Campylobacter pylori, Mucus, and Peptic Ulceration A Dynamic Interaction

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Abstract
Campylobacter pylori, a spiral-shaped bacterium, commonly colonizes the gastric epithelium where it induces chronic gastritis; this organism has also been implicated in the etiology of chronic peptic ulcer disease. Once introduced to the gastric mucosa or an area of gastric metaplasia, it tends to migrate to the vicinity of the epithelial tight junction where it probably utilizes host urea and other substances to sustain itself. Campylobacter pylori also produces a proteolytic enzyme that degrades mucin. As the mucous layer slowly degrades, noxious luminal contents such as acid and pepsin have an opportunity to diffuse closer to the epithelium. We hypothesize that C. pylori, which is sensitive to low-pH environments, eventually migrates away from the compromised area to an area where the mucous layer is still protective. The injured epithelial focus left behind either regenerates its mucous layer and heals, or ulcerates depending upon the balance between other aggressive and protective factors. This interaction between C. pylori and the mucous layer is then repeated at the organism's new location. This hypothesis is consistent with existing data regarding C. pylori. It explains how C. pylori can be present in most duodenal ulcer patients and many gastric ulcer patients, as well as in otherwise healthy individuals. It also explains why ulceration is localized rather than diffuse when it does occur.

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