Although the corpus mucosa of patients with H. pylori associated duodenal ulcer is either mildly or not inflamed, the PGI serum levels were also decreased in duodenal ulcer patients infected
by strains containing Volasertib ic50 Higher number of EPIYA C segments. The results of the present study strengthen the potential role of CagA polymorphism in the development of gastric cancer in agreement with the results GSK621 solubility dmso of the previous studies [18, 19]. However, we can not exclude the possibility that the genetic constitution of the host, more than the bacterium strain, might predispose to atrophic gastritis and the H. pylori strains carrying increasing numbers of EPIYA C repeats would have an advantage over other strains in colonizing the new gastric environment or alternatively a more complex interplay of both mechanisms. In respect to duodenal ulcer, also the results of the studies are discordant [19, 25]. Our results are in agreement with those reported by Basso et al. [19] who also did not BAY 80-6946 find association between the disease and the number of EPIYA C segments in an Italian population. Notably, none patient with duodenal ulcer of our cohort was
colonized by CagA possessing three EPIYA C segments. As suggested by Yamaoka et al. [18], it is possible that strains with higher number of EPIYA C segments may be less resistant to the acid [18]. We also evaluated whether colonization by different strains (mixed infection) could be associated with disease outcomes. We found that gastric cancer patients were significantly more often colonized by mixed strains, whereas patients with duodenal ulcer had a trend toward less mixed strain colonization. One possibility is
that patients with gastric cancer would have areas of gastric mucosa showing cancer transformation, PAK5 alternating with areas of atrophy, intestinal metaplasia, dysplasia, and normal mucosa, each of them representing microenvironments that would be selectively advantageous to mixed infections [32, 33]. Conclusions In conclusion, we found that infection by H. pylori CagA-positive strains harbouring multiple EPIYA C repeats is associated with gastric precancerous lesions and gastric cancer, but not with duodenal ulcer in an ethnically diverse, admixed, Western population. Although infection by H. pylori cagA-positive strains is a risk factor for the mutually exclusive diseases, gastric cancer and duodenal ulcer, CagA strains possessing higher number of EPIYA C segments were associated with gastric cancer, but not with duodenal ulcer. Higher number of EPIYA C segments was also associated with gastric precancerous lesions as demonstrated by histological gastric atrophic and metaplastic changes and decreased serum levels of pepsinogen I.