Pathogenic mechanisms of acid-related diseases: Helicobacter and other spiral organisms

Colonization by Helicobacter pylori is causally related to duodenal ulceration. There is also suggestive evidence that patients who develop malignancy in the upper gastrointestinal tract are more likely to be colonized by the organisms, although to date there is no suggestion of a causal link. H. pylori possess a number of potential virulence factors that singly or together could contribute to gastric inflammation. Evidence from the past year casts doubt on the production of a mucinase enzyme by H. pylori, but has strengthened the role of the organism's urease enzyme as a virulence factor. The current belief is that the urease, by producing ammonia and altering the pH, affects the quality of the mucus barrier, altering its structure. Also, the ammonia can act as a direct cytotoxin for the gastric cells. Further work has strengthened the possible role of a proteinaceous cytotoxin produced by H. pylori as another possible virulence factor by demonstrating that cytotoxin-producing bacteria are more likely to be isolated from patients with ulceration. Further information has been gained about the surface properties of H. pylori and its production of inflammatory mediators, each of which could be important for colonization and stimulation of inflammation, respectively. Finally, there is an increasing appreciation of other mucosa-associated bacteria both in humans and other animals that may induce inflammation in the stomach.