Ca2+ oscillations in neutrophils triggered by immune complexes result from Ca2+ influx.
Although the mechanisms of Ca2+ signalling in neutrophils by certain chemotactic agents have been well characterized, the signalling by immune complexes is poorly understood. Here we demonstrate that immune complex stimulation, acting via Fc receptors, leads to repetitive Ca2+ spiking in neutrophils. Although the initial Ca2+ rise was the result of release of Ca2+ from intracellular stores, subsequent repetitive Ca2+ spikes resulted from transmembrane influx, as they were prevented by removal of extracellular Ca2+ and were accompanied by Mn2+ influx. The transmembrane Ca2+ spikes induced dramatic neutrophil cell shape changes. The Ca2+ spiking phase was inhibited by a phospholipase C (PLC) inhibitor, U73122, and removal of immune complex, but not by cytochalasin B. It was concluded that Ca2+ spiking was dependent upon the initial release of Ca2+ from an intracellular Ca2+ store, and driven by continued binding of immune complex, which triggered pulsatile changes in transmembrane influx.
Davies
E V
EV
Department of Surgery, University of Wales College of Medicine, Cardiff, U.K.
Campbell
A K
AK
Hallett
M B
MB
D000936:Antigen-Antibody Complex / Q000276:immunology*; D002118:Calcium / Q000097:blood*; D002478:Cells, Cultured; D003600:Cytosol / Q000378:metabolism; D006801:Humans; D008345:Manganese / Q000097:blood; D009504:Neutrophils / Q000166:cytology / Q000276:immunology / Q000378:metabolism*; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000502:physiology
D000936:Antigen-Antibody Complex; D008345:Manganese; D010738:Type C Phospholipases; D002118:Calcium