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Blood, Vol. 95 No. 1 (January 1), 2000:
pp. 270-276
Human monocytes express functional receptors for granulocyte
colony- stimulating factor that mediate suppression of monokines
and interferon-
Eva-Maria Boneberg,
Lars Hareng,
Florian Gantner,
Albrecht Wendel, and
Thomas Hartung
From the University of Konstanz, Biochemical Pharmacology; Byk
Gulden Pharmaceuticals, Konstanz, Germany.
In a double-blind, placebo-controlled, randomized study, 10 healthy
men received either a single dose of 480 µg granulocyte colony-stimulating factor (G-CSF) or saline. Blood taken from the
volunteers was stimulated with 10 µg/mL endotoxin and released cytokines were measured by enzyme-linked immunosorbent assay. Expression of G-CSF receptors on leukocytes was examined by flow cytometry and reverse transcriptase-polymerase chain reaction. Functional activity of these receptors was tested by challenging isolated leukocyte populations to release cytokines with endotoxin in
the presence of G-CSF. The G-CSF treatment attenuated the release of
the proinflammatory cytokines tumor necrosis factor (TNF)- , interleukin (IL)-12, IL-1 , and interferon (IFN)- in ex vivo lipopolysaccharide (LPS)-stimulated whole blood. In blood from untreated volunteers the presence of G-CSF in vitro also attenuated the
LPS-stimulated release of these cytokines. G-CSF in vitro also
attenuated TNF- release from elutriation-purified monocytes. In the
presence of 10 ng/mL recombinant TNF-, the attenuation of
LPS-inducible IFN- release by G-CSF was blunted in whole blood. However, G-CSF had no such effect on IFN- release from isolated lymphocytes stimulated with anti-CD3 or a combination of TNF- and
IL-12. G-CSF receptor expression was detected in human neutrophils and
monocytes but not in lymphocytes by means of RT-PCR as well as flow
cytometry. These results indicate that G-CSF receptors expressed on
monocytes are functional in modulating monokine release. We conclude
that the attenuation of IFN- release from lymphocytes is not a
direct effect of G-CSF on these cells but is rather due to the
inhibition of monocytic IL-12 and TNF- release by G-CSF. (Blood.
2000;95:270-276)
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