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Lipoxin A4 Induces Neutrophil‐Dependent Cytotoxicity for Human Endothelial Cells
Author(s) -
BRATT J.,
LERNER R.,
RINGERTZ B.,
PALMBLAD J.
Publication year - 1994
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1994.tb03385.x
Subject(s) - umbilical vein , lipoxin , cytotoxicity , arachidonic acid , in vitro , chemistry , incubation , neutrophile , microbiology and biotechnology , calcium , endothelial stem cell , granulocyte , biochemistry , pharmacology , medicine , immunology , biology , receptor , organic chemistry , enzyme
The authors have assessed the capacity of neutrophil granulocytes (PMN) to kill cultured human umbilical–vein endothelial cells (HUVEC) in vitro (as release of 51 Cr) in response to the recently described double dioxygenation product of arachidonic acid, lipoxin A4 (LXA4). LXA4 conferred a marked cytotoxicity, whereas formyl–methionyl–leucyl–phenylalanine (fMLP) was less potent. The LXA4 and fMLP effects were dose dependent, with a maximum at 100 nM (which caused 2.7–and 2.3–fold increases of 51 Cr release, respectively, relative to buffer–treated controls). The LXA4 and fMLP responses increased with the PMN concentration, depended on the fetal calf serum concentration, incubation temperature and duration and the presence of calcium and magnesium ions.