Mucin depletion in inflammatory bowel disease.

McCormick, David A.; Horton, L. W. L.; Mee, A S

doi:10.1136/jcp.43.2.143

Cited by 104 publications

(75 citation statements)

References 13 publications

(1 reference statement)

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“…Moreover, mucin has a ' priming effect ' on the epithelial cells to enhance ITF binding, which might account, at least in part, for the protective function of epithelium-associated mucin in the gastrointestinal tract. Intestinal mucin has been shown to be depleted in patients with IBD [41]. The composition of mucin in patients with Crohn's disease is significantly different from that of normal controls, suggesting that an altered profile of mucin glycoprotein might be present in IBD patients [42,43].…”

Section: Discussionmentioning

confidence: 99%

Intestinal trefoil factor binds to intestinal epithelial cells and induces nitric oxide production: priming and enhancing effects of mucin

Tan

Liu

Hsueh

et al. 1999

Biochemical Journal

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Intestinal trefoil factor (ITF or TFF3), NO and epitheliumassociated mucin have important roles in sustaining mucosal integrity in the gastrointestinal tract. In the present study we examined ITF-binding molecules on IEC-18 cells (an intestinal epithelial cell line) with the use of flow cytometry and localized these molecules on the cell surface by confocal microscopy. Furthermore, we studied the interaction of mucin and ITF and their co-operative effect on NO production by the epithelium.

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Section: Discussionmentioning

confidence: 99%

Intestinal trefoil factor binds to intestinal epithelial cells and induces nitric oxide production: priming and enhancing effects of mucin

Tan

Liu

Hsueh

et al. 1999

Biochemical Journal

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“…In addition, local gene delivery of IL-22 vector significantly enhanced STAT3 activation in the CECs of proximal colon (the injected site) but not distal colon (noninjected site) as defined by the levels of phospho-STAT3 ( Figure 3B and data not shown). Of note, IL-22 gene delivery led to "prompt" attenuation of colitis at the injection but not the noninjection site, as indicated by a significant reduction in the colonic diameter within 2 weeks after IL-22 gene delivery ( Goblet cell depletion, which is prominently observed in UC in comparison with CD (12,29,30), was observed in the diseased colon of TCRαKO mice treated with mock vector ( Figure 3G). Interestingly, IL-22 gene delivery induced a significant restoration of goblet cell expression in TCRαKO mice ( Figure 3, G and H).…”

Section: Insufficient Expression Of Inducible Il-22 Expression In Th2mentioning

confidence: 99%

IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis

Sugimoto¹,

Ogaẃa²,

Mizoguchi³

et al. 2008

J. Clin. Invest.

702

839

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“…In patients with food intolerance, mucous reduction was food intolerance dependent, as the thickness of the mucous layer significantly increased on the elimination diet. It is noteworthy that the loss of the mucous barrier function is typical of the inflammatory bowel diseases, and can facilitate the exposure of the mucosa to luminal agents that perpetuate the inflammation [17,18].…”

Section: Figmentioning

confidence: 99%

Food intolerance and chronic constipation: manometry and histology study

Iacono¹,

Bonventre²,

Scalici³

et al. 2006

European Journal of Gastroenterology & Hepatology

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Background Chronic constipation in children can be caused by cows' milk intolerance (CMI), but its pathogenesis is unknown.Aims To evaluate the histology and manometry pattern in patients with food intolerance-related constipation.Patients and methods Thirty-six consecutive children with chronic constipation were enrolled. All underwent an elimination diet and successive double-blind food challenge. All underwent rectal biopsy and anorectal manometry.Results A total of 14 patients were found to be suffering from CMI and three from multiple food intolerance. They had a normal stool frequency on elimination diet, whereas constipation recurred on food challenge. The patients with food intolerance showed a significantly higher frequency of erosions of the mucosa, and the number of intra-epithelial lymphocytes and eosinophils. The rectal mucous gel layer showed that the food-intolerant patients had a significantly lower thickness of mucous than the other subjects studied. Manometry showed a higher anal sphincter resting pressure and a lower critical volume in food intolerance patients than in the others suffering from constipation unrelated to food intolerance. Both histology and manometry abnormalities disappeared on the elimination diet.Conclusions Food intolerance-related constipation is characterized by proctitis. Increased anal resting pressure and a reduced mucous gel layer can be considered to be contributory factors in the pathogenesis of constipation. Eur

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Mucin depletion in inflammatory bowel disease.

Abstract: The mucin and gland content of 26 rectal biopsy specimens-five normal specimens,

Cited by 104 publications

References 13 publications

Intestinal trefoil factor binds to intestinal epithelial cells and induces nitric oxide production: priming and enhancing effects of mucin

Intestinal trefoil factor binds to intestinal epithelial cells and induces nitric oxide production: priming and enhancing effects of mucin

IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis

Food intolerance and chronic constipation: manometry and histology study

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