Receptor for Advanced Glycation Endproducts Mediates Neutrophil Migration across Intestinal Epithelium

Receptor for advanced glycation endproducts (RAGE) is an Ig superfamily cell surface receptor that interacts with a diverse array of ligands associated with inflammatory responses. In this study, we provide evidence demonstrating that RAGE is involved in inflammatory responses in the intestines. We...

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Bibliographic Details
Published in:Journal of Immunology 2007-02, Vol.178 (4), p.2483-2490
Main Authors: Zen, Ke, Chen, Celia X.-J, Chen, Yi-Tien, Wilton, Rosemarie, Liu, Yuan
Format: Article
Language:English
Subjects:
CD11b Antigen - immunology
CD18 Antigens - immunology
Cell Movement - immunology
Colon - immunology
Colon - pathology
Epithelial Cells - immunology
Epithelial Cells - pathology
Epithelium - immunology
Epithelium - pathology
Humans
Inflammation - immunology
Inflammation - pathology
Intercellular Junctions - immunology
Intercellular Junctions - pathology
Interferon-gamma - immunology
Intestinal Mucosa - immunology
Intestinal Mucosa - pathology
Neutrophils - immunology
Neutrophils - pathology
Receptor for Advanced Glycation End Products
Receptors, Immunologic - immunology
Tumor Necrosis Factor-alpha - immunology
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Summary:Receptor for advanced glycation endproducts (RAGE) is an Ig superfamily cell surface receptor that interacts with a diverse array of ligands associated with inflammatory responses. In this study, we provide evidence demonstrating that RAGE is involved in inflammatory responses in the intestines. We showed that RAGE is expressed in intestinal epithelial cells, primarily concentrated at the lateral membranes close to the apical cell junction complexes. Although RAGE expression was low in epithelium under normal conditions, this protein was up-regulated after treatment with the inflammatory cytokines IFN-gamma and/or TNF-alpha. RAGE expression was also elevated in colon tissue samples from patients with inflammatory bowel diseases. Using in vitro transmigration assays, we found that RAGE mediates neutrophil (polymorphonuclear leukocytes (PMN)) adhesion to, and subsequent migration across, intestinal epithelial monolayers. This activity appears to be mediated by the binding of RAGE to the PMN-specific beta(2) integrin CD11b/CD18. Thus, these results provide a novel mechanism for the regulation of PMN transepithelial migration and may suggest a new therapeutic target for intestinal inflammation.
ISSN:0022-1767
1550-6606
1365-2567
DOI:10.4049/jimmunol.178.4.2483