Effect of leukotriene B4, prostaglandin E2 and arachidonic acid on cytosolic‐free calcium in human neutrophils

PD Lew, JM Dayer, CB Wollheim, T Pozzan - FEBS letters, 1984 - Wiley Online Library
PD Lew, JM Dayer, CB Wollheim, T Pozzan
FEBS letters, 1984Wiley Online Library
Changes in cytosolic free calcium [Ca2+] i and release of beta‐glucuronidase in response to
leukotriene B4 (LTB4) were measured in intact neutrophils loaded with the fluorescent Ca2+
indicator, quin 2. LTB4 (10− 10 M or higher) caused a rapid rise in [Ca2+] i due to influx from
the extracellular medium and release from intracellular pools as well as enzyme release.
PGE2 (3 μM) did not alter [Ca2+] i whereas arachidonic acid (10 μM) raised [Ca2+] i.
Pretreatment of cells with the chemotactic peptide FMLP inhibited the subsequent rise of …
Changes in cytosolic free calcium [Ca2+]i and release of beta‐glucuronidase in response to leukotriene B4 (LTB4) were measured in intact neutrophils loaded with the fluorescent Ca2+ indicator, quin 2. LTB4 (10−10 M or higher) caused a rapid rise in [Ca2+]i due to influx from the extracellular medium and release from intracellular pools as well as enzyme release. PGE2 (3 μM) did not alter [Ca2+]i whereas arachidonic acid (10 μM) raised [Ca2+]i. Pretreatment of cells with the chemotactic peptide FMLP inhibited the subsequent rise of [Ca2+]i induced by LTB4. Since chemotactic peptides activate the lipoxygenase pathway of arachidonic acid metabolism, it may be speculated that endogenous LTB4 generation is involved in neutrophil activation.
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