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Calcium mobilization, degranulation, arachidonic acid metabolism, and leukotriene B4 (LTB4) synthesis were examined as a function of the G-protein coupling state of seven receptors (leukotriene-B4 receptor [BLT1], leukotriene-B4 receptor-like [BLT2], interleukin-8 [IL-8] receptor [CXCR1], CXCR2, CCR2, CCR5, and CCR8) in human neutrophils. Stimulation of neutrophils with the BLT1 agonist, leukotriene B4, induced little calcium mobilization, degranulation, arachidonic acid metabolism, and leukotriene B4 synthesis when cells were pre-incubated with pertussis toxin (0.01 microg/mL), while stimulation with the BLT2 agonist, leukotriene B4, or the IL-8 agonist, human interleukin-8, induced only calcium mobilization and degranulation. Although the BLT1 antagonist, CAY10444, and the BLT2 antagonist, BKY-405, efficiently inhibited LTB4 production by BLT2 agonists, they had no effect on calcium mobilization or degranulation by BLT1 or IL-8 agonists. The CCR2 agonist, L-1781, and the CCR5 agonist, RANTES, induced only calcium mobilization and degranulation. These results indicate that BLT1-, BLT2-, CCR2- and CCR5-specific G-protein-coupled signal transduction systems exist in human neutrophils.Categories
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