Document Detail

Glucosamine suppresses interleukin-8 production and ICAM-1 expression by TNF-alpha-stimulated human colonic epithelial HT-29 cells.
MedLine Citation:
PMID:  18636175     Owner:  NLM     Status:  MEDLINE    
Intestinal epithelial cells play an important role in the mucosal immune reaction in inflammatory bowel diseases via the production and expression of chemokines and adhesion molecules, such as interleukin-8 (IL-8) and intercellular adhesion molecule-1 (ICAM-1), which are involved in the neutrophil infiltration and tissue damage in the inflamed colon. Notably, glucosamine, a naturally-occurring amino monosaccharide, has been shown to exhibit an anti-inflammatory action by inhibiting neutrophil functions. In the present study, to evaluate the anti-inflammatory action of glucosamine on intestinal epithelial cells, we examined the effects of glucosamine on the activation of a human colonic epithelial cell line HT-29. The results revealed that glucosamine suppressed the IL-8 production and ICAM-1 expression by TNF-alpha-activated HT-29 cells. Furthermore, glucosamine inhibited the TNF-alpha-induced phosphorylation of p38MAPK and NF-kappaB p65, and the nuclear translocation of NF-kappaB in the cells. Thus, glucosamine demonstrates inhibitory actions on the inflammatory and signaling molecules (IL-8, ICAM-1, p38MAPK and NF-kappaB) in intestinal epithelial cells. However, glucosamine did not essentially affect the binding of TNF-alpha to its receptor on HT-29 cells. Together, these observations suggest that glucosamine may have the potential to exhibit an anti-inflammatory action on intestinal epithelial cells, by possibly interfering with the activation signaling downstream of the ligand/receptor binding.
Shin Yomogida; Jian Hua; Koji Sakamoto; Isao Nagaoka
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of molecular medicine     Volume:  22     ISSN:  1107-3756     ISO Abbreviation:  Int. J. Mol. Med.     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-07-18     Completed Date:  2008-09-18     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9810955     Medline TA:  Int J Mol Med     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  205-11     Citation Subset:  IM    
Department of Host Defense and Biochemical Research, Juntendo University, School of Medicine, Tokyo, Japan.
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MeSH Terms
Epithelial Cells / cytology,  immunology,  metabolism
Glucosamine / physiology*
HT29 Cells
Intercellular Adhesion Molecule-1 / metabolism*
Interleukin-8 / metabolism*
Intestinal Mucosa / cytology,  immunology*,  metabolism
NF-kappa B / metabolism
Tumor Necrosis Factor-alpha / immunology*
p38 Mitogen-Activated Protein Kinases / metabolism
Reg. No./Substance:
0/Interleukin-8; 0/NF-kappa B; 0/Tumor Necrosis Factor-alpha; 126547-89-5/Intercellular Adhesion Molecule-1; 3416-24-8/Glucosamine; EC Mitogen-Activated Protein Kinases

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