Telocytes in Crohn's disease

Authors

  • Anna Franca Milia,

    1. Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy
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  • Martina Ruffo,

    1. Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy
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  • Mirko Manetti,

    1. Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy
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  • Irene Rosa,

    1. Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy
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  • Dalila Conte,

    1. Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy
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  • Marilena Fazi,

    1. Department of Surgery and Translational Medicine, University of Florence, Florence, Italy
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  • Luca Messerini,

    1. Department of Experimental and Clinical Medicine, Section of Surgery, Histopathology and Molecular Pathology, University of Florence, Florence, Italy
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  • Lidia Ibba-Manneschi

    Corresponding author
    1. Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy
    • Correspondence to: Prof. Lidia IBBA-MANNESCHI, M.D.,

      Department of Experimental and Clinical Medicine, Section of Anatomy and Histology,

      University of Florence, Largo Brambilla 3, 50134 Florence, Italy.

      Tel.: 0039 055 4271827

      Fax: 0039 055 4379500

      E-mail: lidia.ibba@unifi.it

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Abstract

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.

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