Introduction: Cardiopulmonary Bypass (CPB) triggers a robust systemic inflammatory response, marked by elevated serum levels of inflammatory interleukins, which negatively affect endothelial function and target organs. In response to this inflammatory insult, the body activates TregFoxP3 lymphocytes, which regulate inflammation by inhibiting pro-inflammatory interleukins and promoting restorative macrophage activity. Despite this regulatory mechanism, CPB-related inflammation in cardiac surgery is often associated with hemodynamic disturbances. The impact of TregFoxP3 cell levels—whether increased or depleted—on this relationship remains unclear and was therefore evaluated.
Method: This study aimed to assess the effect of CPB on the relationship between TregFoxP3 cells and inflammatory interleukins in patients undergoing cardiac surgery. Blood samples were collected before and after the CPB procedure to measure levels of IL-2, IL-6, IL-8, and TNF-α using chemiluminescence, and TregFoxP3 lymphocytes were quantified via flow cytometry.
Results: A total of 32 patients (mean age 65 ± 5 years), primarily undergoing cardiac valve replacement (80%), were included in the analysis. The average CPB duration was 80 ± 20 minutes, with aortic clamping lasting 60 ± 15 minutes. Following CPB, serum levels of IL-6, IL-8, TNF-α, and TregFoxP3 significantly increased, while IL-2 levels significantly decreased (p = 0.001). Baseline TregFoxP3 levels showed no correlation with inflammatory interleukins; however, post-CPB levels demonstrated a strong and significant positive correlation (r > 0.50, p = 0.001), except for IL-2, which showed a negative association.
Conclusion: The TregFoxP3 lymphocyte response is strongly and significantly correlated with inflammatory interleukin levels following cardiac surgery involving Cardiopulmonary Bypass, highlighting its potential role in modulating postoperative inflammation.