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Modulation of granulocyte survival and programmed cell death by cytokines
and bacterial products
F Colotta, F Re, N Polentarutti, S Sozzani and A Mantovani
Istituto di Ricerche Farmacologiche Mario Negri, Centro Daniela e Catullo
Borgomainerio, Milano, Italy.
Mature circulating polymorphonuclear cells (PMN) have the shortest half-
life among leukocytes and undergo rapid programmed cell death in vitro. In
this study, we have examined the possibility that inflammatory signals
(cytokines and bacterial products) can regulate PMN survival. PMN in
culture were found to rapidly die, with percentages of survival at 24, 48,
72, and 96 hours of 97.3% +/- 1.9%, 36.8% +/- 5.3%, 14.5% +/- 3.1%, and
4.2% +/- 2.9%, respectively (mean +/- SE of 20 different donors). PMN
incubated with interleukin-1 beta (IL-1 beta), tumor necrosis factor,
granulocyte-macrophage colony-stimulating factor (CSF), granulocyte-CSF,
and interferon-gamma (IFN-gamma), but not with prototypic chemoattractants
(fMLP, recombinant C5a, and IL-8), showed a marked increase in survival,
with values ranging at 72 hours of incubation from 89.5% +/- 5.8% for IL-1
beta to 47.6% +/- 6.4% for IFN- gamma. The calculated half-life was 35
hours for untreated and 115 hours for IL-1-treated PMN. PMN activated with
lipopolysaccharide (LPS) or inactivated streptococci also showed a longer
survival compared with untreated cells (94.4% +/- 3.2% and 95.5% +/- 2.4%,
respectively, at 72 hours). PMN surviving in response to LPS or IL-1 beta
retained the capacity to produce superoxide anion when treated with phorbol
esters or fMLP. All inducers of PMN survival protect these cells from
programmed cell death because they reduced cells with morphologic features
of apoptosis and the fragmentation of DNA in multiples of 180 bp. Thus,
certain cytokines and bacterial products can prolong PMN survival by
interfering with the physiologic process of apoptosis. Prolongation of
survival may be important for the regulation of host resistance and
inflammation, and may represent a crucial permissive step for certain
cytokines and microbial products that activate gene expression and function
in PMN.
Volume 80,
Issue 8,
pp. 2012-2020,
10/15/1992
Copyright © 1992 by The American Society of Hematology
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