| BACKGROUND and OBJECTIVE: Helicobacter pylori is not only the main causative agent for gastritis, it is also associated with gastric cancer, gastric ulcer disease, duodenal ulcer disease. H.pylori leads to chronic gastritis in virtually all colonized persons, yet it is not clear why only a minority develop gastric cancer or peptic ulcer disease. The reason of variation of clinical outcomes of H.pylori infection has been becoming an area of intensive investigation.Epidemiologically, virulent strains are linked to the more serious diseases induced by H.pylori infection, but virulent strains can only be responsible for this in part. For example, the infection rates of cagA positive H.pylori in gastric cancer and duodenal ulcer, which seem to be mutually exclusive outcomes of H.pylori infection, are almost the same. The studies in pathological area have demonstrated that the severity and anatomical distribution of gastritis induced by H.pylori and gastric acid conditions of host are associated with the clinical outcomes. Thus, individuals with gastritis predominantly localized to the antrum retain normal (or even high) acid secretion, with a high risk of duodenal ulcer disease, whereas individuals with extensive corpus gastritis develop hypochlohydria and gastric atrophy, which is presumptive precursors of gastric cancer. Alternatively, when gastric acid is high, gastritis is confined to the antral region, there is a high risk of duodenal ulcer disease; when gastric acid is low, gastritis often involves the acid-secreting corpus region with an increased risk of gastric Cancer. The facts above suggest that exogenous (H.pylori is one) or endogenous factors that are associated with gastritis and gastric acidsecretion contribute to the variation of the clinical outcomes of H.pylori infection. Histamine is such an endogenous factor.In gastric mucosa, histamine is the same transmitter for two regulatory systems: the IgE/mast cell system and gastric acid secretion system. Histamine is also linked to the production of interleukin-l-beta, an important pro-inflammatory cytokine and a powerful inhibitor of gastric acid secretion, which is linked to an increased risk of both hypochlohydria induced by H.pylori and gastric cancer. Accordingly, histamine in gastric mucosa may play very important roles in the pathogenesis of H.pylori associated diseases and contributes to the variation of clinical outcomes of H.pylori infection. This has already caught some researcher's eyes. Some studies have showed that mast cells (histamine storing cells) density is much greater in the antrum in the H.pylori infected peptic ulcer subjects than in gastritis subjects. Mast cell density is correlated significantly with the severity of inflammation. Most studies have demonstrated that the histamine content in gastric mucosa in H.pylori positive subjects is lower than that in H.pylori negative subjects. However, many problems remain unclear. There is almost no report about the roles of different histamine receptor in the pathogenesis of H.pylori associated diseases. There may be different expression of different histamine receptors in different H.pylori associated diseases subjects' gastric mucosa. The correlation between histamine receptors expression and severity of gastritis and distribution are also wanted to be investigated. Histamine and its receptors may be involved in the pathogenesis of H.pylori associated disease by influencing the proliferation and apoptosis of gastric epithelial cells. So, the aims of this study were to investigate the problems pointed out above. This study was consisted of two parts. In part one, we mainly studied the histamine H1,H2 receptors gene mRNA expression in the gastric mucosa of subjects with different H.pylori associated diseases. In part two, we established a Mongoliangerbil model infected with H.pylori and investigated the effects of pyrilamine and cimetidine on gastritis, proliferation and apoptosis of gastric epithelial cells.METHODS: Part one-110 patients entered the study. Acco...
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