Immunology of Helicobacter pylori Infection

Abstract

Helicobacter pylori (H. pylori) is the most common infecting microorganism in humans. H. pylori had coexisted with humans for 30,000 years ago and developed extensive survival adaptations. The infection is both active and chronic and leads to several disorders from chronic gastritis to gastric adenocarcinoma. The prevalence of H. pylori infection is still high in developing countries. The burden of disease due to infection is also heavy. The persistence of infection is the basis of diseases. H. infection activates innate and adaptive immune responses but the immune response fails to eradicate the infection. H. pylori is able to evade both innate and adaptive immune responses. It can neutralize gastric acid, elicit autoimmunity toward parietal cells, prevent phagocytosis, induce apoptosis of immune cells, inhibit lymphocyte proliferation, disrupt imbalance between humoral and cellular adaptive immune responses, promote regulatory T cell activity, and trigger genetic rearrangement. Host factor is involved in the incidence of H. pylori infection and its complications. Reinfection after eradication is common. Multiple drug resistance has also emerged. Vaccination is a promising management approach to eradicate H. pylori and prevent diseases it caused. The development of the vaccine itself needs to consider the immune escape mechanism of H. pylori.