title: N-acetylcysteine attenuates TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression in human monocytes.
abstract: We have previously shown that tumor necrosis factor-alpha (TNF-alpha) reduces interleukin-4 (IL-4)-induced Fc epsilon RII expression in human monocytes. It has been shown that TNF-alpha activates nuclear transcriptional factors through the generation of reactive oxygen intermediates (ROIs), and antioxidant N-acetylcysteine (NAC) inhibits TNF-alpha-induced activation of nuclear transcriptional factors. Therefore, we hypothesized that TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression in monocytes might be mediated through the ROIs-activated mechanism. In the present study, to test our hypothesis, we examined the effect of NAC on TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression in human monocytes. NAC attenuated TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression by attenuating TNF-alpha-dependent reduction of Fc epsilon RII mRNA expression. Similarly, the structurally unrelated antioxidant, pyrrolidine dithiocarbamate (PDTC), also effectively attenuated this-reduction. These results indicate that an ROIs-activated and antioxidant-sensitive mechanism might be involved in TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression in monocytes.
authors.affiliation: First Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Hashimoto
authors.forename: Y
authors.initials: Y
authors.lastname: Gon
authors.forename: T
authors.initials: T
authors.lastname: Nakayama
authors.forename: S
authors.initials: S
authors.lastname: Yoshida
authors.forename: S
authors.initials: S
authors.lastname: Hayashi
authors.forename: S
authors.initials: S
authors.lastname: Maruoka
authors.forename: J
authors.initials: J
authors.lastname: Yodoi
authors.forename: T
authors.initials: T
authors.lastname: Horie
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology; D002478:Cells, Cultured; D016166:Free Radical Scavengers / Q000494:pharmacology*; D006801:Humans; D015847:Interleukin-4 / Q000276:immunology*; D009000:Monocytes / Q000187:drug effects* / Q000276:immunology; D011759:Pyrrolidines / Q000494:pharmacology; D017455:Receptors, IgE / Q000032:analysis* / Q000187:drug effects* / Q000235:genetics; D013859:Thiocarbamates / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects* / Q000276:immunology
chemical_list: D000975:Antioxidants; D016166:Free Radical Scavengers; D011759:Pyrrolidines; D017455:Receptors, IgE; D013859:Thiocarbamates; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4; C020972:pyrrolidine dithiocarbamic acid; D000111:Acetylcysteine