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Staphylococcus albus ‐Induced Protein Kinase C Translocation in Human Neutrophils: The Effect of Opsonization, Cytochalasin B, Pertussis Toxin, Intra‐ and Extracellular Calcium, and R59022
Author(s) -
OBEL N.
Publication year - 1992
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.1365-3083.1992.tb02963.x
Subject(s) - protein kinase c , biology , diacylglycerol kinase , pertussis toxin , protein kinase a , microbiology and biotechnology , biochemistry , kinase , g protein , signal transduction
Membrane‐associated protein kinase C has been p[roposed to tbe essential in transmembrane signalling systems activating neutrophils. A main function of the neutrophil is phagocytosis and killing of microorganisms. Nevertheless, previously published reports mainly have described the effect of artificial or soluble stimulators upon neutrophil protein kinase C activity. Therefore membrane‐associated protein kinase C was studied in neutrophils stimulated by Staphylococceualbus. The bacteria were found to induce a striking increase in membrane associated protein kinase C, an effect which depended upon a previous opsonization of the bacteria. Cytochalasin B which inhibits phagocytosis, was shown to abrogate S. albus‐induced protein kinase C translocation. Chelation of intracellular calcium totally abolished S. albus‐induced protein kinases C translocation, a phenomenon that could not exclusively be ascribed to chelation of extracellularcalcium. The diacylglycerol kinase inhibitor R5902, which has been reported to increases endogeneous diacylglycerol accumulation, nearly doubled the effect of S. albus upon membrane associaed protein kinase C. Pertussis toxin in concentrations which completely inhibited fLMP‐induced superoxide generation did not affect S. albus‐induced protein kinase C translocation. It is the cell membrane, a phenomenon that reies upon enhanced diacylglycerol production and calcium transients and occurs independently of pertussis toxin‐inhibitable G‐proteins.