Platelet-activating factor mediated effects on human neutrophil function are inhibited by pertussis toxin.
Pretreatment of human neutrophils with pertussis toxin inhibits platelet-activating factor-mediated chemotaxis, superoxide generation, aggregation, and release of lysozyme. By contrast, superoxide generation observed in the presence of phorbol-12-myristate-13 acetate is unaffected. Our results suggest that a target protein for pertussis toxin, probably a GTP binding protein termed "Ni", is involved in the actions of platelet-activating factor on human neutrophils.
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D001427:Bacterial Toxins / Q000494:pharmacology*; D002449:Cell Aggregation / Q000187:drug effects; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D003571:Cytochalasin B / Q000378:metabolism; D019204:GTP-Binding Proteins / Q000378:metabolism; D006801:Humans; D009113:Muramidase / Q000378:metabolism; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D037342:Pertussis Toxin; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors*; D013481:Superoxides / Q000096:biosynthesis; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D010566:Virulence Factors, Bordetella
D001427:Bacterial Toxins; D010972:Platelet Activating Factor; D010566:Virulence Factors, Bordetella; D013481:Superoxides; D003571:Cytochalasin B; D037342:Pertussis Toxin; D009113:Muramidase; D019204:GTP-Binding Proteins; D013755:Tetradecanoylphorbol Acetate