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Cardiopulmonary Bypass in a Mouse Model: A Novel Approach
Published on: September 22, 2017
Cardiopulmonary bypass induces release of soluble CD40 ligand
Lisa Nannizzi-Alaimo1, Mark H Rubenstein, Veronica L Alves
1COR Therapeutics, South San Francisco, California, USA.
Insights
Cardiopulmonary bypass (CPB) releases soluble CD40 ligand (sCD40L) from platelets, increasing its plasma concentration. This suggests platelet-derived sCD40L may contribute to CPB-associated thrombosis and inflammation.
Area of Science:
- Cardiovascular Surgery
- Hematology
- Immunology
Background:
- Cardiopulmonary bypass (CPB) is associated with platelet activation, thrombosis, and inflammation.
- CD40 ligand (CD40L) is present in platelets, and its soluble form (sCD40L) is released upon activation.
- Platelets are a primary source of sCD40L, a protein implicated in thrombosis and inflammation.
Purpose of the Study:
- To investigate whether soluble CD40 ligand (sCD40L) is released during cardiopulmonary bypass (CPB).
- To determine the source of sCD40L during CPB and its potential role in CPB-associated complications.
Main Methods:
- Blood samples were collected from patients undergoing CPB surgery.
- Plasma levels of sCD40L, interleukin-6, platelet factor 4, and beta-thromboglobulin were measured.
- Platelet CD40L content was analyzed before and after CPB.
Main Results:
- Plasma sCD40L levels significantly increased during and after CPB, peaking at 3.7-fold baseline 2 hours post-procedure.
- Platelet CD40L content decreased by 40% during CPB, indicating release from platelets.
- Levels of inflammatory marker interleukin-6 also increased during CPB.
Conclusions:
- CPB significantly increases plasma sCD40L concentrations.
- The decrease in platelet CD40L suggests platelets are the primary source of released sCD40L during CPB.
- Elevated sCD40L may contribute to the prothrombotic and inflammatory complications observed after CPB.
Background:
Cardiopulmonary bypass (CPB) is known to induce platelet activation, thrombosis, thrombocytopenia, and a systemic inflammatory response. It is known that CD40 ligand (CD40L) exists in platelets, that a soluble form of this protein (sCD40L) is released on platelet activation, that platelets are the primary source of sCD40L in blood, and that sCD40L is involved in thrombosis and inflammation. The present study was designed to determine whether sCD40L is released during CPB. Methods and Results- Blood was obtained from patients undergoing CPB-requiring surgery and analyzed for sCD40L, interleukin-6, and platelet factor 4 and beta-thromboglobulin (markers of platelet activation). Platelets were also isolated and analyzed for their levels of CD40L. Plasma levels of sCD40L increased >1.7-fold (from 0.29 to 0.51 ng/mL, P=0.001) within 1 hour on CPB and increased further to 3.7-fold (to 1.08 ng/mL, P=0.03) 2 hours after the procedure. Half of the released sCD40L was cleared in 2 hours, which allowed the sCD40L to return to approximately baseline levels 8 hours after the procedure. The platelet content of CD40L was decreased by 40% (2.675 to 1.64 ng/10(8) platelets, P=0.001) 1 hour after initiation of CPB and was similar to that observed for platelet factor 4 and beta-thromboglobulin. Interleukin-6, a marker of inflammation, also increased during CPB.
Conclusions:
The present study demonstrates that CPB causes an increase in the concentration of plasma sCD40L. The corresponding decrease in platelet CD40L suggests that this prothrombotic and proinflammatory protein was derived primarily from platelets and may contribute to the thrombotic and inflammatory complications associated with CPB.
