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Effect of ibuprofen and interleukin 2 on transfusion-induced suppression of cell-mediated immunity
1Department of Surgery, University of Utah Medical Center, Salt Lake City 84132.
Transfusion-induced immunosuppression has been associated with excessive production of prostaglandin E and decreased interleukin 2 (IL-2) production. In the present study, allogeneic blood-transfused mice were tested for cell-mediated immunity with the use of a delayed-type hypersensitivity assay. In vivo administration of a cyclo-oxygenase inhibitor, ibuprofen, and murine recombinant IL-2 was initiated on day 0 and continued daily throughout the delayed-type hypersensitivity assay. The results indicate that prostaglandin E may play a primary role in allogeneic blood transfusion-induced suppression, as manifest by normal responses in ibuprofen-treated mice. Supplementation of transfused mice with recombinant IL-2 also preserved immune response, indicating inadequate IL-2 production after transfusion, while receptor expression appears to remain intact.
Transfusion-induced immunosuppression has been associated with excessive production of prostaglandin E and decreased interleukin 2 (IL-2) production. In the present study, allogeneic blood-transfused mice were tested for cell-mediated immunity with the use of a delayed-type hypersensitivity assay. In vivo administration of a cyclo-oxygenase inhibitor, ibuprofen, and murine recombinant IL-2 was initiated on day 0 and continued daily throughout the delayed-type hypersensitivity assay. The results indicate that prostaglandin E may play a primary role in allogeneic blood transfusion-induced suppression, as manifest by normal responses in ibuprofen-treated mice. Supplementation of transfused mice with recombinant IL-2 also preserved immune response, indicating inadequate IL-2 production after transfusion, while receptor expression appears to remain intact.