Mechanisms underlying parasite induced permeability changes of the human erythrocyte membrane - how much is host, how much is parasite?

• Applicant: Professor Dr. Jude Marek Przyborski, since 10/2015
• Subject Area: Parasitology and Biology of Tropical Infectious Disease Pathogens
• Term: from 2011 to 2016
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 198175986

Parasites of mammalian erythrocytes survive in a nutritionally deprived host cell, where they are secluded within a compartment termed the parasitophorous vacuole. They acquire essential solutes from the extracellular milieu by inducing new permeation pathways in the erythrocyte plasma membrane which are either not present or silent in the non-infected cell. We will use Plasmodium falciparum (a human malaria parasite) and Babesia divergens (in humans an opportunistic parasite) as model organisms to characterize the mechanisms involved in the formation of these pathways. In general terms, we wish to understand to what extent these parasites utilise properties of their host cell and to what extent they directly modify the host cell to increase its permeability. Specifically, we want (i) to unravel the mechanisms whereby infections with Plasmodium activate a silent erythrocyte glutamate transporter and (ii) define similarities and differences in nutrient acquisition by Plasmodium and Babesia.

• DFG Programme: Priority Programmes
• Subproject of: SPP 1580: Intracellular Compartments as Places of Pathogen-Host Interaction
• Ehemaliger Antragsteller: Professor Dr. Klaus Lingelbach, until 10/2015 (†)