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A Generic Large-Scale Cause for Platelet Dysfunction and Depletion in Infection

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A Generic Large-Scale Cause for Platelet Dysfunction and Depletion in Infection Published online: 2020-04-12 THIEME 302 A Champion of Host Defense: A Generic Large-Scale Cause for Platelet Dysfunction and Depletion in Infection Martin J. Page, BSc (Hons)1 Etheresia Pretorius, PhD1 1 Department of Physiological Sciences, Stellenbosch University, Address for correspondence Etheresia Pretorius, PhD, Department of Stellenbosch, South Africa Physiological Sciences, Faculty of Science, Stellenbosch University, Private Bag X1 Matieland, Stellenbosch, 7602, South Africa Semin Thromb Hemost 2020;46:302–319. (e-mail: [email protected]). 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 Keywords the execution of its duty. An exaggerated systemic inflammatory response to infection ► platelets can drive platelet dysfunction, where platelets are inappropriately activated and face ► virus immunological destruction. While thrombocytopenia may arise by condition-specific ► bacteria mechanisms that cause an imbalance between platelet production and removal, this ► thrombocytopenia review evaluates a generic large-scale mechanism for platelet depletion as a repercus- ► immune response sion of its involvement at the nexus of responses to infection. – Infections, both bacterial and viral, are associated with a mortality are greatly enhanced.13 15 Similarly, thrombocyto- profound immune response to the infecting pathogen. Plate- penia is associated with a dysregulated host response and lets are important contributors to the multifaceted response to worse outcomes in sepsis patients.16,17 Platelets are also active infection, where they have the ability to modulate various participants in the host response to viruses, and have been – immune cells. Platelets engage the immune system through shown to be protective in viral infections.18 20 direct cell-to-cell interaction and through the release of vari- Platelets possess receptors that allow them to survey for – ous soluble mediators.1 5 Furthermore, platelets participate in danger signals from pathogens (pathogen-associated molecu- – the interaction between pathogens and host defense.6 12 In lar patterns; PAMPs) and cell damage (damage-associated the absence of platelets, bacteremia, tissue damage, and molecular patterns; DAMPs), and trigger hemostatic and Issue Theme Acquired Platelet Copyright © 2020 by Thieme DOI https://doi.org/10.1055/s-0040- published online Dysfunction—Laboratory and Medical Publishers, Inc., 333 1708827. April 12, 2020 Clinical Implications; Guest Seventh Avenue, New York, ISSN 0094-6176. Editors: Anne-Mette Hvas, MD, PhD, NY 10001, USA. Julie Brogaard Larsen, MD, PhD, and Tel: +1(212) 760-0888. Leonardo Pasalic, MBBS, PhD. Platelet Dysfunction and Depletion in Infection Page, Pretorius 303 inflammatory responses against bacterial and viral infec- rationale of this review and ►Table 1 lists the abbreviations tions.3,21,22 During infection, the platelet is activated, mobi- used in this article. lized, and actively participates in the resultant hemostatic and inflammatory responses. These signaling processes involve 23 Platelet and the Immune Response to many feedback loops that self-amplify initial activation, Infections and platelets can manifest dysfunction even in cases where no bacteremia is present.10 These processes are irreversible Acommonfeature ofmany infections, bothviralandbacterial,is and undoubtedly lead to consumption of the platelet. Activa- asystemicinflammatory response that involves a dysregulated tion of platelets leads to their consumption into aggregates proinflammatory biomarker presence in the circulation.3,5,32 with other platelets, leukocytes, and the endothelium.24 Pla- Thesebiomarkers may include cytokines (e.g., interleukins [ILs], telets with bound antibody are targets of phagocytes, and tumor necrosis factor [TNF]-α, and interferons) but also mole- platelets with a bacterial or viral load are sequestrated and also cules originating from bacteria and viruses themselves (e.g., cleared from the circulation. Further, pathogenic compounds proteases, ribonucleic acid [RNA], and membrane components induce apoptosis and cytotoxic effects in platelets.25 In this like lipopolysaccharide [LPS], lipoteichoic acid [LTA], and viral sense, activated platelets and platelets interacting with patho- glycoproteins). The presence of such circulating biomarkers has gens have shortened survival spans and experience increased profound agonistic effects on platelets. destruction. The outcome for the patient will be a decrease in Platelets contribute to the thromboinflammatory response normal circulating platelets, and if this manifests widely through the plethora of membrane and cytosolic molecules enough it can be measured as thrombocytopenia.3,25 that they express and release, which possess hemostatic, – Other mechanisms of platelet decline in infection exist and immunomodulatory, and inflammatory activity.1 4 Platelets include the formation ofautoantibodies against platelet surface possess receptors that enable pathogen sensing, and which proteins, which leads to clearance of immunoglobulin G (IgG)- allow platelets to regulate leukocytes and other cells at the site coated platelets by the reticuloendothelial system,26,27 as well of infection. During platelet activation, degranulation leads to as by impaired platelet production in the bone marrow,3,6 the surface expression of receptors and the release of abundant among others.6 However, a general view of platelet destruction proinflammatory mediators, which contribute to numerous – is the simple characteristic that their involvement in throm- signaling events.1 5 Platelets also adhere and aggregate to botic, hemostatic, immune, and host defense responses is other platelets and to endothelial cells, leukocytes, and eryth- irreversible. Even if platelets are positive contributors to the rocytes.5,9,24 This response is also characteristic during bacte- host response against invading pathogens, they can become rial and viral infections, and can be induced by pathogens dysfunctional, especially in the context of an excessive and directly.33 This section describes the role of platelets in the unbalanced systemic inflammatory response.16,28 Indeed, the immune response. See ►Fig. 2 for a general overview of dysfunctional state of thrombocytopenia is commonly associ- platelet receptors and secretory products. – ated with sepsis and infections.3,29 31 The focus of the current review is platelets and their role in Platelet–Endothelium Interactions: Endowing a infection. We will examine the interaction of platelets, their Proinflammatory Phenotype receptors, and secretory product with bacteria and viruses, Endothelial activation markers are raised during infection, and and discuss how this may contribute to platelet dysfunction are associated with a thrombotic state.34 During activation, and ultimately lead to thrombocytopenia. ►Fig. 1 provides the platelets can bind to the endothelium.24 This especially occurs upon endothelial damage due to trauma or microbial coloniza- tion,35 as well as inviral infections.36 Platelets become activated during the adhesion process, and the inflammatory and mito- genic substances that are released alter the chemotactic, adhe- sive, and proteolytic properties of endothelial cells.37 Platelet adhesion therefore endows the endothelium with a proinflam- matory phenotype.24 Moreover, platelets that are bound to the endothelium can form a bridging connection with circulating leukocytes.24 Overall, these mechanisms amplify and facilitate leukocyte recruitment and enhance inflammation. ►Fig. 3 provides an overview of the contact between platelets and cells at the vascular wall to emphasize the involvementofplateletsin multiple interactions at the vessel wall. Platelet–Leukocyte Interactions: Promoting Immune Cell Effector Functions against Pathogens fl Fig. 1 Layout of the review. During infection, in ammatory stimuli, Interactions between platelets and leukocytes are important and the presence of bacteria, viruses and their products mobilize for the regulation of the immune response and for the clear- platelets to exert their immune, antibacterial, and antiviral actions. However, these processes can also lead to platelet dysfunction and ance of infectious agents. By binding and activating leukocytes, ultimately depletion. platelets promote their effector functions. Coordination of Seminars in Thrombosis & Hemostasis Vol.
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