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Published on: May 23, 2025
Complement factor D is linked to platelet activation in human and rodent sepsis
O Sommerfeld1,2, K Dahlke3,4, M Sossdorf3,4
1Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany. Oliver.Sommerfeld@med.uni-jena.de.
Insights
Complement factor D (CFD) plays a role in platelet activation during sepsis. Higher CFD levels in sepsis patients correlate with increased organ failure and mortality, suggesting a potential therapeutic target.
Area of Science:
- Immunology
- Hematology
- Critical Care Medicine
Background:
- Complement factor D (CFD) has a known regulatory role in infection.
- Its specific physiological functions in coagulopathy and impact on sepsis progression are not fully understood.
Purpose of the Study:
- To investigate the role of CFD in sepsis-induced coagulopathy and its association with host immune response and clinical outcomes.
- To explore the relationship between CFD levels, platelet activation, and mortality in sepsis patients.
Main Methods:
- Sepsis was induced in wild-type and CFD-deficient mice using cecal ligation and puncture.
- Coagulation markers and host-immune responses were assessed in mice.
- CFD levels were measured in patients with sepsis or SIRS and correlated with clinical data and outcomes.
Main Results:
- Septic CFD-deficient mice showed higher thrombin-antithrombin complexes and impaired clot firmness.
- Wild-type mice exhibited increased platelet activation markers, including GPIIb/IIIa surface expression.
- Elevated CFD levels in human sepsis patients correlated with organ failure (SOFA score) and increased mortality.
Conclusions:
- CFD is implicated in platelet activation during sepsis, particularly in wild-type mice.
- High plasma CFD concentrations in sepsis patients are associated with adverse outcomes, including organ failure and mortality.
- These findings highlight CFD as a potential biomarker and therapeutic target in sepsis management.
Background:
The complement factor D (CFD) exerts a regulatory role during infection. However, its physiological function in coagulopathy and its impact on the course of an infection remains unclear.
Materials:
Wild-type and CFD-deficient mice (n = 91) were subjected to cecal ligation and puncture to induce sepsis. At several time points, markers of coagulation and the host-immune response were determined. Furthermore, in patients (n = 79) with sepsis or SIRS, CFD levels were related to clinical characteristics, use of antiplatelet drugs and outcome.
Results:
Septic CFD-deficient mice displayed higher TAT complexes (p = 0.02), impaired maximal clot firmness, but no relevant platelet drop and reduced GPIIb/IIIa surface expression on platelets (p = 0.03) compared to septic wild-type mice. In humans, higher CFD levels (non-survivors, 5.0 µg/ml to survivors, 3.6 µg/ml; p = 0.015) were associated with organ failure (SOFA score: r = 0.33; p = 0.003) and mortality (75% percentile, 61.1% to 25% percentile, 26.3%). CFD level was lower in patients with antiplatelet drugs (4.5-5.3 µg/ml) than in patients without.
Conclusion:
In mice, CFD is linked to pronounced platelet activation, depicted by higher GPIIb/IIIa surface expression in wild-type mice. This might be of clinical importance since high CFD plasma concentrations were also associated with increased mortality in sepsis patients.
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