Platelet α-granules contribute to organ-specific pathologies in a mouse model of severe malaria.

Cerebral malaria (CM) and malaria-associated acute lung injury/acute respiratory distress syndrome (MA-ALI/ARDS) are among the most severe complications of Plasmodium infection. While these disease manifestations are multifactorial, platelets have been described to play a role in the development of both syndromes in humans1,2 and mice3,4. Although the impact of platelets on malaria has been well-studied, questions remains with regard to their contribution to parasite control and immunopathogenesis. Studies have indicated that platelets can kill Plasmodium-infected red blood cells (iRBCs)5-8. However, there are contrasting reports that platelets do not exert any significant control over parasite growth but rather exacerbate malaria immunopathology3,9-12. In this study, we address the role of platelets in the development of severe malaria in three different mouse models of platelet dysfunction/depletion. We show a key role for platelets, and particularly platelet alpha granules (-granules), in mediating organ-specific pathologies during rodent Plasmodium infection.