[Tumor necrosis factor induced enhancement of neutrophil chemotaxis and adhesion through mediating of phospholipase A2 activation].
Recent studies indicate that phospholipase A2 (PLA2) derived lipid mediators regulate a number of neutrophil responses such as chemotaxis, adhesion and degranulation. Since tumor necrosis factor (TNF) is also a key mediator in neutrophil activation, it remains to be shown that PLA2 is involved in the process of TNF activation. Our results shown that TNF (100 ng/ml) given in vitro for 60 min, causes an obvious enhancement of neutrophil chemotaxis towards FMLP, and increased activity of adhesion to glass beads by stimulated release of TXB2 from PMN other than 6-keto-PGF1a. Similar neutrophil activation responses could also be promoted by in vitro addition of arachidonic acid (1 mumol/ml) for 60 min. It was further found that PLA2 inhibitor, 4-bromophencyl bromide (5 mumol/ml), greatly inhibite the TNF induced responces, while cycloxgenase inhibitor indomethathin (85 nmol/ml) was without effect on the activation of TNF. Those results indicated that PLA2 activation was involved in the TNF stimulated enhancement of neutrophil chemotaxis and adhesion.
Yan
G T
GT
Department of Biochemistry, Clinic Basic Institute of Medicine, Great Wall Hospital, Beijing.
Hao
X H
XH
Li
Z J
ZJ
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D002448:Cell Adhesion / Q000187:drug effects; D002634:Chemotaxis, Leukocyte / Q000187:drug effects*; D009504:Neutrophils / Q000378:metabolism; D010741:Phospholipases A / Q000378:metabolism*; D054467:Phospholipases A2; D051381:Rats; D017208:Rats, Wistar; D013929:Thromboxane B2 / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D014409:Tumor Necrosis Factor-alpha; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D010741:Phospholipases A; D054467:Phospholipases A2