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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 €

EC-Contrib. €

Partnership

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Outcomes and
results

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.

tract acetylglucosamine probing combining emerged recurrence anaerobic isotope catabolism sip probiotic outbreaks catabolize cure bacterium acid nutrient conventional outcompete standardized disease difficile human safe enteric decade prevents intestinal relies normal viewed therapies last commensal refractory resolution nanosims microbiota bacterial disturbance secondary ion colonic carbohydrates gram colonization mechanism rates pathogens eradicate strains mass sialic identification vivo colonize sources positive identity alone basis orchestrate stable clostridium infection spectrometry combination antibiotic gut limited fluorescence competition suppresses treat mucosal fish severity hybridization elucidate expansion mortality organisms treatments treatment cdi members situ glcnac alternative mechanisms sugars

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 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.	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

List of publications.
year	authors and title	journal	last update
2017	FÃ¡tima 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; FÃ¡tima 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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