Abstract
Thrombocytopenia is commonly associated with sepsis and infections, which in turn are characterized by a profound immune reaction to the invading pathogen. Platelets are one of the cellular entities that exert considerable immune, antibacterial, and antiviral actions, and are therefore active participants in the host response. Platelets are sensitive to surrounding inflammatory stimuli and contribute to the immune response by multiple mechanisms, including endowing the endothelium with a proinflammatory phenotype, enhancing and amplifying leukocyte recruitment and inflammation, promoting the effector functions of immune cells, and ensuring an optimal adaptive immune response. During infection, pathogens and their products influence the platelet response and can even be toxic. However, platelets are able to sense and engage bacteria and viruses to assist in their removal and destruction. Platelets greatly contribute to host defense by multiple mechanisms, including forming immune complexes and aggregates, shedding their granular content, and internalizing pathogens and subsequently being marked for removal. These processes, and the nature of platelet function in general, cause the platelet to be irreversibly consumed in the execution of its duty. An exaggerated systemic inflammatory response to infection can drive platelet dysfunction, where platelets are inappropriately activated and face immunological destruction. While thrombocytopenia may arise by condition-specific mechanisms that cause an imbalance between platelet production and removal, this review evaluates a generic large-scale mechanism for platelet depletion as a repercussion of its involvement at the nexus of responses to infection.
Highlights
Thrombocytopenia is commonly associated with sepsis and infections, which in turn are characterized by a profound immune reaction to the invading pathogen
While thrombocytopenia may arise by condition-specific mechanisms that cause an imbalance between platelet production and removal, this review evaluates a generic large-scale mechanism for platelet depletion as a repercussion of its involvement at the nexus of responses to infection
Platelets have a key role in sensing and effecting the first wave of responses to microbial and viral threat.[8,9]. This is achieved by the inflammatory activity of platelets and through direct antibacterial and antiviral actions that facilitate the clearance of pathogens from the circulation
Summary
A common feature of many infections, both viral and bacterial, is a systemic inflammatory response that involves a dysregulated proinflammatory biomarker presence in the circulation.[3,5,32] These biomarkers may include cytokines (e.g., interleukins [ILs], tumor necrosis factor [TNF]-α, and interferons) and molecules originating from bacteria and viruses themselves (e.g., proteases, ribonucleic acid [RNA], and membrane components like lipopolysaccharide [LPS], lipoteichoic acid [LTA], and viral glycoproteins). The presence of such circulating biomarkers has profound agonistic effects on platelets. Abbreviation αIIbβ[3] αMβ2 cAMP CAR receptor (s)CD40L cGMP CR2 CR3 CR4 DAMP DNA Eap Efb FcγRIIa GPIb GPVI HIV HLA-DR HRgpA Ig IL LCMV LPS LTA MyD88 NET P-selectin PAF PAMP PAR PF4 PKG PSGL-1 RANTES RgpB RNA ROS SSL TLR TNF TREM-1(L)
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