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Updated: May 30, 2026

Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice

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Streptococcus sanguinis-induced cytokine release from platelets.

A McNicol¹, A Agpalza, E C G Jackson

¹Department of Oral Biology, University of Manitoba, Winnipeg, MB, Canada. mcnicol@ms.umanitoba.ca

Journal of Thrombosis and Haemostasis : JTH

|August 10, 2011

Summary

Bacterial infections, like those from S. sanguinis, activate platelets, promoting blood clots and inflammation. Epinephrine amplifies clot formation but reduces inflammation, linking infection to heart events.

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Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice

Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice

Published on: August 13, 2015

Area of Science:

Cardiovascular Research
Microbiology
Immunology

Background:

Infections are increasingly linked to atherothrombotic disorders.
Platelet activation by bacteria is a potential mechanism.
Oral bacteria, such as S. sanguinis, can stimulate platelet aggregation.

Purpose of the Study:

To investigate if S. sanguinis triggers pro-inflammatory and immune factors from platelets.
To determine if epinephrine enhances S. sanguinis-induced platelet activation.

Main Methods:

Assessed release of cytokines (RANTES, PF4, sCD40L, PDGF-AB, sCD62p) from platelets stimulated by S. sanguinis strains.
Evaluated the effect of epinephrine on platelet aggregation, phosphorylation, and cytokine release.
Utilized wortmannin to investigate signaling pathways involved in platelet activation.

Main Results:

S. sanguinis and S. gordonii strains induced the release of multiple inflammatory mediators.
Epinephrine potentiated S. sanguinis-induced platelet aggregation and specific signaling pathways.
Epinephrine inhibited the release of most inflammatory factors, while wortmannin blocked aggregation and release.

Conclusions:

Platelets exhibit both prothrombotic and pro-inflammatory responses to S. sanguinis.
Epinephrine enhances platelet prothrombotic activity, potentially linking bacteremia to acute coronary events during stress.
Epinephrine's inhibition of the pro-inflammatory response remains mechanistically unclear.