Pathogenesis of Helicobacter pylori

The intensive study of urease, motility, adhesins and stress response proteins, long-known pathogenic factors of Helicobacter pylori, has continued. The increased virulence associated with cagA-positive strains may be explained by the presence of a pathogenicity island for which the CagA protein acts as a serological marker. The pathogenic relevance of vacuolating cytotoxin and its heterogeneity has been further demonstrated. Advances have been made in understanding the mechanism by which the cytotoxin induces epithelial cell vacuolation. The potential role played by lipopolysaccharide in the development of gastritis and H. pylori-associated autoimmunity is now recognized. The availability of the complete genome sequence of H. pylori promises to give new insights into pathogenesis in the future.