DANGER ATP

Regulation of inflammatory response by extracellular ATP and P2X7 receptor signalling: through and beyond the inflammasome

 Coordinatore FUNDACION PARA LA FORMACION E INVESTIGACION SANITARIAS DE LA REGION DE MURCIA 

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

 Nazionalità Coordinatore Spain [ES]
 Totale costo 1˙794˙948 €
 EC contributo 1˙794˙948 €
 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-CoG
 Funding Scheme ERC-CG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-09-01   -   2019-08-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    FUNDACION PARA LA FORMACION E INVESTIGACION SANITARIAS DE LA REGION DE MURCIA

 Organization address address: CALLE LUIS FONTES PAGAN 9
city: MURCIA
postcode: 30003

contact info
Titolo: Dr.
Nome: Pablo
Cognome: Pelegrin Vivancos
Email: send email
Telefono: +34 968369317
Fax: 34968369364

ES (MURCIA) hostInstitution 1˙794˙948.00
2    FUNDACION PARA LA FORMACION E INVESTIGACION SANITARIAS DE LA REGION DE MURCIA

 Organization address address: CALLE LUIS FONTES PAGAN 9
city: MURCIA
postcode: 30003

contact info
Titolo: Mr.
Nome: Juan Pedro
Cognome: Serna Marmol
Email: send email
Telefono: +34 968359774
Fax: +34 968359777

ES (MURCIA) hostInstitution 1˙794˙948.00

Mappa


 Word cloud

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

treat    infection    free    inflammation       nlrp    danger    host    cells    extracellular    vivo    il    atp       release    activation    diseases    signalling    inflammasome    inflammatory   

 Obiettivo del progetto (Objective)

'Inflammatory diseases affect over 80 million people worldwide and accompany many diseases of industrialized countries, being the majority of them infection-free conditions. There are few efficient anti-inflammatory drugs to treat chronic inflammation and thus, there is an urgent need to validate novel targets. We now know that innate immunity is the main coordinator and driver of inflammation. Recently, we and others have shown that the activation of purinergic P2X7 receptors (P2X7R) in immune cells is a novel and increasingly validated pathway to initiate inflammation through the activation of the NLRP3 inflammasome and the release of IL-1β and IL-18 cytokines. However, how NLRP3 sense P2X7R activation is not fully understood. Furthermore, extracellular ATP, the physiological P2X7R agonist, is a crucial danger signal released by injured cells, and one of the most important mediators of infection-free inflammation. We have also identified novel signalling roles for P2X7R independent on the NLRP3 inflammasome, including the release of proteases or inflammatory lipids. Therefore, P2X7R has generated increasing interest as a therapeutic target in inflammatory diseases, being drug like P2X7R antagonist in clinical trials to treat inflammatory diseases. However, it is often questioned the functionality of P2X7R in vivo, where it is thought that extracellular ATP levels are below the threshold to activate P2X7R. The overall significance of this proposal relays to elucidate how extracellular ATP controls host-defence in vivo, ultimately depicting P2X7R signalling through and beyond inflammasome activation. We foresee that our results will generate a leading innovative knowledge about in vivo extracellular ATP signalling during the host response to infection and sterile danger.'

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