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Venous Air Embolism Activates Complement C3 Without Corresponding C5 Activation and Trigger Thromboinflammation in
Benjamin S Storm1,2,3,4, Judith K Ludviksen4, Dorte Christiansen4
1Department of Anesthesia and Intensive Care Medicine, Nordland Hospital, Bodø, Norway.
Frontiers in Immunology
|April 4, 2022
Summary
Air embolism in pigs activated complement C3, leading to increased white blood cells, coagulation, and inflammatory cytokines in lungs. This study suggests C3 inhibition may be a therapeutic strategy for air embolism complications.
Area of Science:
- Cardiovascular Research
- Immunology
- Pulmonary Medicine
Background:
- Air embolism is a known complication of invasive medical procedures.
- In vitro studies show air bubbles activate complement C3, leading to cytokine release, coagulation, and platelet activation.
- In vivo verification of these effects was lacking.
Purpose of the Study:
- To investigate the in vivo effects of air embolism in pigs.
- To examine the impact of air embolism on thromboinflammation.
- To determine the role of complement activation in air embolism response.
Main Methods:
- Intravenous air infusion in landrace pigs (n=29) or sham procedure (n=14).
- Analysis of blood for white blood cells (WBC), complement activation (C3a, C5b-9), cytokines, and hemostasis (TAT, ROTEM).
- Analysis of lung tissue for complement and cytokines using qPCR and immunoassays.
Main Results:
- Air infusion significantly increased WBC, C3a, thrombin-antithrombin (TAT), and altered ROTEM parameters.
- Lung C3a levels and pro-inflammatory cytokines (IL-1β, IL-6, IL-8, TNF) were significantly elevated in air-infused pigs.
- Complement C3 activation occurred without significant C5 activation.
Conclusions:
- Venous air embolism in pigs activates C3, triggering thromboinflammation via a C3-dependent mechanism.
- These findings support the in vivo relevance of C3 activation in air embolism.
- C3 inhibition could be a potential therapeutic strategy to mitigate air embolism-induced thromboinflammation.
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