Lipoxin A4 induces neutrophil-dependent cytotoxicity for human endothelial cells.
The authors have assessed the capacity of neutrophil granulocytes (PMN) to kill cultured human umbilical-vein endothelial cells (HUVEC) in vitro (as release of 51Cr) 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 51Cr 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.
Bratt
J
J
Department of Rheumatology, Karolinska Institute, Stockholm, Sweden.
Lerner
R
R
Ringertz
B
B
Palmblad
J
J
D002478:Cells, Cultured; D003470:Culture Media; D003602:Cytotoxicity, Immunologic / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000276:immunology; D006801:Humans; D006893:Hydroxyeicosatetraenoic Acids / Q000008:administration & dosage / Q000494:pharmacology*; D066298:In Vitro Techniques; D044045:Lipoxins; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects* / Q000276:immunology*
D003470:Culture Media; D006893:Hydroxyeicosatetraenoic Acids; D044045:Lipoxins; C040527:lipoxin A4; D009240:N-Formylmethionine Leucyl-Phenylalanine