scholarly journals Inflammatory bowel disease is associated with changes of enterocytic junctions

2001 ◽  
Vol 281 (1) ◽  
pp. G216-G228 ◽  
Author(s):  
Nikolaus Gassler ◽  
Claudia Rohr ◽  
Armin Schneider ◽  
Jürgen Kartenbeck ◽  
Alfred Bach ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Inflammatory Process ◽  
Mucosal Barrier ◽  
Altered Expression ◽  
Control Subjects ◽  
Mucosal Tissues ◽  
Associated Proteins ◽  
Junctional Protein ◽  
Inflammatory Bowel

Changes of the intestinal mucosal barrier are considered to play a role in the pathogenesis of inflammatory bowel disease (IBD). Our experiments were designed to identify dysregulation of epithelial junctional molecules in the IBD intestinum and to address whether altered expression of these molecules is a primary event in IBD or a phenomenon secondary to the inflammatory process. Noninflamed and inactively and actively inflamed mucosal tissues from patients with ulcerative colitis or Crohn's disease as well as tissues from control subjects were analyzed for the expression of junctional molecules by different methods. Marked downregulation of junctional proteins and their respective mRNAs was observed in actively inflamed IBD tissues. In IBD tissues with inactive inflammation, only a few junctional molecules such as E-cadherin and α-catenin were affected, whereas expression of desmosomal or tight junction-associated proteins appeared almost unchanged. In noninflamed IBD tissues, junctional protein expression was not different from that seen in normal control subjects. In IBD, downregulation of junctional molecule expression is apparently associated with the inflammatory process and does not likely represent a primary phenomenon.

scholarly journals Altered expression of cell adhesion molecules in uninvolved gut in inflammatory bowel disease

2008 ◽  
Vol 94 (2) ◽  
pp. 341-347 ◽  
Author(s):  
G. M. SCHUERMANN ◽  
A. E. ABER-BISHOP ◽  
P. FACER ◽  
J. C. LEE ◽  
D. S. RAMPTON ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Bowel Disease ◽  
Cell Adhesion Molecules ◽  
Altered Expression ◽  
Inflammatory Bowel

Altered expression of fucosyl-transferases in inflammatory bowel disease

2001 ◽  
Vol 120 (5) ◽  
pp. A525
Author(s):  
Keith Leiper ◽  
Sameena Javeed ◽  
Yamini Krishna ◽  
Jonathan M. Rhodes ◽  
Barry J. Campbell
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Altered Expression ◽  
Inflammatory Bowel

scholarly journals An objective in vivo diagnostic method for inflammatory bowel disease

2018 ◽  
Vol 5 (3) ◽  
pp. 180107 ◽  
Author(s):  
Sophie C. Payne ◽  
Robert K. Shepherd ◽  
Alicia Sedo ◽  
James B. Fallon ◽  
John B. Furness
Keyword(s):  
Inflammatory Bowel Disease ◽  
Real Time ◽  
Bowel Disease ◽  
Experimental Models ◽  
Mucosal Barrier ◽  
Trinitrobenzene Sulfonic Acid ◽  
Inflammatory Damage ◽  
Mucosal Barrier Function ◽  
Inflammatory Bowel

Inflammatory damage to the bowel, as occurs in inflammatory bowel disease (IBD), is debilitating to patients. In both patients and animal experimental models, histological analyses of biopsies and endoscopic examinations are used to evaluate the disease state. However, such measurements often have delays and are invasive, while endoscopy is not quantitatively objective. Therefore, a real-time quantitative method to assess compromised mucosal barrier function is advantageous. We investigated the correlation of in vivo changes in electrical transmural impedance with histological measures of inflammation. Four platinum (Pt) ball electrodes were placed in the lumen of the rat small intestine, with a return electrode under the skin. Electrodes placed within the non-inflamed intestine generated stable impedances during the 3 h testing period. Following an intraluminal injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS), an established animal model of IBD, impedances in the inflamed region significantly decreased relative to a region not exposed to TNBS ( p  < 0.05). Changes in intestinal transmural impedance were correlated ( p  < 0.05) with histologically assessed damage to the mucosa and increases in neutrophil, eosinophil and T-cell populations at 3 h compared with tissue from control regions. This quantitative, real-time assay may have application in the diagnosis and clinical management of IBD.

Neutrophil transmigration in inflammatory bowel disease is associated with altered expression of intercellular junction proteins

2001 ◽  
Vol 120 (5) ◽  
pp. A187
Author(s):  
Torsten Kucharzik ◽  
Shaun V. Walsh ◽  
Jason Chen ◽  
Charles A. Parkos ◽  
Asma Nusrat
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intercellular Junction ◽  
Altered Expression ◽  
Inflammatory Bowel ◽  
Junction Proteins

scholarly journals The Emerging Role of Noncoding RNAs in Pediatric Inflammatory Bowel Disease

