HOMEOEPITH

Homeostasis and rupture of the gut epithelium in the presence of commensals and pathogens

 Coordinatore INSTITUT PASTEUR 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore France [FR]
 Totale costo 2˙356˙350 €
 EC contributo 2˙356˙350 €
 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-2008-AdG
 Funding Scheme ERC-AG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-02-01   -   2014-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    INSTITUT PASTEUR

 Organization address address: RUE DU DOCTEUR ROUX 25-28
city: PARIS CEDEX 15
postcode: 75724

contact info
Titolo: Dr.
Nome: Marie-Laure
Cognome: Rosso
Email: send email
Telefono: +33 1 40 61 95 26
Fax: +33 1 44 38 39 40

FR (PARIS CEDEX 15) hostInstitution 2˙356˙350.00
2    INSTITUT PASTEUR

 Organization address address: RUE DU DOCTEUR ROUX 25-28
city: PARIS CEDEX 15
postcode: 75724

contact info
Titolo: Prof.
Nome: Philippe
Cognome: Sansonetti
Email: send email
Telefono: +33 1 45688342
Fax: +33 1 45688953

FR (PARIS CEDEX 15) hostInstitution 2˙356˙350.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

model    inflammatory    bacterial    flora    molecular    renewal    cellular    biology    intestinal    microorganism    commensals    innate    affect    pathogens    epithelial    infectious    cell    mouse   

 Obiettivo del progetto (Objective)

'The molecular cross talks occuring at the interface between the intestinal epithelium and bacterial flora will be studied at two levels : (i) how commensals and pathogens affect innate immune signalling, thereby leading to tolerance of the resident microbiota, and inflammatory rejection of the pathogens. The theme of commensals and pathogens regulating this innate response, particularly how they respectively strengthen or weaken the network of humoral and cellular epithelial defense systems will be central here. (ii) How, in molecular and cellular terms, bacteria affect epithelial renewal. The gut of a germ-free mouse and of a conventional mouse show dramatic differences marked by global immaturity and slow epithelial renewal in absence of flora. In front of pathogens, the actual role plaid in the disease in altering the kinetics of epthelial repair is unknown. The aim of this project is to study how commensals and pathogens affect intestinal epithelial renewal, particularly the key steps of the whole developmental process such as lineages decisions, entry in cycle and proliferation, migration and final differentiation, decision to engage in cell death. In order to address these fundamental questions, we will study a commensal microorganism : Lactobacillus casei, and a pathogenic microorganism : Shigella flexneri as model organism, and will develop several novel systems such as reverse genetics of Lactobacilli, development of intestinal crypt models in vitro to study bacterial interactions, and development of a mouse model showing susceptibility to human-specific enteroinvasive pathogens. This project aims at interfacing microbiology, cell biology, and development biology around the concept of microbes manipulating intestinal epithelial homeostaesis. It also includes a strong component of therapeutic development aimed at identifying novel anti-infectious strategies and options to speed up epithelial restitution upon infectious-inflammatory damages.'

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