H. pylori is the most common pathogen colonizing humans today. Colonization with H. pylori can lead to detrimental outcomes including gastric adenocarcinoma, MALT lymphoma, peptic ulcer disease and atrophic gastritis. H. pylori is the only bacteria classified by the World Health Organization as a carcinogen. Yet, H. pylori’s classification as a bone fide pathogen has been questioned due to an inverse correlation between H. pylori colonization and immune-mediated diseases, such as allergic airway disease and inflammatory bowel disease. These divergent outcomes can be attributed to a number of factors including host, environment and pathogen.

My laboratory has made noteworthy contributions to understanding which host factors drive gastritis during chronic H. pylori infection. Specifically, our research has described how cytokines produced by proinflammatory T cells influence control of H. pylori colonization and gastritis. A major role of these T cells and the cytokines they produce is to recruit innate immune cells which lead to increased inflammation. Some stresses of the immune response include sequestration of nutrient metals (nutritional immunity), oxidative stress and metabolic stress. Despite the chronic immune response, H. pylori persists for the life of the host. A fundamental gap in our knowledge is how H. pylori responds to and flourishes under the pressures of the host’s immune response and how diet modifications might alter those host responses.