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Thrombocytopenia impairs host defense during murine Streptococcus pneumoniae pneumonia
Florry E van den Boogaard1, Marcel Schouten, Sacha F de Stoppelaar
11Center for Experimental and Molecular Medicine (CEMM), Academic Medical Center, Amsterdam, The Netherlands. 2Center for Infection and Immunity Amsterdam (CINIMA), Academic Medical Center, Amsterdam, The Netherlands. 3Department of Pathology, Academic Medical Center, Amsterdam, The Netherlands. 4Department of Intensive Care Medicine, Academic Medical Center, Amsterdam, The Netherlands. 5Laboratory of Experimental Intensive Care and Anesthesiology (LEICA), Academic Medical Center, Amsterdam, The Netherlands. 6Division of Infectious Diseases, Academic Medical Center, Amsterdam, The Netherlands.
Objectives:
Streptococcus pneumoniae is the most common causative pathogen in community-acquired pneumonia. In patients, thrombocytopenia is correlated with an adverse outcome of pneumonia. Platelets can modulate the host response to infection in several ways, that is, by facilitating clot formation, production of antimicrobial proteins, and interaction with neutrophils. We studied the effect of thrombocytopenia during murine pneumococcal pneumonia.
Design:
Animal study.
Setting:
University research laboratory.
Subjects:
Mice.
Interventions:
Pneumonia was induced by intranasal inoculation of S. pneumoniae. Platelets were depleted by anti-mouse thrombocyte serum; controls received nonimmunogenic serum. In separate studies, mice were treated with the platelet P2Y12 receptor inhibitor clopidogrel or placebo.
Measurements And Main Results:
Thrombocytopenic mice (platelet counts < 1% of uninfected controls) showed a reduced survival during pneumococcal pneumonia (27% vs 75% among controls; p = 0.003), which was associated with higher bacterial loads in lungs, spleen, and blood. Thrombocytopenic mice showed enhanced coagulation activation (thrombin-antithrombin complexes) in plasma. Proinflammatory cytokine levels were higher in plasma but not in lungs of thrombocytopenic mice. Although clopidogrel treatment strongly prolonged the bleeding time, it did not impact on bacterial loads during pneumococcal pneumonia.
Conclusions:
Platelets play a protective role during pneumococcal pneumonia independent of their aggregation.
Insights
Platelets protect against pneumococcal pneumonia by reducing bacterial load and improving survival. This protective role is independent of platelet aggregation, highlighting their broader function in host defense against bacterial infections.
Area of Science:
- Infectious Disease
- Hematology
- Immunology
Background:
- Streptococcus pneumoniae is a leading cause of community-acquired pneumonia.
- Thrombocytopenia, or low platelet count, is linked to worse outcomes in pneumonia patients.
- Platelets influence infection response through clot formation, antimicrobial protein release, and neutrophil interaction.
Purpose of the Study:
- To investigate the role of thrombocytopenia in murine pneumococcal pneumonia.
- To understand how platelet depletion affects host defense and disease progression.
Main Methods:
- Pneumonia induced via intranasal Streptococcus pneumoniae inoculation in mice.
- Platelets depleted using anti-mouse thrombocyte serum; controls received nonimmunogenic serum.
- Mice treated with clopidogrel (platelet P2Y12 inhibitor) or placebo in separate studies.
Main Results:
- Thrombocytopenic mice had significantly reduced survival (27% vs 75%) and higher bacterial loads in lungs, spleen, and blood.
- Enhanced coagulation activation (thrombin-antithrombin complexes) observed in thrombocytopenic mice.
- Proinflammatory cytokines increased in plasma but not lung tissue of thrombocytopenic mice.
Conclusions:
- Platelets play a crucial protective role in pneumococcal pneumonia.
- This protective effect is independent of platelet aggregation.
- Findings suggest platelets are vital for combating S. pneumoniae infection.
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