MUCUS AND METABOLISM

The relationship between the intestinal mucosal barrier and gut microbiota in metabolic diseases

Coordinatore	GOETEBORGS UNIVERSITET    more  Organization address address: VASAPARKEN city: GOETEBORG postcode: 405 30 contact info Titolo: Dr. Nome: Ellen Cognome: Rydberg Email: send email Telefono: +46 31 786 6470 Fax: +46 31 786 4355
Nazionalità Coordinatore	Sweden [SE]
Totale costo	197˙811 €
EC contributo	197˙811 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2013-IEF
Funding Scheme	MC-IEF
Anno di inizio	2014
Periodo (anno-mese-giorno)	2014-04-01   -   2017-03-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	GOETEBORGS UNIVERSITET  Organization address address: VASAPARKEN city: GOETEBORG postcode: 405 30 contact info Titolo: Dr. Nome: Ellen Cognome: Rydberg Email: send email Telefono: +46 31 786 6470 Fax: +46 31 786 4355	SE (GOETEBORG)	coordinator	197˙811.60

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 Obiettivo del progetto (Objective)

'Obesity is a world-wide epidemic and currently about 350 million people suffer from diabetes, resulting in more than 3 million deaths per year. While the gut microbiota has been identified as a contributing factor to obesity and insulin resistance in mice and humans, the underlying disease-causing mechanisms are yet to be defined. The aim of this proposal is to investigate the interactions between the gut microbiota and the intestinal mucosal barrier in metabolic disease. The human intestine is colonized by a complex microbial community with up to 1000 different species. While its composition is specific for each individual, a core gut microbiota is shared between humans. However, the composition of gut microbiota is altered in individuals who are obese, diabetic or suffer from cardiovascular disease. The high density of the gut microbiota provides a continuous challenge and potential threat to the gut epithelium. As only one single, mucus-covered cell layer separates microbes from human tissue the mucosal barrier is essential in preventing microbial translocation. One epithelial defense mechanism is the secretion of antimicrobial peptides (AMPs). These endogenous peptide antibiotics have broad-spectrum antimicrobial activity and can also modulate the composition of gut microbiota. In this proposal I will focus on the intestinal barrier between host and microbiota. I will test if and how the shifted microbial composition in metabolic diseases is associated with alterations in mucosal AMP production and function. Furthermore, I will analyze mucosa-associated microbiota in metabolic disease by using mouse models and samples from human patients. Also, I will compare the peptide repertoire in the mucus of different mouse models and human diabetes patients to identify alterations in the composition that are associated with metabolic disease. The planned investigations will help to better understand the relationship between the mucosal host barrier and metabolic disease.'