Platelets are most identified as the cellular mediator of thrombosis. It is becoming increasingly evident that platelets also have complicated roles in vascular inflammatory and infectious diseases. Platelets have been linked to initiating or accelerating the pathogenesis of diverse pathologies, such as atherosclerosis acute and chronic transplant rejection, arthritis, influenza, and malaria infection. Platelets may also have protective roles in killing microbes, such as bacteria. Malaria kills over 500 000 people per year, so understanding the multifaceted roles for platelets in malaria infection is of critical importance.
Recent literature has on the surface made the role of platelets in malaria infection somewhat confusing, with seemingly contradictory studies indicating a protective role for platelets in malaria infection by direct parasite killing, although others have indicated that platelets have an adverse proinflammatory role. However, what can appear to be mechanistic discrepancies are likely best explained through a better understanding and appreciation of platelet immune functions, especially in the context of the disease outcome or model systems used.
In this review, we will first briefly highlight platelet immune cell functions. We will then discuss how platelet immune and inflammatory functions may affect responses to malaria infection in a disease outcome and animal model context.
Aab Cardiovascular Research Institute, University of Rochester School of Medicine, Rochester, New York, USA
Correspondence to Craig N. Morrell, DVM, PhD, University of Rochester, Box CVRI, 601 Elmwood Avenue, Rochester, NY 14642, USA. Tel: +1 585 276 9921; e-mail: Craig_Morrell@urmc.rochester.edu