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Human GM-CSF primes neutrophils for enhanced oxidative metabolism in
response to the major physiological chemoattractants
RH Weisbart, L Kwan, DW Golde and JC Gasson
Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a T cell-
derived lymphokine which induces hematopoietic precursor cells to
proliferate in vitro and differentiate to neutrophils and macrophages.
GM-CSF also inhibits the motility of mature neutrophils (NIF-T activity),
and primes neutrophils to enhance oxidative metabolism in response to the
bacterial chemoattractant, N-formyl-methionyl-leucyl- phenylalanine
(f-MLP). The present study was designed to determine whether this
lymphokine also enhances neutrophil oxidative metabolism in response to the
other major physiological chemoattractants which include complement-derived
C5a, and the 5-lipoxygenation product of arachidonic acid, leukotriene B4
(LTB4). Superoxide anion production was measured as superoxide
dismutase-inhibitable cytochrome C reduction. Purified biosynthetic GM-CSF
enhanced superoxide anion production by neutrophils in response to f-MLP,
C5a desArg, and LTB4. In contrast to several other factors which prime
neutrophils, GM-CSF did not prime for an enhanced oxidative response to
phorbol myristate acetate (PMA). These results suggest that GM-CSF may be
an endogenous regulator of neutrophil inflammatory responses induced by the
major physiological chemoattractants.
Volume 69,
Issue 1,
pp. 18-21,
01/01/1987
Copyright © 1987 by The American Society of Hematology
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