Related Experiment Video
Updated: Jul 12, 2026

Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids
Published on: June 2, 2023
Decrease in binding for the neuropeptide VIP in response to marked inflammation of the mucosa in ulcerative colitis.
Maria Jönsson1, Orjan Norrgård, Magnus Hansson
1Department of Integrative Medical Biology, Anatomy, Umeå University, SE-901 87 Umeå, Sweden. maria.jonsson@anatomy.umu.se
Vasoactive intestinal peptide (VIP) binding decreases in inflamed intestinal tissues of ulcerative colitis patients. This reduction may impair VIP's beneficial effects in severe inflammation.
Area of Science:
- Neurogastroenterology
- Immunology
- Gastroenterology
Background:
- Vasoactive intestinal peptide (VIP) plays a role in gut neuroimmunomodulation.
- Ulcerative colitis (UC) involves significant intestinal inflammation and mucosal damage.
Purpose of the Study:
- To investigate VIP binding in the sigmoid colon of UC patients compared to non-UC controls.
- To determine the relationship between mucosal inflammation/derangement and VIP binding levels.
Main Methods:
- Immunohistochemistry was used to examine VIP binding in sigmoid colon specimens.
- In vitro receptor autoradiography was employed to quantify VIP binding.
Main Results:
- VIP binding was notably present in the mucosa of both patient groups.
- Significantly lower VIP binding levels were observed in areas with severe inflammation and mucosal derangement in UC patients.
Conclusions:
- Severe mucosal derangement in ulcerative colitis is associated with a distinct decrease in VIP binding.
- Reduced VIP binding in inflamed areas may lead to diminished trophic and anti-inflammatory effects of VIP in UC.
More Related Videos
07:32An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
Published on: December 3, 2020
08:58Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
Published on: January 5, 2017
Related Concept Videos
Inflammatory Bowel Disease II: Ulcerative Colitis
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Inflammatory Bowel Disease I: Ulcerative Colitis
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...
Peptic Ulcer Disease II: Pathophysiology