Helicobacter pylori: 20 years on.

Helicobacters are a new genus of bacteria, inhabiting the interface between mucosa and lumen of the gut. Microaerophilic, spiral, flagellated and urease positive, they possess features necessary for colonisation of the juxtamucosal mucus environment. Helicobacter pylori is the major pathogenic species. Once attached to the gastric epithelial cells, it incites an immune response characterised histologically by the development of active gastritis and immunologically by the presence of specific IgG. Persistence of infection is ensured by attachment to tissue antigens (eg Lewis B), a vacuolating toxin (VacA) which assists the free passage of urea through epithelial cells, and a cytotoxin (CagA) which is actually injected into the epithelial cells via a Type IV secretion system. Finally, during the typical lifelong chronic infection, two important diseases occur. H. pylori alters gastric physiology to cause acid hypersecretion and peptic ulcer. Secondly, it damages the acid secreting mucosa leading to atrophic gastritis and gastric cancer risk.