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Cited by 549

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

IL-22 is increased in active Crohn’s disease and promotes proinflammatory gene expression and intestinal epithelial cell migration

Brand, Stephan, Beigel, Florian, Olszak, Torsten, Zitzmann, Kathrin, Eichhorst, Sören T., Otte, Jan-Michel, Diepolder, Helmut, Marquardt, Andreas, Jagla, Wolfgang, Popp, Andreas, Leclair, Stéphane, Herrmann, Karin, Seiderer, Julia, Ochsenkühn, Thomas, Göke, Burkhard, Auernhammer, Christoph J., Dambacher, Julia·2006·American Journal of Physiology-Gastrointestinal and Liver Physiology
DOI 10.1152/ajpgi.00513.2005
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Abstract

IL-22 is produced by activated T cells and signals through a receptor complex consisting of IL-22R1 and IL-10R2. The aim of this study was to analyze IL-22 receptor expression, signal transduction, and specific biological functions of this cytokine system in intestinal epithelial cells (IEC). Expression studies were performed by RT-PCR. Signal transduction was analyzed by Western blot experiments, cell proliferation by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay and Fas-induced apoptosis by flow cytometry. IEC migration was studied in wounding assays. The IEC lines Caco-2, DLD-1, SW480, HCT116, and HT-29 express both IL-22 receptor subunits IL-22R1 and IL-10R2. Stimulation with TNF-α, IL-1β, and LPS significantly upregulated IL-22R1 without affecting IL-10R2 mRNA expression. IL-22 binding to its receptor complex activates STAT1/3, Akt, ERK1/2, and SAPK/JNK MAP kinases. IL-22 significantly increased cell proliferation ( P = 0.002) and phosphatidylinsitol 3-kinase-dependent IEC cell migration ( P < 0.00001) as well as mRNA expression of TNF-α, IL-8, and human β-defensin-2. IL-22 had no effect on Fas-induced apoptosis. IL-22 mRNA expression was increased in inflamed colonic lesions of patients with Crohn’s disease and correlated highly with the IL-8 expression in these lesions ( r = 0.840). Moreover, IL-22 expression was increased in murine dextran sulfate sodium-induced colitis. IEC express functional receptors for IL-22, which increases the expression of proinflammatory cytokines and promotes the innate immune response by increased defensin expression. Moreover, our data indicate intestinal barrier functions for this cytokine-promoting IEC migration, which suggests an important function in intestinal inflammation and wound healing. IL-22 is increased in active Crohn’s disease and promotes proinflammatory gene expression and IEC migration.

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Metadata

Authors
Brand, S., Beigel, F., Olszak, T., Zitzmann, K., Eichhorst, S. T., Otte, J.-M., Diepolder, H., Marquardt, A., Jagla, W., Popp, A., Leclair, S., Herrmann, K., Seiderer, J., Ochsenkühn, T., Göke, B., Auernhammer, C. J., & Dambacher, J.
Venue
American Journal of Physiology-Gastrointestinal and Liver Physiology
Publisher
American Physiological Society
Published
2006-04
Volume
290
Issue
4
Pages
G827-G838
ISSN
  • 0193-1857 (ISSN-L)
  • 1522-1547
DOI
10.1152/ajpgi.00513.2005
OpenAlex
W2104201959
Cited by
549
References
4
FWCI
13.96
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: IL-22 is increased in active Crohn’s disease and promotes proinflammatory gene expression and intestinal epithelial cell migration. https://app.cochat.ai/papers/10.1152/ajpgi.00513.2005
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Brand, S., Beigel, F., Olszak, T., Zitzmann, K., Eichhorst, S. T., Otte, J.-M., Diepolder, H., Marquardt, A., Jagla, W., Popp, A., Leclair, S., Herrmann, K., Seiderer, J., Ochsenkühn, T., Göke, B., Auernhammer, C. J., & Dambacher, J. (2006). IL-22 is increased in active Crohn’s disease and promotes proinflammatory gene expression and intestinal epithelial cell migration. American Journal of Physiology-Gastrointestinal and Liver Physiology. https://doi.org/10.1152/ajpgi.00513.2005

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.