Thromb Haemost 2009; 102(04): 735-742
DOI: 10.1160/TH09-01-0049
Wound Healing and Inflammation/Infection
chattauer GmbH

Pneumococcal association to platelets is mediated by soluble fibrin and supported by thrombospondin-1

Silke Niemann*
1   Department of Anaesthesiology and Intensive Care, Experimental and Clinical Haemostasis, University Hospital of Muenster, Muenster, Germany
,
Beate E. Kehrel*
1   Department of Anaesthesiology and Intensive Care, Experimental and Clinical Haemostasis, University Hospital of Muenster, Muenster, Germany
,
Christine Heilmann
2   Institute of Medical Microbiology, University Hospital of Muenster, Muenster, Germany
,
Claudia Rennemeier
3   Research Center for Infectious Diseases, University of Wuerzburg, Wuerzburg, Germany
4   Present address: Department of Obstetrics and Gynaecology, University of Wuerzburg, Wuerzburg, Germany
,
Georg Peters
2   Institute of Medical Microbiology, University Hospital of Muenster, Muenster, Germany
,
Sven Hammerschmidt
3   Research Center for Infectious Diseases, University of Wuerzburg, Wuerzburg, Germany
5   Present address: Department Genetics of Microorganisms, University of Greifswald, Greifswald, Germany
› Author Affiliations
Financial support: Deutsche Forschungsgemeinschaft, Collaborative Research Center 293, Project A6 to BK, CH, and GP, and Collaborative Research Center 479 to SH.
Further Information

Publication History

Received: 20 January 2009

Accepted after major revision: 16 June 2009

Publication Date:
24 November 2017 (online)

Summary

Platelets and coagulation are involved in bacterial colonisation of the host. Streptocococcus pneumoniae (pneumococcus) are important etiologic agents of respiratory tract infections in humans. The formation of pneumococci-platelet associations may facilitate haematogenous dissemination of pneumococci by providing an adhesive surface on damaged endothelium. However, the formation of platelet-pneumococci associations and the factors involved in this process have not been described so far. The formation of platelet-pneumococci associates was analysed and quantified using flow cytometry. Binding of pneumococci to platelets was significantly increased after activation of platelets with thrombin, while platelet activation by ADP or collagen did not promote formation of platelet-pneumococci associates. In addition to be a platelet agonist, thrombin cleaves fibrinogen, which results in the generation of fibrin. The simultaneous formation of fibrin and activation of platelets was shown to be a prerequisite for a high number of platelet-pneumococci associates. Moreover, exogenously added human thrombospondin-1 (TSP-1) significantly enhanced the association of pneumococci with activated platelets. Soluble fibrin and TSP-1 are key co-factors of platelet-pneumococci-association. Similar results were recently demonstrated for S. aureus-platelet adhesion. Consequently, we hypothesise that the described mechanism of platelet-bacteriaassociation might represent a general and important strategy of Gram-positive bacteria during development of invasive diseases.

* Both authors contributed equally to the study.


 
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