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

Darling, T. K., Schenk, M. P., Zhou, C., Maloba, F. M., Mimche, P. N., Gibbins, J. M. ORCID: https://orcid.org/0000-0002-0372-5352, Jobe, S. M. and Lamb, T. J. (2020) Platelet alpha-granules contribute to organ-specific pathologies in a mouse model of severe malaria. Blood Advances, 4 (1). pp. 1-8. ISSN 2473-9529 doi: 10.1182/bloodadvances.2019000773

Abstract/Summary

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.