Induction of interleukin-10 during extracorporeal circulation

Problem

The extracorporeal circulation (ECC) causes changes in cellular and cytokine pattern in addition to activation of complement system. These alterations result in a temporary depression of immunity and a perioperative susceptibility to infections. T lymphocytes required for both cell-mediated immune response and the production of antibody by B lymphocytes, are composed of two distinct subsets: Th1 and Th2 cells. Th1 cells produce IL-2 and interferon-γ and execute cell-mediated immune response; whereas Th2 cells produce IL-4, IL-5 and IL-10 and assist in antibody production for humoral immunity. While the influence of ECC in production and changes of several interleukins are known, it is still unclear if ECC induces IL-10 production and contribute to depression of immunity.

Material and methods

Twenty patients undergoing open heart operations without evidence of a concomitant malignant or immunologic disease; HIV and HBV seronegative were studied. EDTA-blood samples were drawn on six occasions. WBC was performed and FACS analysis enrolled. IL-10 was measured after cryopreservation of plasma by quantitative 'sandwich' enzyme immunoassay technique (sensitivity 1 pg/ml).

Results

The total leukocyte count decreases at the institution of ECC (3521 ± 871) and remains nearly unchanged through the aortic clamping time (3503 ± 1370). After removal of aortic clamp a significant leucocytosis occurs (8085 ± 3571), through 3.POD (10708 ± 3606). The phasic changes of leukocytes is mainly caused by identical course of neutrophils. IL-10 shows a monophasic course with a peak concomitant to removal of aortic clamp (45.5 ± 49.6 pg/ml) and falls to preoperative levels at 3.POD (3.2 ± 4.5 pg/ml).

Conclusion

The increased level of IL-10 during the ECC indicates an activation of Th2 cells. IL-10 inhibits the production of IFN-γ, induces the differentiation of Th2 cells from uncommitted T cells. The inhibitory effect of IL-10 on Th1 cell differentiation causes a further depression of cell-mediated immunity during the early postoperative phase.