Abstract
Platelets have received increasing attention for their role in the pathophysiology of infectious disease, inflammation, and immunity. In sepsis, a low platelet count is a well-known biomarker for disease severity and more recently authors have focused their attention on the active role of platelets in the pathogenesis of multi-organ failure. Septic shock is characterised by a dysregulated inflammatory response, which can impair the microcirculation and lead to organ injury. Being at the crossroads between the immune system, clotting cascade, and endothelial cells, platelets seem to be an appealing central mediator and possible therapeutic target in sepsis. This review focuses on the pathogenic role of platelets in septic organ dysfunction in humans and animal models.
Highlights
Sepsis is a complex syndrome characterized by a disordered immune, endocrine, and metabolic response to infection
The severity of organ dysfunction has a prognostic value, and in clinical practice is usually classified according to the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score [2]
In this review the following questions will be considered: What are the possible mechanisms of platelet dysfunction leading to multi-organ failure during sepsis? What evidence do we have for these mechanisms? Is platelet function a potential therapeutic target in sepsis?
Summary
Sepsis is a complex syndrome characterized by a disordered immune, endocrine, and metabolic response to infection. This exaggerated response can lead to multi-organ failure (MOF), shock, and death. Platelets are able to release cytokines, recruit leukocytes, interact with bacteria and the endothelium, and contribute to microthrombi formation [16] These mechanisms are adaptive and protective in the context of a localized infection, but become dysregulated and “maladaptive” during sepsis, contributing to organ damage [17]. In this review the following questions will be considered: What are the possible mechanisms of platelet dysfunction leading to multi-organ failure during sepsis? In this review the following questions will be considered: What are the possible mechanisms of platelet dysfunction leading to multi-organ failure during sepsis? What evidence do we have for these mechanisms? Is platelet function a potential therapeutic target in sepsis?
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