Literature DB >> 18483078

The role of the novel Th17 cytokine IL-26 in intestinal inflammation.

J Dambacher1, F Beigel, K Zitzmann, E N De Toni, B Göke, H M Diepolder, C J Auernhammer, S Brand.   

Abstract

BACKGROUND AND AIMS: Interleukin 26 (IL-26), a novel IL-10-like cytokine without a murine homologue, is expressed in T helper 1 (Th1) and Th17 cells. Currently, its function in human disease is completely unknown. The aim of this study was to analyse its role in intestinal inflammation.
METHODS: Expression studies were performed by reverse transcription-PCR (RT-PCR), quantitative PCR, western blot and immunohistochemistry. Signal transduction was analysed by western blot experiments and ELISA. Cell proliferation was measured by MTS (3-(4,5-dimethylthiazol-2-yl)-5-(carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay. IL-26 serum levels were determined by an immunoluminometric assay (ILMA).
RESULTS: All examined intestinal epithelial cell (IEC) lines express both IL-26 receptor subunits IL-20R1 and IL-10R2. IL-26 activates extracellular signal-related kinase (ERK)-1/2 and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) mitogen-activated protein (MAP) kinases, Akt and signal transducers and activators of transcription (STAT) 1/3. IL-26 stimulation increases the mRNA expression of proinflammatory cytokines but decreases cell proliferation. In inflamed colonic lesions of patients with Crohn's disease, an elevated IL-26 mRNA expression was found that correlated highly with the IL-8 and IL-22 expression. Immunohistochemical analysis demonstrated IL-26 protein expression in colonic T cells including Th17 cells expressing the orphan nuclear receptor RORgammat, with an increased number of colonic IL-26-expressing cells in active Crohn's disease.
CONCLUSION: Intestinal cells express the functional IL-26 receptor complex. IL-26 modulates IEC proliferation and proinflammatory gene expression and its expression is upregulated in active Crohn's disease, indicating a role for this cytokine system in the innate host cell response during intestinal inflammation. For the first time, IL-26 expression is demonstrated in colonic RORgammat-expressing Th17 cells in situ, supporting a role for this cell type in the pathogenesis of Crohn's disease.

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Year:  2008        PMID: 18483078     DOI: 10.1136/gut.2007.130112

Source DB:  PubMed          Journal:  Gut        ISSN: 0017-5749            Impact factor:   23.059


  78 in total

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2.  The presence of fistulas and NOD2 homozygosity strongly predict intestinal stenosis in Crohn's disease independent of the IL23R genotype.

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Journal:  J Gastroenterol       Date:  2010-04-29       Impact factor: 7.527

Review 3.  Mechanisms of Cholera Toxin in the Modulation of TH17 Responses.

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Review 5.  Th17 Cells in Helicobacter pylori Infection: a Dichotomy of Help and Harm.

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6.  Cytokine-induced alterations of gastrointestinal motility in gastrointestinal disorders.

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Review 7.  The role of Th17 lymphocytes in the autoimmune and chronic inflammatory diseases.

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8.  Intestinal neuroendocrine cells and goblet cells are mediators of IL-17A-amplified epithelial IL-17C production in human inflammatory bowel disease.

Authors:  M Friedrich; J Diegelmann; J Schauber; C J Auernhammer; S Brand
Journal:  Mucosal Immunol       Date:  2014-12-10       Impact factor: 7.313

9.  VPR-254: an inhibitor of ROR-gamma T with potential utility for the treatment of inflammatory bowel disease.

Authors:  Leo R Fitzpatrick; Jeff Small; Robert O'Connell; George Talbott; Gordon Alton; Jim Zapf
Journal:  Inflammopharmacology       Date:  2019-09-23       Impact factor: 4.473

Review 10.  Cellular mediators of inflammation: tregs and TH17 cells in gastrointestinal diseases.

Authors:  Franco Pandolfi; Rossella Cianci; Danilo Pagliari; Raffaele Landolfi; Giovanni Cammarota
Journal:  Mediators Inflamm       Date:  2010-02-08       Impact factor: 4.711

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