Related Experiment Video
Updated: Jul 19, 2026

Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Helicobacter pylori in vivo causes structural changes in the adherent gastric mucus layer but barrier thickness is
J L Newton1, N Jordan, L Oliver
1Department of Physiological Sciences, University of Newcastle-upon- Tyne, UK.
Background:
It has been proposed that a pathogenic effect of Helicobacter pylori is a weakening of the protective mucus barrier; however, this remains controversial.
Aims:
To clarify the effects of H pylori infection on the mucus gel barrier in vivo.
Methods:
Mucus gel polymeric structure and the thickness of the adherent mucus barrier were measured in endoscopic biopsy samples in subjects with and without H pylori infection.
Results:
There was a significant 18% reduction in the proportion of polymeric gel forming mucin in the adherent mucus layer in H pylori positive compared with negative subjects. There was no change in the adherent mucus thickness between H pylori positive and negative subjects without gastric atrophy (mean (SD): 104 (26) micron, 106 (30) micron, respectively). There was however a significant reduction in mucus thickness in those H pylori positive subjects with underlying gastric atrophy (84 (13) micron, p=0.03) compared with those without atrophy.
Conclusions:
A partial breakdown in gel forming structure of the gastric mucus barrier does occur in H pylori infection per se but this is insufficient to cause a collapse of the mucus barrier.
Related Concept Videos
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Mucosal Barrier of the Stomach
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Peptic Ulcer Disease II: Pathophysiology
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.
Peptic Ulcer
Gastritis II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology

