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Platelets activate a pathogenic response to blood-stage Plasmodium infection but not a protective immune response

Irene Gramaglia, Joyce Velez, Valery Combes, Georges E. R. Grau, Melanie Wree and Henri C. van der Heyde

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  • RE: Platelets activate a pathogenic response to blood-stage Plasmodium infection but not a protective immune response.
    • Brendan J McMorran, Associate Professor The Australian National University
    • Other Contributors:
      • Simon J Foote, Professor and Director

    In the article by Gramaglia et al (blood-2016-08-733519), the authors conclude that platelets do not kill intraerythrocytic Plasmodium or control the growth of these parasites in murine malaria models. These findings substantially contradict previous studies [1-4], as well as our own [5]. We would like to point out a number of technical and analytical issues in the paper that may explain these contrasting findings.

    There are several technical differences between their and previous studies, including different mouse and Plasmodium strains, which can affect parasite virulence, growth and sequestration, and host response characteristics (in the case of the murine infections) and platelet adhesion molecules such as PfEMP1 (in the case of the P. falciparum-platelet co-culture experiments). The parasitemias used in the co-culture study were also very high (cf. our and Peyron’s studies, which used <1% [2, 5]); this limits the power to detect a platelet effect.

    In the Pca and Pba parasitemia studies, the day 0 parasitemias are based on unsubstantiated assumptions that the entire inoculum reaches the circulation, and that all these parasites are viable. The day 3&4 parasitemias appear too low for accurate quantification using their described method (eg. 0.2% parasitemia derives from observing only 2 iRBC per 1000 RBC counted). The log parasitemia curves are not linear as claimed; some data points are obscured (Fig1B & S1B). The parasite replication rates d...

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    Conflict of Interest:
    None declared.