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- W2526202021 abstract "During inflammation polymorphonuclearcells (PMNs) are exposed to agonistic stimuli including activated complement, kallikrein, arachidonic acid metabolites, monokines, and platelet-activating factor (PAF). We report that PAF not only directly activates PMNs but in miniscule quantities (1012 mol/i) “primes” them as well, that is, permits PMNs to respond to subsequent stimuli that would be otherwise ineffectual. PAF priming of responses including superoxide generation. elastase release. and aggregation is time dependent and is maximal within five minutes. PAF need not be present during the subsequent exhibition of PMN agonists. but priming is inhibited by cold and is also inhibited by the PAF receptor antagonists BN 52021 . 1-652. and kadsurenone. An intact PAF molecule is required because lyso-PAF and methoxy-PAF do not prime PMN responses. PAF priming is associated with both enhanced" @default.
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- W2526202021 date "2016-01-01" @default.
- W2526202021 modified "2023-09-26" @default.
- W2526202021 title "Factor Primes Neutrophil Responses to Agonists: Role in Promoting Neutrophil-Mediated Endothelial Damage" @default.
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