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To understand pathogenesis of H. pylori in stomach diseases including gastric cancer, molecular bacteriological studies are important. The studies are greatly advanced by information of the whole genome sequence of this bacterium in 1997. Various methods of gene manipulation to identify the genes involved in pathogenesis are now available such as transformation followed by construction of knockout mutants, complementation using H. pylori-E. coli shuttle vectors, random insertion mutagenesis, and RT-PCR or proteome analysis of in vivo-expressed genes. The molecular mechanism of persistent infection of H. pylori is discussed in light of recent findings on molecular mechanisms of bacterial attachment and colonization as well as on gastric physiology.

The ammonia concentration in the gastric juice from H. pylori positive cases was significantly higher than that from negative cases, and there was positive correlation between number of H. pylori, gastritis score and ammonia concentration in gastric juice. It is suggested that ammonia in gastric juice which is produced by powerful urease activity of H. pylori is one of the pathogenic factors in gastritis. We succeeded in producing a urease-negative mutant strain of H. pylori. This strain did not colonize gastric mucosa of Cynomolgus monkeys. H. pylori survival time in vitro was increased at pH 2.0 in the presence of urea. These results suggest that urease facilitates colonization of gastric mucosa by H. pylori, and prolongs the survival of H. pylori in an acidic environment.