Conference Agenda
Overview and details of the sessions of this conference. Please select a date or location to show only sessions at that day or location. Please select a single session for detailed view (with abstracts and downloads if available).
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CP15: Drugs & Drug Resistance 2 - 10 min talks sponsored by Institute for Biomedicine and Glycomics, Griffith University Location: Lecture Theatre 1 Session Chair: Jacinta Macdonald, Griffith University Session Chair: Rohith Kutty, Griffith University | |
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Anti‑plasmodial peptide induces polarity and fluidity changes in host and parasite membranes without translocation 1: 1Division of Immunology and Infectious Disease, The John Curtin School of Medical Research, Australian National University, Acton, Canberra 2601, Australia; 2: 2Centre for Advanced Microscopy, The Australian National University, Canberra ACT, 2601, Australia; 3: 3Institute for Molecular Bioscience, Centre of Excellence for Innovations in Peptide and Protein Science, The University of Queensland, St Lucia, Queensland 4067, Australia Platelet Factor 4 Derived Internalisation Peptide (PDIP), based on the antimicrobial peptide-like domain of human PF4, exhibits activity against Plasmodium. PDIP rapidly kills parasites by penetrating Plasmodium-infected erythrocytes and destroying the digestive vacuole. Why PDIP penetrates only infected but not healthy erythrocytes and destroys only the digestive vacuole is unclear. We hypothesised that differences in lipid composition between infected erythrocyte and parasite membranes alter membrane polarity and fluidity, thereby facilitating PDIP’s differential interactions. To test this, we used the membrane dyes Nile Red and Laurdan, which report polarity and fluidity through emission‑wavelength shifts quantified as ratiometric indices. These ratios were measured for uninfected and Plasmodium-infected erythrocyte membranes, and the intracellular parasite, with and without PDIP treatment. We found comparable fluidity between infected and uninfected erythrocyte membranes. Polarity differed significantly, ranking from most to least: intracellular parasite > uninfected > and infected erythrocyte membranes. These polarity differences may contribute to PDIP’s ability to selectively enter infected cells and suggested that parasites contain more polar lipids that may facilitate PDIP’s activity. PDIP treatment significantly increased polarity and reduced fluidity for all membrane types. This indicates a non-specific interaction of the peptide independent of translocation that alters membrane properties non-destructively. | |