ENIGMO

"Gut microbiota, innate immunity and endocannabinoid system interactions link metabolic inflammation with the hallmarks of obesity and type 2 diabetes"

 Coordinatore UNIVERSITE CATHOLIQUE DE LOUVAIN 

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 Nazionalità Coordinatore Belgium [BE]
 Totale costo 1˙494˙640 €
 EC contributo 1˙494˙640 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2013-StG
 Funding Scheme ERC-SG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-10-01   -   2018-09-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITE CATHOLIQUE DE LOUVAIN

 Organization address address: Place De L'Universite 1
city: LOUVAIN LA NEUVE
postcode: 1348

contact info
Titolo: Mrs.
Nome: Anne
Cognome: Bovy
Email: send email
Telefono: 3210473873
Fax: 3210473830

BE (LOUVAIN LA NEUVE) hostInstitution 1˙494˙640.00
2    UNIVERSITE CATHOLIQUE DE LOUVAIN

 Organization address address: Place De L'Universite 1
city: LOUVAIN LA NEUVE
postcode: 1348

contact info
Titolo: Prof.
Nome: Patrice Daniel
Cognome: Cani
Email: send email
Telefono: 32474900562
Fax: 3227637359

BE (LOUVAIN LA NEUVE) hostInstitution 1˙494˙640.00

Mappa


 Word cloud

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evidence       intestinal    metabolic    inflammation    ecb    preliminary    immune    innate    host    linking    data    microbiota    tlr    gut    tone    therapeutic    obesity    metabolism    linked    myd    mechanisms    induced   

 Obiettivo del progetto (Objective)

'Obesity and type 2 diabetes are characterized by metabolic inflammation and an altered endocannabinoid system (eCB) tone. We have provided evidence that gut microbiota modulate both intestinal and adipose tissue eCB system tone. Insulin resistance and inflammation have been linked to microbiota-host interaction via different Toll-Like Receptors (TLR’s). Our preliminary data show that tamoxifen-induced epithelial intestinal cells deletion of the key signalling adaptor MyD88 (myeloid differentiation primary-response gene 88), that encompass most of the TLR’s, protect mice against diet-induced obesity and inflammation. A phenomenon closely linked with changes in the intestinal eCB system tone and antimicrobial peptides production. Moreover, we discovered that the recently identified bacteria living in the mucus layer, namely Akkermansia muciniphila, plays a central role in the regulation of host energy metabolism by putative mechanisms linking both the intestinal eCB system and the innate immune system. Thus these preliminary data support the existence of unidentified mechanisms linking the innate immune system, the gut microbiota and host metabolism. In this high-risk/high-gain research program, we propose to elucidate what could be one of the most fundamental processes shared by different key hallmarks of obesity and related diseases. A careful and thorough analysis of the molecular and cellular events linking gut microbiota, the innate immune system and eCB system in specific organs has the potential to unravel new therapeutic targets. We anticipate the key role of MyD88 and the enzyme NAPE-PLD (N-acylphosphatidylethanolamine phospholipase-D) involved in the synthesis of N-acylethanolamines family to be key determinant in such pathophysiological aspects. Thus, these approaches could provide different perspectives about disease pathogenesis and knowledge-based evidence of new therapeutic options for obesity and associated metabolic disorders in the future.'

Altri progetti dello stesso programma (FP7-IDEAS-ERC)

FAILFLOW (2008)

Failure and Fluid Flow in Porous Quasibrittle Materials

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7TREIMHO (2013)

7kDa TSLP as a novel type of anti-inflammatory agent to re-establish immune homeostasis

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NOVARIPP (2014)

Novel properties of antigen receptors and instruments to modulate lymphoid function in physiological and pathological conditions

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