Recently we have studied arachidonic acid metabolism in human mast cells and have shown that cells prelabeled with 3H-arachidonic acid display phospholipid remodeling (arachidonic acid is lost from phosphotidylcholine and phosphotidylinositol) and metabolize released arachidonic acid by both cyclooxygenase and lipoxygenase enzymes. The major cyclooxygenase metabolite produced by purified human lung mast cells is prostaglandin D2, the major lipoxygenase product produced by these cells is leukotriene C4, with smaller amounts of leukotriene B isomers and 5-hydroxyeicosatetranoic acid (5 HETE) also observed. While the human basophil is very similar to the mast cell in that it also contains significant amounts of histamine and generates large quantities of leukotriene C4 after activation, it is different in that it generates little or no prostaglandin D2. Both cell types apparently have the ability to secrete proteins with kininogenase and TAME (tosyl arginine methyl ester)-esterase enzymatic activities. Mast cells and basophils also differ in their response to pharmacologic agents. The human basophil responds to indomethacin and the lipoxygenase product 5 HPETE by increasing the release of both histamine and leukotriene C after antigen triggering; the mast cell does not. Incubation of the human basophil overnight in the presence of dexamethasone results in a marked reduction in the amount of histamine and leukotriene C4 released from these cells, while similar treatment of the human lung mast cells does not affect histamine release, prostaglandin D2 release or the release of slow-reacting substance of anaphylaxis.
|Original language||English (US)|
|Issue number||5 SUPPL.|
|State||Published - Jan 1 1985|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine
- Cardiology and Cardiovascular Medicine