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*
Clinical Services Program, SAIC Frederick, and
Data Management Services, National Cancer Institute, Frederick, MD 21702; and
Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892
Human exudative neutrophils have greatly increased stores of the
neutrophil chemoattractant IL-8 compared with peripheral blood cells,
but the mechanism for the increase is not defined. In this report, we
show that treatment of peripheral blood neutrophils with the
chemotactic peptide fMLP or with leukotriene B4 or
fibrinogen results in little increase in the production of IL-8 by
peripheral blood neutrophils. However, a chemotactically active dose of
fMLP (5 x 10-9 M) or leukotriene B4
(1 x 10-7 M) in the presence of a physiological
concentration (2 mg/ml) of fibrinogen results in a receptor-mediated,
pertussis toxin-sensitive, synergistic 30-fold increase in IL-8
synthesis. The levels of IL-8 attained are comparable to those observed
in exudative cells. Higher concentrations of fMLP (1 x
10-7 M) are associated with reduced IL-8 protein synthesis
without IL-8 degradation, indicating a sensitive regulatory mechanism
for IL-8 production. Treatment of neutrophils with fibrinogen and fMLP
resulted in minimal changes in the steady state levels of mRNA for
macrophage inflammatory protein-1
and -1
and monocyte
chemoattractant protein-1. In contrast, in the presence of
fibrinogen, the steady-state level of neutrophil IL-8 mRNA increased
8-fold with 5 x 10-9 M fMLP but was not decreased
with 1 x 10-7 M fMLP, suggesting that neutrophils
are specifically adapted to modulate neutrophil IL-8 synthesis through
transcriptional and posttranscriptional mechanisms. The data indicate
that fibrinogen can function not only as a substrate in the clotting
cascade, but also as an important effector during the evolution of the
innate immune response.
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