title: Glucosamine improved atopic dermatitis-like skin lesions in NC/Nga mice by inhibition of Th2 cell development.
abstract: Dysregulated Th subset responses, characterized by Th2-dominant allergic inflammation, are thought to be central to the pathogenesis of atopic dermatitis (AD). Glucosamine has been shown to have immunosuppressive properties, but its effect on AD has not been examined. In this study, the immunoregulatory effects of glucosamine, using dermatophagoides farinae (Df)-induced AD-like skin lesions in NC/Nga mice, were investigated. The clinical scores were reduced significantly by the treatment with glucosamine at 10 and 20 mg/day. Histological analysis of the skin also revealed that treatment of glucosamine at 10 and 20 mg/day significantly reduced the inflammatory cellular infiltrate, including mast cells and eosinophils. The levels of serum IgE and Th2 cytokines in spleen cells were reduced, whereas no significant change was detected in IFN-γ, a Th1 cytokine. To determine the mechanism associated with inhibition of the Th2 immune response, the effects of glucosamine on the selective differentiation pathway of the Th subset in vitro was examined in NC/Nga mice. The results showed that glucosamine suppressed the differentiation of naïve CD4(+) T cells to Th2 cells in vitro. On the basis of in vivo and in vitro results of the NC/Nga mice, the immunobiological effects of glucosamine on peripheral blood mononuclear cells from patients with AD were examined. The production of Th2 cytokines, such as IL-4 and IL-5, was significantly decreased after in vitro administration of glucosamine, which suggest that glucosamine might be a useful immunomodulatory agent for the treatment of human AD.
authors.affiliation: Medical Science Research Center, Dongguk University Research Institute of Biotechnology, Goyang, South Korea.
authors.forename: C-H
authors.initials: CH
authors.lastname: Kim
authors.forename: K A
authors.initials: KA
authors.lastname: Cheong
authors.forename: C D
authors.initials: CD
authors.lastname: Park
authors.forename: A-Y
authors.initials: AY
authors.lastname: Lee
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D002454:Cell Differentiation / Q000187:drug effects / Q000276:immunology; D016207:Cytokines / Q000032:analysis; D003876:Dermatitis, Atopic / Q000188:drug therapy* / Q000276:immunology*; D050990:GATA3 Transcription Factor / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D005944:Glucosamine / Q000494:pharmacology*; D006651:Histocytochemistry; D007073:Immunoglobulin E / Q000097:blood; D007166:Immunosuppressive Agents; D008297:Male; D051379:Mice; D039981:Pyroglyphidae / Q000276:immunology; D012333:RNA, Messenger / Q000737:chemistry / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020825:T-Box Domain Proteins / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D018418:Th2 Cells / Q000187:drug effects* / Q000276:immunology; D000098815:T-bet Transcription Factor
chemical_list: D016207:Cytokines; D050990:GATA3 Transcription Factor; C494748:Gata3 protein, mouse; D007166:Immunosuppressive Agents; D012333:RNA, Messenger; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D007073:Immunoglobulin E; D005944:Glucosamine