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Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
Published on: April 6, 2017
Aggregating and prostanoid-releasing effects of platelet-activating factor and leukotrienes on human
Abstract:
Aggregating and prostanoid-releasing properties of the inflammatory mediators, platelet-activating factor (PAF) and leukotrienes B4, C4 and D4 were studied in human polymorphonuclear leukocytes (PMNL) and in human platelet-rich plasma. Leukotriene B4 (LTB4) and PAF both induced a reversible aggregation of human PMNL with concomitant stimulation of PGE2 formation, whereas LTC4 had no effect on human PMNL. Arachidonic acid (AA) caused an irreversible aggregation of PMNL which was accompanied by formation of both PGE2 and TXB2. Inhibition of TXB2 synthesis by indomethacin or by OKY-1581, a thromboxane synthetase inhibitor, had no effect on the PMNL aggregation induced by LTB4, PAF or AA. Leukotrienes B4, C4 and D4 caused neither aggregation nor TXB2 release in human platelet-rich plasma. PAF, on the other hand, induced a dose-dependent, reversible platelet aggregation which was not accompanied by TXB2 formation nor inhibited by OKY-1581. The present study indicates that in addition to inducing PMNL aggregation, LTB4 is capable of releasing arachidonate metabolites from human PMNL but not from human platelets. Also the responses of PMNL and platelets to PAF seem to differ as the PAF-induced PMNL aggregation was accompanied by increased prostanoid formation whereas the PAF-induced reversible platelet aggregation was obviously independent from arachidonate metabolism.
Insights
Platelet-activating factor (PAF) and leukotriene B4 (LTB4) induce human polymorphonuclear leukocyte (PMNL) aggregation and prostanoid release. PAF also causes platelet aggregation, but this response is independent of arachidonate metabolism.
Area of Science:
- Immunology
- Inflammation Research
- Cellular Signaling
Background:
- Platelet-activating factor (PAF) and leukotrienes (LTs) are key inflammatory mediators.
- Their roles in human polymorphonuclear leukocytes (PMNL) and platelets require further elucidation.
Purpose of the Study:
- To investigate the aggregating and prostanoid-releasing properties of PAF and LTB4, LTC4, LTD4.
- To compare the effects of these mediators on human PMNL and platelet-rich plasma.
Main Methods:
- Human PMNL and platelet-rich plasma were incubated with PAF, LTB4, LTC4, LTD4, and arachidonic acid (AA).
- Aggregation and prostanoid (PGE2, TXB2) formation were measured.
- Inhibition studies using indomethacin and OKY-1581 were performed.
Main Results:
- LTB4 and PAF induced reversible PMNL aggregation with PGE2 formation; LTC4 had no effect.
- AA caused irreversible PMNL aggregation with PGE2 and TXB2 formation.
- LTB4, LTC4, LTD4 did not affect platelets, while PAF induced reversible platelet aggregation independent of TXB2.
- Inhibitors of TXB2 synthesis did not affect PMNL aggregation.
Conclusions:
- LTB4 induces PMNL aggregation and releases arachidonate metabolites from PMNL, but not platelets.
- PAF induces PMNL aggregation with prostanoid release and platelet aggregation independent of arachidonate metabolism.
- PMNL and platelet responses to PAF differ significantly regarding arachidonate metabolism.
