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Equipe : Biologie cellulaire comparative des Apicomplexes

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We study the host-pathogen interaction of Plasmodium falciparum causative agent of human malaria and Theileria annulata causative agent of tropical theileriosis. Our focus is on how the presence of these intracellular pathogens impacts on their respective host cells and how this underpins disease virulence. In P. falciparum-infected red blood cells we examine how infection alters cAMP production and how changes in cAMP levels impact on intra-erythrocyte parasite development with an emphasis on how cAMP regulates infected host cell redox balance and plasma membrane dynamics. In Theileria annualata-infected leukocytes we examine how different autocrine loops contribute to infected macrophage virulence and how their oxidative stress status impacts on pathogenicity.




In both Theileria-infected leukocytes and Plasmodium-infected erythrocytes we focus on how infection alters cAMP levels of both the host cell and the parasite and how changes in cAMP alter the infected host cell phenotype. Increasing cAMP levels leads to the activation of PKA and we study the consequences of cAMP-induced phosphorylation of both parasite and host cell proteins on the infected host cell phenotype. Plasmodium falciparum-infection of red blood cells leads to a rise in intracellular cAMP and PKA-mediated phosphorylation of a number of red blood cell cytoskeletal proteins and increased adhesion of infected erythrocytes to brain endothelial cells. One objective is to understand how PKA-mediated phosphorylation of red blood cell cytoskeletal proteins impacts on alterations in plasma membrane dynamics of infected erythrocytes. Another objective is to understand how alterations in cAMP levels impact on the redox status of the infected host cell. With Theileria we compare virulent to attenuated macrophages with the objective of identifying those virulence traits that have been lost during the attenuation process. Once a particular trait has been identified we can reconstitute that trait in attenuated macrophages and examine what aspect of virulence has been regained (gain of function). Alternatively, we can ablate a particular trait in virulent macrophages (loss of function) and examine how loss of the trait has altered a particular aspect of the virulence phenotype.

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