Platelets, Bacterial Adhesins and the Pneumococcus

Systemic infections with pathogenic or facultative pathogenic bacteria are associated with activation and aggregation of platelets leading to thrombocytopenia and activation of the clotting system. Bacterial proteins leading to platelet activation and aggregation have been identified, and while plat...

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Main Authors: Kristin Jahn, Thomas P. Kohler, Lena-Sophie Swiatek, Sergej Wiebe, Sven Hammerschmidt
Format: Article
Language:English
Published: MDPI AG 2022-03-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/11/7/1121
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author Kristin Jahn
Thomas P. Kohler
Lena-Sophie Swiatek
Sergej Wiebe
Sven Hammerschmidt
author_facet Kristin Jahn
Thomas P. Kohler
Lena-Sophie Swiatek
Sergej Wiebe
Sven Hammerschmidt
author_sort Kristin Jahn
collection DOAJ
description Systemic infections with pathogenic or facultative pathogenic bacteria are associated with activation and aggregation of platelets leading to thrombocytopenia and activation of the clotting system. Bacterial proteins leading to platelet activation and aggregation have been identified, and while platelet receptors are recognized, induced signal transduction cascades are still often unknown. In addition to proteinaceous adhesins, pathogenic bacteria such as <i>Staphylococcus aureus</i> and <i>Streptococcus pneumoniae</i> also produce toxins such as pneumolysin and alpha-hemolysin. They bind to cellular receptors or form pores, which can result in disturbance of physiological functions of platelets. Here, we discuss the bacteria-platelet interplay in the context of adhesin–receptor interactions and platelet-activating bacterial proteins, with a main emphasis on <i>S. aureus</i> and <i>S. pneumoniae</i>. More importantly, we summarize recent findings of how <i>S. aureus</i> toxins and the pore-forming toxin pneumolysin of <i>S. pneumoniae</i> interfere with platelet function. Finally, the relevance of platelet dysfunction due to killing by toxins and potential treatment interventions protecting platelets against cell death are summarized.
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spelling doaj.art-d707fbbaa4104095878e9b856f7b6aac2023-11-30T23:03:46ZengMDPI AGCells2073-44092022-03-01117112110.3390/cells11071121Platelets, Bacterial Adhesins and the PneumococcusKristin Jahn0Thomas P. Kohler1Lena-Sophie Swiatek2Sergej Wiebe3Sven Hammerschmidt4Center for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, Interfaculty Institute for Genetics and Functional Genomics, University of Greifswald, 17489 Greifswald, GermanyCenter for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, Interfaculty Institute for Genetics and Functional Genomics, University of Greifswald, 17489 Greifswald, GermanyCenter for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, Interfaculty Institute for Genetics and Functional Genomics, University of Greifswald, 17489 Greifswald, GermanyCenter for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, Interfaculty Institute for Genetics and Functional Genomics, University of Greifswald, 17489 Greifswald, GermanyCenter for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, Interfaculty Institute for Genetics and Functional Genomics, University of Greifswald, 17489 Greifswald, GermanySystemic infections with pathogenic or facultative pathogenic bacteria are associated with activation and aggregation of platelets leading to thrombocytopenia and activation of the clotting system. Bacterial proteins leading to platelet activation and aggregation have been identified, and while platelet receptors are recognized, induced signal transduction cascades are still often unknown. In addition to proteinaceous adhesins, pathogenic bacteria such as <i>Staphylococcus aureus</i> and <i>Streptococcus pneumoniae</i> also produce toxins such as pneumolysin and alpha-hemolysin. They bind to cellular receptors or form pores, which can result in disturbance of physiological functions of platelets. Here, we discuss the bacteria-platelet interplay in the context of adhesin–receptor interactions and platelet-activating bacterial proteins, with a main emphasis on <i>S. aureus</i> and <i>S. pneumoniae</i>. More importantly, we summarize recent findings of how <i>S. aureus</i> toxins and the pore-forming toxin pneumolysin of <i>S. pneumoniae</i> interfere with platelet function. Finally, the relevance of platelet dysfunction due to killing by toxins and potential treatment interventions protecting platelets against cell death are summarized.https://www.mdpi.com/2073-4409/11/7/1121<i>Streptococcus pneumoniae</i>platelet killingplatelet activationpore formationsurface proteinstoxin
spellingShingle Kristin Jahn
Thomas P. Kohler
Lena-Sophie Swiatek
Sergej Wiebe
Sven Hammerschmidt
Platelets, Bacterial Adhesins and the Pneumococcus
Cells
<i>Streptococcus pneumoniae</i>
platelet killing
platelet activation
pore formation
surface proteins
toxin
title Platelets, Bacterial Adhesins and the Pneumococcus
title_full Platelets, Bacterial Adhesins and the Pneumococcus
title_fullStr Platelets, Bacterial Adhesins and the Pneumococcus
title_full_unstemmed Platelets, Bacterial Adhesins and the Pneumococcus
title_short Platelets, Bacterial Adhesins and the Pneumococcus
title_sort platelets bacterial adhesins and the pneumococcus
topic <i>Streptococcus pneumoniae</i>
platelet killing
platelet activation
pore formation
surface proteins
toxin
url https://www.mdpi.com/2073-4409/11/7/1121
work_keys_str_mv AT kristinjahn plateletsbacterialadhesinsandthepneumococcus
AT thomaspkohler plateletsbacterialadhesinsandthepneumococcus
AT lenasophieswiatek plateletsbacterialadhesinsandthepneumococcus
AT sergejwiebe plateletsbacterialadhesinsandthepneumococcus
AT svenhammerschmidt plateletsbacterialadhesinsandthepneumococcus