Packed red blood cell (PRBC) transfusion has been invoked previously with i
mmunosuppression and increased infections, but it has now been demonstrated
that stored PRBCs (>14 days) can prime PMNs and provoke multiple organ fai
lure. Recently, the role of PMNs in the genesis of MOF has been extended to
their release of inflammatory cytokines, notably IL-1, IL-8, TNF alpha, an
d secretory phospholipase A(2) (sPLA(2)). We hypothesize that stored PRBCs
can act as a second event via stimulating the release of inflammatory cytok
ines from PMNs. Isolated human PMNs were incubated for 24 h in RPMI with ei
ther 20% fresh plasma or plasma from 42 day old PRBC (day of outdate) and r
elease of IL-8, IL-1 beta, TNF alpha, and sPLA(2) were measured. Plasma fro
m stored PRBCs contained small amounts of IL-8, sPLA(2), and TNF alpha (102
.1 +/- 5.6 pg/ml, 87.6 +/- 6.0 pg/ml and 9.7 +/- .7 pg/ml), Levels of IL-1
beta were below detection (<1 pg/ml). Day 42 PRBC plasma stimulated signifi
cant PMN release of both IL-8 and sPLA(2) as compared to both control and d
ay 0 plasma (*P < .05), but PRBC plasma did not stimulate PMN release of ei
ther IL-1 beta or TNF alpha. Transfused blood is emerging as an inflammator
y agent that is capable of producing PMN priming. In this study we have dem
onstrated that PRBC plasma selectively activates PMNs to release both IL-8
and sPLA(2). Thus, transfusion of PRBCs may represent a preventable inflamm
atory insult via modification of both blood banking and transfusion practic
es.