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Influence of Platelet Activating Factor and a Nonmetabolizable Analogue on Superoxide Production by Bone Marrow Derived Macrophages
Author(s) -
Storch J.,
Ferber E.,
Munder P.G.
Publication year - 1988
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.44.5.385
Subject(s) - reprint , superoxide , planck , the republic , production (economics) , bone marrow , biology , library science , physics , immunology , computer science , theology , philosophy , biochemistry , economics , enzyme , macroeconomics , quantum mechanics , astronomy
Serum‐free cultured macrophages could be stimulated for lucigenin‐dependent chemiluminescence by platelet activating factor (PAF) and phorbol myristate acetate (PMA). Stimulation with PMA resulted in a desensitization against PAF, whereas prestimulation with PAF had no influence on a following response caused by PMA. The PAF analogue, 1‐O‐octadecyl‐2‐O‐methyl‐ rac ‐glycero‐3‐phosphocholine (Et‐18‐OCH 3 ), did not induce chemiluminescence by itself and desensitized the cells against PAF, like substimulating concentrations of PAF. PAF and PMA responsiveness was rapidly modulated in a similar manner during adherence of the cells to polystyrene tubes. At higher concentrations, Et‐18‐OCH 3 as well as lysophosphatidylcholines potentiated PMA‐induced chemiluminescence. The PAF analogue was most effective. Although PMA‐induced chemiluminescence was stimulated at least 5‐fold by Et‐18‐OCH 3 , this compound Increased the PMA‐induced activation of protein kinase C only 1.39‐fold. The priming effect of Et‐18‐OCH 3 was not reduced in the absence of extracellular Ca 2+ and after cell membrane depolarisation.