The bacterium Helicobacter pylori colonises the stomach of man and induces
a strong inflammatory response. Differences in the possession of pathogenic
ity determinants by H. pylori isolates could account in part for the differ
ent clinical outcomes of infection. The main H. pylori pathogenic factors,
i.e. urease, the cytotoxin VacA, and the genes involved in virulence contai
ned in the pathogenicity island (PAI) cag, may promote tissue damage and ul
ceration, and could contribute to gastric cancer development. Strains with
the mosaic vacA allelic type s1a/m1 and possessing the cag insertion are co
nsidered endowed with increased inflammatory potential, and are more likely
to be isolated from patients with peptic ulcer and gastric cancer. The pre
sence in H. pylori cag PAI of operons involved in the stimulation of gastri
c epithelial cells to secrete high levels of inflammatory cytokines, in mob
ilisation of DNA, and formation of secretory mechanisms and conjugation app
arati, could contribute to increase the risk of gastric cancer development
in patients infected by this microorganism.