Helicobacter pylori can multiply in autophagic vesicles
Helicobacter pylori, a Gram-negative, flagellated, microaerophilic bacterium, can selectively colonize in the human stomach. Its infection is widespread throughout the world, and is present in about 50% of the global human population with 80% in developing countries and 20-50% in industrialized countries. Infection of the stomach with H. pylori induces a local immune response with infiltration of the mucosa by macrophages, neutrophils and lymphocytes. Although the innate and adaptive immune responses are activated, the bacterium is rarely eliminated and infections can last for decades if left untreated. Most infections are asymptomatic, but overt diseases can occur in 10-20 % of infected individuals. The disease spectrum ranges from gastritis to peptic ulceration disease. A long-term chronic infection will increase the risk to gastric adenocarcinoma and mucosa-associated lymphoid-tissue lymphoma. It has been classified as a class I carcinogen by the WHO. Despite intensive studies, and the award of the 2005 Nobel Prize in Physiology for the discovery of the bacterium H. pylori by Robin Warren and Barry Marshall, our understanding of H. pylori-infection-caused disease is still limited. H. pylori has evolved several mechanisms to increase its adherence and persistence in the host. In addition, it must also evade immune clearance. Elimination of H. pylori by phagocytes is inefficient because H. pylori exhibits several virulence factors to evade opsonization, retard phagocytosis, and disrupt membrane trafficking and phagosome maturation after internalization of the microorganism.