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Demonstration of reversible priming of human neutrophils using platelet-
activating factor
E Kitchen, AG Rossi, AM Condliffe, C Haslett and ER Chilvers
Department of Medicine (RIE), University of Edinburgh Medical School, Rayne
Laboratory, United Kingdom.
Exposure of neutrophils to agents such as lipopolysaccharide, tumor
necrosis factor-alpha (TNF-alpha), and the granulocyte-macrophage
colony-stimulating factor causes a major upregulation of subsequent
agonist-induced NADPH oxidase activation. This priming effect is a
prerequisite for neutrophil-mediated tissue damage and has been widely
considered to be an irreversible process. We have investigated the
potential for neutrophils to recover from a priming stimulus by studying
the effects of platelet-activating factor (PAF). PAF did not stimulate
respiratory burst activity directly, but caused a rapid (maximal at 10
minutes) and concentration-dependent (EC50 50.2 nmol/L) increase in
N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated superoxide anion
release. At time-points > 10 minutes, this priming effect spontaneously
declined, with return to basal levels of fMLP- stimulated superoxide anion
generation by 120 minutes. An identical priming time-course was observed
with N-methyl carbamyl PAF, a nonmetabolizable analogue of PAF, indicating
that the transient nature of PAF-induced priming was not secondary to PAF
metabolism. Two structurally diverse PAF receptor antagonists (UK-74,505
and WEB 2086), added 10 minutes after PAF addition, increased the rate of
decay of the priming effect. In contrast, TNF-alpha-induced priming, which
was of a similar magnitude to that observed for PAF, was slower to evolve
(maximal at 30 minutes) and remained constant for at least 120 minutes. The
reversible nature of PAF-induced priming was confirmed by demonstrating
that PAF-, but not TNF-alpha-, induced cell polarization (shape change) and
CD11b-dependent neutrophil binding of albumin-coated latex beads was also
transient, with return to basal, unstimulated levels by 120 minutes.
Furthermore, cells that had spontaneously deprimed following PAF exposure
retained their capacity to be fully reprimed by a subsequent addition of
either PAF or TNF-alpha. These data imply that neutrophil priming is not an
irreversible event: the demonstration of a cycle of complete priming,
depriming, and repriming offers the potential for functional recycling of
neutrophils at sites of inflammation.
Volume 88,
Issue 11,
pp. 4330-4337,
12/01/1996
Copyright © 1996 by The American Society of Hematology
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