Effects of protein kinase inhibitors on the stimulated neutrophil responses by degraded immunoglobulin G

Abstract

Effects of protein kinase C inhibitors, staurosporine and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride and protein tyrosine kinase inhibitors, genistein, tyrphostin and 2,5-dimethylcinnamate on the neutrophil responses stimulated by immunoglobulin G (IgG), complement C5a or platelet-activating factor were studied. After receptor binding, the role of protein kinase C and protein tyrosine kinase in the stimulation of neutrophil responses, superoxide production and lysosomal enzyme release in degraded IgG-activated neutrophils may be similar to chemoattractant-stimulated cells. In contrast to complement C5a or platelet-activating factor, protein tyrosine kinase appears to play an important role in the regulation of intracellular Ca2+ mobilization in neutrophils activated by degraded IgG rather than by protein kinase C.