Altered expression of mucins throughout the colon in ulcerative colitis.

Smithson, J; Campbell, A. M. G.; Andrews, Jane M.; Milton, J.D.; Pigott, Rod; Jewell, D P

doi:10.1136/gut.40.2.234

Cited by 36 publications

(35 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…IBDs are known to alter the expression of mucins throughout the colon (10,(34)(35)(36). Alterations in mucin expression may play a role in the pathogenesis of IBD (34)(35)(36)(37).…”

Section: Discussionmentioning

confidence: 99%

Mucosal function in rat jejunum and ileum is altered by induction of colitis

Amit-Romach

Reifen²,

Uni³

2006

Int J Mol Med

View full text Add to dashboard Cite

Abstract. Many studies dealing with trinitrobenzene sulfonic acid (TNBS) colitis in rats have been carried out refering only to the colon. In humans, ulcerative colitis (UC) can extend a variable distance into the terminal ileum in a phenomenon known as backwash ileitis (BWI). The aim of this study was therefore to examine the effect of TNBSinduced colitis on different aspects of the rat ileum and jejunum. We hypothesized that TNBS administration would lead to a systemic influence on the small intestine. Rats were induced colitis by administration of 0.25 ml of 2,4,6-trinitrobenzene sulfonic acid and 72 h after colitis induction animals were sacrificed. Segments were taken of the colon, ileum and jejunum. In addition to mucin mRNA expression, morphological changes were observed in the jejunum and ileum. We examined the mRNA expression and biochemical activity of brush border enzyme, sucrase iso-maltase and aminopeptidase, in all three segments. The villous surface area of colitis-induced rats was smaller in jejunum and ileum compared to control. In the jejunum of TNBS-induced rats, goblet-cell volume increased and their density decreased. The relative amount of MUC2 mRNA decreased in the jejunum, ileum and colon of colitis rat. However, MUC3 mRNA expression increased in the ileum and colon of these rats. Sucrase isomaltase expression and activity decreased in the ileum of TNBS-induced rats, while aminopeptidase activity was lower in the jejunum. These observations suggest that intrarectal administration of TNBS to rats influences not only their colon and terminal ileum, but also the proximal ileum and jejunum. Involvement of the ileum and jejunum in TNBSinduced colitis may be related to the systemic reaction of the immune system and mucosa to colitis.

show abstract

“…IBDs are known to alter the expression of mucins throughout the colon (10,(34)(35)(36). Alterations in mucin expression may play a role in the pathogenesis of IBD (34)(35)(36)(37).…”

Section: Discussionmentioning

confidence: 99%

Mucosal function in rat jejunum and ileum is altered by induction of colitis

Amit-Romach

Reifen²,

Uni³

2006

Int J Mol Med

View full text Add to dashboard Cite

show abstract

“…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

View full text Add to dashboard Cite

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

show abstract

“…Most UC patients have colitis only in the distal colon (14). Although the reasons for this regional variation are unknown, UC patients have deterioration of the mucus layer and abnormal mucin expression in the distal colon (1,(15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

Loss of intestinal core 1–derived O-glycans causes spontaneous colitis in mice

Fu¹,

Wei²,

Wen³

et al. 2011

J. Clin. Invest.

298

294

View full text Add to dashboard Cite

Mucin-type O-linked oligosaccharides (O-glycans) are primary components of the intestinal mucins thatform the mucus gel layer overlying the gut epithelium. Impaired expression of intestinal O-glycans has been observed in patients with ulcerative colitis (UC), but its role in the etiology of this disease is unknown. Here, we report that mice with intestinal epithelial cell-specific deficiency of core 1-derived O-glycans, the predominant form of O-glycans, developed spontaneous colitis that resembled human UC, including massive myeloid infiltrates and crypt abscesses. The colitis manifested in these mice was also characterized by TNF-producing myeloid infiltrates in colon mucosa in the absence of lymphocytes, supporting an essential role for myeloid cells in colitis initiation. Furthermore, induced deletion of intestinal core 1-derived O-glycans caused spontaneous colitis in adult mice. These data indicate a causal role for the loss of core 1-derived O-glycans in colitis. Finally, we detected a biosynthetic intermediate typically exposed in the absence of core 1 O-glycan, Tn antigen, in the colon epithelium of a subset of UC patients. Somatic mutations in the X-linked gene that encodes core 1 β1,3-galactosyltransferase-specific chaperone 1 (C1GALT1C1, also known as Cosmc), which is essential for core 1 O-glycosylation, were found in Tn-positive epithelia. These data suggest what we believe to be a new molecular mechanism for the pathogenesis of UC.

show abstract

Altered expression of mucins throughout the colon in ulcerative colitis.

Abstract: Background/Aims-Regional differences

Cited by 36 publications

References 31 publications

Mucosal function in rat jejunum and ileum is altered by induction of colitis

Mucosal function in rat jejunum and ileum is altered by induction of colitis

Food intolerance and chronic constipation: manometry and histology study

Loss of intestinal core 1–derived O-glycans causes spontaneous colitis in mice

Contact Info

Product

Resources

About