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

14 Jan 2020
Darling TK, Schenk MP, Zhou CC, Maloba FM, Mimche PN, Gibbins JM, Jobe SM, Lamb TJ


Cerebral malaria and malaria-associated acute lung injury/acute respiratory distress syndrome 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 mice.3,4 Although the impact of platelets on malaria has been well studied, questions remain 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 immunopathology.3,9-12 In this study, we address the role of platelets in the development of severe malaria in 3 different mouse models of platelet dysfunction/depletion. We show a key role for platelets, particularly platelet α-granules, in mediating organ-specific pathologies during rodent Plasmodium infection.