V Strugala1, P W Dettmar, J P Pearson. 1. Epithelial Group, Institute for Cell and Molecular Biology, Medical School, Framlington Place, University of Newcastle Upon Tyne, Newcastle Upon Tyne, UK. vicki.strugala@technostics.com
Abstract
BACKGROUND: The colon is covered by a mucus barrier that protects the underlying mucosa and alterations in this mucus barrier have been implicated in the aetiology of inflammatory bowel disease (IBD). This study investigated the thickness and continuity of the mucus barrier in ulcerative colitis (UC) and Crohn's disease (CD) in comparison to normal controls. METHODS: Rectal biopsies were taken from 59 patients and cryostat sections stained with periodic acid-Schiff's/Alcian blue to visualise the mucus layer. Mucus thickness and continuity and goblet cell density were measured using light microscopy. RESULTS: An essentially continuous adherent mucus layer was observed in normal human rectum and there was no change in the mucus barrier in quiescent UC. In active UC there was a trend for the mucus layer to become progressively thinner and significantly more discontinuous as disease severity increased. In severe active UC the mucus layer thickness and goblet cell density were significantly reduced compared with normal controls while the percentage discontinuity significantly increased. CONCLUSION: It is not until severe UC that there is a global change in mucosal protection as a consequence of large regions lacking mucus, a decrease in secretory potential caused by a loss of goblet cells and a thinner, less effective mucus layer even when it is present.
BACKGROUND: The colon is covered by a mucus barrier that protects the underlying mucosa and alterations in this mucus barrier have been implicated in the aetiology of inflammatory bowel disease (IBD). This study investigated the thickness and continuity of the mucus barrier in ulcerative colitis (UC) and Crohn's disease (CD) in comparison to normal controls. METHODS: Rectal biopsies were taken from 59 patients and cryostat sections stained with periodic acid-Schiff's/Alcian blue to visualise the mucus layer. Mucus thickness and continuity and goblet cell density were measured using light microscopy. RESULTS: An essentially continuous adherent mucus layer was observed in normal human rectum and there was no change in the mucus barrier in quiescent UC. In active UC there was a trend for the mucus layer to become progressively thinner and significantly more discontinuous as disease severity increased. In severe active UC the mucus layer thickness and goblet cell density were significantly reduced compared with normal controls while the percentage discontinuity significantly increased. CONCLUSION: It is not until severe UC that there is a global change in mucosal protection as a consequence of large regions lacking mucus, a decrease in secretory potential caused by a loss of goblet cells and a thinner, less effective mucus layer even when it is present.
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