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European Journal of Cardio-Thoracic Surgery, Vol 10, 61-67, Copyright © 1996 by European Association for Cardio-thoracic Surgery

ARTICLES

An imbalance in T-helper cell subsets alters immune response after cardiac surgery

A Markewitz, E Faist, S Lang, L Hultner, C Weinhold and B Reichart
Department of Cardiac Surgery, University of Munich, Germany.

Growing evidence indicates that cell-mediated immunity is altered after cardiac surgery with cardiopulmonary bypass (CPB). The objective of this prospective randomized study was to investigate (1) if an imbalance in T-helper cell (TH) subsets, i.e. TH1/TH2, may be responsible for these alterations and (2) if they can be counteracted. Twenty patients formed control group A. Twenty group B patients received indomethacin and thymopentin for immunomodulation. In vitro tests included measurements of TH, interleukin (IL)-2 as a cytokine primarily produced by TH1 cells, and IL-6 as a cytokine primarily produced by TH2. Delayed-type hypersensitivity (DTH) skin response and specific antibody (AB) production were used as in vivo tests for TH1- and TH2-induced immune response, respectively. Postoperatively, group A patients showed a persistent, significant reduction of TH, IL-2 synthesis and DTH skin response as compared to baseline values, while IL-6 synthesis remained unaltered and AB production increased (P < 0.05). In group B patients no change in TH, IL-2 and IL-6 synthesis, or DTH skin response was observed (P < 0.05 vs A). Postoperative AB production increased significantly in group B. These results indicate a significant suppression of TH1-induced cell-mediated immune response following CPB, while TH2-induced response remains normal. A normal TH2 response may be helpful for recovery following cardiac surgery by cleaning the body of the byproducts of CPB. A suppression of TH1 response may gain clinical significance whenever a postoperative infection requires this response, but can be effectively counteracted by immunomodulatory intervention with indomethacin and thymopentin.

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