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Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastrointestinal mucus (GIMu) is a viscoelastic gel, which covers the surface of the entire digestive tract. The main component of GIMu is mucin, which is a high molecular weight glycoprotein. Mucin is composed of a central peptide core with polysaccharide chains arranged radially from the core ("bottle brushappearance"). The carbohydrates are very hydrophilic and, therefore, able to bind large amounts of water, which partly accounts for the gel-forming properties of GIMu. GIMu has an important function as a barrier against large particles, H+ ions and pepsin, carcinogens, certain macromolecules and microorganisms. GIMu seems to be involved in the pathogenesis of gastroduodenal ulceration, inflammatory bowel disease, gastrointestinal malignancies, gallbladder stones and infectious diarrhoeal diseases. GIMu is also an important factor in maintaining the normal microbial intestinal homeostasis. In the future, a more detailed knowledge about the molecular structure and function of GIMu may lead to new diagnostic and therapeutic strategies for gastrointestinal diseases.
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PMID:[Gastrointestinal mucus]. 892 51

We have described a novel macrophage-derived mucin secretagogue (MMS-68) that mediates mucin secretion in colon cancer cell lines and explants of normal and inflammatory bowel disease (IBD) mucosa. We compared MMS-68 induced mucin release with other known intestinal mucin secretagogues in normal colon explants and in the HT-29 colon cancer cell line, and to study the effects of MMS-68 on mucin release from inflamed and uninflamed ulcerative colitis (UC) and Crohn's disease (CD) mucosa. In normal colonic explants and HT-29 cells, each of the secretagogues including, MMS-68-induced mucin release two- to fivefold more than culture medium alone. In HT-29 cells, MMS-68 plus leukotriene C4 (LTC4) induced a 50% increase in mucin release over either secretagogue alone, and MMS-68 plus platelet-activating factor (PAF) markedly enhanced mucin release by eightfold over either secretagogue. In colonic explants from patients with UC and CD, the mucin release in response to MMS-68 was similar to that of normal colonic explants. Likewise, in isolated epithelial cells from CD and UC (whether involved or uninvolved), MMS-68-induced release was similar to that of epithelial cells isolated from normal colonic mucosa. The number of MMS-68-producing macrophages was lower in uninflamed UC mucosa compared with inflamed UC mucosa and CD mucosa. The mucin secretagogue activity of MMS-68 is comparable to that of other known secretagogues, and PAF can have a synergistic effect on this activity. Whole tissue explants and isolated colonic epithelial cells from patients with IBD respond at least as well as their normal counterparts to MMS-68. MMS-68 may play a role in mucin secretion in normal and inflamed colonic tissue.
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PMID:Mucin secretion in inflammatory bowel disease: comparison of a macrophage-derived mucin secretagogue (MMS-68) to conventional secretagogues. 955 23

The aim of this study was to assess the effect of plaunotol, an anti-ulcer agent, on trinitrobenzene sulfonic acid (TNB)- and acetic acid-induced colonic lesions in rats. Plaunotol significantly reduced the severity of colonic mucosal lesions induced by TNB at a dose of 600 mg/kg/day. Moreover, plaunotol, at a dose of 600 mg/kg/day, significantly depressed the myeloperoxidase activity of the lesioned area induced by TNB of the rat colon. In the model of colitis induced by acetic acid, plaunotol reduced the area of lesions dose-dependently and significantly at doses of 60, 200 and 600 mg/kg/day as assessed by macroscopic observation. Microscopic observation showed obvious changes by administration of plaunotol such as reduction of epithelial cell necrosis, decreased mucin production and a decreased infiltration of a large number of neutrophils. In conclusion, plaunotol showed a protective effect against colonic lesion formation induced by TNB and acetic acid in rats. This study suggests the possibility that plaunotol may be effective and useful for treatment of inflammatory bowel disease in humans.
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PMID:[Effect of plaunotol on trinitrobenzene sulfonic acid and acetic acid induced colonic lesions in rats]. 978

Ulcerative colitis (UC), a common form of inflammatory bowel disease, is a multifactorial disorder with significant genetic influence. Recently, evidence of linkage on chromosome 7q near the intestinal mucin gene MUC3 was reported by an affected sib-pair analysis. Previous reports indicate a possible mucin abnormality in UC patients, but whether genetic differences in a specific mucin gene are associated with UC is unknown. Here we analysed polymorphisms of variable number of tandem repeats (VNTRs) within this gene using DNAs obtained from 243 Japanese (75 patients with UC and 168 controls), and to confirm the result we undertook a two-stage examination using 328 Caucasian samples (72 and 85 with UC in the first and second stages, respectively, and 171 controls). When the frequency of patients carrying one or two rare VNTR alleles was compared with that of controls, a significant increase was found first in Japanese patients (odds ratio 2.72, 95% CI 1.17-6.32, P = 0. 0308). In Caucasians, the odds ratio was 2.80 (95% CI 1.36-5.75, P = 0.0079) in the first stage, 2.43 (95% CI 1.20-4.92, P = 0.0196) in the second stage and 2.60 (95% CI 1.41-4.80, P = 0.0024) in total. The overall odds ratio was 2.64 (95% CI 1.60-4.33, P = 0.0001). This result suggests that rare alleles of the MUC3 gene may confer genetic predisposition to UC.
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PMID:Association of ulcerative colitis with rare VNTR alleles of the human intestinal mucin gene, MUC3. 993 38

