Abstract
Ulcerative colitis (UC) is characterized by chronic relapsing intestinal inflammation finally leading to extensive tissue fibrosis and resulting in a stiff colon unable to carry out peristalsis or to resorb fluids. Telocytes, a peculiar type of stromal cells, have been recently identified in the human gastrointestinal tract. Several roles have been proposed for telocytes, including mechanical support, intercellular signalling and modulation of intestinal motility. The aim of the present work was to investigate the presence and distribution of telocytes in colonic specimens from UC patients compared with controls. Archival paraffin-embedded samples of the left colon from UC patients who underwent elective bowel resection and controls were collected. Tissue sections were stained with Masson's trichrome to detect fibrosis. Telocytes were identified by CD34 immunohistochemistry. In early fibrotic UC cases, fibrosis affected the muscularis mucosae and submucosa, while the muscularis propria was spared. In advanced fibrotic UC cases, fibrosis extended to affect the muscle layers and the myenteric plexus. Few telocytes were found in the muscularis mucosae and submucosa of both early and advanced fibrotic UC colonic wall. In the muscle layers and myenteric plexus of early fibrotic UC, telocytes were preserved in their distribution. In the muscularis propria of advanced fibrotic UC, the network of telocytes was reduced or even completely absent around smooth muscle bundles and myenteric plexus ganglia, paralleling the loss of the network of interstitial cells of Cajal. In UC, a loss of telocytes accompanies the fibrotic remodelling of the colonic wall and might contribute to colonic dysmotility.
Highlights
Inflammatory bowel diseases, including Crohn’s disease (CD) and ulcerative colitis (UC), are complex diseases in which the interaction of genetic, environmental and microbial factors drives chronic relapsing and remitting intestinal inflammation that leads to extensive tissue fibrosis [1, 2]
The histopathological analysis of surgical samples obtained from all UC patients confirmed the presence of mucosal/submucosal lesions typical of UC, including erosions, widespread surface epithelial damage, goblet cell depletion, cryptitis, frank crypt abscesses, crypt distortion and/or destruction, as well as a marked infiltration of inflammatory and immune cells in the muscularis mucosae and submucosa (Fig. 1A–C)
In advanced fibrotic UC cases, an increased deposition of the extracellular matrix was observed in the muscularis mucosae, which appeared markedly thickened, and widespread in the submucosa (Fig. 1C and F)
Summary
Inflammatory bowel diseases, including Crohn’s disease (CD) and ulcerative colitis (UC), are complex diseases in which the interaction of genetic, environmental and microbial factors drives chronic relapsing and remitting intestinal inflammation that leads to extensive tissue fibrosis [1, 2]. This is relevant for small bowel CD. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine
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