Related Experiment Video
Updated: Jun 18, 2026
06:31
Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids
Published on: June 2, 2023
Epithelial apoptosis: cause or consequence of ulcerative colitis?
Jakob Benedict Seidelin1, Ole Haagen Nielsen
1Department of Gastroenterology, Medical Section, Herlev Hospital, University of Copenhagen, Denmark. jseidelin@dadlnet.dk
Scandinavian Journal of Gastroenterology
|December 5, 2009
Summary
In ulcerative colitis (UC), epithelial apoptosis is linked to local inflammation, not disease severity. Colonocytes develop protective mechanisms against apoptosis during active UC.
Area of Science:
- Gastroenterology
- Cell Biology
- Immunology
Background:
- Epithelial apoptosis is elevated in ulcerative colitis (UC), potentially playing a role in pathogenesis.
- The role of apoptosis in UC is debated: is it a primary defect or secondary to inflammation?
Purpose of the Study:
- To investigate the relationship between epithelial apoptosis rates and clinical characteristics in UC patients.
Main Methods:
- Colonic epithelial cells from 20 UC patients and 20 controls were cultured.
- Apoptosis was quantified using flow cytometry and Fas ligand stimulation.
- Disease activity was assessed via endoscopy, histology, and serological markers.
Main Results:
- Epithelial apoptosis rates correlated significantly with macroscopic and microscopic inflammation.
- No correlation was found between apoptosis rates and disease extent, clinical course, or surrogate markers of disease activity.
- Increased microscopic inflammation showed an inverse correlation with apoptosis response to Fas ligand.
Conclusions:
- Epithelial apoptosis in UC is primarily driven by the local inflammatory response.
- Colonocytes exhibit upregulated cytoprotective mechanisms that reduce apoptosis susceptibility during active UC.
Related Concept Videos
01:20Inflammatory Bowel Disease II: Ulcerative Colitis
Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
01:27Inflammatory Bowel Disease I: Ulcerative Colitis
Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
01:24Peptic Ulcer Disease II: Pathophysiology
Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
01:28Peptic Ulcer Disease II: Pathophysiology
Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
01:30Apoptosis
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
01:25Inflammatory Bowel Disease III: Crohn's Disease
Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...