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Related Concept Videos

Irritable Bowel Syndrome I: Introduction01:17

Irritable Bowel Syndrome I: Introduction

Irritable Bowel Syndrome (IBS) is characterized by functional disturbances in the gastrointestinal system, presenting a cluster of symptoms without evident structural or biochemical abnormalities. It primarily affects the large intestine and may cause abdominal pain, bloating, excessive gas, diarrhea, constipation, or both.
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Inflammatory bowel disease is a group of chronic disorders marked by recurrent inflammation of the gastrointestinal tract due to an abnormal immune response against gut microflora. This leads to tissue damage. The two main forms are Crohn’s disease and ulcerative colitis.Crohn’s DiseaseCrohn’s disease is a relapsing inflammatory disorder that can affect any part of the GI tract, from the mouth to the anus. It involves all layers of the bowel wall (transmural) and shows “skip lesions” in which...
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Crohn's disease
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Immunostaining to Visualize Murine Enteric Nervous System Development
07:54

Immunostaining to Visualize Murine Enteric Nervous System Development

Published on: April 29, 2015

Enteric nervous system abnormalities in inflammatory bowel diseases.

V Villanacci1, G Bassotti, R Nascimbeni

  • 12nd Department of Pathology, Spedali Civili and University of Brescia, Brescia, Italy.

Neurogastroenterology and Motility
|May 22, 2008
PubMed
Summary

Inflammatory bowel diseases (IBD) like Crohn's disease and ulcerative colitis show abnormal enteric nervous system (ENS) cell densities. These changes, including increased neurons and interstitial cells of Cajal (ICC), suggest the ENS plays a role in IBD pathogenesis.

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Area of Science:

  • Gastroenterology
  • Neuroscience
  • Immunology

Background:

  • Abnormalities in the enteric nervous system (ENS) are noted in inflammatory bowel diseases (IBD).
  • Previous studies lacked systematic analysis of ENS cell density distribution in IBD.
  • The ENS, comprising neurons, enteroglial cells, and interstitial cells of Cajal (ICC), regulates gut function.

Purpose of the Study:

  • To systematically examine the density of neurons, enteroglial cells, and ICC in the ENS plexuses.
  • To compare cell densities in involved and non-involved tissues from Crohn's disease (CD) and ulcerative colitis (UC) patients versus controls.
  • To investigate the potential pathogenetic role of the ENS in IBD.

Main Methods:

  • Immunohistochemistry was used on tissue samples from 16 CD, 16 UC patients, and controls.
  • Antibodies against neuron-specific enolase, S100, C-Kit, and CD3 were employed.
  • Blind analysis by two pathologists quantified cell types in different ENS plexuses.

Main Results:

  • Crohn's disease (CD) showed increased neuronal cell bodies, enteroglia, and ICC in the deep muscular plexus.
  • Non-involved CD tissues exhibited decreased enteroglial cells.
  • Ulcerative colitis (UC) displayed increased ICC and enteroglial cells in diseased muscularis propria.

Conclusions:

  • The study confirms ENS cell abnormalities in IBD patients.
  • Reduced enteroglia in non-involved tissues suggests a pathogenetic role for the ENS in IBD.
  • ENS alterations contribute to the complex pathophysiology of IBD.