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Expression of CD11b (MAC-1) and CD162 (PSGL-1) on monocytes is decreased under conditions of deep hypothermic
Stefanie Swoboda1, Joachim Gruettner2, Siegfried Lang3
1Pharmacy Department of the University Hospital of Heidelberg, Heidelberg, Germany.
Insights
Deep hypothermic circulatory arrest (DHCA) reduces inflammatory markers on monocytes. This study shows hypothermia decreases CD11b and CD162 expression, potentially mitigating inflammatory responses during cardiac surgery.
Area of Science:
- Cardiovascular Surgery
- Immunology
- Cell Biology
Background:
- Deep hypothermic circulatory arrest (DHCA) protects organs during complex cardiac surgeries.
- Leukocytes mediate inflammatory responses during ischemia, involving cell adhesion molecules.
- Temperature significantly impacts inflammatory cell activation, but its effect on leukocyte markers during DHCA is unknown.
Purpose of the Study:
- To investigate the effect of hypothermia on monocyte cell adhesion molecule expression under DHCA conditions.
- To assess changes in CD11b, CD54, and CD162 expression on monocytes at different temperatures.
Main Methods:
- Simulated DHCA conditions using blood samples from 11 healthy volunteers.
- Incubation at 36°C (normothermia) and 18°C (hypothermia) for 30 minutes.
- Flow cytometry analysis of monocyte surface markers (CD11b, CD54, CD162).
Main Results:
- Monocyte CD11b expression significantly decreased at 18°C compared to 36°C (P<0.001).
- Monocyte CD162 expression was significantly lower at 18°C than at 36°C (P<0.001).
- No significant difference in CD54 expression was observed between the two temperatures.
Conclusions:
- Deep hypothermia significantly reduces CD11b and CD162 expression on monocytes in a simulated DHCA model.
- This reduction may inhibit leukocyte-endothelial and leukocyte-platelet interactions.
- These findings suggest a potential beneficial anti-inflammatory mechanism of DHCA in reducing tissue damage.
Abstract:
Deep hypothermic circulatory arrest (DHCA) is a common technique used to protect vital organs during surgical interventions on the thoracic aorta or during surgery for complex congenital heart disease. Activated leukocytes are key mediators of inflammatory responses during ischemia. Intercellular crosstalk between leukocytes, platelets and endothelial cells is mediated by cell adhesion molecules. These molecules trigger complex cell-cell interaction mechanisms and initiate the release of proinflammatory molecules. One parameter that is known to have a significant impact on inflammatory cell activation and the production of proinflammatory markers is temperature. However, to the best of our knowledge, no data have yet been published on the effect of hypothermia on leukocyte surface markers during DHCA. Thus, the aim of the present study was to investigate the effect of hypothermia on the expression of cell adhesion molecules on monocytes under DHCA conditions in vitro. Blood samples collected from 11 healthy volunteers were incubated in a well-established model simulating circulatory arrest at 36°C and 18°C for 30 min. The expression of cluster of differentiation (CD) molecule 11B (CD11b), CD54 and CD162 on monocytes was measured as the mean fluorescence intensity (MFI) using flow cytometry. The expression level of CD11b on monocytes was significantly decreased following the incubation of the blood samples at 18°C compared with the level in blood samples incubated at 36°C (P<0.001). After 30 min of blood stasis in the circulatory arrest model, the expression level of CD162 on monocytes was significantly lower in the blood samples incubated at 18°C than in those incubated at 36°C (P<0.001). No association was identified between temperature and the surface expression of CD54 on monocytes following 30 min of stasis. These findings demonstrate that deep hypothermia decreases the expression of CD11b and CD162 on monocytes in an experimental setup simulating the conditions of DHCA. This may be the result of the inhibition of leukocyte-endothelial and leukocyte-platelet interactions, which may be a beneficial aspect of deep hypothermia that affects the inflammatory response and tissue damage during DHCA.
