many enteric pathogens, I focus here on competition for limited nutrient sources, such as the gut mucosal sugars N-acetylglucosamine (GlcNAc) and sialic acid, as a mechanism by which the members of the gut microbiota can eradicate C. difficile. I will investigate in detail the importance of GlcNAc catabolism, both alone and in combination with the catabolism of sialic acid, for C. difficile expansion in the gut. Furthermore, by combining stable isotope probing (SIP) and fluorescence in situ hybridization (FISH) with high resolution secondary ion mass spectrometry (NanoSIMS) I propose to identify commensal members of the gut microbiota that can efficiently catabolize these mucosal carbohydrates in vivo and to evaluate the ability of the identified organisms to outcompete C. difficile. Thus, this work will contribute to elucidate the mechanisms by which the gut microbiota prevents C. difficile colonization and to identify members of the gut microbiota that can be the basis for an effective, safe and standardized treatment to cure CDI.

 Publications

year authors and title journal last update
List of publications.
2017 Fátima C. Pereira, David Berry
Microbial nutrient niches in the gut
published pages: 1366-1378, ISSN: 1462-2912, DOI: 10.1111/1462-2920.13659
Environmental Microbiology 19/4 2019-07-24
2017 Ladurner, Angela; Zehl, Martin; Grienke, Ulrike; Hofstadler, Christoph; Faur, Nadina; Fátima C Pereira; Berry, David; Dirsch, Verena M.; Rollinger, Judith M.
Allspice and Clove As Source of Triterpene Acids Activating the G Protein-Coupled Bile Acid Receptor TGR5
published pages: , ISSN: 1663-9812, DOI: 10.3389/fphar.2017.00468
Frontiers in Pharmacology 1 2019-07-24

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