POSSIBLE ROLE OF ARACHIDONIC-ACID IN HUMAN NEUTROPHIL AGGREGATION AND DEGRANULATION

  • 1 January 1979
    • journal article
    • research article
    • Vol. 96  (3) , 799-809
Abstract
Chemotactic factors stimulate neutrophils to aggregate, and in presence of cytochalasin B, to degranulate. Arachidonic acid also stimulates human neutrophils to aggregate but does not stimulate cytochalasin B-treated or untreated cells to degranulate. The effect of 3 blockers of arachidonic acid metabolism on these cellular responses was examined. The arachidonic acid analog 5,8,11,14-eicosatetraynoic acid and indomethacin, but not aspirin, inhibited the arachidonic acid-induced aggregation response and degranulation responses evoked by C5a [fragment a of complement component 5] or a synthetic oligopeptide chemotactic factor. Arachidonic acid may be a precursor of bioactive metabolites that stimulate aggregation and foster neutrophil degranulation responses. These metabolites may be neutrophil function mediators. Agents that block their formation may thereby inhibit aggregation and degranulation.