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Competition between the enteric pathogen Clostridium difficile and the commensal...

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

31/08/2017

UNIVIE

166K€

Presupuesto del proyecto: 166K€

Líder del proyecto

UNIVERSITAT WIEN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2017-08-31

MSCA-IF-2014-EF: Marie Skłodowska-Curie Individual F...

I+D

Cerrada hace 10 años

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No hay información privada compartida para este proyecto. Habla con el coordinador.

1 Participantes

UNIVIE

166.16K€ | Lider

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Duración del proyecto: 28 meses Fecha Inicio: 2015-04-22
Fecha Fin: 2017-08-31

Líder del proyecto

UNIVERSITAT WIEN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 166K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto 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.

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