Journal
CELLS
Volume 11, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/cells11030424
Keywords
platelet; platelet activation; infection; critical care
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In addition to their role in hemostasis, platelets also play a significant role in the immune response. Thrombocytopenia, a decrease in platelet count, is a known risk factor for mortality and disease severity. Platelets' response to infections goes beyond a simple decrease in count, involving changes in morphology, receptor expression, and aggregation.
Beyond their role in hemostasis, platelets have emerged as key contributors in the immune response; accordingly, the occurrence of thrombocytopenia during sepsis/septic shock is a well-known risk factor of mortality and a marker of disease severity. Recently, some studies elucidated that the response of platelets to infections goes beyond a simple fall in platelets count; indeed, sepsis-induced thrombocytopenia can be associated with-or even anticipated by-several changes, including an altered morphological pattern, receptor expression and aggregation. Of note, alterations in platelet function and morphology can occur even with a normal platelet count and can modify, depending on the nature of the pathogen, the pattern of host response and the severity of the infection. The purpose of this review is to give an overview on the pathophysiological interaction between platelets and pathogens, as well as the clinical consequences of platelet dysregulation. Furthermore, we try to clarify how understanding the nature of platelet dysregulation may help to optimize the therapeutic approach.
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