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Updated: May 11, 2026
Humanized Mouse Model to Study Bacterial Infections Targeting the Microvasculature
Published on: April 1, 2014
Platelets promote bacterial dissemination in a mouse model of streptococcal sepsis
Fredrik Kahn1, Sinead Hurley, Oonagh Shannon
1Division of Infection Medicine, Department of Clinical Sciences, Lund University, SE-22184 Lund, Sweden.
Abstract:
Platelets have been reported to contribute to inflammation and inflammatory disorders. In the present study, we demonstrate that platelets contribute to the acute response to bacterial infection in a mouse model of invasive Streptococcus pyogenes infection. Thrombocytopenia occurred rapidly in infected animals and this was associated with platelet activation, formation of platelet-neutrophil complexes and neutrophil activation. In order to assess the role of platelets during infection, platelets were depleted prior to infection. Platelet-depleted animals had significantly decreased platelet-neutrophil complex formation and neutrophil activation in response to infection. Importantly, significantly fewer bacteria disseminated to the blood, lungs, and spleen of platelet-depleted animals. Platelet-depleted animals did not decrease as significantly in weight as the infected control animals. The results demonstrate a previously unappreciated role for platelets during the pathophysiological response to infection, whereby S. pyogenes bacteria bind to platelets and platelets facilitate bacterial dissemination.
Insights
Platelets play a key role in the acute response to Streptococcus pyogenes infection by facilitating bacterial spread. Reducing platelet levels limits bacterial dissemination and reduces disease severity in mice.
Area of Science:
- Immunology
- Hematology
- Microbiology
Background:
- Platelets are known to contribute to inflammation and inflammatory disorders.
- Their specific role in acute bacterial infection responses requires further elucidation.
Purpose of the Study:
- To investigate the role of platelets in the acute response to invasive Streptococcus pyogenes infection in a mouse model.
- To determine if platelets facilitate bacterial dissemination and influence disease severity.
Main Methods:
- Induction of invasive Streptococcus pyogenes infection in a mouse model.
- Assessment of thrombocytopenia, platelet activation, and platelet-neutrophil complex formation.
- Depletion of platelets prior to infection to evaluate their role in bacterial dissemination and host response.
Main Results:
- Infection led to rapid thrombocytopenia, platelet activation, and formation of platelet-neutrophil complexes.
- Platelet depletion significantly reduced platelet-neutrophil complex formation and neutrophil activation.
- Fewer bacteria disseminated to the blood, lungs, and spleen in platelet-depleted mice, which also showed less weight loss.
Conclusions:
- Platelets play a significant, previously unappreciated role in the acute response to Streptococcus pyogenes infection.
- Streptococcus pyogenes bacteria bind to platelets, which then facilitate bacterial dissemination.
- Targeting platelet-host interactions could be a therapeutic strategy for bacterial infections.
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