Gastric pathology

Direct bacterial cytotoxicity due to Helicobacter pylori cytotoxins and ammonia production along with inflammation-mediated damage contribute to the epithelial changes in H. pylori gastritis. Over-expression of both cathepsin E and HLA-DR in H. pylori-infected surface-foveolar cells suggests an additional role for the epithelium in the processing and presenting of H. pylori antigens to immunocompetent cells. The same epithelial cells produce interleukin-8, a powerful chemotactic factor for neutrophils, which is likely to contribute to inflammation-mediated epithelial damage. Following the eradication of H. pylori there is a rapid and permanent disappearance of both granulocytic activity and degenerative epithelial lesions. In other areas it has been shown that H. pylori and non-steroidal anti-inflammatory drugs (NSAIDs) are independent causes of gastritis and NSAIDs do not influence colonization rates. H. pylori gastritis is also believed to represent a risk factor for gastric cancer. Especially high rates of H. pylori colonization are to be found in early gastric cancer of diffuse type.