12. Pdv. 707 D. Olivares

Helicobacter pylori is a bacterium that chronically colonizes the gastric epithelium and infects approximately half of the human population worldwide. This pathogen is responsible for chronic gastritis and a high percentage of peptic ulcers, and its presence has been correlated to gastric cancer development (1-4). Several factors have been associated with this germ’s aggressiveness and hence implicated in epithelial damage, including vacuolizing cytotoxin (VacA), cytotoxinassociated gene A (cagA), surface lipopolysaccharide (LPS), bacterial urease, flagella, surface adhesins, oxidizing radicals, and citokines produced by leukocytes in response to infection. On the other hand, there is increasing evidence that H. pylori species are genetically diverse, that such diversity is associated with different aggresiveness degrees on the mucosa, and hence with gastric mucosal inflammation to different extents and a variety of clinical prognoses for infected patients (5). H. pylori genoma includes more than 1,000 preserved genes and strain-specific genes. This bacterium may acquire or lose exogenous DNA, and thus follows an ongoing microevolution model allowing high genetic variability, which may result in strains adapted to multiple adverse environments. Such variability also results from a high recombination rate during colonization of one host by non-related H. pylori species, in addition to a high frequency of mutation (6-11). The objective of this paper is to review the characteristics, and both the in vivo and in vitro effects, of major bacterial factors related to H. pylori virulence on human epithelial cells, as well as the effects deriving from H. pylori’s intrinsic genetic variability.