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Platelets, Aspirin, and Malaria

Platelets contribute to the host defense against malarial parasites — an effect blocked by aspirin and other antiplatelet agents.

Thrombocytopenia, a common manifestation of malaria, is associated with increased parasite density and poor outcome. Platelets produce microbicidal peptides active against a variety of bacteria. Now, researchers in Australia have investigated whether these blood components play a role in host defense against malaria.

Experiments in mice showed that animals genetically deficient in platelets were significantly more susceptible to death from Plasmodium chabaudi infection than were isogenic non–platelet-deficient mice, even though immunologic responses appeared to be unchanged. Similarly, aspirin-treated mice were more susceptible to death from P. chabaudi infection than were placebo-treated animals. In an in vitro model of Plasmodium falciparum infection of human red blood cells (RBCs), coincubation with purified human platelets inhibited parasite growth in a dose-dependent manner. Various platelet antagonists including aspirin abrogated the antiparasitic activity of human platelets. Both in vivo and in vitro, platelets selectively bound to Plasmodium-infected RBCs, and the percentage of dead intraerythrocytic parasites was greater in the presence than in the absence of normal numbers of platelets.

Comment: These findings suggest that platelets kill intraerythrocytic malarial parasites and thus mediate survival. Such observations raise concern about the use of aspirin as an antipyretic in patients with malaria. Moreover, they raise questions about the role of platelets in controlling other intraerythrocytic parasites, such as Babesia.

— Richard T. Ellison III, MD

Published in Journal Watch Infectious Diseases February 18, 2009

Citation(s):

McMorran BJ et al. Platelets kill intraerythrocytic malarial parasites and mediate survival to infection. Science 2009 Feb 6; 323:797.

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