Impact of Helicobacter pylori Virulence on the Outcome of Gastroduodenal Diseases: Lessons from the Microbiologist

Abstract

Two main pathogenic factors have been described in Helicobacter pylori strains: the cag pathogenicity island (cag PAI) and the vacuolating cytotoxin VacA. The cag PAI is comprised of approximately 40 open reading frames probably originating from another species. It encodes a type IV secretion system, i.e., an apparatus derived from pili which may contribute to the transfer of bacterial molecules to epithelial cells. One of the most well known is the CagA protein which is involved in cell actin rearrangement. Another important property is the induction of interleukin 8, a proinflammatory mediator, which is the consequence of other cag PAI genes. VacA has also been the subject of numerous studies. In vitro, it leads to vacuoles in epithelial cells from the late endosome compartment. However, its main impact could be to induce apoptosis by acting on mitochondria, as was shown in a recent study. The presence of cag PAI as well as VacA has been associated with a higher pathogenic potential of H. pylori strains. Indeed, both are often found simultaneously, but it may well be that the combination of the two, with specific adherence properties, increases even more the pathogenicity of the strains.