title: Molecular pathogenesis of Helicobacter pylori infection: the role of bacterial virulence factors.
abstract: Helicobacter pylori is one of the most common pathogens affecting humankind, infecting approximately 50% of the world's population. Of those infected, many will develop asymptomatic gastritis, but 10% develop gastric or duodenal ulcers. The clinical outcome of the infection may involve a combination of bacterial factors, host factors and environmental factors. In the process of development of gastritis, ulceration and cancer, several cellular and molecular steps follow each other. Infection, acid survival, adhesion, cytotoxicity, epithelial cell turnover changes, inflammation, regeneration or pathological alteration towards erosions, ulceration, and cancer can be observed on the cellular level. Bacterial factors like urease, AmiE, AmiF, hydrogenase and arginase are needed for survival in the acidic gastric environment. The bacterial flagellae are essential to move the bacteria towards the epithelial surface. Adhesive factors like BabA, SabA and ureaseA are necessary for adhesion against MHC-II complexes and Le antigens. The bacteria VacA and CagA are cytotoxic factors. The Cag type IV secretion system delivers these proteins inside the epithelial cells. After disruption of epithelial cell junctions, the bacteria can pass through the gastric wall facing direct immune response from neutrophils, lymphocytes, mast cells and dendritic cells. This review describes and summarizes our present molecular biological information and knowledge about the Helicobacter infective component, cell functions and processes. The possible role of host counter responses and interactions with gastric epithelia and immune cells are also detailed.
authors.affiliation: Molecular Medicine Research Unit, Semmelweis University and the Hungarian Academy of Sciences, 2nd Department of Medicine, Budapest, Hungary. mb@bel2.sote.hu
authors.forename: Bela
authors.initials: B
authors.lastname: Molnar
authors.forename: Orsolya
authors.initials: O
authors.lastname: Galamb
authors.forename: Ferenc
authors.initials: F
authors.lastname: Sipos
authors.forename: Katalin
authors.initials: K
authors.lastname: Leiszter
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Tulassay
mesh_terms: D000375:Aging / Q000473:pathology; D000818:Animals; D004847:Epithelial Cells / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000472:pathogenicity*; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D037521:Virulence Factors / Q000378:metabolism*
chemical_list: D037521:Virulence Factors