Helicobacter pylori induces infiltration of the gastric mucosa by polymorphonuclear cells and macrophages, as well as T and B lymphocytes. Paradoxically, this robust immune/inflammatory response cannot clear the infection, and thus leaves the host prone to complications resulting from chronic inflammation. One adverse consequence of this inflammatory response may be gastric cancer, as inflammation has been implicated in the development of intestinal metaplasia and mutations in oncogenes that precede the development of gastric adenocarcinoma. The gastric inflammatory response is affected somewhat, by the strain of H. pylori that infects the host. Thus, the more severe clinical manifestation associated with some strains may be attributed to the higher grade of inflammation that they induce. Both H. pylori and cytokines induced during infection can stimulate the recruitment and activation of inflammatory cells including neutrophils and macrophages. When activated, these cells produce inflammatory mediators that include reactive oxygen species (ROS). These mediators impart an oxidative stress on the cells in the immediate vicinity, in this case, the gastric epithelium. Normally, oxidative stress is neutralized by natural antioxidants such as vitamin C, however, levels of this antioxidant in the gastric juice are decreased during infection. The increased levels of oxidants and decreased antioxidants create a stress that can change many processes in the gastric epithelium. For example, an accumulation of intracellular ROS regulates the expression of many genes and can induce DNA damage. Point mutations in the DNA that disrupt the expression and function of genes that inhibit cell growth (i.e. p53) are believed to contribute to the pathogenesis of gastric cancer. Several studies suggest that epithelial cell turnover is affected by the inflammatory response to H. pylori. This notion is supported by studies describing an increase in both epithelial cell proliferation, as well as cell death by apoptosis, in response to infection. Apoptosis is a regulated process of cell death that is triggered by H. pylori as well as various inflammatory mediators, including tumour necrosis factor and interferon-gamma. Activated T-cells also kill gastric epithelial cells directly. Moreover, the host response increases the expression of receptors for H. pylori and thus increases bacterial binding and the induction of apoptosis by the bacteria. There are several other immune/inflammatory responses that contribute to epithelial cell damage mucosa and the pathogenesis of gastric cancer. For example, gastric B cells produce autoreactive antibodies that bind to gastric epithelial cells. As a consequence of this antigen-antibody complex formation, complement becomes activated suggesting that some of the inflammation and epithelial cell damage is attributable to immune-complex formation. Epithelial cell death can then stimulate the proliferative response of epithelial cell precursors. In summary, the proposed model may explain how the gastric inflammatory response contributes to the pathogenesis of cancer. This model raises the possibility that it could be preferable to identify the patients at highest risk of developing gastric cancer and then apply an intervention that eliminates the infection and inflammatory response. Alternatively, clinical interventions should at least attenuate the oxidative stress that is directly attributed to inflammation. These mechanisms have to be examined in the paediatric population.