The role of innate memory in Helicobacter pylori infection

Wider research context
Infection with Helicobacter pylori (H. pylori) affects almost half of the world's population and is a major cause of stomach cancer. Although immune cells react strongly to this gastric bacterium, H. pylori is still one of the rare pathogens that can evade elimination by the host and cause chronic inflammation. Mechanisms that allow H. pylori to finally evade elimination by the immune system are still not fully understood and are in the focus of this project.
Hypotheses / research questions / objectives
Based on preliminary data showing that H. pylori infection imprints innate immune cells in a way that makes the cells hypersensitive to LPS 24 hours after priming, but renders them highly refractory to a delayed LPS challenge after a 6-days resting phase, we hypothesize that, by so far unknown mechanisms, H. pylori induces very distinct innate memory responses which might promote chronic H. pylori-induced inflammation. We assume that the long-lasting tolerance of innate immune cells after H. pylori priming may be linked to the impaired ability of antigen-presenting cells to prime protective T cell responses, which might contribute to the inability of immune cells to terminally clear the pathogen.