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Immunosuppressive effects of glucosamine

Academic Article
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Overview

authors

  • Ma, L. L.
  • Rudert, W. A.
  • Harnaha, J.
  • Wright, M.
  • Machen, J.
  • Lakomy, R.
  • Qian, S. G.
  • Lu, L. N.
  • Robbins, Paul D.
  • Trucco, M.
  • Giannoukakis, N.

publication date

  • October 2002

journal

  • Journal of Biological Chemistry  Journal

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.

subject areas

  • Adenosine Triphosphate
  • Animals
  • Cyclosporine
  • DNA-Binding Proteins
  • Dendritic Cells
  • Dose-Response Relationship, Drug
  • Flow Cytometry
  • Glucosamine
  • Humans
  • Immunosuppressive Agents
  • Jurkat Cells
  • Mice
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • NFATC Transcription Factors
  • Nuclear Proteins
  • Tacrolimus
  • Time Factors
  • Transcription Factors
  • Transplantation Tolerance
  • beta-Galactosidase
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Identity

International Standard Serial Number (ISSN)

  • 0021-9258

Digital Object Identifier (DOI)

  • 10.1074/jbc.M204924200

PubMed ID

  • 12176986
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Additional Document Info

start page

  • 39343

end page

  • 39349

volume

  • 277

issue

  • 42

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