| Since Helicobacter pylori (H. pylori, Hp) was isolated from human gastric mucosa, it has become one of the research focus in the field of gastroenterology. So far H. pylori is identified as one of the principal pathogens of gastroduodenal diseases. H. pylori infection is associated with divergent clinical outcomes that range from asymptomatic gastritis to more serious conditions such as peptic ulcer disease and gastric neoplasia. The balance between epithelial cell proliferation and apoptosis sustains the integrity of gastric mucosa. H. pylori infection could disrupt this equilibrium by a predominant apoptosis resulting in peptic ulcers (in the acute phase) or atrophic gastritis (in the chronic phase), or by an excessive proliferation ultimately promoting the development of gastric cancer. In addition to bacterial pathogens, increased levels of gastric cytokines such as IL-1β, IL-8 and IL-10, derived from mucosal inflammatory or immune reactions stimulated by H. pylori infection, may be involved in the pathogenesis of H. pylori-related gastroduodenal diseases. H. pylori-induced gastritis can alter gastric physiology, resulting in increase or decrease of acid secretion. These changes in physiology are also related to the divergent disease outcomes, with increase of acid secretion leading to duodenal ulcer disease and decrease of acid secretion being a risk factor for gastric cancer. On the basis of such background, the aim of this study is in attempt to explore the effect of H. pylori and H. pylori-related cytokines (IL-1β, IL-8 and IL-10) on gastric epithelial cell proliferation/apoptosis and isolated parietal cell acid secretion in vitro. 1. Modulation of gastric epithelial cell proliferation/apoptosis by H. pylori and H. pylori-related cytokinesIn the study, both human gastric epithelial cell line GES-1 and gastric cancer cell line AGS were incubated with either Hp (NCTC 11637, VacA~+/CagA~+) or exogenous...
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