To investigate the pathogenesis of inflammatory bowel disease, it is critical to develop a system that uses simple and reproducible models for analyzing the "normal" mucosal defense mechanism. In the present study, germ-free mice were conventionalized by the oral administration of microorganisms prepared from the feces of genetically identical mice. Histological assessment and mucin characterization of small intestine and colon were then carried out. Histological findings in the gut were site-dependent and clearly time-dependent. Acute inflammation was most evident in the cecum. The cecal mucosa exhibited hyperplastic changes in epithelial cells, infiltration of polymorphonuclear cells, crypt abscesses, and epithelial projections on the epithelial surface 7 days after conventionalization. Some of the changes were similar to those seen in human ulcerative colitis. The histological findings in the conventionalized mice were comparable to those in specific pathogen-free mice after 28 days. Mucin histochemistry revealed that bacterial colonization altered the number of rectal goblet cells and the mucin composition in a time-dependent fashion. Although this model shares only some characteristics of human inflammatory bowel disease, it is unique in demonstrating the acquisition of mucosal defense. Understanding of this process is critical for the elucidation of inflammatory bowel disease pathogenesis.
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PMID:Colonization of microflora in mice: mucosal defense against luminal bacteria. 1020 11

Idiopathic inflammatory bowel disease is a chronic relapsing condition. The role of stress in causing relapses of inflammatory bowel disease remains controversial. We now show that colitis induced in mice by dinitrobenzenesulfonic acid (DNBS) resolves by 6 weeks, but can subsequently be reactivated by stress plus a sub-threshold dose of DNBS, but not by DNBS alone. Stress reduced colonic mucin and increased colon permeability. Susceptibility to reactivation by stress required CD4+ lymphocytes and could be adoptively transferred. We conclude that stress reactivates experimental colitis by facilitating entry of luminal contents that activate previously sensitized CD4 cells in the colon.
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PMID:The role of CD4+ lymphocytes in the susceptibility of mice to stress-induced reactivation of experimental colitis. 1050 22

The concordance rate of monozygotic twins showed that the occurrence of ulcerative colitis required both internal and environmental conditions. Genetic studies revealed that IBD1 locus on chromosome 16 and IBD2 locus on chromosome 12 showed highly suspicious susceptibility for inflammatory bowel disease. The other possible internal factors include antineutrophil cytoplasmic antibodies and mucin abnormality. Many environmental factors have been reported to cause relapse. These are viral and bacterial infection, medicine such as antibiotics, non-steroidal anti-inflammatory drugs and aminosalicylates, colonic ischemia, post-examination state, psychological stress, winter season, travel and overwork.
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PMID:[Influencing factors on occurrence and relapse in ulcerative colitis]. 1057 4

Inflammatory bowel disease (IBD) of humans is a chronic and devastating disease of unknown etiology. Models of acute colitis in animals have been achieved by intrarectal administration of agents such as 2,4,6-trinitrobenzenesulfonic acid (TNBS) into rat colon. This agent induces focal inflammation and alterations in the colon with features similar to those found in chronic inflammatory diseases in humans. The aim of this study was to assess the effect of TNBS administration on histological and ultrastructural features of the rat colon, especially in areas not affected by transmural inflammation. Also in areas without transmural inflammation, we observed a significant increase in crypt diameter and in the number and area of the goblet cells, as well as alterations in the contents of mucin in goblet cells. We conclude that TNBS treatment in rats led to severe changes in normal architecture of the colon and also in damaged areas where no direct inflammation was produced.
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PMID:Experimental colitis induced by trinitrobenzenesulfonic acid: an ultrastructural and histochemical study. 1063 May 7

Muciphages (mucin-containing macrophages), first described in 1966 by Azzopardi & Evans, are a common feature of biopsies of large intestinal mucosa, even in the absence of other abnormalities such as active inflammation or evidence of chronic inflammatory bowel disease. Should they be mentioned in diagnostic reports? Do muciphages reliably indicate previous mucosal disease, now quiescent? In the following articles, Salto-Tellez & Price review what is known about muciphages and conclude that they reflect previous occult and clinically unimportant mucosal damage and that, in an otherwise normal colorectal mucosa, they have no diagnostic significance; and Shepherd draws attention to a wide range of clinically much more significant mucosal infiltrates that could be mistakenly regarded as muciphages and thus overlooked.
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PMID:What is the significance of muciphages in colorectal biopsies? The significance of muciphages in otherwise normal colorectal biopsies. 1084 99

Muciphages (mucin-containing macrophages), first described in 1966 by Azzopardi & Evans, are a common feature of biopsies of large intestinal mucosa, even in the absence of other abnormalities such as active inflammation or evidence of chronic inflammatory bowel disease. Should they be mentioned in diagnostic reports? Do muciphages reliably indicate previous mucosal disease, now quiescent? In the following articles, Salto-Tellez & Price review what is known about muciphages and conclude that they reflect previous occult and clinically unimportant mucosal damage and that, in an otherwise normal colorectal mucosa, they have no diagnostic significance; and Shepherd draws attention to a wide range of clinically much more significant mucosal infiltrates that could be mistakenly regarded as muciphages and thus overlooked.
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PMID:What is the significance of muciphages in colorectal biopsies? Muciphages and other mucosal accumulations in the colorectal mucosa. 1084


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