Possible mechanisms of allogeneic blood transfusion-associated postoperative infection

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Four possible mechanisms have been reported to underlie the apparent association of allogeneic blood transfusion (ABT) with postoperative bacterial infection. These are (1) a transfusion-related immunomodulatory (TRIM) effect of ABT mediated by immunologically active allogeneic white blood cells (WBCs) that downregulate the recipient's immune function, thereby predisposing to infection; (2) a TRIM effect of ABT mediated by soluble biologic response modifiers released in a timedependent manner from WBC granules or membranes into the supernatant flud of red blood cells (RBCs) during storage; (3) a TRIM effect of ABT mediated by soluble HLA peptides that circulate in allogeneic plasma; and (4) a related non-TRIM effect of ABT, whereby ABT causes postoperative organ dysfunction that predisposes to infection. The available clinical studies examining the association of ABT with postoperative infection were not designed to specifically test 1 or more of these 4 hypotheses. Thus, it is difficult to make inferences from the published data about the specific mechanism(s) that may underlie the purported association of ABT with infection. To permit such inferences, future studies of the association of ABT with postoperative infection should consider 2 outcomes (ie, postoperative organ dysfunction in addition to postoperative infection), as well as 3 possible exposures (ie, allogeneic WBCs, soluble biologic response modifiers originating in WBC granules or membranes, and/or soluble HLA molecules circulating in allogeneic plasma).

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