title: Glucosamine suppresses interleukin-8 production and ICAM-1 expression by TNF-alpha-stimulated human colonic epithelial HT-29 cells.
abstract: 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.
authors.affiliation: Department of Host Defense and Biochemical Research, Juntendo University, School of Medicine, Tokyo, Japan.
authors.forename: Shin
authors.initials: S
authors.lastname: Yomogida
authors.forename: Jian
authors.initials: J
authors.lastname: Hua
authors.forename: Koji
authors.initials: K
authors.lastname: Sakamoto
authors.forename: Isao
authors.initials: I
authors.lastname: Nagaoka
mesh_terms: D004847:Epithelial Cells / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D005944:Glucosamine / Q000502:physiology*; D019073:HT29 Cells; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D016209:Interleukin-8 / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D016209:Interleukin-8; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D048051:p38 Mitogen-Activated Protein Kinases; D005944:Glucosamine