Activation-dependent redistribution of cellular components alters susceptibility of human neutrophils to cross-linking agents.
Contrary to resting cells, neutrophils stimulated with concanavalin A resist inhibition by bifunctional N-hydroxysuccinimide esters. Con A prestimulated, cross-linker-treated cells released superoxide upon restimulation with PMA but did not respond to chemotactic peptides. Although rates of PMA-elicited NADPH oxidase activity were lowered by the treatment, the activation parameters, namely lag times of the reaction, were not altered. The protection by Con A against blockade by cross-linkers developed concomitantly to the activation of NADPH oxidase and indicated redistribution of cross-linker-susceptible cellular components responsible for activation with PMA. The identity of these components is discussed.
D003208:Concanavalin A / Q000494:pharmacology; D003432:Cross-Linking Reagents / Q000494:pharmacology*; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects; D008565:Membrane Proteins / Q000378:metabolism; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D019255:NADPH Oxidases; D009504:Neutrophils / Q000187:drug effects*; D013481:Superoxides / Q000096:biosynthesis; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D003432:Cross-Linking Reagents; D008565:Membrane Proteins; D003208:Concanavalin A; D013481:Superoxides; D009240:N-Formylmethionine Leucyl-Phenylalanine; D009247:NADH, NADPH Oxidoreductases; D019255:NADPH Oxidases; D013755:Tetradecanoylphorbol Acetate