Telocytes in Crohn's disease
Article first published online: 19 NOV 2013
© 2013 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Journal of Cellular and Molecular Medicine
Volume 17, Issue 12, pages 1525–1536, December 2013
How to Cite
Milia, A. F., Ruffo, M., Manetti, M., Rosa, I., Conte, D., Fazi, M., Messerini, L. and Ibba-Manneschi, L. (2013), Telocytes in Crohn's disease. Journal of Cellular and Molecular Medicine, 17: 1525–1536. doi: 10.1111/jcmm.12177
- Issue published online: 25 DEC 2013
- Article first published online: 19 NOV 2013
- Manuscript Accepted: 2 OCT 2013
- Manuscript Received: 3 SEP 2013
- Regione Toscana. Grant Number: 248639/Q20.70.20
- Crohn's disease;
- interstitial cells of Cajal;
Crohn's disease (CD) is a relapsing chronic inflammatory disorder that may involve all the gastrointestinal tract with a prevalence of terminal ileum. Intestinal lesions have a characteristic discontinuous and segmental distribution and may affect all layers of the gut wall. Telocytes (TC), a peculiar type of stromal cells, have been recently identified in a variety of tissues and organs, including gastrointestinal tract of humans and mammals. Several roles have been proposed for TC, including mechanical support, spatial relationships with different cell types, intercellular signalling and modulation of intestinal motility. The aim of our study was to investigate the presence and distribution of TC in disease-affected and -unaffected ileal specimens from CD patients compared with controls. TC were identified by CD34/PDGFRα immunohistochemistry. In affected CD specimens TC disappeared, particularly where fibrosis and architectural derangement of the intestinal wall were observed. In the thickened muscularis mucosae and submucosa, few TC entrapped in the fibrotic extracellular matrix were found. A discontinuous network of TC was present around smooth muscle bundles, ganglia and enteric strands in the altered muscularis propria. At the myenteric plexus, the loss of TC network was paralleled by the loss of interstitial cells of Cajal network. In the unaffected CD specimens, TC were preserved in their distribution. Our results suggest that in CD the loss of TC might have important pathophysiological implications contributing to the architectural derangement of the intestinal wall and gut dysmotility. Further functional studies are necessary to better clarify the role of TC loss in CD pathophysiology.