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Erythrocytes increase leukotriene C 4 release from human eosinophils: characterization and examination of possible mechanisms
Author(s) -
Raible Donald G.
Publication year - 1994
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.56.1.65
Subject(s) - eosinophil , leukotriene c4 , leukotriene , immunology , basophil , biology , calcium , pertussis toxin , immunoglobulin e , chemistry , antibody , biochemistry , receptor , asthma , g protein , organic chemistry
There has been considerable interest in the role of eosinophils in the pathogenesis of asthma and allergic diseases. While examining the conditions necessary for the release of leukotriene C 4 (LTC 4 ) from human eosinophils activated by immunoglobulin G‐Sepharose (IgG‐Seph), we observed that red blood cells (RBCs) potentiated eosinophil LTC 4 release. The time course of IgG‐Seph‐stimulated LTC 4 release was prolonged in the presence of RBCs. After 45 min of incubation, eosinophils without RBCs released 0.95 ± 0.11 ng/10 6 cells, and those with RBCs released 3.69 ± 0.67 ng/10 6 cells. Control experiments indicated that the effect was not due to platelet contamination of the RBCs and could not be reproduced with RBC supernatants or RBC membrane ghosts. An interesting characteristic of this interaction was that the eosinophils and RBCs had to be in close contact for the enhancement to occur. We also observed that at low calcium concentrations (0.6 mM), the eosinophils had to be primed with fMLP for the RBC effect to occur, but priming was not required at higher calcium concentrations. Several possible mechanisms that would explain the RBC effect on eosinophil LTC 4 release were examined: (1) RBCs block the metabolism of LTC 4 ; (2) RBCs protect the eosinophils from oxidative damage; (3) RBCs provide a substrate (or enzyme) that allows increased eosinophil LTC 4 production. These mechanisms failed to explain our observation that erythrocytes enhance eosinophil LTC 4 release, however, suggesting that alternative mechanisms are responsible for this effect J. Leukoc. Biol. 56: 65–73; 1994.