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Cardiopulmonary bypass during cardiac surgery modulates systemic inflammation by affecting different steps of the
Jan Rossaint1, Christian Berger, Hugo Van Aken
1Department of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, Münster, Germany.
Insights
Cardiopulmonary bypass (CPB) impairs selectin-mediated leukocyte rolling but enhances chemokine-induced recruitment. Understanding these mechanisms of systemic inflammation after CPB is crucial for developing new therapies.
Area of Science:
- Cardiovascular Surgery
- Immunology
- Cellular Biology
Background:
- Cardiopulmonary bypass (CPB) in cardiac surgery activates leukocytes, potentially causing organ dysfunction via increased leukocyte recruitment.
- Leukocyte extravasation involves capturing, rolling, adhesion, and transmigration, but CPB's molecular impact on these steps is unclear.
- Investigating the specific molecular mechanisms of leukocyte recruitment affected by CPB-induced systemic inflammation is essential.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying increased leukocyte recruitment during CPB.
- To determine which steps of the leukocyte recruitment cascade are altered by CPB-induced systemic inflammation.
Main Methods:
- Whole blood from healthy volunteers and cardiac surgery patients (CPB and off-pump coronary artery bypass - OPCAB) was analyzed.
- Flow chamber experiments, transmigration assays, and biochemical analyses were employed.
- Investigated effects on selectin- and chemokine-induced leukocyte recruitment.
Main Results:
- CPB abrogated selectin-induced slow leukocyte rolling on E-selectin/ICAM-1 and P-selectin/ICAM-1.
- Chemokine-induced leukocyte arrest and transmigration were significantly increased by CPB.
- Reduced phosphorylation of PLCγ2, Akt, and p38 MAP kinase impaired rolling; Mac-1 upregulation on neutrophils increased transmigration.
Conclusions:
- CPB disrupts intracellular signaling, abrogating selectin-mediated leukocyte rolling.
- Increased leukocyte recruitment post-CPB is primarily due to enhanced chemokine-induced arrest and transmigration.
- Understanding CPB-related inflammation mechanisms can guide therapeutic development for improved patient outcomes.
Background:
It is known that the use of a cardiopulmonary bypass (CPB) during cardiac surgery leads to leukocyte activation and may, among other causes, induce organ dysfunction due to increased leukocyte recruitment into different organs. Leukocyte extravasation occurs in a cascade-like fashion, including capturing, rolling, adhesion, and transmigration. However, the molecular mechanisms of increased leukocyte recruitment caused by CPB are not known. This clinical study was undertaken in order to investigate which steps of the leukocyte recruitment cascade are affected by the systemic inflammation during CPB.
Methods:
We investigated the effects of CPB on the different steps of the leukocyte recruitment cascade in whole blood from healthy volunteers (n = 9) and patients undergoing cardiac surgery with the use of cardiopulmonary bypass (n = 7) or in off-pump coronary artery bypass-technique (OPCAB, n = 9) by using flow chamber experiments, transmigration assays, and biochemical analysis.
Results:
CPB abrogated selectin-induced slow leukocyte rolling on E-selectin/ICAM-1 and P-selectin/ICAM-1. In contrast, chemokine-induced arrest and transmigration was significantly increased by CPB. Mechanistically, the abolishment of slow leukocyte rolling was due to disturbances in intracellular signaling with reduced phosphorylation of phospholipase C (PLC) γ2, Akt, and p38 MAP kinase. Furthermore, CPB induced an elevated transmigration which was caused by upregulation of Mac-1 on neutrophils.
Conclusion:
These data suggest that CPB abrogates selectin-mediated slow leukocyte rolling by disturbing intracellular signaling, but that the clinically observed increased leukocyte recruitment caused by CPB is due to increased chemokine-induced arrest and transmigration. A better understanding of the underlying molecular mechanisms causing systemic inflammation after CPB may aid in the development of new therapeutic approaches.
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