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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Granulocyte colony-stimulating factor directly affects human monocytes and modulates cytokine secretion.

OBJECTIVE: Recent reports have indicated that monocytes express receptors for the granulocyte colony-stimulating factor (G-CSF). The direct effects of G-CSF on cytokine secretion in monocytes were examined. MATERIALS AND METHODS: A monocytic cell line NOMO-1 that secretes multiple cytokines upon stimulation with lipopolysaccharide (LPS) was used. Normal human monocytes were purified by negative selection using magnetic beads. Cells pretreated with or without G-CSF were stimulated with LPS, and the subsequent concentrations of cytokines and chemokines in supernatants were determined by sandwich enzyme-linked immunosorbent assay. RESULTS: NOMO-1 cells were found to express receptors for G-CSF. Although G-CSF stimulation did not induce cytokine secretion, pretreatment with G-CSF significantly attenuated LPS- stimulated secretion of the proinflammatory cytokines tumor necrosis factor-alpha and interleukin (IL)-12 in NOMO-1 cells. Simultaneously, however, G-CSF pretreatment apparently enhanced LPS- induced secretion of IL-10 and monocyte chemoattractant protein-1, whereas secretions of IL-1beta, IL-6, and IL-8 were unaffected. When normal human monocytes from healthy volunteers were similarly examined, marked individual variations in LPS-induced secretion of cytokines were observed. Although some exceptions exist, a similar tendency as to the effects of G-CSF treatment on cytokine secretions as that in NOMO-1 cells was observed in human monocytes. CONCLUSIONS: Our data suggest that G-CSF directly affects monocytes and modulates their cytokine secretion. NOMO-1 cells can provide an alternate model for in vitro culture of monocytes to investigate the effects of G-CSF on cytokine secretion by these cells.[1]


  1. Granulocyte colony-stimulating factor directly affects human monocytes and modulates cytokine secretion. Saito, M., Kiyokawa, N., Taguchi, T., Suzuki, K., Sekino, T., Mimori, K., Suzuki, T., Nakajima, H., Katagiri, Y.U., Fujimura, J., Fujita, H., Ishimoto, K., Yamashiro, Y., Fujimoto, J. Exp. Hematol. (2002) [Pubmed]
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