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Published on: March 23, 2018
Successful restoration of cell-mediated immune response after cardiopulmonary bypass by immunomodulation
1Department of Cardiac Surgery, University of Munich, Germany.
Insights
Cardiopulmonary bypass suppresses immune response by decreasing T cells and interleukin-2. Combined indomethacin and thymopentin therapy effectively counteracted these immunosuppressive effects, restoring immune function.
Area of Science:
- Immunology
- Cardiovascular Surgery
- Pharmacology
Background:
- Cardiopulmonary bypass (CPB) is known to induce significant immunosuppression.
- The specific mechanisms and T-lymphocyte alterations following CPB require further elucidation.
- Postoperative immune dysfunction can increase the risk of complications.
Purpose of the Study:
- To quantify the immunosuppressive effects of CPB.
- To identify the underlying mechanisms of postoperative immunosuppression.
- To evaluate an immunomodulatory intervention for counteracting CPB-induced immune suppression.
Main Methods:
- Prospective randomized trial involving 60 patients undergoing CPB.
- In vitro and in vivo immunological assays including T-cell subset analysis, cytokine synthesis, and skin antigen testing.
- Intervention groups received indomethacin alone, or indomethacin combined with thymopentin, versus a control group.
Main Results:
- CPB decreased CD4+ T cells and interleukin-2 receptor expression, while increasing CD8+ T cells and monocytes.
- Reduced interleukin-1, interleukin-2, and gamma-interferon synthesis were observed, indicating impaired cell-mediated immunity.
- The combined indomethacin and thymopentin regimen successfully restored immune parameters, unlike indomethacin alone.
Conclusions:
- CPB significantly downregulates cell-mediated immune responses.
- Combined immunomodulatory therapy with indomethacin and thymopentin effectively counteracts CPB-induced immunosuppression.
- This therapy protects human lymphocytic interleukin-2 synthesis, a key immune regulatory mechanism.
Abstract:
The objectives of this prospective randomized trial were to quantify immunosuppressive effects of cardiopulmonary bypass, to identify mechanisms responsible for postoperative immunosuppression, and to investigate the effects of immunomodulatory intervention on these mechanisms. Sixty patients were studied after cardiopulmonary bypass. Immunomodulatory therapy consisted of the cyclooxygenase inhibitor indomethacin, which blocks the downregulating agent prostaglandin E2, and thymopentin, which enhances T-lymphocytic activity. Twenty patients each received indomethacin either alone or combined with thymopentin. Twenty patients served as the control population. Our in vitro studies showed a decrease of CD4+ helper/inducer T cells and interleukin-2 receptor expression on T lymphocytes, while CD8+ suppressor/cytotoxic T cells and monocytes increased. Additionally, a depression of interleukin-1 and interleukin-2 synthesis as well as concurrent low gamma-interferon serum concentrations could be documented. These results indicate a downregulation of cell-mediated immune response. As an in vivo correlate of the immunomechanistic alterations, patients demonstrated an impaired delayed-type hypersensitivity response to an antigen skin test battery. These changes in immunoreactivity could be successfully counteracted by the combined immunomodulatory regimen, whereas sole indomethacin treatment could only partially restore depressed host defense parameters. With this study we could demonstrate for the first time that human lymphocytic interleukin-2 synthesis, which represents the key event among forward regulatory immune mechanisms, can be protected via in vivo immunoaugmentatory therapy and that this therapy can successfully counteract immunosuppressive effects of cardiopulmonary bypass.
