Activation of human neutrophils by the air pollutant sodium sulfite (Na2SO3): Comparison with immature promyelocytic HL-60 and DMSO-differentiated HL-60 cells reveals that Na2SO3 is a neutrophil but not a HL-60 cell agonist
M. Pelletier et al., Activation of human neutrophils by the air pollutant sodium sulfite (Na2SO3): Comparison with immature promyelocytic HL-60 and DMSO-differentiated HL-60 cells reveals that Na2SO3 is a neutrophil but not a HL-60 cell agonist, CLIN IMMUNO, 96(2), 2000, pp. 131-139
Sulfite exposure can induce inflammatory responses characterized by an infl
ux of neutrophils into the airways leading to lung malfunctions. Studies fo
cusing on sodium sulfite (Na2SO3)/neutrophil interactions have shown that t
his chemical possesses proinflammatory properties based on its ability to i
nduce a respiratory burst. Information regarding how this chemical could al
ter other neutrophil responses/functions as well as its role on immature pr
omyelocytic cells is currently lacking in the literature. In this study, we
report that Na2SO3 can induce tyrosine phosphorylation events in human neu
trophils but not in both HL-60 and HL-60 + DMSO. As a positive control, GMC
SF was found to induce tyrosine phosphorylation of a particular protein of
120-130 kDa in both HL-60 and HL-60 + DMSO cells testifying that these cell
s were responsive. In addition, we report that Na2SO3 does not alter neutro
phil phagocytosis and that this chemical increases the release of the proin
flammatory cytokine IL-8 but not TNF-alpha. Paradoxically, we found that Na
2SO3 acts as a potent inhibitor of de novo neutrophil protein synthesis in
a concentration-dependent fashion (0.1, 1, or 10 mM) as assessed by SDS-PAG
E from metabolically [S-35]-labeled cells. In contrast to mature neutrophil
s, we found that Na2SO3 does not modulate de novo protein synthesis in HL-6
0 cells treated with low concentrations (0.1 or 1 mM) and that this polluta
nt was toxic at 10 mM: as judged by a drastic decrease of total protein con
tent stained with Coomassie blue. We conclude that Na2SO3 can activate huma
n neutrophils and that its proinflammatory potential is further supported b
y its ability to increase IL-8 production. In addition, our results clearly
indicate that HL-60 and HL-60 + DMSO respond differently than mature human
neutrophils to the inflammatory pollutant Na2SO3. Extrapolation of data ob
tained with HL-60 (and/or HL-60 + DMSO) to neutrophils should be taken with
caution. Our data obtained with Na2SO3 are an example. (C) 2000 Academic P
ress.