Host factor: Genetic polymorphism

Abstract

Proinflammatory cytokines and anti-inflammatory cytokines are produced in gastric mucosa from inflammatory cells activated by Helicobacter pylori (H. pylori) infection. Polymorphisms in these genes are associated with individual differences in cytokine messenger RNA levels, which result in different gastric mucosal inflammation, different acid inhibition, and different gastroduodenal disease risks in response to H. pylori infection. Of the inflammatory cytokines, polymorphisms related to interleukin (IL)-1ß and tumor necrosis factor (TNF)-a, IL-10, and IL-8 gene have been reported to be associated with the risk of gastric cancer. A functional polymorphism within toll-like receptor 4 (TLR4) has also been demonstrated to increase the risk for gastric atrophy and gastric cancer. However, the prevalence of cytokine gene genotypes differs between Western and Asian populations, and the role of genetic polymorphism on gastric cancer related to H. pylori might be different between race and geographic region.