AUTOPHAGTUBERCULOSIS

MOLECULAR MECHANISMS OF AUTOPHAGY REGULATION IN TUBERCULOSIS

Coordinatore	CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE    more  Organization address address: Rue Michel -Ange 3 city: PARIS postcode: 75794 contact info Titolo: Ms. Nome: Armelle Cognome: Barelli Email: send email Telefono: +33 561336080 Fax: +33 562172901
Nazionalità Coordinatore	France [FR]
Totale costo	100˙000 €
EC contributo	100˙000 €
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-2011-CIG
Funding Scheme	MC-CIG
Anno di inizio	2011
Periodo (anno-mese-giorno)	2011-08-01   -   2015-07-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE  Organization address address: Rue Michel -Ange 3 city: PARIS postcode: 75794 contact info Titolo: Ms. Nome: Armelle Cognome: Barelli Email: send email Telefono: +33 561336080 Fax: +33 562172901	FR (PARIS)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'Mycobacterium tuberculosis (M.tb), etiologic agent of tuberculosis (TB), is still the leading cause of mortality by single bacterial infection worldwide. Annually, these air-borne bacilli kill almost 2 million people around the globe. M.tb is an extremely successful pathogen that have developed several strategies to neutralize the host immune defenses. One of significance is the block of phagosome maturation which results in survival and replication of M.tb inside macrophages. Autophagy is a cellular lysosomal degradative process which plays a fundamental role in immune responses to M.tb infection. Indeed, multiple reports show that extracellular inducers of autophagy promote phagosome maturation and killing of M.tb by macrophages. Furthermore, autophagy enhances BCG vaccine efficiency and antigen presentation. Although, M.tb succumbs to induced-autophagy, a recent study indicates that virulent M.tb can also modulate basal autophagy to survive intracellularly. Despite important progresses made in the research field of autophagy and mycobacterial infection, how M.tb regulates autophagy and its role in virulence remains largely unknown. To gain further insights into M.tb-autophagy interplay, we propose to decipherer the molecular mechanisms involved in autophagy regulation by M.tb using original, interdisciplinary and complementary approaches. We will (1) examine the correlation between virulence, pathogenicity of mycobacteria and autophagy modulation in human macrophages; (2) determine autophagy signaling pathways regulated by M.tb; (3) identify new M.tb factors that modulate autophagy. This project proposal will expand our understanding of the intricate relationship between M.tb and autophagy and its role in virulence which should help in the future design of innovative therapeutics for the fight against TB. Moreover, manipulating host autophagy might be one significant alternative for elimination of multi- and extensively-drug-resistant M.tb strains (M/XDR-TB).'