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  • Title: Histochemical demonstration of desialation and desulphation of normal and inflammatory bowel disease rectal mucus by faecal extracts.
    Author: Rhodes JM, Black RR, Gallimore R, Savage A.
    Journal: Gut; 1985 Dec; 26(12):1312-8. PubMed ID: 2867955.
    Abstract:
    Experiments were carried out to assess the susceptibility of normal and inflammatory bowel disease rectal mucus to desulphation and desialation by faecal extracts and by bacterial sialidase. The effects were assessed histochemically using a combined high iron diamine (HID) and alcian blue (AB) stain for sulphomucins and sialomucins. Rectal mucus in biopsies from controls (irritable bowel syndrome) and patients with ulcerative colitis or Crohn's disease was resistant to desialation by Clostridium perfringens sialidase, but susceptible to desialation and desulphation by bacteria-free extracts of normal faeces. Periodic acid-Schiff (PAS) staining of adjacent sections similarly treated showed retention of neutral mucus. One faecal extract selectively desulphated all 42 biopsies, causing the goblet cells to change from HID positive to AB positive, suggesting that most, or all HID positive cells also contain sialomucins. This alters the interpretation of previous histochemical studies. Faecal extracts from patients with active ulcerative colitis (n = 6) had desialating and desulphating effects similar to faecal extracts from normal subjects (n = 6). Ulcerative colitis (n = 21), Crohn's disease (n = 18), and control (irritable bowel syndrome) (n = 17) rectal biopsies all showed similar susceptibility to desulphation by a pooled normal faecal extract, but rectal biopsies from patients with Crohn's disease proved more resistant to desialation than control or ulcerative colitis biopsies (p less than 0.02). These studies imply that colonic mucus undergoes continual desulphation and desialation in vivo as a result of faecal enzyme activity that is probably mainly of bacterial origin. Altered susceptibility of colonic mucus to this may be important in the pathogenesis of colonic disease.
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