H.pylori infection leads to gastric inflammation, characterised histologically by surface epithelial degeneration and infiltration of the gastric mucosa by acute and chronic inflammatory cells. H.pylori adherence, the production of a vacoulating cytotoxin and bacterial enzymes all contribute to epithelial damage. Recruitment and activation of immune cells in the underlying mucosa involves H.pylori chemotaxins, epithellial-derivees chemoticatic peptides (chemokines) such as IL-8 and GRO-α and pro-inflammatory cytokines liberated by mononuclear phagocytes(TNα IL-1 and IL-6)as part of non-specific immunity. Antigen-specific cellular immunity results in a predominant Th1 lymphocyte response with an increase in IFN γ secreting T-helper cells, which may serve to damp down inflammation.Molecular mimicry of host structures by H. pylori with the generation of specific immunity directed against self-antigens may also contribute to host injury. Progress in molecular biology has revealed considerable genomic diversity amongst H. pylori strains, with cag+ bacteria being associated with increased chemokine and cytokine responses and more severe degrees of gastric inflammation. Strain hetereogeneity may contribute towards the wide spectrum of disease manifestati'ons encountered in clinical practice.