LIPID & INFECTION

The function and dynamic of cholesterol during Plasmodium liver stage infection

 Coordinatore INSTITUTO DE MEDICINA MOLECULAR 

 Organization address address: AVENIDA PROF EGAS MONIZ
city: LISBOA
postcode: 1649 028

contact info
Titolo: Dr.
Nome: Margarida
Cognome: Pinto Gago
Email: send email
Telefono: -7999081
Fax: -7999082

 Nazionalità Coordinatore Portugal [PT]
 Totale costo 0 €
 EC contributo 148˙048 €
 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-IEF-2008
 Funding Scheme MC-IEF
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-04-22   -   2011-04-21

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    INSTITUTO DE MEDICINA MOLECULAR

 Organization address address: AVENIDA PROF EGAS MONIZ
city: LISBOA
postcode: 1649 028

contact info
Titolo: Dr.
Nome: Margarida
Cognome: Pinto Gago
Email: send email
Telefono: -7999081
Fax: -7999082

PT (LISBOA) coordinator 148˙048.66

Mappa


 Word cloud

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

infection    cholesterol    diseases    malaria    bi    host    plasmodium    infectious    sporozoite    prophylactic    sr    cell    liver    hepatocyte   

 Obiettivo del progetto (Objective)

'Plasmodium parasites are the causative agents of malaria, amongst the most prevalent and severe human infectious diseases. Liver infection by Plasmodium sporozoites is the first obligatory step of malaria and a quite attractive target for prophylactic strategies against the disease. At this stage, each sporozoite invades a single hepatocyte and develops into thousands of merozoites that are released into the bloodstream. Preliminary results of the host laboratory clearly show that a hepatocyte receptor, SR-BI, plays a crucial role both in invasion and development of Plasmodium in the liver. In its physiological role, SR-BI is a central component of the cholesterol uptake by cells. Thus, the overall aim of this project is to reveal whether and how cholesterol uptake by SR-BI is critical for hepatocyte infection by Plasmodium. By using various cell biology approaches, we propose to: 1) describe the chronology of cholesterol requirements during the infection, 2) investigate the SR-BI and cholesterol organization and dynamic at the sporozoite-host cell interphase and 3) determine the role of SR-BI in delivering cholesterol for Plasmodium development inside hepatocytes. Achieving this plan of work will, hopefully, provide a rationale for a potential SR-BI/cholesterol-based anti-malarial prophylactic intervention, and contribute to the European excellence by reaching one of the main goals of the 7th Framework Programme regarding Action to Confront Infectious Diseases.'

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