Molecular and cellular activities of Helicobacter pylori pathogenic factors

Abstract

Stomach infection with pathogenic strains of Helicobacter pylori causes in some patients severe gastroduodenal diseases. These bacteria produce various virulence factors and, here, we review the recent acquisition on the biochemical mode of action of three major factors. We discuss the role of urease both as buffer of the stomach pH and as source of ammonia. The vacuolating toxin alters the endocytic pathway of non-polarized cells, inducing the release of acid hydrolases, the depression of extracellular ligand degradation and of antigen processing and, in the presence of ammonia, swelling of late-prelysosomal compartments. In polarized epithelial monolayers, vacuolating toxin induces an increase of the paracellular permeability, independent of vacuolation. The neutrophil activating protein induces the production of oxygen radicals in human neutrophils and could contribute to the damage of the stomach mucosa. The activities of these factors are discussed in terms of the need of the bacterium of increasing the supply of nutrients from the stomach lumen and from the mucosa.