Joint project
SPP 1580 TP - Intracellular compartments as places of pathogen-host-interactions - Teilprojekt: Mechanisms underlying parasite induced permeability changes of the human erythrocyte membrane - how much is host, how much is parasite?
Funder: German Research Foundation
Period: 2011-2015
URI: https://gepris.dfg.de/gepris/projekt/198175986
Detailed description:
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.
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.
Coordinating organisation / Consortium Leader
- University of Bonn
Cooperation partners with funding
1 of 5
- Bernhard Nocht Institute for Tropical Medicine
- Charité - Universitätsmedizin Berlin
- Friedrich-Loeffler-Institut
- Goethe University Frankfurt
- Hans Knöll Institute
