It is estimated that almost half of the world’s population is infected with the gastric bacterium Helicobacter pylori (H. pylori). A persistent, lifelong infection with H. pylori is the primary risk factor for the development of peptic ulcer disease and gastric cancer. H. pylori infection induces inflammation and oxidative stress responses in the host, which can result in DNA damage that may activate oncogenic pathways.
The purpose of my postdoc project, in Anna Arnqvist lab, is to elucidate the molecular mechanisms in H. pylori that enable it to adapt to the stomach, leading to lifelong infection and the development of severe gastric disease. As a model system, we use the SabA adhesion protein, which binds to the sLex-receptor present in inflamed and premalignant tissue.