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Plasmodium vivax: paroxysm-associated lipids mediate leukocyte aggregation
Nadira Karunaweera1, Deepani Wanasekara, Vishvanath Chandrasekharan
1Malaria Research Unit, Department of Parasitology, Faculty of Medicine, University of Colombo, Colombo, Sri Lanka. nadira@parasit.cmb.ac.lk
Malaria Journal
|May 23, 2007
Summary
Recurrent Plasmodium vivax malaria paroxysms cause leukocyte aggregation via host cytokines and parasite lipids. A novel cholesterol/triglyceride toxin, distinct from GPI moieties, drives this P. vivax malaria complication.
Area of Science:
- Malariology
- Immunology
- Biochemistry
Background:
- Paroxysms in Plasmodium vivax malaria are febrile episodes linked to erythrocyte rupture.
- These events release parasite and host factors, potentially influencing leukocyte behavior.
Purpose of the Study:
- To investigate the formation of leukocyte aggregates during Plasmodium vivax malaria paroxysms.
- To identify the specific host and parasite factors mediating this aggregation phenomenon.
Main Methods:
- Incubation of leukocytes with plasma from paroxysm or control states.
- Immune depletion and reconstitution experiments to identify mediating factors.
- Biochemical characterization of active plasma components.
Main Results:
- Leukocyte aggregates formed exclusively in plasma from paroxysms.
- Mediators included host cytokines (TNF-alpha, GM-CSF, IL-6, IL-10) and two lipid fractions (phospholipid-rich and cholesterol/triglyceride-rich).
- The cholesterol/triglyceride fraction showed potent activity independently of cytokines, suggesting a novel toxin.
Conclusions:
- Leukocyte aggregation is associated with P. vivax paroxysms, mediated by cytokines and parasite-derived lipids.
- A novel, highly active cholesterol/triglyceride malarial toxin is identified, distinct from known GPI moieties.
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