Helicobacter pylori infection is associated with divergent clinical outcomes that range from simple asymptomatic gastritis to more serious conditions such as peptic ulcer disease and gastric neoplasia. The key determinants of these outcomes are the severity and distribution of the H pylori induced gastritis. Gastritis that is largely confined to the antral region is associated with excessive acid secretion and a high risk of duodenal ulcer disease.1 In contrast, gastritis that involves the acid secreting corpus region leads to hypochlorhydria, progressive gastric atrophy, and an increased risk of gastric cancer.2 The association of H pylori with such variable outcome poses a fascinating scientific challenge, the unravelling of which will not only explain how ulcers and gastric cancer develop but will also act as a paradigm for gene-environment interactions in most human diseases. The proinflammatory cytokine interleukin (IL)-1β is emerging as a key mediator of many pathophysiological events that characterise host-environment interactions. In this article we discuss the role of IL-1β in H pylori associated disease.

The key pathophysiological event in H pyloriinfection is initiation of an inflammatory response. Bacteria or their products trigger this inflammatory process and the main mediators are cytokines. Cytokines, including interleukins, are soluble peptide molecules that mediate the interaction between immunocompetent and haematopoietic cells and between the immune and neuroendocrine systems.3 They are produced by a variety of activated cells and exert their biological effects through binding to specific receptors on target cells. IL-1β is the archetypal pleiotropic cytokine being produced by many cells and exerting its biological effects on almost all cell types.4 IL-1β is a potent proinflammatory cytokine and is involved in the host's response to many antigenic challenges.