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Prolongation of survival of human polymorphonuclear neutrophils by
granulocyte-macrophage colony-stimulating factor is caused by inhibition of
programmed cell death
MA Brach, S deVos, HJ Gruss and F Herrmann
Department of Internal Medicine 1, University of Freiburg Medical Center,
Germany.
In the absence of appropriate stimuli, polymorphonuclear neutrophils (PMN)
undergo programmed cell death (PCD), also termed apoptosis. We show that
granulocyte-macrophage colony-stimulating factor (GM-CSF), but not the
chemotactic factors formyl-methionyl-leucyl-phenylalanine (FMLP),
recombinant human (rh) C5a, transforming growth factor (TGF)- beta, and
interleukin-8 (IL-8), or other cytokines including IL-3, IL- 4, IL-6, and
G-CSF, maintains viability of PMN in culture by preventing these cells from
undergoing PCD. Prevention from PCD by GM-CSF was associated with induction
of RNA and protein synthesis in PMN. Inhibition of RNA and protein
synthesis by actinomycin-D and cycloheximide impeded the protection of
apoptosis by GM-CSF. Similarly, neutralization of GM-CSF biologic activity
by a specific antiserum abrogated GM-CSF-mediated inhibition of PCD.
Volume 80,
Issue 11,
pp. 2920-2924,
12/01/1992
Copyright © 1992 by The American Society of Hematology
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