Pro- and anti-inflammatory control of M-CSF-mediated macrophage differentiation

• Verfasst von: Popova, Anna [VerfasserIn]
• Verfasst von: Kzhyshkowska, Julia [VerfasserIn]
• Verfasst von: Nurgazieva, Dinara [VerfasserIn]
• Verfasst von: Goerdt, Sergij [VerfasserIn]
• Verfasst von: Gratchev, Alexei [VerfasserIn]
• Titel: Pro- and anti-inflammatory control of M-CSF-mediated macrophage differentiation
• Verf.angabe: Anna Popova, Julia Kzhyshkowska, Dinara Nurgazieva, Sergij Goerdt, Alexei Gratchev
• Jahr: 2011
• Umfang: 9 S.
• Fussnoten: Available online 15 June 2010 ; Gesehen am 10.01.2023
• Titel Quelle: Enthalten in: Immunobiology
• Ort Quelle: München : Elsevier, 1979
• Jahr Quelle: 2011
• Band/Heft Quelle: 216(2011), 1-2, Seite 164-172
• ISSN Quelle: 1878-3279
• DOI: doi:10.1016/j.imbio.2010.06.003
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Cell Culture Techniques
• Sach-SW: Cell Differentiation
• Sach-SW: Cell Separation
• Sach-SW: Cells, Cultured
• Sach-SW: Cytokines
• Sach-SW: Dexamethasone
• Sach-SW: Flow Cytometry
• Sach-SW: Gene Expression Regulation
• Sach-SW: Humans
• Sach-SW: Immune Tolerance
• Sach-SW: Inflammation
• Sach-SW: Macrophage Colony-Stimulating Factor
• Sach-SW: Macrophages
• Sach-SW: Receptor, Macrophage Colony-Stimulating Factor
• Sach-SW: Th1-Th2 Balance
• K10plus-PPN: 1830674927

Abstract

Macrophages play a key role in inflammation, tissue regeneration and tolerance. Their differentiation is regulated by tissue cells derived CSF-1 (M-CSF). The ability of macrophages to use autocrine M-CSF to control their differentiation and function remained controversial. In this study we investigated the regulation of M-CSF production by Th1 and Th2 cytokines (IFN-γ and IL-4) and tolerogenic stimuli - glucocorticoid dexamethasone in primary human monocyte derived macrophages. We show that IFN-γ and IL-4 efficiently induce production of M-CSF while glucocorticoid inhibited it in a dose dependent manner. Since glucocorticoid inhibits production of inflammatory cytokines we tested whether this effect is a result of inhibited M-CSF production. We showed that exogenous M-CSF rescues the ability of glucocorticoid-treated macrophages to produce TNF and IL-6 in response to LPS. These data indicate that glucocorticoid-treated macrophages retain the ability to respond to M-CSF. Analyzing the mechanism of this responsiveness, we showed that dexamethasone up-regulates surface expression of M-CSF receptor - CSF-1R. We conclude that the ability of macrophages to produce M-CSF secures macrophage differentiation under Th1 and Th2 conditions if tissue cells are unable to supply enough M-CSF. Increased surface expression of CSF-1R in tolerogenic conditions guarantees response to minute amounts of exogenous M-CSF.