Plasmodium parasite exploits host aquaporin-3 during liver stage malaria infection

• DOI: 10.1371/journal.ppat.1007057
• Publication Date: 2018-05-18T17:28:00Z
• Authors: Dora Posfai; Kayla Sylvester; Anupama Reddy; Jack G. Ganley; Johannes Wirth; Quinlan E. Cullen; Tushar Dave; Nobutaka Kato; Sandeep S. Dave; Emily R. Derbyshire
• Keywords: Plasmodium (life cycle)

Within the liver a single Plasmodium parasite transforms into thousands of blood-infective forms to cause malaria. Here, we use RNA-sequencing identify host genes that are upregulated upon berghei infection hepatocytes with hypothesis pathways hijacked benefit development. We found expression aquaporin-3 (AQP3), water and glycerol channel, is significantly induced in Plasmodium-infected compared uninfected cells. This aquaglyceroporin localizes parasitophorous vacuole membrane, compartmental interface between pathogen, temporal pattern correlates parasite's expansion liver. Depletion or elimination AQP3 reduces P. burden during stage chemical disruption by known inhibitor, auphen, falciparum asexual blood load. Further this inhibitor as probe suggests AQP3-mediated nutrient transport an important function for study reveals previously unknown potential route host-dependent acquisition which was discovered mapping transcriptional changes occur throughout infection. The dataset reported may be leveraged additional factors essential highlights Plasmodium's dependence on within hepatocytes.