The role of interleukin-I beta in Helicobacter pylori-associated disease

Helicobacter pylori infects half the world's population and is associated with serious human diseases including peptic ulcer disease and gastric neoplasia. The clinical outcome is largely dependent on the severity and distribution of the H. pylori-induced gastritis. The reasons for such variable clinical outcomes remain poorly understood. Bacterial virulence factors contribute to the pathogenicity but do not explain the divergent outcomes. There is emerging evidence that host genetic factors play a key role in determining the clinical outcome to H. pylori infection. In particular, proinflammatory genotypes of the interleukin-1 beta (IL-1beta) gene are associated with increased risk of gastric cancer and its precursors. The effects are most likely mediated through induction of hypochlorhydria and severe corpus gastritis with subsequent development of gastric atrophy. In this article we discuss the role of IL-1beta and other host genetic factors in the pathogenesis of H. pylori-related disease.