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Activation of polymorphonuclear neutrophils by immune complex: possible involvement in development of transfusion‐related acute lung injury
Author(s) -
Nishimura M.,
Ishikawa Y.,
Satake M.
Publication year - 2004
Publication title -
transfusion medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.471
H-Index - 59
eISSN - 1365-3148
pISSN - 0958-7578
DOI - 10.1111/j.0958-7578.2004.00527.x
Subject(s) - immunology , transfusion related acute lung injury , immune system , human leukocyte antigen , tumor necrosis factor alpha , apoptosis , antiserum , receptor , medicine , antigen , biology , lung , biochemistry , pulmonary edema
summary. Transfusion‐related acute lung injury (TRALI) is a serious side‐effect of transfusion. We presumed that immune complex (IC)‐activated polymorphonuclear neutrophils (PMNs) are involved in the development of TRALI. The aim of this study is to examine the various effects of ICs on normal human PMNs. ICs used here were artificially formed by combining soluble human leucocyte antigen (HLA) class II‐positive serum and anti‐HLA class II antiserum. The abilities of ICs to trigger PMNs and induce the production of soluble mediators and the involvement of the Fc receptor (FcR) in the activation of PMNs by ICs were investigated. Moreover, the ability of the culture supernatant of PMNs incubated with ICs regarded to induce the apoptosis of lung microvascular endothelial (LME) cells was examined. The results proved that PMNs are triggered by ICs resulting in the acceleration of the production of tumour necrosis factor‐α (TNF‐α), perforin and Fas ligand, in which FcR on PMNs appears to be involved. Furthermore, the culture supernatants of PMNs cultured with ICs were revealed to induce the apoptosis of LME cells. In conclusion, the ICs used here were proved to induce PMNs to release cytotoxic factors upon activation. These results suggest that ICs are mediators of the development of TRALI.