Platelets, Bacterial Adhesins and the Pneumococcus

Cells

Sergej Wiebe¹  Kristin Jahn¹  Sven Hammerschmidt¹  Thomas P. Kohler¹  Lena-Sophie Swiatek¹ 

[1] Center for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, Interfaculty Institute for Genetics and Functional Genomics, University of Greifswald, 17489 Greifswald, Germany;

关键词: Streptococcus pneumoniae;    platelet killing;    platelet activation;    pore formation;    surface proteins;    toxin;   

DOI  :  10.3390/cells11071121

来源: DOAJ

【 摘 要 】

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 Staphylococcus aureus and Streptococcus pneumoniae 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 S. aureus and S. pneumoniae. More importantly, we summarize recent findings of how S. aureus toxins and the pore-forming toxin pneumolysin of S. pneumoniae 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.

【 授权许可】

Unknown