English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Leukoagglutinating antibodies have been implicated in the development of transfusion-related acute lung injury. In the present study, human neutrophil leukotriene generation was provoked by an anti-5b immunoglobulin G, isolated from a multiparous donor plasma that caused noncardiogenic lung edema during transfusion therapy. In 5b-positive polymorphonuclear neutrophils (PMNs), the antibody stimulated marked arachidonic acid metabolism, dependent on the presence of plasma as the complement source. Quantity and profile of lipid mediators (leukotriene B4 and its omega-oxidation products, 5-hydroxyeicosatetraenoic acid, and nonenzymatic hydrolysis products of leukotriene A4) corresponded to those repeatedly described after PMN in vitro stimulation with the artificial calcium ionophore A23187. Anti-5b challenge of PMNs sequestered in the microvasculature of perfused rabbit lungs did, however, induce a markedly modified metabolite profile. Nonenzymatic hydrolysis products of leukotriene A4 were not detected, and 5-hydroxyeicosatetraenoic acid was markedly reduced. In contrast, cysteinyl leukotrienes were measured as predominant compounds, with rapid appearance of leukotriene C4 and more protracted generation of leukotriene E4. Leukotriene B4 and its omega-oxidation products were released with similar kinetics, but in lower amounts, as compared with the isolated PMN stimulation. Anti-5b challenge of PMNs coincubated with pulmonary artery endothelial cells in vitro, but not stimulation of either cell type alone, provoked marked generation of cysteinyl leukotrienes. These findings suggest modulation of PMN 5-lipoxygenase metabolism in favor of leukotriene A4 transfer to adjacent acceptor cells with subsequent enzymatic conversion to cysteinyl leukotrienes under conditions of lung vascular sequestration. Endothelial cells appear to serve as predominant cooperative cells under circumstances of blood-free lung perfusion. PMN-related transcellular eicosanoid synthesis may be involved in the pathogenesis of transfusion-evoked acute lung injury.

circulation research

Human leukoagglutinating antibody evokes cooperative leukotriene synthesis in pulmonary microvasculature. Model of transfusion-related acute lung injury.