Abstract
We have further investigated the role of arachidonic acid metabolism in the release of inflammatory mediators from human basophils. 5,8,11-Eicosatriynoic acid, which selectively inhibits the lipoxygenase pathway of arachidonic acid metabolism, caused a dose-dependent inhibition of histamine release from human basophils induced by several immunologic (i.e., antigen and anti-IgE) and nonimmunologic (i.e., formyl methionine-containing peptide and the Ca 2+ ionophore A23187) stimuli. In contrast, the nonsteroidal antiinflammatory drug, indomethacin, which blocks only the cyclooxygenase pathway of arachidonic acid metabolism, enhanced or had little effect on histamine release from basophils induced by the same stimuli. It appears that the product(s) of the arachidonic acid metabolism, generated via a lipoxygenase pathway, plays an essential role in the biochemical control of basophil activation and secretion, irrespective of the nature of the stimuli utilized.
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