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Reproduction of transfusion-related acute lung injury in an ex vivo lung
model [see comments]
W Seeger, U Schneider, B Kreusler, E von Witzleben, D Walmrath, F Grimminger and J Neppert
Department of Internal Medicine, Justus-Liebig-University, Giessen, FRG.
Leukoagglutinins are implicated in transfusion-related acute lung injury
(TRALI). In the present study, severe lung vascular leakage was reproduced
by application of a leukoagglutinating antibody of anti-5b specificity in
an ex vivo lung model. The antibody originated from a multiparous
donor-plasma, observed to cause noncardiogenic edema during transfusion
therapy. Heated full plasma (anti-5b-titer 1/128) or purified
immunoglobulin G fraction was used for the studies. Ex vivo isolated rabbit
lungs were perfused with albumin buffer, and human granulocytes (PMN) were
admixed to the recirculating perfusate. In presence of anti-5b antibody
plus 5b-positive PMN plus rabbit plasma as complement-source, severe lung
edema occurred after a latent period of 3 to 6 hours. Pulmonary artery
pressure was only transiently and moderately increased, and the leakage
reaction could be traced back to a several-fold increase in lung vascular
permeability. In contrast, no vascular leakage was noted in lungs perfused
in the absence of anti-5b antibody, PMN, or rabbit plasma. Moreover, no
permeability increase occurred on use of 5b-negative PMN. This reproduction
of TRALI in an ex vivo lung model corroborates the role of
leukoagglutinating antibodies in initiating PMN-dependent respiratory
distress and suggests a contribution of concomitant complement activation.
Volume 76,
Issue 7,
pp. 1438-1444,
10/01/1990
Copyright © 1990 by The American Society of Hematology
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