Increased expression of CCL20 in human inflammatory bowel disease - PubMed (original) (raw)

doi: 10.1023/B:JOCI.0000018066.46279.6b.

Othmar Ludwiczek, Sandra Holzmann, Alexander R Moschen, Günter Weiss, Barbara Enrich, Ivo Graziadei, Stefan Dunzendorfer, Christian J Wiedermann, Elisabeth Mürzl, Eveline Grasl, Zerina Jasarevic, Nikolaus Romani, Felix A Offner, Herbert Tilg

Affiliations

• PMID: 14997037
• DOI: 10.1023/B:JOCI.0000018066.46279.6b

Increased expression of CCL20 in human inflammatory bowel disease

Arthur Kaser et al. J Clin Immunol. 2004 Jan.

Abstract

Inflammatory bowel disease (IBD) constituting Crohn's disease (CD) and ulcerative colitis (UC) is related to a dysregulated T cell response. CCL20 attracts memory T lymphocytes and dendritic cells. We asked whether CCL20 expression is altered in IBD. Colonic biopsies were obtained from 114 subjects with IBD, non-IBD colitis, irritable bowel syndrome, and healthy controls. CCL20 and CCR6 mRNA expression was measured by Taqman-PCR, and protein secretion from colonic explant cultures (CEC) and its regulation by TNF-alpha by ELISA. CCL20, CCR6, and Langerin were identified by immunohistochemistry and immunofluorescence. CCL20 mRNA and protein were severalfold increased in involved CD and UC but not in non-IBD colitis. TNF-alpha increased and anti-TNF-alpha decreased CCL20 release in healthy control CEC but not in involved IBD colonic specimens. CCL20 localized to follicle-associated epithelium, and CCR6 to the adjacent mantle zone of lymphoid follicles. Furthermore, abundant numbers of Langerin(+) immature dendritic cells were identified in the subepithelial space of IBD specimens. CCL20 might regulate the attraction of T lymphocytes and dendritic cells in IBD.

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