title: Immunosuppressive effects of glucosamine.
abstract: Glucosamine is a naturally occurring derivative of glucose and is an essential component of glycoproteins and proteoglycans, important constituents of many eukaryotic proteins. In cells, glucosamine is produced enzymatically by the amidation of glucose 6-phosphate and can then be further modified by acetylation to result in N-acetylglucosamine. Commercially, glucosamine is sold over-the-counter to relieve arthritis. Although there is evidence in favor of the beneficial effects of glucosamine, the mechanism is unknown. Our data demonstrate that glucosamine suppresses the activation of T-lymphoblasts and dendritic cells in vitro as well as allogeneic mixed leukocyte reactivity in a dose-dependent manner. There was no inherent cellular toxicity involved in the inhibition, and the activity was not reproducible with other amine sugars. More importantly, glucosamine administration prolonged allogeneic cardiac allograft survival in vivo. We conclude that, despite its documented effects on insulin sensitivity, glucosamine possesses immunosuppressive activity and could be beneficial as an immunosuppressive agent.
authors.affiliation: Department of Surgery, T. E. Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
authors.forename: Linlin
authors.initials: L
authors.lastname: Ma
authors.forename: William A
authors.initials: WA
authors.lastname: Rudert
authors.forename: Jo
authors.initials: J
authors.lastname: Harnaha
authors.forename: Marietta
authors.initials: M
authors.lastname: Wright
authors.forename: Jennifer
authors.initials: J
authors.lastname: Machen
authors.forename: Robert
authors.initials: R
authors.lastname: Lakomy
authors.forename: Shiguang
authors.initials: S
authors.lastname: Qian
authors.forename: Lina
authors.initials: L
authors.lastname: Lu
authors.forename: Paul D
authors.initials: PD
authors.lastname: Robbins
authors.forename: Massimo
authors.initials: M
authors.lastname: Trucco
authors.forename: Nick
authors.initials: N
authors.lastname: Giannoukakis
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D016572:Cyclosporine / Q000627:therapeutic use; D004268:DNA-Binding Proteins / Q000378:metabolism; D003713:Dendritic Cells / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005434:Flow Cytometry; D005944:Glucosamine / Q000378:metabolism / Q000627:therapeutic use*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D019169:Jurkat Cells; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D050778:NFATC Transcription Factors; D009687:Nuclear Proteins; D016559:Tacrolimus / Q000627:therapeutic use; D013997:Time Factors; D014157:Transcription Factors / Q000378:metabolism; D023001:Transplantation Tolerance; D001616:beta-Galactosidase / Q000378:metabolism
chemical_list: D004268:DNA-Binding Proteins; D007166:Immunosuppressive Agents; D050778:NFATC Transcription Factors; D009687:Nuclear Proteins; D014157:Transcription Factors; D016572:Cyclosporine; D000255:Adenosine Triphosphate; D001616:beta-Galactosidase; D005944:Glucosamine; D016559:Tacrolimus