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.

Association of Helicobacter pylori infection with the Lewis and ABO blood groups in dyspeptic patients

“…It also has geographic diversity and is more frequent in European than Japanese H. pylori isolates 2930. The babA distinguishes both H-type 1 and Lewis B blood-group antigens on gastric mucosa of secretor persons, initiating the first steps of the infection.…”

Brain-gut axis in the pathogenesis ofHelicobacter pyloriinfection

“…pylori infection occurs via the oral route and, like other contagions, depends on the balance between bacteria virulence (urease, AmiE, AmiF, hydrogenase and arginase, BabA, SabA and ureaseA), host immunity and environmental factors [62] . The brain-gut axis may modulate the local immunological resistance related to gastric and gut-associated lymphoid tissue (neuroendocrine-immune crosstalk).…”

Sperm Parameters and Semen Levels of Inflammatory Cytokines in Helicobacter pylori–infected Men

“…26 After disruption of epithelial cell junctions, the bacteria can pass through the gastric wall facing direct immune response from lymphocytes, mast cells, neutrophils, and dendritic cells. 27 Tests carried out in animals experimentally infected have confirmed that H pylori constituents and substances secreted by the microorganisms may penetrate into the blood vessels and sensitize macrophages and other white blood cells. 28,29 Once sensitized, immune cells may gain access to the portal circulation and the lymphatic system and could eventually reach the gonad district and go over the damaged tight junctions.…”