Premium
HOCI production by human neutrophils activated by surface‐associated IgG: Requirement for influx of extracellular calcium
Author(s) -
Blackburn Warren D.,
Chatham W. Winn
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.55.6.793
Subject(s) - egta , extracellular , calcium , biology , biochemistry , granule (geology) , pertussis toxin , lactoferrin , microbiology and biotechnology , chemistry , g protein , signal transduction , paleontology , organic chemistry
Abstract Neutrophils produce large quantities of HOCI when stimulated by surface‐associated immunoglobulin G, a result not seen when neutrophils are stimulated with soluble complexes of IgG. Compared with unactivated cells or cells stimulated with soluble aggregates of IgG, a significant influx of extracellular 45 Ca 2+ was observed in cells activated by surface‐associated IgG. Removal of extracellular calcium with EGTA almost completely blocked HOCI production. Similarly, treatment of neutrophils with lanthanum, which has been shown to interfere with calcium channels, also effectively blocked HOCI production. These results were not secondary to an overall decrease in activation, as superoxide production and release of the specific granule protein lactoferrin and the azurophilic granule protein myeloperoxidase were not significantly altered by lanthanum or EGTA. Production of H 2 O 2 , the precursor of HOCI, was similarly decreased by both EGTA and lanthanum. Induction of extracellular calcium influx with a calcium ionophore in the presence of soluble aggregates of IgG resulted in HOCI production. Production of HOCI is not sensitive to inhibition by pretreatment of cells with pertussis toxin. These observations indicate that the differences in the biological responses of human neutrophils to surface‐associated IgG compared with soluble aggregates of IgG are associated with differing signaling events, including influx of extracellular calcium. J. Leukoc. Biol . 55: 793–797; 1994.