ABSTRACT
Gastric metaplasia is the replacement of the absorptive columnar cells, which normally cover the duodenal villi, by cells rich in neutral mucin similar to those which normally line the stomach. There is strong evidence that Helicobacter pylori play an important role in the pathogenesis of duodenal ulcer (DU) disease. D. R. Cave and M. Vargas found that cultured H. pylori produce a protein substance which inhibits uptake of aminopyrine into rabbit gastric glands. The immunological response to H. pylori partly reflects responses to specific proteins, but H. pylori also release substances which may directly attract and stimulate immunocytes. Gastrin release may be increased because H. pylori diminish the sensitivity of parietal cells to gastrin. H. pylori infection undoubtedly generates alkali, which might also disrupt the mucus layer and make it more permeable to acid. Some of the familial traits that have been described in DU disease might be explained by familial infection with H. pylori.
