Abstract

Inflammatory response to Helicobacter pylori is characterized by infiltration of neutrophils, monocytes, and lymphocytes into the gastric mucosa. Interleukin-8 (IL-8), a prototype of the CXC-chemokine subfamily, may be a key modulator in inducing neutrophil migration and activation in H. pylori-infected gastric mucosa. IL-8 is produced by gastric epithelial cells in response to H. pylori infection, and IL-8 expression is induced by local production of proinflammatory cytokines and attachment of H. pylori organisms to the gastric epithelial cell surface. Multiple genes in the H. pylori cag pathogenicity island seem to be involved in inducing the epithelial IL-8 response to H. pylori attachment. Activation of the transcription factor, nuclear factor kappaB (NF-kappaB), is associated with this IL-8 response. Reactive oxygen intermediates whose production is increased in H. pylori-infected gastric mucosa may also modulate IL-8 expression in the gastric mucosa. Recent reports also suggest that the local production of CC-chemokines, another chemokine subfamily, is important in H. pylori-associated gastritis.