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A mechanistic role for leptin in human dendritic cell migration: Differences between ileum and colon in health and Crohn's disease
Al-Hassi, Hafid Omar Bernardo, D Murugananthan, AU Mann, ER English, NR Jones, A Kamm, MA Arebi, N Hart, AL Blakemore, AIF
Al-Hassi, Hafid Omar
Bernardo, D
Murugananthan, AU
Mann, ER
English, NR
Jones, A
Kamm, MA
Arebi, N
Hart, AL
Blakemore, AIF
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Other contributors
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Epub Date
Issue Date
2012-11-21
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Abstract
Dendritic cells (DC) migrate to lymph nodes on expression of C-C motif chemokine receptor 7 (CCR7) and control immune activity. Leptin, an immunomodulatory adipokine, functions via leptin receptors, signaling via the long isoform of receptor, LepRb. Leptin promotes DC maturation and increases CCR7 expression on blood DC. Increased mesenteric fat and leptin occur early in Crohn's disease (CD), suggesting leptin-mediated change in intestinal CCR7 expression on DC as a pro-inflammatory mechanism. We have demonstrated CCR7 expression and capacity to migrate to its ligand macrophage inflammatory protein 3β in normal human ileal DC but not colonic or blood DC. In CD, functional CCR7 was expressed on DC from all sites. Only DC populations containing CCR7-expressing cells produced LepRb; in vitro exposure to leptin also increased expression of functional CCR7 in intestinal DC in a dose-dependent manner. In conclusion, leptin may regulate DC migration from gut, in homeostatic and inflammatory conditions, providing a link between mesenteric obesity and inflammation. © 2013 Society for Mucosal Immunology.
Citation
Al-Hassi, H., Bernardo, D., Murugananthan, A. et al. (2013) A mechanistic role for leptin in human dendritic cell migration: differences between ileum and colon in health and Crohn’s disease. Mucosal Immunol 6, pp. 751–761. https://doi.org/10.1038/mi.2012.113
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Research Unit
PubMed ID
23168838 (pubmed)
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Journal article
Language
en
Description
© 2012 The Authors. Published by Springer Nature. This is an open access article available under a Creative Commons licence.
The published version can be accessed at the following link on the publisher’s website: https://doi.org/10.1038/mi.2012.113
Series/Report no.
ISSN
1933-0219
EISSN
1935-3456
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Sponsors
We thank The Broad Medical Research Program of the Broad Foundation, USA, the Medical Research Council Trust, UK, St Mark’s Hospital Foundation, UK, the Biotechnology and Biological Research Council Institute Strategic Program for Gut Health and Food Safety BB/J004529/1 and the Brigid Balfour Fund for funding this study. A.I.F.B. is also funded by Diabetes UK and the BRC at the Imperial College Healthcare Trust.
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Licence for published version: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International