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Interleukin 34: a new modulator of human and experimental inflammatory bowel disease
IBD (inflammatory bowel disease), where CD (Crohn's disease) and UC (ulcerative colitis) represent the two main forms, are chronic inflammatory conditions of the intestine. Macrophages play a central role in IBD pathogenesis and are regulated by major differentiation factors such as CSF-1 (colo...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557398/ https://www.ncbi.nlm.nih.gov/pubmed/25896238 http://dx.doi.org/10.1042/CS20150176 |
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author | Zwicker, Stephanie Martinez, Gisele L. Bosma, Madeleen Gerling, Marco Clark, Reuben Majster, Mirjam Söderman, Jan Almer, Sven Boström, Elisabeth A. |
author_facet | Zwicker, Stephanie Martinez, Gisele L. Bosma, Madeleen Gerling, Marco Clark, Reuben Majster, Mirjam Söderman, Jan Almer, Sven Boström, Elisabeth A. |
author_sort | Zwicker, Stephanie |
collection | PubMed |
description | IBD (inflammatory bowel disease), where CD (Crohn's disease) and UC (ulcerative colitis) represent the two main forms, are chronic inflammatory conditions of the intestine. Macrophages play a central role in IBD pathogenesis and are regulated by major differentiation factors such as CSF-1 (colony-stimulating factor 1) in homoeostasis and inflammation. IL (interleukin)-34 has recently been discovered as a second ligand for CSF-1R (CSF-1 receptor). However, expression and involvement of IL-34 in IBD remain unknown. In the present paper, we investigated the expression of IL34, CSF1 and their shared receptor CSF1R in normal human ileum and colon, in inflamed and non-inflamed tissues of CD and UC patients, and in a mouse model of experimental colitis. We found distinct expression patterns of IL34 and CSF1 in ileum and colon, with higher IL34 in ileum and, in contrast, higher CSF1 in colon. Furthermore, IL34 and CSF1 expression was increased with inflammation in IBD patients and in experimental colitis. In humans, infiltrating cells of the lamina propria and intestinal epithelial cells expressed IL-34, and TNF-α (tumour necrosis factor α) regulated IL-34 expression in intestinal epithelial cells through the NF-κB (nuclear factor κB) pathway. These data demonstrate the expression pattern of IL-34 in ileum and colon and suggest IL-34 as a new modulator of inflammation in IBD. |
format | Online Article Text |
id | pubmed-4557398 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-45573982015-09-11 Interleukin 34: a new modulator of human and experimental inflammatory bowel disease Zwicker, Stephanie Martinez, Gisele L. Bosma, Madeleen Gerling, Marco Clark, Reuben Majster, Mirjam Söderman, Jan Almer, Sven Boström, Elisabeth A. Clin Sci (Lond) Original Paper IBD (inflammatory bowel disease), where CD (Crohn's disease) and UC (ulcerative colitis) represent the two main forms, are chronic inflammatory conditions of the intestine. Macrophages play a central role in IBD pathogenesis and are regulated by major differentiation factors such as CSF-1 (colony-stimulating factor 1) in homoeostasis and inflammation. IL (interleukin)-34 has recently been discovered as a second ligand for CSF-1R (CSF-1 receptor). However, expression and involvement of IL-34 in IBD remain unknown. In the present paper, we investigated the expression of IL34, CSF1 and their shared receptor CSF1R in normal human ileum and colon, in inflamed and non-inflamed tissues of CD and UC patients, and in a mouse model of experimental colitis. We found distinct expression patterns of IL34 and CSF1 in ileum and colon, with higher IL34 in ileum and, in contrast, higher CSF1 in colon. Furthermore, IL34 and CSF1 expression was increased with inflammation in IBD patients and in experimental colitis. In humans, infiltrating cells of the lamina propria and intestinal epithelial cells expressed IL-34, and TNF-α (tumour necrosis factor α) regulated IL-34 expression in intestinal epithelial cells through the NF-κB (nuclear factor κB) pathway. These data demonstrate the expression pattern of IL-34 in ileum and colon and suggest IL-34 as a new modulator of inflammation in IBD. Portland Press Ltd. 2015-05-15 2015-08-01 /pmc/articles/PMC4557398/ /pubmed/25896238 http://dx.doi.org/10.1042/CS20150176 Text en © 2015 The author(s) has paid for this article to be freely available under the terms of the Creative Commons Attribution Licence (CC-BY)(http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Paper Zwicker, Stephanie Martinez, Gisele L. Bosma, Madeleen Gerling, Marco Clark, Reuben Majster, Mirjam Söderman, Jan Almer, Sven Boström, Elisabeth A. Interleukin 34: a new modulator of human and experimental inflammatory bowel disease |
title | Interleukin 34: a new modulator of human and experimental inflammatory bowel disease |
title_full | Interleukin 34: a new modulator of human and experimental inflammatory bowel disease |
title_fullStr | Interleukin 34: a new modulator of human and experimental inflammatory bowel disease |
title_full_unstemmed | Interleukin 34: a new modulator of human and experimental inflammatory bowel disease |
title_short | Interleukin 34: a new modulator of human and experimental inflammatory bowel disease |
title_sort | interleukin 34: a new modulator of human and experimental inflammatory bowel disease |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557398/ https://www.ncbi.nlm.nih.gov/pubmed/25896238 http://dx.doi.org/10.1042/CS20150176 |
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