2020 ◽  
Vol 26 (7) ◽  
pp. 985-993 ◽  
Author(s):  
Petr Jabandziev ◽  
Julia Bohosova ◽  
Tereza Pinkasova ◽  
Lumir Kunovsky ◽  
Ondrej Slaby ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Expression Profiles ◽  
Significant Proportion ◽  
Noncoding Rnas ◽  
Inflammatory Disorder ◽  
Altered Expression ◽  
Clinical Biomarkers ◽  
Inflammatory Bowel ◽  
Pediatric Ibd

Abstract Prevalence of inflammatory bowel disease (IBD), a chronic inflammatory disorder of the gut, has been on the rise in recent years—not only in the adult population but also especially in pediatric patients. Despite the absence of curative treatments, current therapeutic options are able to achieve long-term remission in a significant proportion of cases. To this end, however, there is a need for biomarkers enabling accurate diagnosis, prognosis, and prediction of response to therapies to facilitate a more individualized approach to pediatric IBD patients. In recent years, evidence has continued to evolve concerning noncoding RNAs (ncRNAs) and their roles as integral factors in key immune-related cellular pathways. Specific deregulation patterns of ncRNAs have been linked to pathogenesis of various diseases, including pediatric IBD. In this article, we provide an overview of current knowledge on ncRNAs, their altered expression profiles in pediatric IBD patients, and how these are emerging as potentially valuable clinical biomarkers as we enter an era of personalized medicine.

Prevalence and Relative Risk of Malignancy in Relatives of Inflammatory Bowel Disease Patients and Control Subjects

1998 ◽  
Vol 27 (3) ◽  
pp. 211-214 ◽  
Author(s):  
G. Riegler ◽  
R. Carratù ◽  
M. Tartaglione ◽  
F. Morace ◽  
R. Manzione ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Relative Risk ◽  
Bowel Disease ◽  
Control Subjects ◽  
Risk Of Malignancy ◽  
Inflammatory Bowel ◽  
And Control

Altered expression of angiogenetic factors in Vegf-Ets-1 cascade in inflammatory bowel disease

2003 ◽  
Vol 124 (4) ◽  
pp. A325
Author(s):  
Konno Shiho ◽  
Iizuka Msahiro ◽  
Sasaki Kenji ◽  
Sato Akiko ◽  
Horie Yasuo ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Altered Expression ◽  
Inflammatory Bowel

scholarly journals Studies on the Interleukin-10 Gene in Animal Models of Colitis

2001 ◽  
Vol 15 (8) ◽  
pp. 557-558
Author(s):  
Hugh J Freeman
Keyword(s):  
Inflammatory Bowel Disease ◽  
Animal Models ◽  
Bowel Disease ◽  
Inflammatory Process ◽  
Intestinal Inflammation ◽  
Therapeutic Potential ◽  
Interleukin 10 ◽  
Necrosis Factor Alpha ◽  
Inflammatory Bowel ◽  
Deficient Mice

Cytokines play a role in the inflammatory process in colitis and may have therapeutic potential. Interleukin-10 (IL-10) has both immunomodulatory and anti-inflammatory properties. IL-10-deficient mice develop intestinal inflammation with increased tissue levels of other cytokines, including tumour necrosis factor-alpha. In patients with inflammatory bowel disease, impaired IL-10 production by lamina propria T cells occurs and human recombinant IL-10 improves clinical parameters in inflammatory bowel disease (eg, Crohn's disease). There seem to be conflicting results in differing animal models, and the timing of administration of IL-10 relative to onset of colitis may be critical, possibly due to rapid clearance of IL-10. Interestingly, in IL-10 gene-deficient mice raised in germ-free conditions, the intestinal inflammatory changes normally observed in conventional nongerm-free conditions are not detected, suggesting a role for luminal bacteria in the pathogenesis of the inflammatory process.

scholarly journals Intestinal Permeability in Inflammatory Bowel Disease: Pathogenesis, Clinical Evaluation, and Therapy of Leaky Gut

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Andrea Michielan ◽  
Renata D’Incà
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Permeability ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Mucosal Barrier ◽  
Mucosal Inflammation ◽  
Confocal Laser Endomicroscopy ◽  
Confocal Laser ◽  
Sugar Absorption ◽  
Inflammatory Bowel

The pathogenesis of inflammatory bowel disease (IBD) is multifactorial with data suggesting the role of a disturbed interaction between the gut and the intestinal microbiota. A defective mucosal barrier may result in increased intestinal permeability which promotes the exposition to luminal content and triggers an immunological response that promotes intestinal inflammation. IBD patients display several defects in the many specialized components of mucosal barrier, from the mucus layer composition to the adhesion molecules that regulate paracellular permeability. These alterations may represent a primary dysfunction in Crohn’s disease, but they may also perpetuate chronic mucosal inflammation in ulcerative colitis. In clinical practice, several studies have documented that changes in intestinal permeability can predict IBD course. Functional tests, such as the sugar absorption tests or the novel imaging technique using confocal laser endomicroscopy, allow anin vivoassessment of gut barrier integrity. Antitumor necrosis factor-α(TNF-α) therapy reduces mucosal inflammation and restores intestinal permeability in IBD patients. Butyrate, zinc, and some probiotics also ameliorate mucosal barrier dysfunction but their use is still limited and further studies are needed before considering permeability manipulation as a therapeutic target in IBD.

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