Platelets, cell fragments traditionally thought of as important only for hemostasis, substantially and dynamically contribute to the immune system’s response to infection. In addition, there is increasing evidence that externally active platelet entities, including platelet granules and platelet extracellular vesicles (PEVs), play a role not only in hemostasis, but also in inflammatory actions previously ascribed to platelets themselves. Given the functions of platelets and PEVs during inflammation and infection, their role in sepsis is being investigated. Sepsis is a condition marked by the dysregulation of the body’s normal activation of the immune system in response to a pathogen. The mechanisms for controlling infection locally become detrimental to the host if they are applied systemically. Similar to cells traditionally ascribed to the immune system, including neutrophils, lymphocytes, and macrophages, platelets are instrumental in helping a host clear an infection, but are also implicated in the uncontrolled amplification of the immune response that leads to sepsis. Clearly, the function of platelets is more complicated than its simple structure and primary role in hemostasis initially suggest. This review provides an overview of platelet and platelet extracellular vesicle structure and function, highlighting the complex role platelets and PEVs play in the body in the context of infection and sepsis.
- blood platelets
- platelet activation
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EWJK and CH are joint first authors.
EWJK and CH contributed equally.
Contributors Each author participated in the literature search, review of the literature, creation of the figures, writing of the manuscript and has approved the manuscript as submitted. EWJK and CH contributed equally to this manuscript as co-first authors.
Funding EWJK is currently receiving support through a Ruth L. Kirschstein National Research Service Award (NRSA) Institutional Research Training Grant awarded to the Children’s Research Institute Hematology Training Program by the National Heart, Lung and Blood Institute (NHLBI) of the National Institutes of Health (5T32HL110841-07).
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Commissioned; externally peer reviewed.
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