Dopamine suppresses IL-12 p40 production by lipopolysaccharide-stimulated macrophages via a β-adrenoceptor-mediated mechanism

György Haskó, Csaba Szabó, Zoltán H. Németh, Edwin A. Deitch

    Research output: Contribution to journalArticle

    64 Scopus citations

    Abstract

    In this study, we examined the effect of dopamine on the production of IL-12 p40 by lipopolysaccharide (LPS)-stimulated J774.1 macrophages and mouse peritoneal macrophages. Treatment of J774.1 cells with dopamine (0.01-100 μM) decreased the release of IL-12 p40, in a concentration-dependent manner. The attenuating effect of dopamine on IL-12 p40 production appeared to be pretranslational, because dopamine decreased mRNA accumulation of IL-12 p40. The inhibitory effect of dopamine on IL-12 p40 production by J774.1 macrophages was not mediated by dopamine receptors, because dopamine receptor antagonists were unable to reverse the dopamine-induced suppression of IL-12 p40 production. Since the β-adrenoceptor antagonist propranolol completely prevented the inhibitory effect of dopamine on IL-12 p40 production, the suppressive effect of dopamine on IL-12 p40 production by J774.1 cells is mediated by β-adrenoceptors. In contrast to J774.1 cells, propranolol only partially reversed the inhibitory effect of dopamine on IL-12 production by peritoneal macrophages. Furthermore, dopamine stimulated the production of the anti-inflammatory cytokine IL-10 in both J774.1 cells and peritoneal macrophages. While the stimulatory effect of dopamine on IL-10 production by J774.1 cells was β-adrenoceptor-mediated, dopamine increased IL-10 production by peritoneal macrophages via both β-adrenoceptor-dependent and independent mechanisms. These results indicate that dopamine has multiple anti-inflammatory effects mediated by both β-adrenoceptor dependent and independent mechanisms.

    Original languageEnglish (US)
    Pages (from-to)34-39
    Number of pages6
    JournalJournal of Neuroimmunology
    Volume122
    Issue number1-2
    DOIs
    StatePublished - Jan 29 2002

    Keywords

    • Adrenergic
    • Endotoxin
    • Inflammation
    • Monocyte

    ASJC Scopus subject areas

    • Immunology and Allergy
    • Immunology
    • Neurology
    • Clinical Neurology

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